cotton - PDF

					                                                          [2006] WASC 270



JURISDICTION                 : SUPREME COURT OF WESTERN AUSTRALIA
                               IN CIVIL

CITATION                     : ELLIS, Executor of the Estate of PAUL STEVEN
                               COTTON (DEC) -v- THE STATE OF SOUTH
                               AUSTRALIA & ORS [2006] WASC 270

CORAM                        : EM HEENAN J

HEARD                        : 29, 30 & 31 AUGUST, 1, 2, 5 - 9, 12 - 16 & 19 - 23
                               SEPTEMBER 2005

DELIVERED                    : 8 DECEMBER 2006

FILE NO/S                    : CIV 2314 of 2000

BETWEEN                      : TERESA ELLIS, Executor of the Estate of PAUL
                               STEVEN COTTON (DEC)
                               Plaintiff

                                AND

                                THE STATE OF SOUTH AUSTRALIA
                                First Defendant

                                AMACA PTY LTD (ACN 000 035 512) formerly
                                JAMES HARDIE & COY PTY LTD
                                Second Defendant

                                MILLENNIUM INORGANIC CHEMICALS LTD
                                (ACN 008 683 627) formerly SCM CHEMICALS
                                LTD
                                Third Defendant




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                                                      [2006] WASC 270



Catchwords:
Employer's liability - Asbestos - Lung cancer - Death - Estate claim - Law
Reform (Miscellaneous Provisions) Act 1941 - Fatal Accidents Act 1949 -
Dependants' claim - Overlap between statutory causes action - Employment in
industry involving exposure to asbestos - Two periods of employment -
Employment in laying of cement and asbestos water pipes in South Australia,
working, cutting and grinding pipes in field - Later employment in mineral
sands factory producing titanium dioxide within large industrial premises with
asbestos cladding, insulation and roofing

Death due to progressive lung cancer - No asbestosis - No pleural thickening or
plaques - Deceased formerly a smoker - Tobacco smoking a significant cause of
fatal lung cancer - Extent of exposure to asbestos in working environments -
Relatively low levels of exposure - Potential cumulative effects of exposure -
Potential interaction of tobacco smoking and exposure to asbestos fibres as
multiplying the toxic effect of both substances - Significance of statistical
attempts to estimate harmful concentrations of asbestos fibres in working
environments - Short-comings in statistical quantifications - Attempts
retrospectively to estimate statistical concentration of asbestos fibres in each of
plaintiff's two working environments - Causation - Contributory negligence -
Voluntary assumption of risk - Onus of proof - Standard of proof - Damages -
Significance of early onset of cancer disease after exposure to asbestos in either
workplace - Cumulative effects of exposure to asbestos with respect to potential
liability of each employer - Helsinki Protocol - Award criteria

Damages

Legislation:
Civil Liability Act 1936 (SA)
Crown Proceedings Act 1992 (SA)
Fatal Accidents Act 1959 (WA)
Law Reform (Contributory Negligence and Apportionment of Liability) Act 2001
(SA)
Law Reform (Contributory Negligence and Torfeasors' Contribution) Act 1947
(WA)
Law Reform (Miscellaneous Provisions) Act 1941 (WA)
Survival of Causes of Action Act 1940 (SA)




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                                                              [2006] WASC 270

Result:
Judgment for plaintiff in both sets of claims

 (a) In the estate claim against the

        first defendant for $361,573.09
        second defendant for $331,952.16
        third defendant for $196,573.09

(b) In the claims for wrongful death against the

        first defendant for $240,321
        second defendant for $199,789
        third defendant for $196,455

Category: A


Representation:

Counsel:
   Plaintiff                       :    Mr J R C Gordon
   First Defendant                 :    Ms C J Thatcher
   Second Defendant                :    Mr G M Watson SC & Ms J M Kubacz
   Third Defendant                 :    Mr A J Power

Solicitors:
   Plaintiff                       :    Slater & Gordon
   First Defendant                 :    State Solicitor for Western Australia
   Second Defendant                :    Minter Ellison
   Third Defendant                 :    Phillips Fox



Case(s) referred to in judgment(s):

Adelaide Stevedoring Company v Forst (1940) 64 CLR 538
Astley v Austrust Ltd (1999) 197 CLR 1
Australian Capital Territory v Kitt [2004] NSWCA 444; (2004) 43 MVR 249
Badger v Ministry of Defence [2005] EWHC 2941; [2006] 3 All ER 173


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                                                [2006] WASC 270

Barker v Corus (UK) Ltd [2006] UKHL 20; [2006] 2 WLR 1027
Barker v Corus (UK) Ltd [2006] UKHL 20; [2006] 3 All ER 785
Beavis v Apthorpe [1963] NSWR 1176
Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307
Bennett v Minister for Community Welfare (1992) 176 CLR 408,
Betts v Whittingslowe (1945) 71 CLR 637
Birkholz v R J Gilbertson Pty Ltd (1985) 38 SASR 121
Bonnington Castings Ltd v Wardlaw [1956] AC 613
Campbells Cash & Carry v Fostif Pty Ltd [2006] HCA 41; (2006) 229 ALR 58
Chapman v Hearse (1961) 106 CLR 112
Chappel v Hart [1998] HCA 55; (1998) 195 CLR 232
City of Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155
Clarke v Chandler Clay Pty Ltd (1984) A Tort Rep 80-631
Cole v South Tweed Heads Rugby League Football Club Ltd [2004] HCA 29;
         (2004) 217 CLR 469
Commonwealth v McLean (1996) 41 NSWLR 389
CSR Ltd v Culkin, unreported; FCt SCt of WA; Library No 940570; 18 October
         1994
Dalby v Wallaby Grip Ltd [2002] NSWDDT 15
De Sales v Ingrilli [2002] HCA 52; (2002) 212 CLR 338
Direct Engineering Services Pty Ltd v A Goninan & Co Ltd [2006] WASC 105
Distillers Co (Bio-Chemicals) Ltd v Thompson [1971] 1 NSWLR 83; [1971]
         AC 458
Dumais v Hamilton [1998] ABCA 218
E M Baldwin & Son Pty Ltd v Plane [1999] NSWCA 130; (1999) 17 NSWCCR
         434
Fairchild v Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32
Fox v Wood (1981) 148 CLR 438
Gammell v Wilson [1982] AC 27
Goodwin v Nominal Defendant (1979) 54 ALJR 84
Grant v Sun Shipping Co Ltd [1948] AC 549
Haar v Uneedus Scaffolding Pty Ltd, unreported; SCt of VIC (O'Bryan J);
         30 March 1990
Haigh v State Government Insurance Office (Qld) [1962] Qd R 534
Henville v Walker [2001] HCA 52; (2001) 206 CLR 459
Hole v Hocking [1962] SASR 128
ICI Australia Operations Pty Ltd v Walsh (1997) A Tort Rep 81-452
In the Matter of TNN Limited & Ors and In the Matter of the Companies Act
         1985 [2006] EWHC 1447
Insurance Commissioner v Joyce (1948) 77 CLR 39
John Pfeiffer Pty Ltd v Rogerson [2000] HCA 36; (2000) 203 CLR 503
Jones v Bradley [2003] NSWCA 81


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                                                   [2006] WASC 270

Jongen v CSR Ltd (1992) A Torts Rep 81-192
Joslyn v Berryman [2003] HCA 34; (2003) 214 CLR 552
Judd v Amaca Pty Ltd (No 2) (2003) 25 NSWCCR 488
Margolis v Imperial Tobacco Ltd & Ors - UK Court of Appeal [2000] EWCA
        Civ 114
McDonald (Executrix of the estate of late T G H McDonald) v State Rail
        Authority (NSW) [1998] NSWDDT 4; (1998) 16 NSWCCR 695
McGhee v National Coal Board [1973] 1 WLR 1
McGilvray v Amaca Pty Ltd (formerly James Hardie & Coy Pty Ltd) [2001]
        WASC 345
McKain v R W Miller & Co (SA) Pty Ltd (1991) 174 CLR 1
McKew v Holland & Hannen & Cubitts (Scotland) Ltd [1969] 3 All ER 1621
McLachlan v Purchas & Ors, unreported; FCt SCt of WA; Library No 980749;
        21 December 1998
Misiani (as Executor of the Will of Misiani (Dec)) v Welshpool Engineering Pty
        Ltd (In Liq) [2003] WASC 263
Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383
Murray v Shuter [1976] QB 972
Nance v British Columbia Electric Railways Co Ltd [1951] AC 601
Naxakis v Western General Hospital [1999] HCA 22; (1999) 197 CLR 269
Neilson v Overseas Projects Corporation of Victoria Ltd [2005] HCA 54; (2005)
        223 CLR 33
Nguyen v Nguyen (1990) 169 CLR 245
O'Connor v S P Bray Ltd (1937) 56 CLR 464
Orica Ltd v CGU Insurance Ltd (2003) 59 NSWLR 14
Paris v Matkovich, unreported; FCt SCt of WA; Library No 980614; 27 October
        1998
Public Trustee v Zoanatti (1945) 70 CLR 266
Purkess v Crittenden (1965) 114 CLR 164
Re Full Board of the Guardianship and Administration Board [2003] WASCA
        268; (2003) 27 WAR 475
Refalo v Stevedoring Industry Finance Committee [2002] NSWDDT 20
Regie Nationale des Usines Renault SA v Zhang [2002] HCA 10; (2002) 210
        CLR 491
Reindel v James Hardie & Co Pty Ltd [1994] 1 VR 619
Robertson v Hobart Police and Citizens Youth Club (1984) A Tort Rep 80-629
Roggenkamp v Bennett (1950) 80 CLR 292
Rosenberg v Percival [2001] HCA 18; (2001) 205 CLR 434
Rufo v Hosking [2004] NSWCA 391; (2004) 61 NSWLR 678
Seltsam Pty Ltd v Ghaleb [2005] NSWCA 208; (2005) 3 DDCR 1
Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262
Shire of Brookton v Water Corporation [2003] WASCA 240


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                                                [2006] WASC 270

South Tweed Heads Rugby League Club Ltd v Cole [2002] NSWCA 205;
       (2002) 55 NSWLR 113
Sweedman v Transport Accident Commission [2006] HCA 8; (2006) 80 ALJR
       646; (2006) 224 ALR 625
Sydney County Council v Furner (1991) 7 NSWCCR 210
TC (by his Tutor Sabatino) v State of New South Wales [2001] NSWCA 380
Thompson v Johnson & Johnson Pty Ltd [1991] 2 VR 449
Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720; (1976) 10 ALR
       303
Vaughan v Olver [1977] Qd R 1
Voth v Manildra Flour Mills Pty Ltd (1990) 171 CLR 538
Western Australia v Watson [1990] WAR 248
Westralian Caterers v Eastment Ltd (1992) 8 WAR 139
Wilsher v Essex Area Health Authority [1988] AC 1074
Wylie v South Metropolitan College of TAFE [2003] WASCA 34
Wynbergen v Hoyts Corporation Pty Ltd [1997] HCA 52; (1997) 149 ALR 25


Case(s) also cited:

Adams v Ascot Iron Foundry Pty Ltd [1968] 3 NSWR 305; (1968) 72 SR
        (NSW) 120
AMP General Insurance Ltd v Roads & Traffic Authority of New South Wales
        [2001] NSWCA 186; (2001) 22 NSWCCR 247
Attorney-General v Gilbert [2002] 2 NZLR 342
Australian Blue Asbestos Ltd v Rees, unreported; FCt SCt of WA; Library No
        4283; 9 October 1981
Australian Iron & Steel Ltd v Connell (1959) 102 CLR 522
Australian Safeway Stores Pty Ltd v Zaluzna (1987) 162 CLR 479
Bale v Seltsam Pty Ltd, unreported; CA Qld; 8 March 1996
Bale v Seltsam Pty Ltd, unreported; SCt of Qld (White J); 14 December 1995
Bankstown Foundry Pty Ltd v Braistina (1986) 160 CLR 301
Barker v Saint-Gobain Pipelines plc [2004] EWCA Civ 545; [2005] 3 All ER
        661
Barrow v CSR Ltd; Heys v CSR Ltd, unreported; SCt of WA (Rowland J);
        Library No 7231; 4 August 1988
BI (Contracting) Pty Ltd v Strikwerda [2005] NSWCA 288; (2005) 3 DDCR
        149
Black v Motor Vehicle Insurance Trust [1986] WAR 32
Blomley v Ryan (1956) 99 CLR 362
Bowen v Tutte (1990) A Tort Rep 81-043


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                                                 [2006] WASC 270

Browne v Cockatoo Dockyard Pty Ltd [1999] NSWDDT 19; (1999) 18
        NSWCCR 618
Chance v Alcoa of Australia Ltd (1990) A Tort Rep 81-017
Chandler v Water Corporation [2001] WASC 166
Clark v Kramer [1986] WAR 54
Cockatoo Dockyard Pty Ltd v Browne [2001] NSWCA 58; (2001) 21 NSWCCR
        544
Commonwealth of Australia v Ryan [2002] NSWCA 372
Commonwealth of Australia v Stoilkovski, unreported; FCt SCt of Vic;
        19 March 1981
CSR Ltd v Wren (1997) 44 NSWLR 463
CSR Ltd v Young (1998) 16 NSWCCR 56
Cuthill v State Electricity Commission of Victoria [1981] VR 908
Dahl v Grice [1981] VR 513
Davies v Adelaide Chemical and Fertiliser Co Ltd [1946] 74 CLR 541
Donoghue v Folkstone Properties Ltd [2003] EWCA Civ 231; [2003] QB 1008
Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317
Dow Jones & Company Inc v Gutnick [2002] HCA 56; (2002) 210 CLR 575
Dwan v Farquhar [1988] 1 Qd R 234
EMI (Australia) Ltd v Bes [1970] 2 NSWR 238
Ewins v BHP Billiton Ltd [2005] SASC 95; (2005) 91 SASR 303
Fernandez v Tubemakers of Australia Ltd [1975] 2 NSWLR 190
Finn v Commonwealth of Australia (2002) 24 NSWCCR 614
Footner v Broken Hill Associated Smelters Pty Ltd (1983) 33 SASR 58
Foyster v Goynich [1984] WAR 80
General Cleaning Contractors Ltd v Christmas [1953] AC 180
Grove v Bestobell Industries Pty Ltd [1980] Qd R 12
Hall v Tarlinton (1978) 19 ALR 501
Hamilton v Nuroof (WA) Pty Ltd (1956) 96 CLR 18
Havenaar v Havenaar [1982] 1 NSWLR 626
Hetherington v Mirvac Pty Ltd [1999] NSWSC 443; (1999) A Tort Rep 81-514
HG v The Queen [1999] HCA 2; (1999) 197 CLR 414
Hughes v Lord Advocate [1963] AC 837
I & L Securities Pty Ltd v HTW Valuers (Brisbane) Pty Ltd [2002] HCA 41;
        (2002) 210 CLR 109
Imperial Chemical Industries of Australia & New Zealand Ltd v Murphy (1973)
        47 ALJR 122
James Hardie & Co Pty Ltd v Hall (1998) 43 NSWLR 554
James Hardie & Coy Pty Ltd v Roberts [1999] NSWCA 314; (1999) 47
        NSWLR 425
Jones v Dunkel (1959) 101 CLR 298
Jones v James Hardie & Co Pty Ltd [1966] 2 NSWR 85


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                                               [2006] WASC 270

Jones v Watney, Combe, Reid & Co (1912) 28 TLR 399
Jsekarb Pty Ltd v Plane (1999) 18 Leg Rep SL4a
Julia Farr Services Inc v Hayes [2003] NSWCA 37; (2003) 25 NSWCCR 138
Kember v Thackrah [2000] WASCA 198
Kilgannon v Sharpe Bros Pty Ltd (1986) 4 NSWLR 600
Kolodziejczyk v Grandview Pty Ltd [2002] NSWCA 267; (2002) A Tort Rep
        81-673
Latimer v A E C Ltd [1952] 2 QB 701
Lawson v Flavel [2001] WASCA 272
Levi v Colgate-Palmolive (1941) 41 SR (NSW) 48
Lock v Lock [2001] WASCA 20
Maclenan v Segar [1917] 2 KB 325
Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705
Margerson v J W Roberts Ltd, unreported; UKCA; 2 April 1996
Margerson v J W Roberts Ltd, unreported; UKQBD (Holland J); 27 October
        1995
McNeill v Seltsam Pty Ltd [2005] NSWDDT 43; (2005) 3 DDCR 85
Medlin v State Government Insurance Commission [1995] HCA 5; (1995) 182
        CLR 1
Miletic v Capital Territory Health Commission [1995] HCA 13; (1995) 130
        ALR 591
Morgan v Tame [2000] NSWCA 121; (2000) 49 NSWLR 21
Moriarty v Evans Medical Supplies Ltd [1958] 1 WLR 66
Murdoch v SG Sayer Pty Ltd [1961] WCR 182
Nagle v Rottnest Island Authority (1993) 177 CLR 423
Naismith v London Film Productions Ltd [1939] 1 All ER 794
National Insurance Co of New Zealand Ltd v Espagne (1961) 105 CLR 569
Nicholson v Atlas Steel Foundry and Engineering Co Ltd [1957] 1 WLR 613
Nolan v Hamersley Iron Pty Ltd [2000] WASCA 304; (2000) 23 WAR 287
Nominal Defendant v Gardikiotis [1995] HCA 56; (1996) 186 CLR 49
O'Connor v Commissioner for Government Transport (1954) 100 CLR 225
Olson v CSR Ltd, unreported; DDT (NSW) (O'Meally J); 24 December 1994
Page v Smith [1996] AC 155
Planet Fisheries Pty Ltd v La Rosa (1968) 119 CLR 118
Pollock v Wellington (1996) 15 WAR 1
Power v Snowy Mountains Hydro Electric Authority (1956) 57 SR (NSW) 9
Prast v Town of Cottesloe [2000] WASCA 274; (2000) 22 WAR 474
R v Henry [1999] NSWCCA 111; (1999) 46 NSWLR 346
R v O'Connor (1980) 146 CLR 64
Rae v Broken Hill Proprietary Co Ltd (1957) 97 CLR 419
Restuccia v Workers Compensation (Dust Diseases) Board (2005) 2 DDCR 691



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Reynolds v Katoomba RSL All Services Club Ltd [2001] NSWCA 234; (2001)
        53 NSWLR 43
Rhesa Shipping Co SA v Edmunds ("The Popi M") [1985] 1 WLR 948
Richards v State of Victoria [1969] VR 136
Richters v Motor Tyre Service Pty Ltd [1972] Qd R 9
Rolls Royce Industrial Power (Pacific) Ltd v James Hardie & Coy Ltd [1999]
        NSWDDT 5; (1999) 18 NSWCCR 653
Rowe v McCartney [1976] 2 NSWLR 72
RTA v AMP [2001] NSWCA 186
Rundle v State Rail Authority (2002) NSWCA 354
Seltsam Ltd v Minahan (1996) 13 NSWCCR 410
Sherman v Nymboida Collieries Pty Ltd (1963) 109 CLR 580
Sherson & Associates Pty Ltd v Bailey [2000] NSWCA 275; (2001) A Tort Rep
        81-591
Simpson v Midalco Pty Ltd, unreported; FCt SCt of WA; Library No 7421;
        7 December 1988
St George Club Ltd v Hines [1962] ALR 39
State Electricity Commission of Victoria v Johnson, unreported; SCt of Vic; No
        6031 of 1994; 31 October 1995
State Government Insurance Commission (South Australia) v Laude (1984) 37
        SASR 31
Stokes v Guest, Keen and Nettlefold (Bolts & Nuts) Ltd [1968] 1 WLR 1776
Sutherland Shire Council v Heyman (1985) 157 CLR 424
Sydney County Council v Furner (1991) 7 NSWCCR 210
Tame v State of New South Wales; Annetts v Australian Stations Pty Ltd [2002]
        HCA 35; (2002) 211 CLR 317
Thompson v Smiths Shiprepairers (North Shields) Ltd [1984] QB 405
Tomlinson v Congleton Borough Council [2002] EWCA Civ 309; [2004] 1 AC
        46
Tomlinson v Congleton Borough Council [2003] UKHL 47; [2004] 1 AC 46
Vacwell Engineering Co Ltd v BDH Chemicals Ltd [1971] 1 QB 88
Van Der Sluice v Display Craft Pty Ltd (2002) NSWCA 204
Vozza v Tooth & Co Ltd (1964) 112 CLR 316
Wilson v Tyneside Window Cleaning Co [1958] 2 QB 110
Wintle v Conaust (Vic) Pty Ltd [1989] VR 951
Workers' Compensation (Dust Diseases Board) v Kelly [2000] NSWCA 57;
        (2000) 20 NSWCCR 234
Wright v Dunlop Rubber Co Ltd (1972) 13 KIR 255
Wyong Shire Council v Shirt (1980) 146 CLR 40
X & Y v Pal (1991) 23 NSWLR 26




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                                                           Table of Contents

Introduction .............................................................................................................................. 12
The estate claims and the dependants' claims........................................................................... 17
Choice of applicable law .......................................................................................................... 18
Grant of representation and testamentary distribution ............................................................. 21
The periods of the deceased's employment with the defendants .............................................. 23
Personal background ................................................................................................................ 27
Family and Dependants ............................................................................................................ 28
History of deceased's health ..................................................................................................... 29
Deceased's smoking history - effects of cigarette smoking...................................................... 38
Varieties of asbestos ................................................................................................................. 39
Composition of asbestos in water pipes ................................................................................... 44
Composition of asbestos at the third defendant's premises at Australind ................................ 44
Asbestos - complete carcinogen or promoter ........................................................................... 45
Lung cancer - divisible or indivisible disease .......................................................................... 47
Paul Cotton's employment with the South Australian Engineering and Water Supply
Department ............................................................................................................................... 52
Paul Cotton's employment with the third defendant and extent of exposure to asbestos......... 66
   1. The workers at Australind ................................................................................................ 79
   2. The Matprolab Reports of March and August 1990........................................................ 90
   3. Air monitoring ............................................................................................................... 107
   4. Complaints about asbestos at Australind site ................................................................ 109
   5. Asbestos insulation removal.......................................................................................... 111
   6. Chronology of asbestos removal activities at Australind .............................................. 113
Quantitative estimates of asbestos exposure .......................................................................... 120
   1. The WAIT AID Study................................................................................................... 123
   2. The Amdel Report ......................................................................................................... 125
   3. The A/C Pipe Producers Association Report ................................................................ 126
   4. The James Hardie Asbestos Cement Cutting Tool Study of February 1980.................. 128
   5. Ontario Royal Commission Report ............................................................................... 128
   6. Japanese Study of 1993 ................................................................................................. 129
The occupational hygienists ................................................................................................... 129
   1. Mr M H Kottek .............................................................................................................. 129
   2. Professor de Klerk ......................................................................................................... 135
   3. Mrs Janet Sowden.......................................................................................................... 139
   4. Mr Geoffrey Pickford .................................................................................................... 145
   5. Mr Paul Foley................................................................................................................ 147
   6. Mr Alan John Rogers..................................................................................................... 150
Results of Attempts at Quantitative Assessment of Asbestos Exposure ................................ 159
Specialist medical opinion - clinical and epidemiological..................................................... 159
   1. Professor A W Musk, AM ............................................................................................. 160
   2. Professor K Wan............................................................................................................ 164
   3. Dr James Leigh.............................................................................................................. 169
   4. Dr Peter Kendall ............................................................................................................ 173
   5. Professor Geoffrey Berry .............................................................................................. 173
   6. Professor R M Fox......................................................................................................... 187
Conclusions ............................................................................................................................ 192



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Scientific literature ................................................................................................................. 195
The Helsinki Protocol and the AWARD Criteria ................................................................... 210
Adelaide Workshop on Asbestos-Related Diseases (AWARD Criteria)............................... 213
Other literature........................................................................................................................ 222
Knowledge of the hazards of asbestos - scientific literature relied upon by Dr James Leigh 223
The scientific literature relied upon by Mr Kottek ................................................................. 225
Further Conclusions ................................................................................................................ 232
Liability for negligence, breach of contract or breach of statutory duty................................ 242
Knowledge of the hazards of asbestos.................................................................................... 257
Evidence of Mr Peter Russell ................................................................................................. 261
Knowledge about risks of asbestos......................................................................................... 265
Newspaper and media publications ........................................................................................ 271
Findings of negligence, breach of contract and breach of statutory duty against each of the
three defendants ...................................................................................................................... 272
Differential risks ..................................................................................................................... 274
Approach to causation............................................................................................................ 280
More aspects of causation ...................................................................................................... 298
Contributory negligence and voluntary assumption of risk - the effects of smoking ............ 305
Significance of anti-smoking campaigns ................................................................................ 310
Contributory negligence ......................................................................................................... 321
Further amendments to apportionment legislation................................................................. 328
Damages - estate claims and dependants' claims ................................................................... 329
   1. Estate claim - South Australia ....................................................................................... 335
   2. Estate claim - Western Australia ................................................................................... 338
   3. Dependants' claims ........................................................................................................ 339
   4. Dependants' claims from the date of death until judgment ........................................... 342
   5. Loss of superannuation benefits .................................................................................... 346
   6. Dependants' claims for loss of services rendered by the deceased................................ 347
Forms of orders or judgment .................................................................................................. 353




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EM HEENAN J


        EM HEENAN J:

Introduction
1            The plaintiff has sued each of the three defendants claiming damages
        for personal injuries and loss suffered by her late husband Paul Steven
        Cotton and, in addition, for damages for herself and his four dependant
        children consequent upon his death on 6 January 2002. In May 2000, at
        the unusually young age of 43 years, the late Steven Cotton was found to
        be suffering from inoperable cancer in the right lung and abdomen.
        Following this diagnosis he underwent extensive courses of chemotherapy
        and eventually radiotherapy which, to some extent, ameliorated the
        progress of the disease but were themselves very debilitating. The cancer
        metastasised to his brain causing a series of grand mal epileptic fits which
        were eventually brought under control but he died as a result of the
        disease leaving a family of his de facto widow, the plaintiff, and their four
        daughters then aged from 16 to 5 years.
2             Mr Cotton had smoked cigarettes regularly since he was 17 years of
        age and only gave up that practice after the diagnosis of his lung disease
        in May 2000. This 26 year period of regular smoking, in the opinion of
        all the medical consultants, contributed significantly to the development
        of his lung cancer but, in the view at least of the plaintiff's physicians and
        oncologists, the level and extent of the smoking would not ordinarily be
        expected to result in the development of such a lung cancer at this early
        age, the more common presentation of a cigarette-induced lung cancer
        appearing for a person, with Mr Cotton's history of smoking, in his fifties
        or sixties. Accordingly, the diagnosis of Mr Cotton's cancer led to a
        retrospective inquiry about whether or not he had ever been particularly
        exposed to asbestos in a working or other environment because such
        exposure is also a recognised cause of lung cancer, and more potent when
        associated with regular cigarette smoking.

3             In fact Mr Cotton had been employed by the Engineering and Water
        Supply Department of South Australia ("EWSD") for three years between
        September 1975 and October 1978 working for most of that time in laying
        and fitting cement and asbestos water pipes in various parts of the
        Adelaide metropolitan area. This work had involved cutting, filing or
        rasping pipe ends on the work site in conditions which, it is alleged, gave
        rise to quantities of dust and other particles containing asbestos some of
        which were probably inspired by the deceased and other workmen on the
        site. The plaintiff's case is that no warnings were given about the danger
        of working in conditions involving exposure to cement/asbestos dust and


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EM HEENAN J


        that no precautions were taken to avoid or minimise the dust problem.
        The first defendant, the State of South Australia, operated and conducted
        the Engineering and Water Supply Department of that State at the time
        and was the deceased's employer. The plaintiff's case is that the cement
        asbestos water pipes which were supplied to the EWSD during those years
        were manufactured and delivered by James Hardie & Coy Pty Ltd - by
        which name the second defendant Amaca Pty Ltd was then called. The
        plaintiff's case against the second defendant is that no warnings were
        given nor any precautions taken or recommended about the methods of
        installation, use or fabrication of its cement asbestos water pipes by any
        end user.

4            After leaving the employment of the EWSD in Adelaide in October
        1978 Mr Steven Cotton took other employment, mainly on sheep stations
        in outback South Australia and in the Northern Territory, before settling
        in Katherine where he met the plaintiff. The couple and three of their
        children who by then had been born moved to Western Australia in 1989
        or 1990 and eventually settled in the Bunbury region, although moving
        several times within that locality, where Mr Cotton obtained employment
        with SCM Chemicals Ltd as the third defendant was then known. The
        period under review in this litigation covers the change of name of the
        third defendant from SCM Chemicals Ltd ("SCM") to Millennium
        Inorganic Chemicals Ltd (its present name) and therefore, throughout the
        evidence there are many references to the third defendant in both names
        and this variable usage is also followed in these reasons.

5             The industrial operation undertaken by the third defendant was the
        production of titanium dioxide (Ti O2), a brilliant white pigment used in
        painting and many other chemical and industrial uses. The product, as
        finally prepared by the third defendant, is very fine white powder packed
        in bags for delivery or shipment. The process of the production of the
        Ti O2 which mostly concerns this litigation occurred within a very large
        industrial building or shed (some 200m x 20m x 10m) known as the Band
        Drier Room ("BDR"). Within that operation large volumes of a viscous
        slurry of the product would be fed via various conveyors through a drying
        process which removed liquid leaving a very friable chalk-like solid
        product. This was then readily crushed to the final powder form which
        was placed in bags for distribution.
6            This process, essentially a drying process, was carried out on a very
        large scale and the source of heat was from steam, generated elsewhere,
        and passed into the operating areas through large steam pipes which were
        used to heat the slurry and convert it into the cake-like solid. In the early


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        years the many large steam pipes in the factory were covered in asbestos
        cladding and asbestos was also used in insulating doors to the Band Drier
        machine within which this drying process was concentrated. In addition,
        the very extensive overhead roof of this large building was covered with
        asbestos cement sheeting.

7            The evidence for the plaintiff is that, within this working
        environment, the condition of the asbestos lagging on the steam pipes was
        deteriorating and that strips of the insulation would often, indeed all the
        time, break from the overhead lagged piping, and that the fragments and
        associated shredding would fall onto the floor of the workplace below. In
        addition, the opening and closing of the doors to the heating appliances in
        the BDR resulted in the asbestos insulation within them wearing and
        shedding, giving rise to further fragmentation of the insulation in the
        workplace. The plaintiff's case also is that the asbestos roof material was
        ageing and deteriorating and the dust and fragments from the overhead
        roof would also fall to the floor below. Shifts of workmen, including the
        plaintiff, were regularly required to sweep up the floor, clear it of these
        fragments and deposits and did so simply by the use of brooms. This
        process itself generated dust in which the plaintiff worked without any
        warning from the employer or any protection against the risk of
        respiration in an area containing dusty fragments of asbestos, including
        airborne asbestos particles.

8            During the time that Mr Cotton was working with SCM Chemicals
        the company took extensive steps to remove or reduce the risk of asbestos
        exposure to its workforce. There were a series of initiatives described by
        the third defendant. Firstly, independent consultants were brought in to
        assess and then to remove the asbestos lagging on the steam pipes and this
        was done, in controlled conditions, in late 1991 and early 1992. Next,
        another group of consultants were brought in to remove and replace the
        asbestos cement sheeting on the roofs and to install asbestos-free roofing
        material. That was done from about 1994 in stages until 1998. Finally,
        the asbestos insulation behind the metal sheeting on the doors to the
        heating appliances within the BDR was removed and a form of
        asbestos-free rock wool insulation was installed, again under controlled
        conditions in or about 1996. Consequently, the third defendant maintains
        that it was not possible, or at least it was highly improbable, that the
        deceased was exposed to ambient asbestos fibres during his employment
        with it which could have caused or contributed towards the development
        of his fatal lung cancer. The timing and duration of the asbestos removal
        programmes are, however, rather more complicated and extensive and are
        examined in detail later in these reasons.

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9            At this point it is enough simply to note that the plaintiff alleges that
        the harmful and carcinogenic properties of asbestos were well-known in
        public health circles and in industry long before his first employment with
        EWSD in Adelaide in 1975 and that, by that time, any employer who
        conducted a system of work which exposed employees to uncontrolled
        ambient atmospheric asbestos particles, asbestos dust or asbestos products
        was both negligent and in breach of relevant statutory provisions then
        applying or relating to occupational health and safety.
10           There is an issue in this case as to whether or not the levels of
        exposure, if any, occurring in the workplaces in which Mr Cotton was
        employed transgressed then applicable regulatory standards, but,
        otherwise, all the parties to this litigation have accepted that the harmful
        effects of asbestos in workplaces, and indeed elsewhere, were well-known
        by 1975.

11            Each of the defendants denies that Mr Cotton was exposed to
        asbestos, whether in the two periods of employment identified or, in the
        first period of employment by asbestos cement products supplied by the
        second defendant. More significantly, in the light of the evidence
        examined later, each defendant also denies that any exposure to asbestos
        which Mr Cotton experienced, during either of the two periods of
        employment in Adelaide and Bunbury respectively, whether alone or in
        combination with each other, or in combination with his tobacco smoking,
        caused or contributed to the development of his lung cancer and his death.
12            The real point upon which this case appears to me to turn is whether
        or not the plaintiff has established to the requisite degree of proof that
        Mr Cotton's death was caused or contributed to by such exposure to
        asbestos as he actually experienced. This must be shown as distinct from
        a position where all that the plaintiff can demonstrate is that there may
        have been an elevated risk of Mr Cotton developing asbestos-induced
        lung disease without any proof that in the circumstances of this case, that
        risk actually materialised. This issue loomed very large in the trial and
        was the subject of a great quantity of expert opinion from diagnostic
        clinical physicians, from epidemiologists, from occupational hygienists
        and epidemiological statisticians. As will be seen later in these reasons
        the controversy developed into a complicated scientific argument over the
        establishment or acceptance of criteria sufficient to allow a diagnosis of
        asbestos-induced lung disease, and in particular lung cancer, and attempts
        at quantification of levels of atmospheric asbestos contamination
        sufficient to warrant a conclusion that a particular lung cancer, a disease
        known to result from one or more quite separate and distinct causes, did in


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        this particular instance develop because of, or because of the contribution
        of, alleged asbestos contamination.
13            The more is this controversy significant in the present case because,
        unlike asbestos-induced lung diseases such as mesothelioma or asbestosis,
        or even lung cancers associated with pleural plaques, themselves
        indicative of pleural irritation due to asbestos fibrosis or inspiration, there
        is no unequivocal diagnostic finding or feature of Mr Cotton's case which
        directly demonstrates asbestos as the principal, or a material, contributing
        cause. That is by no means uncommon in lung cancers where it is known
        that asbestos can be a cause, or a precipitating or promoting factor, but it
        does raise the question of whether or not Mr Cotton's lung cancer can be
        shown to have probably been caused or contributed to by the alleged
        periods of asbestos exposure during his working life. To a large degree
        each of the defendants tacitly asserts that Mr Cotton's fatal disease was
        caused solely by his smoking or that, at least, it is not possible for the
        plaintiff to prove on the probabilities that any occupational asbestos
        exposure contributed materially to it.
14           In addition to these main defences, the first and second defendants
        plead volenti asserting that Mr Cotton's long history of cigarette smoking
        must be regarded by him as a voluntary assumption of the risk of
        developing lung cancer or another fatal disease. To an extent this plea
        seems misplaced because the plaintiff has never alleged that the first or
        second defendants caused or is any way responsible for the deceased's
        smoking or its effects. However, the defence may be applicable if all that
        the evidence can establish is that the level of asbestos exposure to which
        Mr Cotton was subjected whilst employed by the EWSD was harmless for
        anyone who was not a chronic smoker and that, as a chronic smoker with
        an elevated susceptibility to the effects of asbestos, Mr Cotton knew and
        willingly accepted the risk involved in working in an environment with
        ambient asbestos. However that is not the way upon which the first
        defendant advanced this plea.

15           Similarly, the first defendant alleges that the cause of the deceased's
        cancer was a novus actus interveniens for which it was not responsible. In
        effect this appears to be a plea that it was the subsequent period of
        exposure of the deceased to asbestos at the workplace of SCM Chemicals
        near Bunbury which, if there was any asbestos contribution to the fatal
        lung disease, was the cause and not any earlier exposure during the
        employment with the EWSD. However, each defendant also alleges that
        Mr Cotton's smoking was a significant contributory cause of his fatal
        disease and that his engagement in tobacco smoking, particularly in the


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        light of a long history of public health warnings of the hazards of smoking
        canvassed elaborately in the evidence, constituted contributory
        negligence.

The estate claims and the dependants' claims
16           The claims against the first and second defendant arise out of a series
        of events which, putting aside the long latency of asbestos-induced
        diseases before the presentation of symptoms and disability, occurred
        during Mr Cotton's employment with the EWSD in Adelaide between
        September 1975 and October 1978. Conversely, and again putting to one
        side the initiating or contributing effect, if any, of prior exposure to
        asbestos in South Australia, the claims against the third defendant arise
        from the period of the deceased's employment in Western Australia with
        SCM/Millennium between April 1990 and his death in January 2002. In
        respect of each of the two sets of claims the plaintiff seeks damages on
        behalf of the estate of Steven Cotton (deceased) for pain and suffering,
        economic loss and other special damages which Mr Cotton himself
        suffered or incurred up to the date of his death. These claims, "the estate
        claims", are brought against the first and second defendants under the
        provisions of the Survival of Causes of Actions Act 1940 (SA) and against
        the third defendant pursuant to the Law Reform (Miscellaneous
        Provisions) Act 1941 (WA).
17            The distinct and special statutory cause of action for loss of
        dependency following the death of Mr Cotton is brought against the first
        and second defendants pursuant to the Civil Liability Act 1936 (SA)
        (which, uniquely, allows recovery of an allowance for solatium) and the
        Fatal Accidents Act 1959 (WA). Both causes of action for the alleged
        breaches of duty by the employer in South Australia are brought against
        the first defendant pursuant to the Crown Proceedings Act 1992 (SA).
        Similarly, in relation to both sets of claims, the defences of contributory
        negligence advanced against the first and second defendants rely upon the
        provisions of the Wrongs Act 1936 (SA) now the Civil Liability Act 1936
        (SA) and, in relation to the claim against the third defendant, reliance is
        placed upon the Law Reform (Contributory Negligence & Tortfeasors'
        Contribution) Act 1947 (WA). As set out below, there are some
        differences in the nature and extent of damages recoverable in an estate
        claim and in a dependant's claim because of differences in the detail of the
        applicable legislation in South Australia and in Western Australia.




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Choice of applicable law
18            However, it is now clear that, notwithstanding that this action has
        been brought and determined in this Court of Western Australia, the
        provisions of the legislation relating to the place of the alleged tort or
        breach of duty apply to the determination of the existence and
        quantification of the respective claims for damages - John Pfeiffer Pty
        Ltd v Rogerson [2000] HCA 36; (2000) 203 CLR 503; 172 ALR 625;
        Regie Nationale des Usines Renault SA v Zhang [2002] HCA 10; (2002)
        210 CLR 491 and Sweedman v Transport Accident Commission [2006]
        HCA 8; (2006) 80 ALJR 646; (2006) 224 ALR 625. No question of the
        jurisdiction of this Court to entertain and determine the claims brought out
        of the alleged breaches of duty in South Australia exists and the
        authorities cited establish that the choice of law rules, both as to the law
        relating to the alleged liability of the defendants and the quantum, if any,
        of damages recoverable in the event of liability will be the respective laws
        of the States in which the alleged breaches of duty occurred.

19           This follows not only because laws relating to defences such as
        contributory negligence or to quantum of damages have been treated as
        being substantive rather than procedural notwithstanding the decision in
        McKain v R W Miller & Co (SA) Pty Ltd (1991) 174 CLR 1 which
        recognised and preserved the former distinction between substantive law
        and procedural law, the latter being provided by the lex fori, because that
        result was superseded by the decision in John Pfeiffer (supra). Hence
        laws which previously may have been regarded as procedural, such as the
        discount rate to be applied for the assessment of damages involving future
        occurring economic loss, and indeed whether a component of interest may
        be added to an award of damages, or parts of it, and if so for what period
        and at what rates, should now be regarded as being matters of substantive
        law to be governed by the operative provisions of the lex loci delicti -
        John Pfeiffer (supra) 203 CLR 503 at 542 [97] - [103].

20           In relation to the estate claims the legislation in Western Australia in
        most cases excludes the recovery of damages for pain and suffering, any
        bodily or mental harm or curtailment of the expectation of life. Also in
        the case of the estate claims the legislation of both States in most cases
        excludes recovery of damages for loss of earning capacity after the date of
        death. The consequence, therefore, subject to the exceptions to be
        mentioned, is that in the estate claims, if successful, the plaintiff may
        recover damages for:




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              •       medical, hospital and other therapeutic expenses incurred
                      for or on behalf of the deceased until his death;
              •       loss of earning capacity, if any, to the date of death; and

              •       funeral expenses;
              •       and (in the South Australian claims only) general
                      damages.
        Also available are damages for the recovery of the value of voluntary
        services. Excluded are the costs of obtaining a grant of probate or
        administration and the costs of administration: Gammell v Wilson [1982]
        AC 27 at 47 but funeral expenses may be recovered because of the
        provisions of the statutes. In neither jurisdiction are exemplary damages
        recoverable as part of the estate claim (Law Reform Act WA, s 4(2)(a),
        Survival of Causes of Action Act 1940 (SA), s 3(1)(b)).
21           In relation to certain claims for damages (but not this one) where the
        death results from a latent injury which is attributable to the inhalation of
        asbestos which has been caused by the act or omission giving rise to the
        cause of action where proceedings in respect of that cause of action had
        been instituted before his death and were still pending at the time of death,
        the estate action may include (in Western Australia) damages for pain or
        suffering or for any bodily or mental harm suffered by him or curtailment
        of his expectation of life. This is only possible where the death occurs
        after the commencement of the provisions of the Law Reform
        (Miscellaneous Provisions (Asbestos Diseases)) Act 2002 which came
        into operation on 21 March 2002, that is after the death of Steven Cotton.
        For those estate claims in which damages for future economic loss is
        recoverable the discount rate for the calculation of damages is fixed at
        6 per cent (Law Reform Act, s 5(1)(e)).

22           In South Australia, however, under s 3(2) of the Survival of Causes
        of Action Act 1940 (as amended), if a person commences an action for
        damages in respect of a dust-related condition and dies as a result of that
        condition before the action is finally determined, damages for pain and
        suffering, bodily and mental harm and curtailment of expectation of life
        are recoverable for the benefit of the estate of the person. In the SA
        legislation a dust-related condition means a disease specified in the
        schedule or any other pathological condition of the lungs, pleura or
        peritoneum which is attributable to dust and the schedule specifically
        includes asbestos-induced carcinoma as one of several prescribed dust
        diseases.


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23           Under the legislation of which Lord Campbell's Act is the prototype,
        no non-pecuniary loss is recoverable and exemplary damages are
        excluded - Reindel v James Hardie & Co Pty Ltd [1994] 1 VR 619. But
        in South Australia, unlike in Western Australia, there is provision for the
        payment of a solatium - Wrongs Act 1936 (SA), s 23A - s 23C, but the
        allowance for a surviving spouse is capped at $4200 - Wrongs Act
        Amendment Act 1975 (SA) - and the maximum is conventionally awarded
        in South Australia in most cases - see Luntz, "Assessment of Damages for
        Personal Injuries and Death", 4th ed, [9.7.2]. However, the plaintiff did
        not seek any such allowance in this case and no party addressed any
        submission to this point.

24           Despite the dual claims, it is established that the benefits accruing to
        dependants by reason of the death of the deceased must be taken into
        account in reduction of the claim for dependency under the dependants'
        action so that, where there is recovery of damages in an estate action
        which goes to benefit the dependants entitled under the dependants' action
        there must be, pro tanto, a reduction of the damages in the latter claim.
25           The present action was commenced by Steven Cotton in person
        before his death and, since then, has been continued by the plaintiff, his
        de facto widow and executrix. After his death the claims were expanded,
        by amendment, to include the fatal accident claims under the legislation of
        both States.

26           It follows from the foregoing, therefore, that if the plaintiff is
        successful in her claims against all the defendants, the estate claim against
        the third defendant cannot include any component for loss of expectation
        of life, damages for pain and suffering or loss of amenity or loss of
        earning capacity subsequent to the date of death, but that under the
        applicable law of South Australia the estate claim will accommodate each
        and all of those heads of damages. Similarly, if the plaintiff is successful
        in her actions against each of the defendants, the dependants' claim,
        against the first and second defendants arising from the alleged breaches
        of duty in South Australia may include a component for solatium but no
        such component will be recoverable against the third defendant in relation
        to the alleged breaches of duty occurring in Western Australia. All this
        will give rise to some complexities of calculation if and when it is
        necessary to set off the benefits derived under the estate claims from the
        damages recoverable under the dependants' claims and in determining the
        different extent of the liabilities of the several defendants for the several
        causes of action. The details of these calculations will be addressed later
        when the quantification of damages, if recoverable, is undertaken.


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27           I therefore accept the submissions of the plaintiff and both the first
        and second defendants that the law applicable to both the estate claim and
        the dependants' claim for damages arising out of the deceased's
        employment in South Australia is the law of the place of the alleged
        wrong - that is, the law of South Australia: Distillers Co (Bio-Chemicals)
        Ltd v Thompson [1971] 1 NSWLR 83; [1971] AC 458; Voth v Manildra
        Flour Mills Pty Ltd (1990) 171 CLR 538 at 567 and John Pfeiffer Pty
        Ltd v Rogerson (2000) 203 CLR 503 at [87]. Each of those claims now
        originates in or derives from statute law, rather than from common law;
        namely the Survival of Causes of Action Act 1940 (SA) for the estate
        claim, and the Wrongs Act (now the Civil Liability Act 1936 (SA)) for the
        dependants' claim. As they provide the substantive law, this also
        determines that the law relating to the measure or quantum of damages,
        discount rates and other rules for the quantification of damages applying
        in South Australia shall apply to the determination of any damages
        recoverable in this first action - a proposition confirmed by subsequent
        decisions of the High Court in Neilson v Overseas Projects Corporation
        of Victoria Ltd [2005] HCA 54; (2005) 223 CLR 331; Campbells Cash &
        Carry v Fostif Pty Ltd [2006] HCA 41; (2006) 229 ALR 58 and
        Sweedman v Transport Accident Commission [2006] HCA 8; (2006) 224
        ALR 625. None of the parties contended other than to the effect that the
        law of South Australia should be applied in relation to the claims against
        the first and second defendants, including liability and quantification of
        damages, if any. Furthermore, pursuant to the law of South Australia, any
        claims of damages arising from the estate claim or the dependants' action
        are subject to the potential apportionment for contributory negligence of
        the deceased - see s 27A(8) and (9) in the Civil Liability Act 1936.

Grant of representation and testamentary distribution
28           In September 2005, that is during this trial, the plaintiff applied for a
        grant of probate of a will of Paul Steven Cotton which was dated only
        "1989" without specifying the day or month of execution. This document,
        said to be Mr Cotton's last will and testament, appointed Teresa Ellis as
        his sole executor and the sole beneficiary of his entire estate. The
        application for probate was supported by an affidavit from the plaintiff
        annexing a statement of the deceased's assets and liabilities. That
        statement purported to place a value on the present claim for damages of
        $360,561.68 which was listed as part of the moveable property of the
        deceased. Putting that to one side the only other assets were:




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              Jewellery and personal effects                        $1000
              Commonwealth Bank Everyday Account                      $200
              1989 Nissan Pintara Station Wagon                     $1000
                                                                    $2200
              Liabilities:

              William Barrett & Sons - funeral expenses             $5209
              Legal fees due to Slater & Gordon, lawyers            $2000
                                                                    $7209
              Deficit                $5009

29            By the completion of the trial no grant of probate had been made, but
        the position was left by the parties that the court would be notified, or
        could ascertain, if and when a grant of probate was made in which case
        the title of the plaintiff to sue on behalf of the estate would be established
        and would become retrospective to the date of death - see Administration
        Act, s 8 and Re Full Board of the Guardianship and Administration
        Board [2003] WASCA 268; (2003) 27 WAR 475 at 491. The action is to
        be brought by the personal representative of the deceased but if no grant
        of representation has been made within six months of the death the action
        may be brought by any dependant - Fatal Accidents Act, s 9 and Civil
        Liability Act 1936 (SA), s 23 and s 27.

30            Since the end of the trial I have had notice, through the Court's own
        processes, that probate of the will of the deceased was granted to the
        plaintiff on 27 September 2005. The matter was left on the basis that the
        parties had liberty to apply in relation to any matter arising from the
        pending grant for probate. No attempt has been made to avail of this
        opportunity and, accordingly, as I am satisfied that a grant of probate has
        been made, as described, and I conclude that the plaintiff has the standing
        to bring and pursue the estate claims.
31            The evidence is that the deceased's car was taken over and used by
        the family before being sold for a modest amount and that no advantage
        was derived from his other assets which were utilised to defray expenses
        associated with the administration of his estate. There is no surplus for
        division to the sole beneficiary: the widow. I have no hesitation in
        concluding that the only assets of value are the claims for damages
        instituted by the deceased himself and pursued by this current litigation.
        To the extent that the estate claims succeed the damages will become an

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        asset of the estate distributable to Teresa Elizabeth Ellis alone.
        Accordingly, in the dependants' claims, the widow will have to bring to
        account against any assessed loss of dependency, the value of the benefit
        derived from the estate action which will diminish and may well
        extinguish that claim. By contrast, however, the four daughters w   ould
        have their respective losses of dependency undiminished because none
        succeeds to any benefit under her father's will.

The periods of the deceased's employment with the defendants
32           Paul Steven Cotton was first employed by the EWSD of South
        Australia at its Marden depot in the eastern suburbs of Adelaide on
        4 September 1975. His initial role in that employment was as a gardener
        for about six months but from early March 1976 he joined a gang of pipe
        layers whose responsibilities were to lay water or sewerage pipes in
        suburban areas and to do so by laying asbestos cement piping, usually of
        about four inches in diameter, and that the task involved cutting and
        shaping these pipes in the field - processes which generated quantities of
        dust containing asbestos and cement fibres.
33           The controversy about the frequency and concentration of exposure
        to dust containing asbestos particles can be deferred for the present but it
        was certainly a daily occurrence for the five day working week which the
        deceased put in during this interval of a little over two and a half years.
34           Despite an issue arising on the pleadings over the identity of the
        manufacture and supply of the cement and asbestos pipes used for these
        purposes by the EWSD, the evidence clearly establishes that the pipes
        were manufactured by the second defendant under its name of James
        Hardie & Coy Pty Ltd at its Elizabeth manufacturing plant in South
                                                                            h
        Australia and were supplied direct by the second defendant to t e first
        defendant for use in the Adelaide water and sewerage system. The only
        doubt which arose about the source of the pipes can be attributed to the
        deceased Steven Cotton himself who, when giving evidence before the
        Workers' Compensation Workcover Review Directorate on 16 October
        2000 in proceedings in which the identity of the supplier or manufacturer
        of the pipes was not a material issue, said that he believed that the pipes
        had come from Humes. However, other evidence established that the
        pipes which Humes manufactured were made of cement only, were of a
        much larger diameter and were manufactured in Tasmania. The only
        cement asbestos pipes sought and installed by the EWSD of South
        Australia at the time were Hardie's cement and asbestos pipes from
        Elizabeth.


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35           The facts of significance emerging from this history are that
        Mr Cotton had an aggregate period of exposure to ambient dust containing
        asbestos particles on a regular week day basis for two and a half years and
        that the commencement of the period of exposure in March 1976 is
        slightly more than 24 years before the diagnosis of his lung cancer in
        May 2000, signifying that this is within the possible period for the latency
        of his lung disease if it were entirely asbestos caused. He had, of course,
        commenced smoking about the time he turned 17 in October 1973. His
        period of exposure to asbestos dust when employed by the first defendant
        coincided with a time when he was smoking regularly. He had indeed
        been smoking regularly for about two and a half years before he
        commenced working with those pipes.
36            On moving to Western Australia in 1990 Mr Steven Cotton first
        obtained employment with the third defendant, then SCM, on 19 April
        1990 when he was engaged as a full-time casual employee and worked in
        that role until 19 February 1991. His employment then ceased but he was
        re-engaged, again on a full-time casual basis on 14 October 1991, and
        worked until 28 January 1993. There was then a short break of two weeks
        before he was re-engaged on 11 February 1993, later being made a
        full-time permanent employee and working continuously for the third
        defendant until the diagnosis of his disease on 8 May 2000.
37            Immediately upon the diagnosis being made he was classified as
        totally and permanently incapable of further work but remained in the
        employ of the third defendant and in receipt of workers' compensation and
        other benefits until his death on 6 January 2002. Consequently, the
        aggregate period of his employment with the third defendant before the
        diagnosis of his disease was about 10 years and three weeks - from April
        1990 until early May 2000, including two periods totalling about
        8½ months for the interruptions to that employment. In other words there
        was a maximum period of about nine years and four months during which
        he was working on the Australind work site. Not all of this involved
        actual or potential exposure to asbestos because Mr Cotton was working
        in other places besides the large factory which has been described as the
        BDR. Nevertheless, the asbestos removal programmes had been carried
        out in stages so that, according to the third defendant, the working
        environment was largely asbestos free by 1997. This means a total
        possible period of exposure to asbestos during his employment with the
        third defendant of about 6½ years. This also coincided with a time when
        the deceased maintained his daily smoking habit.




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38           This period of potential exposure to asbestos while in the employ of
        the third defendant, provisionally estimated at about six and a half years
        duration, began not earlier than 11½ years after he had stopped working
        with the concrete asbestos pipes while with the EWSD in Adelaide. If the
        deceased's lung cancer was wholly caused by exposure to asbestos during
        his employment with the third defendant, then the maximum latency
        period before diagnosis would be just over 10 years which, as some expert
        evidence later examined suggests, would be rather short. However, it is
        not possible to undertake an adequate consideration of this case by
        attempting to segregate factors such as the separate episodes of alleged
        exposure to asbestos, assumed latency periods or other circumstances
        because the evidence shows that a combination of causes acting together,
        rather than any one alone, could have caused the disease.
39           The description of the form of cancer suffered by Mr Cotton was
        given by Professor Musk as "non small cell carcinoma with features of
        squamous cell carcinoma". The pathologist Dr Shilkin reported that the
        tumour was a "poorly differentiated squamous cell carcinoma of the
        lung". Professor Musk testified that there are a variety of carcinogenic
        tumours including squamous carcinoma, large cell (or adeno-carcinoma)
        and small cell carcinoma, but that it is not possible to identify the cause or
        precipitant of the cell mutations leading to the development of the cancer
        from the particular variety of the lung tumour. Similarly, the site of the
        origin of the development of the tumour in the lung will not reveal the
        cause of the tumour either. Professor Musk explained how that,
        sometimes, the diagnostician may find evidence of asbestos in the lung
        biopsy which may lead one to think of asbestos as a cause of the tumour
        but even this may not be determinative and that the ultimate diagnosis is
        essentially a clinical one.
40           The exact pathogenesis of lung cancer whether caused by smoking or
        by asbestos or a combination of both is not fully understood, yet the
        causal relationship has been known to medicine and industry for many
        years.     The plaintiff's lung cancer is quite distinct from other
        asbestos-related lung diseases such as mesothelioma and asbestosis.
        Mesothelioma is a cancer of the mesothelia cells, that is cells in the wall
        of the lung and the lining of the chest wall. This disease was endemic in
        Turkey where there were large exposures to asbestos in the form of
        aryionite. The mechanism of the disease was thought to be that the
        inspiration of asbestos fibres results in them becoming lodged in air sacs
        within the lung which are only microns away from the pleural surfaces
        resulting in a migration of the asbestos fibres from the sacs to the pleura
        and mutation in the lining of the chest wall or mesothelium. This form of

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        carcinoma is readily recognisable as asbestos caused and has been studied
        in considerable detail resulting in a large measure of international
        consensus about cause and latency period.

41            Like other forms of asbestos-induced disease lung cancer is dose
        related and the studies have led to various attempts to establish protocols
        for the diagnosis of asbestos-induced lung cancer, one of which is the
        Helsinki Protocol upon which the defendants place great reliance as
        excluding any permissible attribution of asbestos as a cause of
        Mr Cotton's lung cancer. However, the plaintiff's treating consultants and
        other expert witnesses respond, first, by observing that the Helsinki
        Protocol was only ever an attempt to reach a diagnostic consensus for the
        recognition of lung cancer and then only for a particular form of statutory
        compensation then available in Scandinavian countries. They observe
        that there are limitations and uncertainties about the Helsinki Protocols
        but that they are not appropriate to exclude cases such as the present.
42            Professor Musk also distinguishes the disease of asbestosis from the
        cancer suffered by Mr Cotton. While asbestosis is also dose related, it is a
        form of interstitial fibrosis caused by the inspiration of asbestos fibres
        causing microscopic irritation and scarring to the lung tissues. It
        sometimes may lead to consequent mutation and a form of cancer from
        this fibrotic origin. There was no asbestosis discovered in the
        investigations of Mr Cotton, nor were any pleural plaques reported on
        X-ray. These are formations involved in the thickening of the lung tissues
        in various areas and are thought to indicate the effects of accumulated
        irritation of the cells in those areas by asbestos fibre deposits which had
        been inspired over time but which may have been partly or totally
        expelled through mucous effusions and other protective responses of the
        body itself. Professor Musk explained, and all the other consultants
        accepted, that all three diseases, lung cancer, mesothelioma and
        asbestosis, were dose responsive in the sense that the higher the dose of
        exposure to asbestos the greater the risk of contracting the disease and that
        there was an approximately logarithmically linear relationship between
        the total dose exposure over time and the development of the disease. To
        identify the relationship as being logarithmically linear, of course, denotes
        it as being exponential in the sense that the greater the aggregate
        exposure, the greater the risk at an ever increasing magnitude.
43            Professor Musk maintained that there was no demonstrated threshold
        of exposure to asbestos at which the risk of lung cancer or other asbestos
        related disease disappeared or was regarded as tolerable. While accepting
        this proposition in general, a number of the consultants for the defendants


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        nevertheless advanced theses which involved, to a greater or lesser extent,
        propositions that exposure at less than certain levels (the identification
        which was a further source of controversy) meant that attribution of
        asbestos as a cause of the carcinoma is not justifiable. These theses, in
        effect, if not overtly, advanced the argument that the plaintiff should fail
        unless a minimum degree of aggregate exposure to asbestos could be
        demonstrated.

Personal background
44           Paul Steven Cotton was born at Adelaide on 6 October 1956. He
        lived with his family in a brick house in an Adelaide suburb and there is
        no suggestion of any special exposure to asbestos or to asbestos fibres
        during his childhood or adolescence beyond the background levels of
        exposure experienced by all members of the general population. He left
        school at the age of 16 and his subsequent employment history was as
        follows:
              •       1972 - employment with a Mr Ted Hamood in a wood
                      factory. There his role was to pick up pieces of wood, to
                      stack wood and to sweep up. The work area was a tin
                      shed.
              •       1972 - employment as a brickies labourer with a builder
                      Mr Bob Bennett. His role was to carry bricks and
                      materials and to perform general manual labour.

              •       1972 - Employment as a general hand at Mt Victor
                      Station. Mr Cotton's role was as a general cowboy
                      mustering sheep and fixing fences.
              •       1972 - employment as a general hand on McCoy Station
                      performing the same general work as at Mt Victor Station
                      for the same employer.
              •       1975 - employment at the South Australian Engineering
                      and Water Supply Department. Initially, for a period of
                      six months, Mr Cotton was engaged in the gardening
                      department but he then transferred to a pipe laying gang
                      from the Marden depot where his work involved cutting
                      and laying asbestos concrete pipes throughout various
                      regions of the eastern suburbs of Adelaide and sometimes
                      beyond. This period of employment relates to the



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                      plaintiff's claim for damages against the first and second
                      defendants and it lasted until 1978.
              •       1978 - stock work with Delamere River Ranch in the
                      Northern Territory.
              •       1979 - gardening and general labouring work for the
                      Katherine Town Council.
              •       1983 - employment as a general hand at meat works
                      involved in trimming hides and general clean-up. The
                      meat work sheds were constructed of brick and tin and he
                      was not conscious of any exposure to chemicals.
              •       1984 - Astral Plumbing - employed to carry materials and
                      dig trenches and holes to lay pipes in position. The pipes
                      worked on were PVC and he was not involved in the use
                      of adhesives or the heating or burning of pipes.

              •       1990 - employment with SCM Chemicals - Millennium
                      Inorganic Chemicals until retirement in 2002. This
                      relates to the claim for damages against the third
                      defendant and more detailed descriptions of this are set
                      out later.
        After moving to Western Australia in about 1990 Mr Cotton and his
        family lived at Dardanup in a brick and tile home at 10 Trustee Place.
        From there the family moved to 20 Main Way, Clifton Park, in Bunbury
        and this, too, is a brick and tile home.
45            On the evidence which he gave in the Workers' Compensation
        Review proceedings (Exhibit 2) and in his statutory declaration of 2001
        (Exhibit 1) Mr Cotton said that he began smoking at the age of 17 but that
        he quit smoking after his diagnosis with cancer in May 2000. On his
        evidence, he smoked regularly about 15 cigarettes (less than a pack) per
        day. Counsel for the third defendant refers to a reference in Exhibit 57
        (clinical notes from Sir Charles Gairdner Hospital, recording a statement
        of smoking 20 per day).

Family and Dependants
46          Paul Steven Cotton met the plaintiff Teresa Elizabeth Ellis at
        Katherine in about 1981. She had been born in the United Kingdom and
        came to Western Australia with her mother at the age of 10 and grew up,
        was educated and, initially, was employed in the Perth area. When she


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        was about 18 or 19 years of age she embarked on travel throughout the
        Northwest and into the Northern Territory and it was there that she met
        Paul Cotton. They started living together about eight months later and
        remained together until his death. The couple had four children:
              •       Amy Rae Cotton        - born 8 May 1985
              •       Kristie Lee Cotton    - born 12 December 1986
              •       Mandy Jane Cotton     - born 10 October 1988
              •       Madeline Marie Cotton - born 21 January 1996.
        Initially there was a plan for the two to be married but as they could not
        decide on where to hold the wedding the ceremony was simply put off and
        never actually eventuated. They lived in Katherine with the three children
        they then had before coming to Western Australia in 1989 and it was in
        Perth that Madeline was born. The family lived with Ms Ellis' parents in
        Perth for several months before moving to Bunbury where they lived in an
        SHC home at Withers before moving to a rental property in South
        Bunbury. Paul Cotton was seeking work and soon obtained a position as
        a full-time casual worker at Millennium Inorganic Chemicals, then known
        as SCM Chemicals, at Australind. Later, the family moved to Stanbury
        Crescent in Bunbury, later to Dardanup in about 1993 or 1994, then to
        another home in Dardanup before moving back to 20 Main Way, Clifton
        Park, Bunbury, where the family was living when Paul Cotton died.
47           Mrs Ellis describes Paul Cotton as complaining, uncharacteristically,
        of chest pain and feeling tired in about April 2000 and it was this which
        led him to see Dr Mincham who ordered the chest X-rays.

History of deceased's health
48           The medical evidence, beginning with Exhibit 57 - a letter of referral
        to Dr Tribe at SCGH from Dr G Mincham of the general medical practice
        at Bunbury - reveals that Mr Cotton had presented for a routine
        work-screening chest X-ray which had shown right mediastinal masses.
        He was said to be a smoker and had positive hepatitis C serology.
        Dr Mincham asked Dr Tribe to see him for further investigation and
        management. The initial notes at SCGH (Exhibit 57) show that Cotton
        was examined on 8 May 2000 and noted to be a 43-year-old process
        worker for Millennium Organic Chemicals. He had had a chest X-ray on
        27 April 2000 and a reported finding of a mass in the right pera trachial
        and right hilar region. The differential diagnosis was then noted as being
        lymphoma, first grade lung cancer or sarcoidosis. His previous medical


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        history was noted as including hepatitis C from maternal foetal
        transmission. His mother had died from hepatitis C. The family history
        showed a paternal grandmother who died of bowel cancer at the age of 57.
        The patient's own history was that he lived with his wife and four
        daughters in Bunbury, smoked a packet a day but said he would give it up
        and was a non-drinker. On examination he was noted to look well and a
        series of detailed investigations were ordered.

49           The initial chest examination of Paul Cotton by X-ray conducted on
        27 April 2000 was reported by the radiologist, Dr John Pederson
        (Exhibit 225) as follows:
              "Chest:

              Heart size within normal limits. Abnormal soft tissue seen in
              the right para tracheal and right hilar region. The left hilum is
              relatively normal in size.

              There is no parenchymal opacity or pleural fluid.
              Conclusion:

              Abnormal right hilum and right para tracheal lesion. Further
              investigation with CT is recommended. Differential diagnosis
              would include lymphoma, primary lung cancer and possibly
              sarcoidosis although bilateral hilar lymphadenopathy is usually
              present with this disorder."
        There was then a CT scan of the chest performed at Sir Charles Gairdner
        Hospital on 12 May 2000 and reported on by the Radiologist
        Dr Thompson (Exhibit 227) which included the following:

              "In the chest there is a 2 - 3 cm mass located in the anterior
              portion of the right upper lobe.
              In addition, there is a right hilar lymphadenopathy and
              extensive mediastinal lymphadenopathy. A large lymph node
              mass is present in the retrocaval/pretracheal location and nodal
              disease extends up almost to the level of the sternal notch.
              There are contra lateral nodes and subcarinal nodes also.

              Both axillae are clear.




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              The lung windows show two small nodules in the right lung, the
              most anterior of which is quite dense and may well be calcified.
              The other lesion is not necessarily a metastisis and has a rather
              teardrop shape on one scan. Otherwise the lungs are clear.
              Below the diaphragm the spleen is noted to be significantly
              enlarged and contains a 4 cm low density focus in its posterior
              aspect. The liver appears normal but is not seen in its entirety.
              There are some tiny nodes in a retro pancreatic location and
              small retro peritoneal nodes are seen around the aorta and vena
              cava at the level of the renal hilar.
              Conclusion:

              There is evidence of an extensive neoplastic process. The mass
              at the lung and adjacent mediastinal lymphadenopathy suggests
              a lung primary but the large spleen and low density lesion in
              that organ, as well as the extensive abdominal
              lymphadenopathy, suggests lymphoma. Differential would also
              include widespread metastatic disease from some other primary
              such as a melanoma."

50           Later, in May 2001, Dr Peter Leaver of SKG Radiology reported to
        Dr Mincham upon a cranial CT scan conducted after a history of
        headaches lasting three weeks and vomiting. The findings of these axial
        brain scans (Part of Exhibit 84) were:

              "There are two mass lesions situated within the medial aspect of
              the right frontal lobe, associated with marked surrounding
              oedema. The largest lesion, at the level of the frontal horns,
              abuts the anterior falx. This measures 2.5 x 2 x 1.5 cm and
              demonstrates substantial mass affect, with effacement of the
              frontal horns and sub falcine herniation of the right frontal horn.
              Oedema extends into the left hemisphere via the corpus
              callosum. A second, smaller, 1 cm contrast enhancing nodule is
              present more inferomedially within the right frontal lobe.
              Again, this has substantial surrounding oedema and
              displacement of the midline towards the left. No further focal
              enhancing lesion is identified. The right lateral ventricle and
              the right sylvian fissure are generally effaced.




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              Conclusion:

              Two contrast enhancing masses in the right frontal lobe, as
              described, compatible with metastatic disease. Significant mass
              effect is identified in relation to both nodules."
51            In the investigations which were conducted which led to the
        diagnosis of Mr Cotton's lung cancer in May 2000 it was discovered that
        he showed positive symptoms for hepatitis C and for hepatitis B and this
        was reported on by Professor Musk following the consultation of 16 June
        2000. There was some enlargement of his liver but no evidence of hepatic
        fibrosis or other symptoms of liver disease. Doctor Kendall, in his reports
        of 13 October 2000 (Exhibits 67 and 69), reported that the hepatitis C
        infection was due to a blood-borne route of viral infection, probably due
        to a maternal infection which had been transmitted to him in utero. There
        was, therefore, the potentiality for a future liver disease had Mr Cotton not
        died of his lung tumour but there was no clear indication that this was
        imminent or inevitable. The prospect of future liver disease and potential
        for a shorter life expectancy or working life can therefore only be
        regarded as contingencies to be taken into effect in the event that damages
        are recoverable.
52           Similarly, Mr Cotton showed signs of chronic bronchitis and, in the
        extensive medical investigations conducted from May 2000, described
        producing approximately a quarter of a cup of white sputum per day. This
        was, apparently, associated with his long history of tobacco smoking.
        However both Dr Musk and Dr Kendall concluded that there was no
        reduction in lung capacity, that his spirometry tests were within the
        normal range, and that there was no emphysema. Dr Musk excluded any
        chronic obstructive airways disease (COAD). Nor had there been any
        symptoms of breathlessness recorded preceding the diagnosis of lung
        cancer in May 2000 which, it seems, was an entirely unexpected
        development.
53            Mr Cotton, in October 2000 when giving evidence to the
        Conciliation and Review Officer under the provisions of the Workers'
        Compensation Act (Exhibit 2), described (at 47) feeling ill in early 2000
        and, therefore, attending for a company medical examination under the
        auspices of the third defendant. In his words that investigation revealed a
        "big shadow on his lung" leading to the discovery of a cancerous mass in
        his lung and stomach for which he saw Dr Mitcham in Bunbury, Dr Tribe
        at the Sir Charles Gairdner Hospital in Perth and Dr Spinx. He



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        commenced chemotherapy under the direction of Dr Beer at SCGH and
        later by Dr Martin Buck in Bunbury.
54           He was admitted to Sir Charles Gairdner Hospital on 11 May 2000
        and, following the diagnosis, was told that he may only have about six
        months to live. Dr Musk later said that his condition at that time was that
        Mr Cotton had a large cell cancer in the upper lobe of the lung with no
        bony metastatic spread. Enlarged lymph nodes were discovered on
        12 May 2000 but at that point there had been no weight loss. This was a
        Stage IV lung cancer which had spread to the lung and to the abdomen.
        He was placed on chemotherapy and completed three courses of that
        treatment lasting until February 2001 under the supervision of Dr Martin
        Buck who saw him first on 15 September 2000. That was the full course
        of chemotherapy treatment but by 6 July 2001 he had developed brain
        metastases which eventually led to seizures and loss of control.

55           As earlier noted, Mr Cotton died on 6 January 2002 then aged
        45 years. Professor Musk and the other specialist physicians and
        oncologists regarded him as being very young to develop lung cancer and,
        indeed, as being at the lower limit of the reported ranges for the incidence
        of that disease which, while common with chronic smokers, usually did
        not present until their fifties or sixties. Mr Cotton's death certificate
        (Exhibits 32 and 222(5)) shows that the attributed cause of death was
        carcinoma of the lung (squamous cell) (21 months), smoking, asbestos
        exposure (20 years), (contributory causes) cellulitis, hepatitis C and
        nominates the certifying medical practitioner as Dr P Terren, from whom,
        however, no evidence was adduced at the trial.
56           After the initial diagnosis, Mr Cotton was referred to Professor
        A W Musk, head of the Department of Respiratory Medicine at SCGH. In
        a report of 16 June 2000 (Exhibit 56), Professor Musk described the
        presentation as follows:

              "He told me that a routine chest X-ray taken because of his
              work at Millennium Chemicals in Bunbury on the 28th April
              was abnormal, showing a mass in the right upper lobe. He was
              referred by Dr Minchin to the Sir Charles Gairdner Hospital for
              investigation. CT of his chest on 12 May 2000 confirmed a
              mass with extensive mediastinal lymphadenopathy in addition
              to extensive abdominal lymphadenopathy.           Fine needle
              aspiration of the right upper lobe mass on the 16th May 2000
              under CT guidance revealed non small cell carcinoma with
              features of squamous cell carcinoma. A bone scan on the 11th


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              May showed no evidence of metastases. He has commenced on
              chemotherapy with Gemcitabine and Cisplatinum for Stage 4
              non small cell bronchiogenic carcinoma on 22nd May 2000.

              In the past he has been found to be suffering from hepatic
              cirrhosis due to hepatitis C on liver biopsy in November 1999.
              This was attributed to a blood transfusion given to his mother
              before he was born. He has also suffered from arthritis in his
              right wrist since a fracture of his scaphoid at the age of 17. He
              had a lipoma removed from his thigh in January 2000.

              He said that he smoked about 15 cigarettes a day from the age
              of 16 to 43 years, stopping two months ago when he became
              unwell.
              His mother died at the age of 68 from cirrhosis and
              hepato-cellular carcinoma. His father died at the age of 51 from
              bowel cancer. He has a sister and a brother in their early fifties
              who are well. He has daughters aged 15, 13, 11 and 4 who are
              all well ... He says he can still keep up with others of his own
              age when walking and still plays basketball with his children.
              His weight has been steady. He usually has a cough productive
              of about a quarter of a cup of white sputum. There has been no
              haemoptysis. He had some pains across the front of his chest
              prior to commencing on chemotherapy here recently but these
              have improved.
              On examination he appeared heavily built. His pulse was 80
              per minute and regular and blood pressure 120/70 mm Hg. His
              heart sounded normal. There was no lymphadenopathy or
              clubbing. His chest sounded clear.

              His FEV1/FVC today was 3.9/5.3 litres (predicted 4.1/5.0).
              ... His prognosis for survival is about three to six months."

57           Later in October 2000 the solicitors for each of the second defendant
        and the third defendant arranged for Mr Cotton to be examined on their
        behalf by Dr Peter Kendall FRACP, FCC P a consultant physician and
                                               r
        specialist in respiratory medicine. D Kendall reported to the solicitors
        for those defendants separately on 13 October (Exhibits 67 and 69).
        While the two reports are not identical they nevertheless reveal
        Dr Kendall's conclusions. Mr Cotton was seen by Dr Kendall on
        13 October 2000 and at the time Dr Kendall had a copy of the report of


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        Professor Musk of 16 June 2000 already mentioned (Exhibit 56).
        Dr Kendall obtained a history of a fairly normal childhood and of
        Mr Cotton smoking from the age of 17, continuing until recent times with
        an average of about 12 cigarettes a day over those years which,
        Dr Kendall calculated as 12 - 14 pack years. Dr Kendall noted that a
        similar calculation based on a slightly higher incidence of smoking
        described to Dr Musk would produce a calculation of 20 pack years of
        smoking. Cotton had reported a smoker's cough for about five years and
        Dr Kendall noted that his father also smoked, although Mr Cotton denied
        any significant side stream smoke from his father when he was a boy.
58                                   s
             Dr Kendall recorded a being important, the history of hepatitis C
        and cirrhosis of the liver and referred to a liver biopsy having been done
        recently by Dr Martin Reeve in Bunbury before going on to observe:
              "There seems little doubt that he has had asbestos exposure
              whilst working for the South Australian Engineering and Water
              Supply over a period of two years. There is also little doubt that
              he has had some exposure to asbestos while working for
              Millennium Chemicals in the Bunbury region.

              He has been a little short of breath for about a month and was
              feeling quite tired and lethargic at the point when he had a 10
              year medical at work including a chest X-ray. This is when the
              lung cancer was diagnosed earlier this year. He tells me he has
              been having chemotherapy since May and the second-hand
              report from his Oncologist describes a 50% reduction in the size
              of the cancer in his chest and in his abdomen.
              On physical examination he was pale and sallow, chest and
              heart examinations were normal. He has an enlarged liver,
              particularly the left lobe of the liver and he has signs of
              cirrhosis, including many spider naevi."

        The contents of the two reports of Dr Kendall (Exhibits 67 and 69) then
        diverge slightly but, paraphrasing the two, the following points and
        opinions emerge:
              •       There is no doubt that Cotton has lung cancer and that it
                      may be related to asbestos.
              •       His is a well-advanced cancer, being inoperable and
                      therefore not easily curable. It was, however, at that time
                      responding to chemotherapy to some extent.


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              •       At the time he was totally and permanently disabled by
                      his condition.
              •       Although Dr Kendall had not seen the X-rays, Mr Cotton
                      does not appear to have asbestosis or asbestos-related
                      pleural plaques. In Dr Kendall's opinion it was possible
                      to say that lung cancer is caused by exposure to asbestos
                      in the absence of asbestosis or asbestos-related pleural
                      plaques.
        The solicitors for each of the second defendants asked, in slightly
        different ways, for Dr Kendall's opinion about the cause of Mr Cotton's
        cancer. The two explanations which were given, because of the difference
        phraseology in the questions, are to be found respectively in Exhibits 67
        and 69 as follows:
              Exhibit 67:

              "In relation to the cause of Mr Cotton's lung cancer, the
              literature repeatedly supports the notion of a straight line dose
              response curve between cigarette exposure and lung cancer and
              so there is no doubt that his smoking has contributed to his lung
              cancer. By the same token of course with a relatively low
              consumption of cigarettes, it is relatively speaking much less
              likely that he would have developed a lung cancer from
              smoking. In clinical experience it is unusual to see lung cancer
              with an exposure of less than 20 pack years. Again from the
              literature, the risk of developing lung cancer in smokers is much
              higher than the risk of developing lung cancer in people who are
              exposed to asbestos. Furthermore, when one is exposed to both
              noxious stimuli the risk of developing lung cancer is multiplied
              not added."
        And, in Exhibit 69 to the question posed by the solicitors for the second
        defendant, Dr Kendall wrote:
              "In relation to question seven I do not think this is a simple
              problem and I cannot say whether or not his lung cancer is due
              to smoking or inhalation of asbestos products or some other
              cause. Rather I think it is a combination of all three. He has a
              significant risk of developing lung cancer from cigarette
              smoking but his total intake of cigarettes is rather small and
              clinical experience shows that it is unusual to develop a lung
              cancer with less than 20 pack years of cigarette exposure. We


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              certainly see people with lung cancer from very small amounts
              of asbestos exposure. My further postulation is that his immune
              system is probably not normal because of chronic Hepatitis C
              and possibly because he has worked in conditions of low level
              background of ionising radiation. I stress that these last points
              are speculative."
        The allusion to ionising radiation is explained in Exhibit 67 where
        Dr Kendall observed that the work site at Millennium Chemicals was
        associated with a low level of ionising radiation and that this may have
        acted as a catalyst in the development of the lung cancer. Finally, in
        addressing a question about the period of latency before the emergence of
        detectible signs of the disease, Dr Kendall wrote that experience
        demonstrated that a longer latency period is usual, commonly of the order
        of 20 years, but because of the possible factors of immuno suppression
        due to hepatitis or the hypothosised ionising radiation, this may not be the
        case for this patient. Again, with reference to the time incidence of
        exposure to asbestos, Dr Kendall observed that it was more probable that
        the exposure 20 to 30 years before was more important than the exposure
        more recently but that he was not sure that that could be proved.
59           Following the diagnosis of the lung and abdominal cancer at SCGH
        in May 2000, Dr K B Shilkin of the hospital and university pathology
        services reported on Mr Cotton's case to Dr F Heyworth, the chairman of
        the Pneumoconiosis Medical Panel. His report (of 16 June 2000,
        Exhibit 81) followed an examination of nine cytology slides taken from
        bronchial washings and fine needle aspiration biopsy on 11 and 16 May.
        Dr Shilkin reported that the bronchial washings were unhelpful. Tumour
        material was present in the lung aspiration sample and was identifiable in
        both the smears and the cellblock sections. In the smears there were many
        small groups and individual tumour cells. He noticed these to have
        hyperchromatic and pleomorphic nuclei and variable amounts of harsh
        eosinophilic cytoplasm. He observed that these lie in a background of
        considerable necrosis. In the cell block sections there were small sheets
        of cells and groups of just a few cells as well as individual cells lying in a
        necrotic background. Although the cells were poorly differentiated there
        were features of squamous origin, including the appearance of the
        cytoplasm and some intercellular bridges in some areas. Dr Shilkin's
        conclusion was:

              "There is no lung tissue in the biopsy. There is no evidence to
              suggest malignant mesothelioma in this material.            The
              appearances here are of a poorly differentiated carcinoma of the


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              lung in keeping with poorly differentiated squamous cell
              carcinoma.
              In summary, in my opinion, the tumour here is poorly
              differentiated squamous cell carcinoma of the lung."
60           The oncologist, Dr Martin Buck, reported on 23 April 2001 that
        Mr Cotton had then just completed a combination of chemotherapy and
        radiation from a brochogenic carcinoma (Exhibit 82). He had recently
        had tests which indicated that the cancer was inactive but was having a
        brain scan in the near future for investigation of headaches and it was
        thought that the results of that brain scan would significantly affect the
        prognosis. Unfortunately, the CT scan demonstrated multiple cerebral
        metastases from the bronchial primary tumour causing the radiologist,
        Dr Cassidy, to report on 18 June 2001 (Exhibit 83) that the median
        survival following this diagnosis was in the region of three to four
        months.
61           This development was also reported by the general practitioner
        Dr G Mincham on 28 June 2001 (Exhibit 84), who said that the CAT scan
        revealed two cerebral secondaries. As a result, Mr Cotton was referred to
        Dr Cassidy for palliative radiotherapy which caused a cessation in the
        headache and vomiting. Regrettably, the clinical course was complicated
        by the development of grand mal seizures related to the cerebral
        pathology. These were treated with Dilantin and brought under control.
        Dr Mincham ventured the opinion that the prognosis, in the light of these
        developments, was probably a term of three to six months.

62           While living in Bunbury Mr Cotton attended Dr Mincham as his
        general medical practitioner for the usual range of minor medical
        disorders and illnesses. Dr Mincham's notes for the latter part of 1992
        reveal a consultation with Mr Cotton on 31 August 1992 for upper
        respiratory tract infection, sinusitis, cough and a throat inflamed. He was
        prescribed appropriate medication and advised to stop smoking. The
        defendants each rely upon this warning to cease smoking as part of their
        cases alleging contributory negligence.
Deceased's smoking history - effects of cigarette smoking
63           Ascertaining the duration and extent of Steven Cotton's cigarette
        smoking can only be an exercise in estimation and approximation. When
        giving evidence to the Workers' Compensation Review Directorate on
        16 October 2000, after the cancer diagnosis, Mr Cotton said that he started
        smoking when he was 17 and gave up in May 2000 when his lung cancer

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        was diagnosed - Exhibit 2, p 57. However, Professor Musk reported that
        the history he took from Mr Cotton included a statement that he had been
        smoking from the age of 15 years.

64           Despite the statements by Mr Cotton that he quit smoking upon the
        diagnosis of lung cancer, the plaintiff said in evidence that even after the
        diagnosis he smoked occasionally and at intervals. This seems to be a
        demonstration of an addiction to cigarettes which by then had been well
        entrenched rather than any sign of irresponsibility or fatalism because,
        when describing the effects of addiction, Professor Christie mentioned
        that it is a characteristic of addictive behaviour for chronic smokers to
        continue or resume smoking after a major adverse health diagnosis such
        as cancer or heart attack which was smoking-related. There is no
        suggestion that this post diagnosis smoking was anything other than minor
        and occasional or that it affected or accelerated the inevitable
        consequences of the established disease.
65            Other differences about the level of smoking exist in the evidence.
        The plaintiff described Mr Cotton as smoking a 30 cigarette pack of
        cigarettes every two days. In Exhibit 57, the clinical notes taken at Sir
        Charles Gairdner Hospital in May 2000, the level of smoking was
        recorded as 20 per day and Mr Cotton had also said when giving evidence
        at the Workcover hearing that he smoked on average 15 cigarettes a day.
        On this basis, therefore, I consider that I should conclude that by the time
        of the diagnosis of his cancer in May 2000 Mr Steven Cotton had been
        smoking regularly for at least 26 years (that is from the age of 17) and
        quite possibly for a year or two longer. No exact finding about the
        quantity or average rate of consumption is possible but the probabilities
        are that he was smoking, on average somewhere between 15 and 20
        cigarettes a day, and that his own estimate of about half a packet of
        cigarettes a day is the best estimate which can be reached, subject to a
        recognition that it is improbable that it was less than that and that there is
        a need to recognise that it may have been slightly greater.

Varieties of asbestos
66           There are varieties of asbestos mineralisation. Blue asbestos is
        known as Crocidolite and brown asbestos is known as Amosite. Both
        these forms of asbestos are known as amphiboles and are regarded as
        more noxious than other varieties. White asbestos is known as Chrysotile
        and is sometimes known as Serpentinite but is not an amphibole.




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67           In his report (Exhibit 245) Mr Alan Rogers, who has studied and
        written extensively as an occupational hygienist about asbestos lung
        disease, wrote:

              "Asbestos is a general term given to a series of naturally
              occurring fibrous minerals. These fibrous minerals are sourced
              mainly from two rock types. Serpentine rock when found in its
              fibrous form produces the commercial mineral called Chrysotile
              (commonly called white asbestos). Chrysotile accounts for the
              majority (more than 95%) of commercial asbestos production.
              Amphibole rock when fibrised produces a variety of asbestos
              forms depending on the elemental composition of the rock.
              Historically the main commercial types of Amphibole asbestos
              are Crocidolite (blue asbestos) and Amosite (brown/grey
              asbestos). Another fibrous Amphibole called Anthophyllite was
              mined in smaller quantities and fibrous Tremolite as well as
              Anthopyllite is commonly found in non-commercial quantities
              and often as a mineral contaminant throughout many geological
              regions.

              The various forms of asbestos (Chrysotile, Crocidolite,
              Amosite, Anthophyllite and Tremolite) have differing chemical
              and physical properties and hence have different industrial uses.
              The various asbestos types also exhibit differing toxicological
              potencies and have different potential to cause diseases such as
              mesothelioma, lung cancer and asbestos."

68          The chemical formulae for these different varieties of asbestos is
        found in Exhibit 80(1) and they are:
              •       Chrysotile (Mg6 Si4 O10 (OH)8)
              •       Amosite (Fe+++, Mg)7 Si8 O22 (OH)2)
              •       Crocidolite Ma2 (Fe++, Mg)3 Fe+++2 Si8 O22 (OH)2
              •       Anthophyllite (Mg, Fe++)7 Si8 O22 (OH)2
69           A specification for laying asbestos cement pipes below ground was
        published by the EWSD of South Australia in October 1959 (Exhibit 89).
        This confirmed that the fibrolite pipes then in use were manufactured by
        James Hardie & Coy Ltd, at that time at factories in Melbourne and
        Sydney, and were made in various sizes including the four inch diameter
        variety, as described by Mr Cotton. The pipes had a nominal length of
        13 feet or 406 pipes per mile and the 4 inch pipes weighed 0.75 cwt per


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        pipe and came in batches of 220 pipes per load. The trenches were to be
        excavated to a depth sufficient to ensure two feet of clear cover above the
        laid pipe. Four inch pipes were to be laid by hand and the homing of
        pipes effected by crowbar against a wooden block. Smaller pipes were to
        be cut by the use of a hacksaw and larger pipes were to be cut with a
        special cutting tool manufactured by Sassafras Workshops. A laying gang
        was composed of 12 men and it was expected that such a gang would lay
        pipes at the rate of one mile per week, except where rocky conditions
        were encountered when that rate may be reduced by up to one half.

70           Later, an EWSD Construction Branch Newsletter published in 1973
        (Exhibit 90) described the installation of a much larger diameter asbestos
        cement pipe in the country area of South Australia (Christie Creek pipe
        culvert) but referred to the pipes being manufactured by James Hardie &
        Coy Pty Ltd at Elizabeth in South Australia (Exhibit 90). "Hardie's
        Textbook Pipeline Design 1981" (Exhibit 93) described the development
        by some of the leading Australian water authorities of the use of asbestos
        cement pipes for water reticulation and described the composition of the
        pipes as being cement fibre and silica. The fibre was "asbestos" which
        contributes to the mechanical properties of the pipe - tested for fibre
        length, diameter and surface area to determine its effect on the quality of
        the finished pipe. The asbestos materials were silicates of magnesium,
        sodium and iron broken into silk-like fibres of great tensile strength. "The
        fibres are chemically inert, resistant to all common acids and alkalis and
        being poor conductors of heat, are good thermal insulators".

71           Counsel for the first defendant, in her final written submissions,
        par 13, submits that the pipes used in Adelaide at the material time
                      o
        contained up t 15 per cent of asbestos fibre and that the asbestos was
        mainly Chrysotile with some Amosite which was there to add strength to
        the pipes. Her implication is that this comes from the evidence of
        Mr Neagle at t/s 260, but that is not confirmed by the transcript. This
        percentage of asbestos is less than the 20 per cent referred to in James
        Hardie's own literature (Exhibit 94) and the 1975 Australian Standards
        which I have earlier quoted.

72           The evidence of Mr M H Kottek (t/s 733) was to the effect that, from
        his studies and experience, asbestos cement water pipes from the 1970's
        era almost always contained a mixture of Amosite and Chrysotile. The
        report of Dr de Klerk (Exhibit 74(1)) in par 5 stated that the type of
        asbestos in the pipes is likely to have been a mixed type and, at t/s 758,
        Dr de Klerk explained that the pipes probably contained Amosite and
        Chrysotile and probably a little bit of Crocidolite as well. Mrs Sowden, in


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        cross-examination at t/s 1110, said that to the best of her knowledge
        Hardie's asbestos cement types of that era always contained Amosite and
        Chrysotile and said further, at t/s 1112, that she had assumed that the
        asbestos content would have been about 15 per cent and that this was
        typical - 10 - 15 per cent asbestos was a typical concentration of the
        asbestos in AC types and that she knew that James Hardie pipes in the late
        1970's contained Amosite and Chrysotile.               Again, at t/s 1121,
        Mrs Sowden said that she did not think that it was possible that the James
        Hardie pipes contained only Chrysotile and that she thought they always
        contained amphibole as well. Exhibit 157 indicates that the asbestos fibre
        content of these pipes is in the range of between 13.42 per cent and
        14.92 per cent pure asbestos but the origins and original purpose of that
        document were never clearly established. At t/s 1287, in the course of
        cross-examination of Mr G Pickford, the witness said that the asbestos
        cement content of the water pipes consisted of between 8 per cent and
        15 per cent of asbestos fibres. Mr Pickford doubted that any of the
        asbestos pipes contained Crocidolite which was known to be about five or
        ten times dustier in terms of airborne asbestos fibre generation than plain
        Chrysotile - t/s 1293. Finally, in Exhibit 94, a safety memorandum issued
        by the first defendant on 7 August 1979, stated that the asbestos cement
        types which the first defendant produced contained less than 20 per cent
        asbestos fibre.

73            In a report to the second defendant in October 1957 (Exhibit 117)
        there is a brief reference to the effect of these varieties of asbestos in
        relation to asbestosis. At page 4 of that report the author observes that the
        variety of asbestos known as Serpentine, which has small, short fibres is
        comparatively harmless compared with the variety known as amphibole
        (Crocidolite, Amosite and Tremolite) whose fibres are long, and which
        are considered more dangerous.            Those observations were made
        specifically with regard to the cause of asbestosis - a form of pulmonary
        fibrosis due to the blocking of the finer bronchioles by relatively long
        fibres of asbestos (20 micrograms - 250 micrograms) which also appear to
        irritate the bronchial wall and cause fibrosis.

74           As early as 1968 Dr McCullagh, the medical officer for James
        Hardie & Coy Pty Ltd, wrote to the manager of the second defendant in
        Adelaide enclosing a copy of the report which he had prepared following
        a visit to Canada, the United Kingdom and Germany to study the
        biological effects of asbestos (Exhibit 120). That report recognised the
        possibility that Chrysotile was causative of mesothelioma which was then
        under investigation and that lung cancer attributable to asbestos exposure
        may occur in the absence of asbestosis. It also recorded demonstrations

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        that cigarette smoking greatly increased the likelihood of lung cancer in
        the asbestos exposed. In a report written in 1965 the same Dr McCullagh
        summarised the biological effects of asbestosis, following an examination
        of the annals of the New York Academy of Sciences of 1965. In that
        document he recorded that asbestos fibres produced in Australia were
        Crocidolites from Western Australia and a little Chrysotile from New
        South Wales. Chrysotile was used in asbestos cement and other products
        and Crocidolite was also used to make asbestos cement (page 1). At
        par 25 he noted that Amosite and Crocidolite were then held to be the
        most dangerous asbestos forms of carcinogens but it was doubtful whether
        Chrysotile alone was a carcinogen but that, in combination with smoking,
        Chrysotile may more readily cause cancer. Furthermore, in a confidential
        inter-house memorandum of James Hardie of 24 January 1968,
        Dr McCullagh drew attention to then recently published figures
        suggesting a greatly increased risk of fatal lung cancer from the
        combination of exposure to asbestos dust and cigarette smoking - a
        combination said to increase the risk of dying from lung cancer by a factor
        of some 90 times (Exhibit 139). As stated, Chrysotile is sometimes
        referred to as white asbestos, Amosite is brown or grey asbestos and
        Crocidolite is blue asbestos. This is the nomenclature adopted by
        Matprolabs in its survey for the third defendant of the presence of
        asbestos in the BDR shed at the SCM Bunbury plant in March 1990
        (Exhibit 44).
75            This classification also appears in the report to the Asbestos
        Advisory Committee to the Minister of Labour in New Zealand of 1991
        (Exhibit 60) where, at p 12, the Committee reported that asbestos is not a
        single chemical or geological entity but a term used to describe naturally
        occurring fibrous hydrated silicates. According to the Committee there
        are six common varieties, as shown below:

                                            Asbestos
              Serpentine Group ____________________ Amphibole Group

              Chrysotile (White)                                Actinolite
                                                                Tremolite
                                                             Anthophyllite
                                                         Amosite (Brown)
                                                         Crocidolite (Blue)
        The fibres of Amosite and Crocidolite are straight, needle-like structures
        which may split longitudinally to produce very fine fibrils. By contrast,


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        Chrysotile fibres tend to be longer, softer and curlier. This is important
        from the viewpoint of lung dynamics as this property has the effect of
        increasing their diameter and making it less likely that they will reach the
        smaller airways.
76           In this case none of the parties sought to place any great emphasis on
        the presence or absence of a particular variety of asbestos occurring in the
        two working environments in which Mr Cotton operated. Nevertheless, it
        is perhaps desirable that I record the findings, so far as they are possible,
        on the evidence which was adduced.

Composition of asbestos in water pipes
77           There was little in the way of identification of the variety of asbestos
        present in the asbestos cement pipes supplied by the second defendant for
        the first defendant for use in the water and sewerage reticulation
        programme in which Mr Cotton participated with the EWSD. However,
        the publications of the time (Exhibits 41 and 74) showed that the asbestos
        cement pipe then in use contained up to 20 per cent of asbestos fibres
        mixed in combination with Portland cement and silica. The Australian
        AIS Standard 1975 (Exhibit 91) described that content and Exhibit 92
        referred to the forms of asbestos then used for this purpose as being
        asbestos silicates of magnesium, sodium and iron. In combination with
        the writings of Dr McCullagh it seems probable, therefore, that the
        asbestos cement pipe used by the EWSD while Mr Cotton was working in
        its Adelaide operations included a variety of forms of asbestos, including
        Amosite, Chrysotile and Crocidolite.

78           In these circumstances I consider that the plaintiff has established, on
        the probabilities, that all the pipes produced by the second defendant and
        used by the first defendant for its water laying operations in and around
        Adelaide at the time Mr Cotton was employed by the EWSD contained
        mixed asbestos fibres making up between 15 per cent and 20 per cent of
        the entire composition of the asbestos cement product. The asbestos
        content was mixed and definitely included Chrysotile and Amosite and,
        probably, some Crocidolite.
Composition of asbestos at the third defendant's premises at Australind
79           There is more detailed and reliable scientific information in evidence
        about the content of the asbestos at the various locations at the third
        defendant's operations at Australind. Exhibit 44, the Matprolab's report,
        reveals that Chrysotile, Amosite and Crocidolite were found on analysis
        from samples of that site in March 1990 and samples taken from the BDR


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        shed were found to contain Amosite and Chrysotile. Similar analysis
        conducted in April 1995 of samples taken within the BDR (Exhibit 52)
        reported the presence of Chrysotile and Crocidolite. Samples taken from
        the microniser area in August 1995 were shown to contain Amosite,
        Tremolite, Actinolite and Chrysotile (see Exhibit 100) and an analysis of
        air samples from the Australind plant, reported on by Matprolabs
        (Exhibit 247), also revealed the presence of Amosite.

80           Essentially, there were three main sources of asbestos: the lagging
        over the steam pipes and other heating pipes within the BDR and
        elsewhere on the premises; second, the asbestos within the insulation in
        the lagging or seals within the doors to the band drier machine itself and
        in the seals around those doors; and third, the asbestos in the asbestos
        cement sheeting on the roofs of various buildings in the premises and in
        cladding and external and internal walls or divisions within those
        buildings.
81            There is in evidence a series of analysis reports of samples of
        asbestos taken from various places and at various times on the Australind
        site. These are detailed in the Matprolab reports (Exhibits 45, 52 and 113)
        and in subsequent testing of air sampling at the Australind premises over
        extended periods during the asbestos removal programmes. There is also
        the evidence of the workman, Mr Savage, who, more than 30 years ago
        was actually involved in mixing up the lagging which was placed around
        the steam and heating pipes and in applying that insulation to them. He
        described the lagging being mixed from blue asbestos which we know to
        be Crocidolite. The Matprolab report (Exhibit 44) confirms the existence
        of Chrysotile, Amosite and Crocidolite at Australind. Within the BDR
        there was Amosite and Chrysotile and some Crocidolite, the details of
        which are described later in these reasons where the Matprolab reports are
        addressed. It is reasonably clear that, lagging on the heating pipes aside,
        the greater proportion of the asbestos in and around the BDR and
        elsewhere on the Australind site was probably Chrysotile but with small
        amounts of Amosite and Crocidolite.
Asbestos - complete carcinogen or promoter
82           On the controversy of whether asbestos could be a "complete
        carcinogen" or a "promoter" there was a division of opinion among the
        consultants.    Professor Musk and Professor Berry were each
        unequivocally of the view that asbestos could operate as a complete
        carcinogen, that is, to be a sole cause and initiator of lung cancer,
        notwithstanding that the carcinogenesis was not exactly understood


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        scientifically. Professor Fox also seems to have been of the view that
        asbestos could be a complete carcinogen in the sense that it was capable
        of producing lung cancer without the presence or interaction of another
        carcinogen. The difference in Professor Fox's approach, however, was
        that he, unlike the other consultants, believed that any particular lung
        cancer could not be regarded as due to asbestos exposure unless it was
        accompanied by asbestosis. This seems to imply that Professor Fox was
        of the view that the asbestos exposure which produced this fibrosis was
        part, perhaps a preliminary part, of the development of the accompanying
        tumour and that it therefore required the same degree of heavy cumulative
        exposure to asbestos as believed to cause asbestosis.

83            By contrast, Professor de Klerk who, incidentally, rejected the theory
        that asbestosis must be present before a diagnosis of asbestos-induced
        lung cancer could be made, referred to asbestos acting as a promoter,
        rather than as a complete carcinogen, although nothing in his evidence
        suggests that asbestos was incapable of producing the lung cancer in the
        absence of a different carcinogen. It is important to examine the context
        in which Professor de Klerk was addressing these issues because the
        answers which he gave were when addressing the suggestion that, in
        Mr Cotton's case, the latency period was too short to allow asbestos to be
        treated as the cause of his lung cancer. The substance of Professor
        de Klerk's answers to these questions was to the effect that asbestos could
        act at an intermediate or late stage of the multi-stage process of cell
        mutation and so confound the theory of latency, particularly for a man
        who had experienced an earlier discrete period of asbestos exposure.
84            In the light of this evidence I have concluded that in the industrial
        setting where workers are exposed over time to the risk of inhalation of
        asbestos dusts, asbestos should be regarded as being a complete
        carcinogen. That is, in other words, exposure to asbestos alone in those
        circumstances is capable of initiating alone a process of carcinogenesis
        which can lead to the development of a fatal tumour. However, the effect
        of asbestos in this setting should not be confined to that of a sole and
        complete carcinogen because I am satisfied, from the opinions of
        Professors Musk, Berry and de Klerk, together with the scientific
        literature which is reviewed elsewhere in these reasons, that asbestos can
        certainly act in combination with another or other carcinogens such as
        tobacco to magnify and even accelerate the process of carcinogenesis, and
        that it can have this effect even if the carcinogenic process has already
        been initiated by some independent factor. In other words, asbestos in
        such circumstances is capable of, and often does, act both as a complete


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        carcinogen and as a promoter as well as aggravating the effects of other
        carcinogens to which the worker may also be exposed.
Lung cancer - divisible or indivisible disease
85           The notion of a "divisible disease" is important when considering
        attempts to prove the cause or causes of the disease. An "indivisible
        disease" is regarded as one which has only one initiating cause or
        precipitant, so that if contracted further exposure to that or other causes
        will not increase or accelerate the progress of the disease. In cases of
        indivisible disease, where there is the possibility of multiple originating
        causes it will not be sufficient to assert that one of the causal elements
        probably caused the disease in the case in hand unless, on the
        probabilities, the likelihood of any one of the other potential causes being
        the sole and effective cause can be rejected. With a divisible disease,
        however, the condition, if initiated by one cause can be aggravated or
        accelerated by further exposure to that same cause or by other potential
        causative factors, or it may be the case that one or more potential
        causative factors acting together in combination produces or accelerates
        the progress of the disease. In Seltsam Pty Ltd v Ghaleb [2005] NSWCA
        208; (2005) 3 DDCR 1, Ipp JA said at [32] and [33]:
              "[32] The essence of the term 'divisible disease' is that it
              connotes a disease that increases in severity through an ongoing
              process of successive events that inflict harm on the victim.
              Each infliction of harm is separate and independent of the harm
              that has gone before.

              [33] A well-known example of a divisible disease is a hearing
              impediment caused by exposure to excessive noise over a
              lengthy, continuous period where each successive exposure to
              noise separately increases the hearing loss."
        In that case the NSW Court of Appeal was considering a claim by a
        worker for relief from alleged negligently caused asbestos-related pleural
        disease (ARPD). The case proceeded on the basis that ARPD is a
        divisible disease and was treated on that basis by the Court of Appeal,
        leading Ipp JA at [34] to observe:
              "[34] In the case of ARPD, the disease is the consequence of
              inhaling asbestos fibre in circumstances where each successive
              inhalation of asbestos inflicts a further and separate form of
              harm on the victim. As each infliction of harm is an
              independent event, where ARPD has accumulatively been


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              brought about by different tortfeasors over different periods,
              each tortfeasor is separately liable for the separate damage each
              has caused. Such tortfeasors are not jointly, concurrently or
              severally liable to the victim. The damage for which each is
              liable has to be separately proved and separately assessed."

        The contrast between such a disease and an indivisible disease is that
        multiple causative factors in the case of the divisible disease all conduce,
        in combination, to the aggregate harm suffered by the claimant so that the
        situation is one of multiple concurrent and cumulative causes all acting
        together to enhance the progress of the harm so that, if breach of duty or
        negligence is proved, each of the tortfeasors is liable for the ascertainable
        damage caused by its conduct.
86           This approach has been adopted and developed in the United
        Kingdom where it has been subject to detailed analysis in the decision of
        the House of Lords in Wilsher v Essex Area Health Authority [1988] AC
        1074.

87           In the present case comparatively little attention was given in the
        evidence to whether or not Mr Cotton's lung cancer was a divisible or
        indivisible disease. However, at various points in the evidence (t/s 114,
        978, 1551, 1727 and 1728) counsel for the second defendant objected to
        certain evidence which was proposed to be led on the basis that the
        plaintiff did not contend (so the second defendant submitted) that this lung
        cancer was a divisible disease and that, consequently, the approach which
        should be taken to the evidence was, and so he submitted, that only
        evidence suggesting the disease was solely caused by one tortfeasor was
        relevant and evidence, in the form of opinions from experts, about the
        degrees of contribution towards the disease caused by the two periods of
        exposure to asbestos were not relevant. While recognising that this would
        be the consequence if the disease were, in fact, indivisible, I nevertheless
        allowed the evidence to be taken, subject to the objection, as it was not at
        that point certain whether or not there was any consensus about whether
        the disease was divisible or indivisible or whether or not, as the plaintiff
        seemed to be contending, there were concurrent multiple causes involved
        in the alleged breaches of duty by the defendants.
88            However, it is difficult to square this contention by the second
        defendant with the underlying proposition, emerging from the evidence of
        all the consultants, and indeed formulating the basis of all defendants'
        defences, to the effect that insufficient aggregate exposure to asbestos had
        been established by the plaintiff to justify any conclusion that it was
        causative by his lung disease, and that the risks of contracting lung cancer,

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        or indeed other forms of asbestos lung disease, are dose related. Perhaps
        an explanation may be that the risk of suffering a single and sole initiating
        causative event increases in proportion to the aggregate dose/time
        exposure to asbestos while remaining singular and indivisible. On the
        other hand, the concept of increasing aggregate dose over time suggests
        that the many instances of separate exposures act in combination to
        initiate the disease even if subsequent exposures do not aggravate or
        accelerate it. In the present case all the expert opinion accepted that there
        was an enhanced risk of developing lung cancer if one was a person
        exposed to asbestos who was also a chronic smoker and that the
        enhancement of the risk was more than additive being multiplicative. I do
        not see any basis for concluding otherwise than that the smoking and the
        asbestos exposure acting in combination have a greater effect than either
        carcinogen singularly in causing the onset and development of the disease.

89            It is perhaps important to be more specific about the concepts of
        indivisibility and divisibility when related to the lung cancer in this
        particular case because, putting to one side the possibility of some
        unrecognised and unidentifiable cause for this tumour, the attention at this
        trial was devoted to three potential factors as being responsible for
        Mr Cotton's lung cancer, either alone or in combination: first, the
        asbestos exposure in the course of his employment in Adelaide with the
        first defendant; second, the asbestos exposure in the course of his
        employment with the third defendant at Bunbury and, third, the chronic
        smoking which had originated in about 1973, or thereabouts, and which
        coincided with and exceeded each period of exposure to asbestos. On the
        evidence it could not be said that either the asbestos exposure or the
        tobacco smoking was indivisible as the cause of Mr Cotton's lung cancer,
        but I understand the defendants to be contending that separate periods of
        exposure to asbestos at Adelaide and at Bunbury were entirely indivisible.
        I am not satisfied, however, that the plaintiff ever accepted or conceded
        that point, although counsel for the defendants suggested that he had. I
        understand the position of counsel for the plaintiff to have been, at all
        times, that he contended that lung cancer was a divisible disease in the
        sense that a single sole or isolated cause, discrete from any other
        concurrent or aggravating cause, did not exist and that multiple and/or
        cumulative factors had caused Mr Cotton's fatal illness.
90          The significance of this distinction for present purposes has recently
        conveniently been explained In the Matter of TNN Limited & Ors and In
        the Matter of the Companies Act 1985 [2006] EWHC 1447 (Ch). A
        Chancery Division decision of the English High Court would be an
        unexpected source of authority on a matter concerning tortious liability

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        for asbestos-induced lung disease, but this case was an application by
        administrators of several companies which faced large contingent
        liabilities for damages or compensation to former employees for
        asbestos-induced disease. In the course of his judgment, Richards J
        observed at [64] - [65]:

              "[64] Asbestos related diseases may be divided between the
              malignant and the non-malignant. Non-malignant conditions,
              such as asbestosis and pleural thickening, are the result of a
              cumulative exposure to asbestos. Where a claimant with such a
              condition has been exposed to asbestos by more than one
              employer, liability is divided between each employer and the
              employee has a separate claim against each employer for its
              share of the loss. In respect of these divisible diseases, no
              claims for contribution between employers can arise.

              [65] In contrast, malignant diseases, such as mesothelioma and
              lung cancer, may result from a single exposure to asbestos. In
              the present state of scientific knowledge, it is impossible for a
              claimant to establish which of a number of employers is
              responsible for the exposure which caused the disease. In these
              circumstances, the House of Lords held in Fairchild v
              Glenhaven Funeral Service Ltd [2003] 1 AC 32 that, rather than
              the claim failing due to an inability to prove causation against
              any particular employer, the claimant was entitled to claim
              damages against all or any of the employers who had exposed
              him to asbestos, and had materially increased the risk of
              contracting the disease. Until the decision of the House of
              Lords in Barker v Corus (UK) Ltd [2006] 2 WLR 1027, it was
              widely thought, and the Court of Appeal in that case held, that
              the employee could obtain judgment for the full amount of his
              damages against any of the employers, who would then be
              entitled to make contribution claims against the other
              employers. The House of Lords reversed the decision of the
              Court of Appeal and held that the liability to pay damages to the
              claimant must be apportioned among the employers. There will
              not accordingly be contribution claims between employers
              where each employer has exposed an employee to asbestos if
              the exposure occurred on different occasions or over different
              periods of time. There remain circumstances in which
              contribution claims may be made, for example where T & N
              and another person are liable in respect of the same period or
              incident of exposure to asbestos. An example would be the case

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              in which T & N failed to provide adequate safety equipment to
              an employee who was working on the premises of another
              person who in turn failed to provide a safe work place or who
              was liable as occupier of a premises ... "
91           Barker v Corus (UK) Ltd [2006] UKHL 20; [2006] 2 WLR 1027
        was decided by the House of Lords after final submissions had been made
        in this case and, therefore, obviously was not addressed by counsel.
        However, I have received no application from any party that they wished
        to reopen this case, or make oral submissions and I have therefore
        proceeded on the basis of the submissions received.
92            Having regard to the evidence which is later examined in these
        reasons, I have reached the view that considerable care and reserve should
        be exercised before identifying a particular case of lung cancer, alleged to
        be due to asbestos exposure as being within the category of indivisible
        disease, despite the prevalence of the application of that distinction in the
        authorities. The principal reason for my view in this regard is the
        incomplete state of medical scientific knowledge about the details of the
        process of carcinogenesis in many types of asbestos related cancer. If the
        expert scientists and researchers are unable to explain how a particular
        cancer, or a particular type of cancer, resulted from asbestos exposure or
        from exposure to other carcinogens occurring simultaneously, it is very
        difficult to see how it can be established satisfactorily that that particular
        cancer had a single indivisible cause. However, so much depends upon
        the nature and circumstances of the individual disease and its presentation
        by the particular patient. In the case of mesothelioma where the tumour
        can be linked unequivocally solely to the effect of asbestos it may well be
        possible to establish that the disease was caused by one identifiable
        episode or period of exposure and, in such a case, the attribution of the
        description of indivisible disease would be justified. However, in other
        cases where the probable cause of the tumour is the cumulative effect of
        asbestos exposure, whether alone or in combination with other
        carcinogens, over time and where the preponderance of medical opinion is
        that it is the combined effect of those carcinogens working together over
        time which has initiated the incompletely understood mechanism of
        carcinogenesis, then it does not seem to me that that disease can properly
        be described as indivisible and that any breaches of duty by employers or
        others which constitute or contribute to the noxious effects of that
        exposure over the periods when it is probable that the cumulative process
        was occurring are each liable for the damages which result from the
        development of that disease. Quite possibly there may be complicated
        questions of contribution as between the parties whose conduct has led to

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        the exposure of the claimant to such carcinogens during the formative
        process of the tumour but no claims for contribution are being made in the
        present proceedings and it is therefore unnecessary, and perhaps
        undesirable, to attempt to address such issues in the abstract. It is enough,
        in the present case, to conclude that I am satisfied that Mr Cotton's fatal
        lung tumour should not be categorised as an indivisible disease and that
        whether it resulted from the effects of exposure to asbestos alone, to his
        tobacco use alone, or to a combination of the effects of both those
        carcinogens it is almost certainly the result of the cumulative effect of one
        or more of those carcinogens operating over an extended period of
        exposure.

Paul Cotton's employment with the South Australian Engineering and
             Water Supply Department
93            Steven Cotton was employed by the State of South Australia in its
        Engineering and Water Supply Department from 4 September 1975 until
        2 October 1978, mainly in the Adelaide suburban area. For the first six
        months of that employment he worked in the gardening department and
        there is no suggestion that there was occupational exposure to asbestos
        fibres or products during that interval. From about March 1976 onwards,
        however, he was employed as a member of a water main laying gang
        installing 4 inch diameter asbestos cement water pipes in the Adelaide
        suburbs. He continued doing this work until he left the department and it
        is, therefore, this period of about two and a half y ears until 2 October
        1978 of exposure to asbestos products which is alleged to have caused or
        contributed to his fatal lung disease. As there is controversy as to the
        nature, frequency and intensity of the deceased's exposure to asbestos
        during this phase of his employment, it is necessary to examine the
        evidence in detail.
94           The pipe laying operations of the first defendant during this period
        were organised from several different depots in the Adelaide area.
        Mr Cotton was employed and worked from the Marden depot, but other
        depots which performed similar work were the Daube Peake depot; the
        Berri depot, the Fulham Gardens depot, the St Mary's depot, the Happy
        Valley depot and another at Elizabeth. Different gangs worked from the
        different depots but the pipes which were supplied were delivered by
        James Hardie & Coy Pty Ltd from its manufacturing plant in Elizabeth to
        the various depots or to the working sites in the field and were then
        worked on by the gangs during the process of installation.




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95            Generally speaking, the pipes would be laid in trenches which had
        been cut in the ground and this would require the lengths of pipe to be
        fitted, one to another and on occasions cut to fit in appropriate lengths, to
        follow the route of the pipeline and also to be cut where joins or turns in
        the line were required - whether involving "T" joins, angle turns or more
        complicated joins or turns. When the pipe had to be cut for any of these
        purposes it would usually be cut by a special chain disc cutter which
        would be fitted over the pipe and progressively tightened until it cut into
        the pipe sufficiently for the application of force, by a mallet or hammer, to
        break the pipe at the cutting (see illustrations on p 7 of Exhibit 41).
        Occasionally the pipe would be cut by other methods such as by a
        power-driven saw (Exhibit 41, illustration p 5) or by a hacksaw or
        bushman's saw (Exhibit 41, illustration p 6). Once cut by any of these
        methods it would be necessary for the newly cut end of the pipe to be
        bevelled off for later fitting and this was usually done by a manual rasp or
        file (see Exhibit 41, illustration p 9). Cutting the pipe to create a hole for
        connection to another pipe could be done by either using a mechanical
        hole saw or by hole cutting with drilling and rasping (Exhibit 41,
        illustrations at pp 10 and 11). To varying degrees, these processes
        involved the release of fragments, fibres and/or dust from the pipe which
        was being worked upon. On the evidence it was suggested, and I have
        inferred, that these processes not only released visible fragments and dust
        which found their way onto the workmen's clothes, hands and arms but
        also gave rise to smaller airborne particles which were likely to be
        inspired by the workmen performing these tasks, or working nearby
        through the ordinary processes of respiration. Just how much and how
        often inspiration of airborne particles of cement asbestos pipe would
        occur from these processes was controversial in the case, but I am
        satisfied that, inevitably, it occurred to some degree.

96           Of these various operations the most common frequently
        encountered by the deceased was the repetitive operation of pipe cutting
        with a chain and disc cutter followed by manual bevelling of the cut edge
        with a hand rasp. According to Mr Cotton, this was an operation which
        took about one to one and a half hours in total for each cutting (Exhibit 2,
        pp 55 - 56) and involved about two pipe cuts per day for the gang in
        which he was working.
97            There is evidence from Mr Cotton himself on these matters: First in
        a statutory declaration which he made on 17 July 2000 (Exhibit 1) and, in
        more detail, in the evidence which he gave under oath before the
        Conciliation and Review Directorate of Workcover in Western Australia
        on 16 October 2000 and upon which he was cross-examined by a

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        representative of the third defendant in the course of the proceedings in
        which he was seeking workers' compensation. Of his employment by the
        first defendant in the pipe laying operation at Adelaide Mr Cotton said, in
        Exhibit 1:
              "My role here was initially to work as pipe layer in the gang.
              This involved the installation of new asbestos pipes in and
              around Adelaide in South Australia.

              We would commence work at the depot and go to the job site.
              The pipes were delivered on site in large timber boxes. I had to
              remove the asbestos pipes from the packing and lay them along
              the trench in the position. If I had to lay the pipes I would get
              into the trench and fit the collar. To fit the collar I was required
              to coat the two ends to be joined with white grease or sealer and
              push the pipe into the collar. We used a crowbar to lever the
              pipe to ensure the pipe went into the collar the required
              distance.

              When the pipe length did not fit in with the installation for
              example if a fire hydrant was to be put into the line we had to
              cut the asbestos pipe. This was done using a chain pipe cutter,
              which was wrapped around the pipe and tension was applied to
              force a blade into the pipe. The blade would not go completely
              through the pipe. I would then leave the pipe cutter in place and
              tap the pipe with a wooden hammer until it fractured along the
              pipe cutter lines. During the process there was asbestos fibres
              coming away from the pipe, which was at that time in and
              around my face area.
              Once the pipe had been cut I had to use a bastard file to file the
              edges smooth. This generated a lot of dust from the asbestos
              pipe.

              At no stage was it mentioned to me that the asbestos from these
              pipes was dangerous. No respiratory protection was provided at
              this time."
        Mr Cotton's evidence before the Workers' Compensation Directorate was
        to similar effect. He described the water pipes which were being laid by
        the gang as being 4 inch diameter cement and asbestos pipes. He
        described the cutting operation with the chain cutter as resulting in brown
        and grey fibres being released and grey dust being prevalent on the pipe
        surfaces. Once the pipe had been cut it was necessary to file it off to

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        produce a 3 inch long tapered or bevelled edge. This was done while
        standing in the trench and dust from the pipes was generated by the
        process. He said that his shift work involved a five-day week, working
        eight hours each day and that the cutting of the pipes by the methods
        described was a daily event, usually involving about two cuts per day
        which would take half an hour to an hour each and then rasping off, so
        that the complete cutting and rasping exercise would altogether take one
        to one and a half hours on each occasion. This work was done throughout
        the Adelaide suburbs and he would often be half in a trench when working
        on the pipes, with the work being done throughout the year including the
        summer and winter seasons.
98            Mr Cotton confirmed that his first six months of employment with
        the first defendant was with a gardening group and that he was not
        exposed to working with asbestos cement pipes during that period. As
        mentioned elsewhere, he was asked in the course of his evidence about the
        source and composition of the pipes. He answered by saying that they
        were generally referred to by the men, including those making the
        deliveries of the product, as asbestos cement pipes and that he believed
        that they were Humes' pipes. The identity of the manufacturer was not
        pursued in the Workcover proceedings as it was not material, but that is
        the only reference to them being a Humes' product. As the evidence of
        Mr Campbell, set out below, describes, the probabilities are
        overwhelming that they were James Hardie pipes and that James Hardie
        was the only supplier of such pipes to the EWSD at the time.

99            During the course of these proceedings Mr Cotton answered on oath
        interrogatories which had been delivered by the first and second
        defendant. No attempt to tender these interrogatories was made by either
        of those defendants but the plaintiff sought, and I allowed, them to be
        adduced as a statement of a person who had direct personal knowledge of
        the facts described pursuant to s 79C of the Evidence Act any requirement
        for availability for cross-examination being excluded because of his death
        - see Evidence Act, s 79C. In answers to interrogatories delivered by the
        second defendant, which became Exhibit 3(c), there were the following
        questions and answers given by the deceased:
              "Interrogatory 1: During the period [1975 - 1978] what precise
              tasks was the plaintiff performing in carrying out the work
              which caused him to being exposed to asbestos.

              Response 1: Laying water main asbestos cement pipes when
              working on water main installation work (which I did for the
              bulk of the period), repair work on water main asbestos cement

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              pipes (which I did from time to time during the period). The
              tasks associated with laying water main asbestos cement pipes
              which I believe caused me to be exposed to asbestos included:

              (1)     handling the asbestos cement pipes (pulling them out of
                      the packs that the pipes arrived in, placing them in the
                      trenches and handling them to cut, fit and join them);
              (2)     cutting the asbestos cement pipes;

              (3)     filing back the asbestos cement pipes when they were in
                      the trenches so that they would fit into the collar and
                      rubber ring;
              (4)     levering and pushing the pipes with a crowbar in the
                      trenches to get them to join up in the collar and rubber
                      rings;
              The tasks associated with breakdown gang which I believe
              caused me to be exposed to asbestos included the work
              associated with undertaking repairs. In the breakdown gang a
              jackhammer was used to dig around the asbestos cement pipe to
              be repaired, the asbestos cement pipe was then cleaned off with
              a rag; the leak in the pipe was located; the asbestos cement pipe
              was then cut with an angle grinder (powered by an air
              compressor); a piece of new asbestos cement pipe was then cut
              to size to replace the section that had been cut out, again with an
              angle grinder (powered by an air compressor)."
        Then, to interrogatory 2, seeking details of the time spent by the deceased
        in performing those alleged tasks, the answer was:
              "Response 2:
              (a)     ...

              (b)     It is not possible for me to give estimates in terms of
                      hours per day, days per week, weeks per year and years
                      that I spent on each task.
                      When I was in the installation gang laying new pipes (for
                      almost the entire period of my employment with the first
                      defendant)and when I worked on breakdown gang (less
                      frequently than the installation gang- only when I was



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                      called upon to fill in) I worked 8 hours per day, on
                      average 5 days per week on average 48 weeks per year.
                      On installation gang work the trenches were dug
                      mechanically (by workers other than me) and w       hen the
                      installation was complete, the trenches were filled over
                      mechanically (by workers other than me) so that my
                      entire day consisted in working, primarily in the trenches,
                      handling, cutting, filing, fitting and joining the asbestos
                      cement pipes.

                      Other than as outlined I am unable to furnish greater
                      detail in terms of hours per day, days per week, weeks per
                      year and years on each task and, to the extent that the
                      second defendant seeks this degree of detail, I object to
                      providing the same on the basis that such a request is
                      unreasonable and oppressive."
100         To the next interrogatory enquiring about the time spent in using or
        handling asbestos products, the deceased answered:
              "Response 3:

              Throughout the period I used and handled asbestos cement
              pipes while performing the tasks identified in answer to
              Interrogatory 1.    Other than as outlined in answer to
              Interrogatory 2 I am unable to furnish greater detail in terms of
              hours per day, days per week, weeks per year and years that I
              used and handled asbestos cement pipes while performing each
              of the tasks outlined in answer to Interrogatory 1, and to the
              extent that the second defendant seeks this detail, I object to
              providing the same on the basis that such a request is
              unreasonable and oppressive."
        To the next interrogatory which enquired about the time during which the
        plaintiff worked in the vicinity of other workers using or handling
        asbestos, the deceased answered:
              "Response 4:
              I worked in a gang of workers who were doing the same work
              as I was doing. Consequently I worked in the vicinity of other
              workers using or handling asbestos cement pipes. I am
              otherwise unable to furnish greater detail ... "


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        And, then, to an interrogatory enquiring about the time during which the
        plaintiff was exposed to or inhaled asbestos fibres and dust, the deceased
        answered:
              "Response 7:
              I believe that it was throughout the period. Throughout the
              period I worked 8 hours per day; on average 5 days per week;
              on average all days per month other than weekends; on average
              all days in the year other than weekends and annual holidays
              (generally 4 weeks per annum). Other than as outlined in
              answer to Interrogatory 2 I am unable to furnish greater
              detail ... "

101          To the extent to which these answers by the deceased make reference
        to the deceased occasionally working in a repair gang and then working
        with powered cutting or grinding tools which generated cement asbestos
        dust, the defendants submit that evidence should be rejected because it is
        not corroborated by the evidence of any workman who was present with
        Mr Cotton on occasions when that is said to have occurred and, further,
        because Mr Cotton himself did not explicitly mention such occasions or
        the use of power tools when giving evidence in the Workcover
        proceedings. Having noted this controversy, I note, however, that
        Mr Cotton's evidence is consistent with the evidence of other workmen
        whom I accept to be credible, measured and responsible witnesses
        although they were working on different gangs and in different areas for
        the EWSD. Having heard and seen those witnesses, as well as
        Mr Campbell who was called by the first defendant, I have reached the
        conclusions that all of the water laying gangs followed, generally
        speaking, much the same working routines and methods, as one would
        naturally expect for consistency of operation and efficiency in teams of
        workers essentially carrying out the same or similar tasks. No suggestion
        was put to Mr Cotton during his cross-examination in the Workcover
        proceedings that he was dishonest although, of course, this particular issue
        did not arise in those proceedings and he was being cross-examined only
        by representatives of the third defendant. Still there does not appear to me
        to be any reason to doubt his honesty or reliability and I reject the
        submission that this aspect of his testimony should not be accepted.

102          Mr David Tilly, a former team leader employed by the South
        Australian Engineering and Water Supply Department from between 1973
        and 1978 gave evidence and was cross-examined. He worked for the first
        defendant at a construction camp at Dark Peake near the middle of the
        Eyre Peninsular with a 50-man crew for the whole of the period 1973 to

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        1978. His team was involved in laying 15 inch water mains with cement
        asbestos pipes supplied by James Hardie. In addition, his team worked
        with 100 ml or 4 inch pipes as well as 6 inch asbestos cement pipes. His
        team's method of operation was to have four pipe layers, two in the trench
        and two with the pipes and he used a chain cutter or wheel cutter for the
        occasional cutting of pipes which was necessary and, once the cutting had
        been done used an air grinder to even off the edges. Mr Tilly described
        that the actual chain cutter produced very little dust and could take only
        one or two minutes depending upon the size of the pipes being cut. With
        6 inch or 8 inch pipes, once they had been cut, a file would be used to
        shape the ends and that may take eight or nine minutes and would
        generate lots of dust. He described it just as pipe dust or cement coloured
        dust with a consistency of a very fine powder with a tendency to stick to
        whatever it touched. The operations which Mr Tilly described occurred in
        the country outside Adelaide and he had never worked with Mr Cotton or
        at the Marden depot.

103           Mr Ivan Streeter is another former employee of the first defendant,
        having worked with the EWSD from about 1974 until retirement in
        January 1993. He worked at the Berri depot and one of his jobs was to
        make up "T" joints in the asbestos cement pipes to allow a smaller pipe to
        be connected into the larger pipe at a 90 degree angle. To do this he
        would drill an oval hole in the asbestos pipe and rasp the ends of the
        smaller pipes to fit into that junction and fasten the join with fibreglass
        and glue. He explained that on the end of the "T" the men also used lathes
        to grind down the pipes to fit into the collar but that sometimes this would
        be done by hand. All the processes which he described - the drilling, the
        cutting and the use of the lathe - gave off lots of dust. He said the dust
        used to get on everything and that he would have to take the overalls off
        and belt them against a post to get the dust off, resulting in clouds of dust
        rising from them. The pipes which Mr Steeter worked with were about
        17 mm thick and were made at the Hardie's factory at Elizabeth. He
        remembered the name Hardie's being written on the pipes. He rejected the
        suggestion that any of the pipes were manufactured by Humes, although
        he acknowledged that Humes did make cement pipes which were used by
        the Council at Berri for the management of waste water and street
        drainage but he confirmed that the pipes which his team worked on were
        Hardie's products.

104           Peter Neagle was another former employee of the EWSD of the first
        defendant during the period from about 1965 until about 1980. For his
        first 12 months of employment he was a water worker laying water pipes
        and then he was promoted to work as a machine operator when he would

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        dig trenches for the pipes and, having done so, would then assist the pipe
        layers to lay the pipes. He described the Marden depot as servicing the
        eastern metropolitan areas and the Fulham Gardens depot, from which he
        worked, as servicing the northwest metropolitan areas. Each of these
        depots had about half a dozen gangs each made up of about 15 workers,
        including the pipe layers, machine operators and a truck driver. There
        were also service trucks used to attend to burst mains, leaking fire plugs,
        to repair domestic connections and to connect water services to houses.
        He confirmed that the pipes which were laid were asbestos cement pipes
        manufactured by James Hardie and stamped with the James Hardie logo
        and were either collected or delivered from the James Hardie depot a      t
        Elizabeth. He explained that when the men were laying the asbestos
        cement pipes the gang would be handling and cutting them for most of the
        day. He said that an air grinder was used to cut the pipes but that some
        times a manual pipe cutter would be used instead but that this would leave
        a jagged edge so that the air grinder was more commonly used.

105          According to Mr Neagle, dust got into the whole work process. Dust
        from the angle grinder would settle on the dirt in or near the trench and
        when a trench was back filled the dust would get mixed in with the dirt.
        On occasions when the pipe had to be cut to a required length, that would
        be done and then the men would have to grind or manually file the pipe to
        create a bevelled edge that would subsequently slip into the pipe collars
        and joins. With respect to grinding the pipes when domestic services
        were laid, a stopcock had to be screwed into the pipes and this was done
        using the drill which also created asbestos shavings and dust. In his
        experience, filing or bevelling a pipe edge manually was a lengthy time
        consuming task and, because of this, it was more common to machine the
        edges. The use of air grinders occurred in the presence of visiting
        supervisors and engineers but was not prevented. By the late 1970's the
        men were provided with hand lathes instead of grinders, but even these
        created lots of filing shavings and dust. Mr Neagle said that he had never
        seen any Humes pipes in use during his time with the EWSD and that
        other depots, including the Marden depot, would generally perform the
        same type of work.
106           I should observe that I was impressed with the credibility and
        reliability of Mr Neagle and of Mr Streeter and, indeed, of all these former
        employees. They were men who had retired from their employment with
        the first defendant, who had no direct knowledge of or acquaintanceship
        with the deceased who had, of course, left the first defendant's employ
        more than 25 years before. Each had worked for a long time in this
        particular activity and I have no doubts or reservations about the

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        reliability of their testimony. There was some issue about the name of
        "James Hardie" as it was said to appear on these pipes, whether it was in
        red lettering or in black or whether there was a company logo, the initials
        "JH" or the name. I do not think that it is necessary to resolve this
        because I am satisfied that when these witnesses said that they saw the
        name James Hardie on the pipes, their recollection after this period cannot
        be sufficiently precise to distinguish between a logo, an initial or a full
        name, but the substance of their evidence that the pipes bore markings
        identifying them as products of James Hardie is reliable.

107           Mr Tim Cotton, the deceased's older brother, gave evidence
        describing a period when he and the deceased and their parents were
        living in the family home in Firle. Mr Tim Cotton did not work for the
        EWSD but rather for Telecom. He would visit his brother when he was
        working on site for the first defendant every now and again. He described
        that on such visits he saw his brother filing water pipes and shaving them
        down to put collars on the pipes. Because they were working in the same
        areas he would come across his brother only occasionally at intervals of
        three weeks to a month or more, but when he did so he said that he usually
        found Paul Cotton in the trenches handling or fitting the pipes which were
        being laid and that he saw dust coming off the pipes when they were
        being filed down by his brother. He, too, said that the pipes bore a
        Hardie's logo stencilled on their sides.

108          The first defendant called Mr Mark Campbell, an operations officer
        of SA Water, formerly known as the EWSD. He was first employed with
        EWSD in 1975 and from then until 1982 was first a labourer and then a
        supervisor in the sewerage branch. That branch did not use asbestos
        cement pipes but, rather, vitreous clay pipes and later unplasticised PVC
        pipes, but he began working with asbestos cement pipes in about 1982
        when he became a construction maintenance supervisor of a water main
        gang. This was after the time of Mr Cotton's employment, but in the
        1980's there were only about two or three gangs doing construction work
        out of the Marden depot and about five crews doing maintenance on the
        water supply. These numbers were fewer than in the late 1970's because
        in the early 1980's EWSD began outsourcing construction work to private
        contractors.

109         Speaking of his experience of water pipe laying during the years
        1982 - 1986, Mr Campbell said that his gang was responsible for
        excavating the ground, laying the pipes (including the fittings) and
        backfilling the trench. The asbestos cement pipes used during that period
        were manufactured and supplied by James Hardie. There were different


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        diameters, depending upon the requirements of the job, varying from
        80 mm, 100 mm, 150 mm, 250 mm, 350 mm and larger. The AC pipes
        were all of a standard length, approximately 4 metres. In his experience
        there was not a great deal of dust upon the pipes at the time when they
        were delivered and they were usually in a fairly good condition. Mr
        Campbell said that the majority of the pipes were laid without cutting or
        rasping, but cutting was done where a fitting was needed such as a fire
        plug, a "T" branch, an isolation stop valve or a bend. He described the
        process of cutting pipes with a snap cutter and, once the pipe was cut,
        manual rasping being used to form a spigot on the pipe, a process which
        took between two and five minutes and which generated both flakes and
        dust, but mainly dust. In his experience the majority of the rasping of the
        pipe ends was done above ground and not in the trench.
110           Mr Campbell produced a working drawing of a section of piping
        which had been laid in the suburb of Dernancourt in 1978 involving a
        100 mm diameter asbestos cement pipe and approximately 330 metres in
        length. From an examination of this sketch Mr Campbell estimated that a
        minimum of eight and a maximum of 14 pipe cuts would have been
        necessary to install this layout and that it would have taken a pipe laying
        gang about 12 days to complete, using about 83 lengths of AC pipe. The
        point of Mr Campbell's evidence in this respect plainly is that the pipe
        cutting and rasping procedures which the plaintiff alleges occurred in the
        course of her husband's employment were quite limited in duration and
        frequency in the course of his work.

111          No precautions were taken by the first or second defendants, nor
        were any warnings given to employees by either of those defendants about
        the potential risks of working with asbestos cement pipes during this
        period in 1975 to 1978. No protective clothing, no wetting or dampening
        devices were used nor was any advice against using abrasive or
        dust-generating tools or work practices given. Nor was there any
        sampling of dust or asbestos concentrations in the atmosphere or in the
        workplace done.
112           Some retrospective studies were later attempted by James Hardie
        which were conducted in Western Australia and supervised by
        Mr J Lawless (Exhibit 216) to attempt to estimate the nature and intensity
        of dust surrounding pipe layers who were working with asbestos cement
        pipes being laid in open-field operations in the Perth suburban areas in
        1983. Several studies were done and are known as the "WAIT Aid
        Reports". It will be necessary to examine these studies later, because I am
        satisfied that the conditions do not reproduce or approximate the working


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        practices employed by the first defendant's staff when Mr Cotton was
        working on AC pipes in Adelaide between 1976 and 1978. Nevertheless,
        the results which were obtained indicated a very low concentration of
        asbestos fibres per millilitre of air and led to the inference that working
        under such conditions would only generate a low cumulative dose of
        fibre/millilitre years of asbestos contamination.
113          On the basis of this evidence I find that during the course of his
        employment with the first defendant in Adelaide from about March 1976
                             h
        until October 1978 t e deceased, Paul Cotton, was exposed, on a daily
        basis, to fragments and dust arising from operations on asbestos cement
        pipes which he and his fellow workmen were required to lay in the region.
        The pipes which he and his workmen were using were asbestos cement
        pipes manufactured and supplied by the second defendant, under its then
        operating name of James Hardie & Coy Pty Ltd, from its Elizabeth
        manufacturing plant in South Australia. All the pipes used by the EWSD
        upon which Mr Cotton was working were such asbestos and cement pipes
        and were mainly of about 4 inch diameter and 17 mm thickness, although
        it is probable, that occasionally, pipes of larger dimension were
        sometimes used. The work involved was conducted in the field, that is in
        suburban metropolitan areas where new water pipes were being laid in
        developing or established suburbs, or when maintenance, repair or
        modification work was required on existing pipelines in such areas. For
        the whole of this period Mr Cotton was based at the Marden depot in
        Adelaide which serviced the eastern and some of the northern suburban
        areas and that, generally speaking, the work done by crews from the
        Marden depot was similar to and conducted much in the same manner as
        the work done by crews from other depots in the Adelaide region operated
        by the first defendant, all using James Hardie AC pipes and, essentially,
        similar operating methods.

114           This work was conducted during weekdays, that is five days a week
        and 48 working weeks for the year (allowing for annual holidays). Each
        day was an eight hour day spent mainly in the field. The pipes would be
        delivered to the work site by truck, either directly from the James Hardie
        depot at Elizabeth or occasionally from the first defendant's depot where
        stocks were stored. They were unloaded by winch or crane, each pipe
        being of a standard length of four metres. The pipes were to be laid in
        trenches which had been cut by machine operators in the gang. The
        reticulation of the pipe system required the pipes being connected end to
        end with occasional "T" junctions to distributor outlets and with bends,
        other "T" junctions and like connections or configurations being installed
        as required.

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115           When two lengths of pipe were connected, this was done by fitting
        them both into a collar which was sealed. This process seldom required
        cutting or abrasion of the pipe ends or of the collar. However, when the
        pipe had to be cut, for any of the reasons cited or other reasons, this was
        done on site by a variety of methods which are instanced in Exhibit 41. In
        Mr Cotton's experience, however, the general and most frequent method
        of cutting was through the use of a chain cutter which was strapped to the
        pipe, tightened, to make initial cuts which were sufficient to allow the
        pipe to be broken off relatively cleanly by force applied by hammer or
        mallet. When this was done the rough end of the broken pipe had to be
        smoothed and bevelled. This process could be done either by using
        powered handheld grinders or, more commonly, manually by abrasive
        rasping. The latter was the process most generally employed in
        Mr Cotton's experience and was time consuming and generated a lot of
        dust and particles, whereas, by contrast, the use of the wheel-cutting
        device was a much cleaner operation giving off only small quantities of
        asbestos cement fragments and comparatively little dust. Although other
        crews from other depots, particularly in areas outside Adelaide, appear to
        have made greater use of mechanical powered tools for this purpose,
        Mr Cotton's crew usually cut the pipes with a form of wheel pipe cutter as
        illustrated on p 7 of Exhibit 41 and then smoothed or bevelled the
        resulting rough edges manually with hand rasps, as illustrated on p 9 of
        that same exhibit.
116          Slightly different methods were used during Mr Cotton's work by
        members of his crew and, occasionally, the bevelling or grinding work
        made after a cut, particularly when the operation was one of pipe repair
        rather than of installation, involved the use of handheld powered grinders
        or lathes. This was much less common than the routine operations of
        wheel cutting and manual rasping already described. When powered
        grinders or lathes were used, however, considerable quantities of dust and
        fragments would be given off and they clouded the surrounding areas.
        The duration of such an abrasive operation would be much shorter than
        the manual one.

117          Whenever these cutting or abrasion techniques were used the
        resulting fragments of cement and asbestos would be left where they fell,
        so that coatings of such fragments and dust would gather on the pipe ends
        and more particularly on the ground and in the foot of the trenches. Later,
        when the trenches were filled in, these fragments and dust would be
        redisturbed and the operation of burying the pipes could be expected to
        generate and distribute quantities of dust from those sources. It is quite
        impossible to quantify the extent of dust contamination or distribution

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        from these final trench filling operations apart from saying, in the most
        general way, that there must of necessity have been some degree of
        contamination but it is unlikely to have been severe.

118          The pipes themselves, when delivered by truck under protective
        plastic or other wrapping, were coated, to a small extent, by dust which,
        presumably, came from the manufacturing site and probably was of a
        composition which matched that of the pipe. The pipes themselves were
        made of a mixture of Portland Cement, asbestos fibre and silica, the
        asbestos fibre content being approximate 20 per cent or a little less.
        Although there is little evidence on the subject, as described elsewhere the
        asbestos in the pipes was Chrysotile and Amosite, the latter being a form
        of amphibole asbestos. It is probable that there was also a small content
        of Crocidolite in the composition.
119           During a typical working day Mr Cotton, or members of his gang,
        would usually be required to carry out a cutting operation on the four inch
        diameter AC pipes about twice, although this could be more frequent
        depending upon the particular design of the layout and connections
        required for the reticulation being installed. Despite different estimates of
        the times required for these tasks being given by witnesses operating on
        other crews and using slightly different methods, I consider I should
        accept the evidence of the deceased that these combined cutting and
        rasping operations, when required, would each last for about one to one
        and a half hours, meaning that two to three hours per working day would
        be occupied by those functions.

120           These activities, and the incidental activities of refilling the trenches
        and of cutting apertures in pipes already laid with power tools when
        replacements or repairs were required, inevitably generated dust almost
        certainly being of the same composition as the AC pipes themselves, that
        is, containing up to about 20 per cent of mixed asbestos types. I have no
        hesitation in concluding that some quantities of these dusts were probably
        inhaled by Mr Cotton and the other workmen as an unavoidable
        consequence of this activity.
121          Because so much attention has been given by the parties to their
        attempts to quantify the concentration of this asbestos cement dust, I must
        address that issue. In many ways a problem in this case has been the
        constant attempts to ascertain precise concentrations and estimates of
        asbestos contamination in the working atmosphere, a task which seems to
        me to be almost, but not quite, fruitless. The "WAIT Aid" experiments,
        although genuine and conscientious attempts to undertake such a task of


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        estimation, did not, and could not, exactly replicate the conditions under
        which Mr Cotton worked. On the other hand, certain features of the
        working operation, namely that they occurred in the open air, in all
        seasons and when the cutting operations described occupy in time, less
        than half each working day, suggest that this working environment was
        very different to one in which men are working in confined spaces, or
        without adequate ventilation and in which sources of asbestos
        contamination were extensive, such as in a brake manufacturing or
        repairing facility, in a shipyard involving the installation of asbestos
        linings or lagging, or in a workshop where there was constant sawing or
        abrasion of asbestos sheeting or products. Nevertheless, I am satisfied
        that there was a degree of ambient asbestos dust contamination but I can
        only conclude that, generally speaking, it was fairly low and probably
        discontinuous.

Paul Cotton's employment with the third defendant and extent of exposure
              to asbestos
122          The plaintiff's case proceeds on the basis that he was exposed to
        levels of asbestos while in the employ of the third defendant at its
        Australind plant for all or most of the duration of his employment
        between 1990 and his diagnosis of lung cancer in May 2000, but that the
        principal source of asbestos exposure occurred while he was working in
        the Band Drier Room ("BDR"). The third defendant's case, however, is
        that Mr Cotton did not begin working in the BDR before about March or
        April 1992 and before then was working elsewhere where there was no
        occupational exposure to asbestos. Further, the third defendant maintains
        that after then Mr Cotton did not work regularly or continuously in the
        BDR but, rather, only worked there intermittently during shut downs or
        cleaning operations. This has generated an issue over the frequency and
        duration of the periods in which Mr Cotton did work in the BDR as well
        as controversy over the nature and extent of his exposure to asbestos on
        those occasions.

123           Another level of controversy arises from the fact that the third
        defendant was undertaking a series of progressive and extensive
        programmes for removal of asbestos from the Australind operation
        leading to claims by the third defendant that, by about March or April
        1992 all asbestos insulation had been removed from the BDR, and that
        other forms of asbestos had been removed by 1994 so that Mr Cotton's
        exposure to asbestos occurred, at most, for a relatively short period of his
        total employment.



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124          To consider these issues it becomes necessary to undertake a review
        of the evidence of Mr Cotton and other workers who actually operated in
        the environment at the time; to consider the reports of consultants who
        were called in in 1990 to report on and identify asbestos hazards in this
        workplace; to identify and mark the progress of the asbestos removal
        programmes already mentioned and, in addition, to consider the
        significance of scientific tests or air monitoring conducted in various parts
        of the workplace over time but, particularly, during the asbestos removal
        operations.

125          One of the few areas of certainty and lack of controversy in this
        regard is the history of Mr Cotton's employment classification with the
        third defendant. He gave evidence of this in the Workcover proceedings
        and that evidence is not, as I understand it, contested. The employer's
        details, recorded in the personnel records are to be found in the evidence
        of Liz Baggetta, the Human Resources Manager, whose statement of
        evidence (Exhibit 235) was adduced by consent without her being called
        or cross-examined. Mr Cotton commenced his employment with the third
        defendant on 19 April 1990 and the employment terminated on his death
        on 6 January 2002 but from 9 March 2000 (shortly after his diagnosis) he
        was on continuous sick leave. There were two short interruptions to this
        working history resulting in three separate periods of employment as
        follows:

                 (a)       From 19 April 1990 to 19 February 1991 when his
                           employment was terminated because of shortage of work.
                           During that period from 19 April to 30 November 1990 he
                           was engaged on the D shift as a bulk bag packer. From
                           1 December 1990 until 19 February 1991 he was on day
                           work as a plant operator (section 3 - a reference to an area
                           in the plant).
                 (b)       From 14 October 1991 to 28 January 1993. During this
                           time Mr Cotton was employed as a casual worker and his
                           employment was eventually terminated because the casual
                           work was completed. For the whole of that time he was on
                           shift work, initially on B shift, but from 21 September
                           1992 to 27 January 1993 on E and C shifts. He was
                           classified as a "plant operator" and for the period
                           14 October 1991 to 9 March 1992 worked in the Raymond
                           Mill. For the period 10 March 1992 to 27 January 1993 he
                           was operating as a packer 4 or 5.



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                 (c)       From 11 February 1993 to 6 January 2002. Mr Cotton was
                           re-employed as a plant operator and was initially engaged
                           as a casual from 11 February 1993 until 22 November
                           1993. At the latter date he was transferred to the
                           permanent workforce and remained as a permanent
                           employee until his death.
126          During this third period he was first engaged as a plant operator from
        11 February 1993 until 8 August 1993 in the R and D office. He
        transferred to a shift worker - packer 5 on 9 August 1993 and continued
        working shifts as a plant operator packer 5 until 9 October 1995. On
        10 October 1995 he transferred to day work and continued as a day
        worker until his diagnosis, then as a plant operator - shrinkwrap. Day
        workers performed Monday to Friday, usually between the hours of 7 am
        to 3 pm, although his letters of engagement refer to the hours as being
        from 7 am to 3.30 pm, including a half hour unpaid meal break nine days
        per fortnight for permanent workers and from 7 am to 3.30 pm daily
        (including a half hour unpaid lunch break) eight hours per day, five days
        per week for a casual employee. I find that the description of the hours
        and duration of employment set out in the letters of engagement are in fact
        the hours and times worked.

127           The operation conducted by Millennium Inorganic Chemicals Ltd at
        Australind has had a long history. Initially established some time in the
        1960's as plant for the treatment of mineral sands and ilmenite deposits for
        the production of titanium dioxide and other products it was conducted by
        Laporte Titanium. It was later taken over by SCM Chemicals Ltd, as the
        third defendant was then known, and has undergone various upgrades. It
        is a very large industrial plant, spread over a big area comprising many
        separate buildings, tanks, processes, power generation sources,
        workshops, storage areas and other facilities, some under the same roof or
        roofs, some adjoining and some separated by distances varying from short
        to long. Between these many parts runs an extensive pipe system for the
        transportation of the product during various phases of treatment, and for
        water and power reticulation and steam for heating. It is a large and
        complicated refinery-like operation. The areas of principal attention for
        this litigation are towards the end of the industrial process, that is the
        recovery of the refined titanium dioxide TiO 2, its bagging and storage, and
        the cleaning and maintenance of the areas of the plant involved in those
        stages. To say this does not imply that the end phase of the industrial
        processes was at the end of a linear chain of physical works, quite the
        contrary. Various phases of the industrial processes were clustered
        together for efficiency and convenience.


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128          A classification of the various operations on the third defendant's
        refinery site, utilised at the trial, can be found in the Matprolab's reports
        (Exhibits 44 and 113) which were prepared by those consultants in March
        and August 1990 to assess the presence of asbestos and which
        recommended a removal programme. Those two reports dealt with
        discrete areas of the third defendant's operation, distinguishing between:
              •       Band Drier Room (Exhibit 44).

              •       Section 1:
                         Grinding plant
                         Sulphation plant
                         Classification plant
                         Crystalizers/Clarification plant
              •       Section 2:
                         De-watering filters
                         RV filters
                         Moore filtration
                         Hydrolysis
              •       Section 3:
                         Calciners
                         Raymond Mills/Crushing Rolls

              •       Section 4:
                         Sulphur melter & filter plant
                         Acid plant
                         East-West pipe rack and associated external lines
                         Old boiler house
129          Some of the many other discrete areas of the third defendant's
        operation, not included in the above classification, are the microniser
        building (abutting the band drying shed) and the R & D Laboratory, quite
        some distance away. Another classification of buildings or areas of plant
        associated with the asbestos removal programme is set out in Exhibit 257
        (a proposal for asbestos removal of 25 August 1993) which distinguishes
        between:
              •       asbestos insulation removal from the 6 inch steam pipe
                      and 2 inch caustic pipe;
              •       asbestos sheeting removal from:

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                      surface treatment building

                      - Raymond mill area
                      - Microniser building (SD 1)
                      - No 3 packing shed
                      - BD-DWF area
                      - BD building
                      - BD and packing area roofs.

130          That last document outlined an ongoing staged asbestos maintenance
        or removal programme lasting from early 1994 to late 1998. It is
        therefore of importance to appreciate that the various witnesses, when
        giving evidence, alluded, to varying degrees, to different parts of the
        workplace and that different conditions may have applied in separate
        areas. With that caveat, however, it is still possible to conclude that in
        this multi-staged industrial plant there were a number of major buildings,
        many of which were originally built with asbestos cement fibre roofs and
        some with asbestos fibre cement cladding on the walls or internal
        divisions.
131           Throughout the whole plant, and unquestionably in the BDR, there
        were many pipe racks and systems which were heavily bound with
        insulation, much of which originally contained asbestos. This is often
        referred to in the evidence as "asbestos lagging" but it could take several
        forms. A mixture of asbestos cement, or plaster or other binders, was
        mixed and layered over pipes as an insulating coating. Sometimes
        insulation containing asbestos was bound or wrapped around pipes,
        gaskets or other lines. In some instances this "lagging" was sealed by a
        coating of paint or other sealant giving it a durable and non-porous
        exterior but, in many instances, that deteriorated over time, breaking open,
        being damaged and allowing the friable interior contents to shed. In some
        instances the insulating layer around the pipes, of whichever kind, was
        bound with a tarry sealant fabric material to give it greater durability and
        resistance but this, too, was prone to damage or deterioration, exposing
        the underlying insulation to the ravages of the atmosphere which was
        often more than usually corrosive because of high temperatures and
        ventilating steam and other gasses. On other occasions the insulation
        around pipelines was covered by a metal coating presenting even greater
        durability and protection from exterior forces, but this did not entirely
        prevent damage and exposure of the underlying asbestos insulation due to
        deterioration over time and random accidental damage.


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132           The asbestos sheeting on the roofs, including the roof of the BDR,
        was very old. In some instances asbestos cladding on walls or internal
        divisions was of a similar age. This older asbestos cement sheeting was
        noticed to have deteriorated over time, presumably under the influence of
        the elements, but also especially because of the steam-laden atmosphere
        rising from certain operations below, to the extent that it had become both
        fragile and friable. The plaintiff alleges that the roof of the BDR
        constantly shed grey dust onto the areas below which was regularly swept
        up by workmen, including himself.

133          A third general source of asbestos in the working area was the
        fibrous insulation packed into the doors and seals around the doors to the
        band drier itself. It will be sufficient to describe the characteristics and
        size of this source of asbestos in more detail a little later.
134           Within the BDR all three of these different sources of asbestos
        occurred. Asbestos cement sheeting or panels on the roof, and some areas
        of internal partitioning; asbestos lagging or similar insulation bound to
        large steam pipes and other lines passing through the BDR; and fibrous
        insulation containing asbestos within the doors and seals to the band drier
        itself.
135          The BDR was a very large area of the plant, said by some witnesses
        to be up to 250 metres in length (although that may be an overestimate)
        but somewhat narrow in width, as appears from the photographs in
        Exhibit 44. It was fully enclosed by brick walls on all sides, with one
        door on each of the four walls. It was of substantial height, at one end
        being several stories high and the roof was covered with asbestos cement
        sheeting laid over steel frames. There was much supporting steelwork
        within the building and this and other supports carried extensive pipe rack
        systems along and adjacent to the walls. Some, but not all, of these pipes
        were steam pipes and these and others carrying heated contents were
        insulated by the lagging already described.
136          Running longitudinally down the central length of the BDR was the
        band drier itself. This has been referred to variously by witnesses as a
        "giant pizza oven" or "stove". Essentially, it comprised a very large
        metal-sided tunnel sealed on all sides enclosing a metal conveyor system
        which transported containers filled with the slurry of TiO 2. As the
        containers of TiO 2 passed slowly down the length of the band drier they
        were subjected to heating, the source of which was the steam from the
        lagged pipes, and elevated temperature which had the effect of causing the
        moisture in the slurry to evaporate and eventually leave dried TiO 2 in


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        slabs or cakes which could readily by reduced to the white powder which
        constituted the final product of the operation.
137          The heated air blown into the band drier (itself a giant heat
        exchanger) was drawn out by large exhaust fans which carried the
        extracted gas through vents above the band drier, depicted also in the
        photographs in Exhibit 44. This meant that the interior in the band drier
        was a hot pressurised system with many moving parts and there were,
        inevitably, spillages of TiO 2 within the band drier and diffusion of dust
        escaping unintentionally from unavoidable apertures. All-in-all this
        meant that when the band drier was in operation the environment within
        the BDR was hot and dusty and several witnesses made reference to
        vibration occurring in the band drier which accounted for deterioration in
        seals, door frames, exhaust vents and other parts of this big machine.
138           The third defendant's factory operated on a 24 hour a day, 7 days a
        week basis, and, accordingly, generally speaking, the band drier operated
        continuously. Nevertheless, it was necessary from time to time to shut it
        down in order to carry out maintenance or repair and also to clean out the
        interior when a grade change in the TiO 2 being processed was made. On
        each of those occasions the conveyor would be stopped, the source of heat
        turned off and plant operators would be required to carry out the cleaning
        and maintenance. To do this they had access to the interior of the long
        box comprising the band drier by doors located in the vertical sides.
        According to the evidence there were 30 or more of these doors on the
        sides of the band drier and their dimensions were approximately
        1.5m x 1m, or something of that order. These were the hatch doors which
        are illustrated in photograph No 2 on p 6 of Exhibit 44. These hatches or
        doors were made of metal plating and appear to have been several inches
        thick. Within the space between the interior and the exterior of metal
        surface of those doors there were further steam pipes which provided
        radiant heat to the interior of the band drier when in operation. Between
        these pipes and the surfaces there was packed fibrous insulation, some of
        which contained asbestos. Furthermore, to seal the doors in place when
        closed, there were strips of a fabric-like substance or sealer along the
        edges of the door and the fittings into which they were placed. This, too,
        at certain stages included asbestos in its content.

139          Over time the ravages of the working environment, the vibration of
        the system when in operation, and occasional knocks when removing and
        replacing the hatches during these inspection, maintenance, cleaning and
        repair periods caused damage to the these doors. Sometimes the rivets
        popped and the exterior metal sheeting peeled open to some degree. In


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        other instances the fabric seals to the doors and the apertures were broken
        or abraded. Consequently, it was by no means uncommon for the fibrous
        insulation within the doors to be exposed and for the fabric seals to
        become abraded or to shred through constant use. The result was that
        fragments of the contents, including asbestos, would escape and either be
        deposited upon the floor of the BDR or its internal working surfaces or
        become airborne inside that enclosure.

140           Although not stressed by any of the parties, the fact that the interior
        of the band drier operated in a pressurised system also suggests that
        friable fragments of asbestos material which may have come loose from
        any of the sources would probably be disseminated into the atmosphere of
        that building. The hot and dusty conditions inside the BDR have already
        been mentioned. No doubt the greatest component of the dust was TiO 2
        powder itself. Neither the employer nor the workmen regarded this as
        hazardous and indeed the workmen had been assured by the third
        defendant that many studies had revealed that TiO 2 dust was non-toxic
        and did not present any hazard. For this reason face masks or protective
        clothing were not worn by the workmen and, although face masks were
        available (presumably for occasions when there was an extremely dusty
        task to be performed), there was no standing order or instruction for their
        use and they were very seldom worn by the men.
141          This description of the BDR is particular to that area of operation
        because other areas, such as the microniser unit and the packing sheds,
        where Mr Cotton at times worked, did not contain the band drier or any
        similar machine heavily insulated and working under pressure.
        Nevertheless, it is evident that many other parts of the third defendant's
        operation at Australind contained asbestos roofed, and sometimes asbestos
        walled, buildings or areas and that insulated steam lines clad with asbestos
        lagging ran through, or close to, many of these other areas. The plaintiff's
        contention, in the present case, is that Mr Cotton worked in an
        environment where he was exposed to airborne asbestos particles which
        he probably inspired, and that these came from:
              "Dust shed from the deteriorating asbestos roofs above the
              working places; particles of asbestos lagging which had broken
              open and were shedding onto the work space and the floor
              below; particles of asbestos insulation coming from the interiors
              of the hatch doors on the band drier and from the fabric seals to
              those doors."




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        In particular, the plaintiff alleges that it was common place for pieces of
        asbestos lagging from the overhead pipe systems to fall onto the floor of
        the band drier room and that, during cleaning operations, Mr Cotton was
        required to sweep up the floor, generating dust in the process, and to
        shovel the sweepings into bags. These floor deposits, according to the
        plaintiff, must have comprised a mixture of TiO 2 powder, fragments from
        the roof, broken fragments from the asbestos lagging on the pipes, and
        sheddings of insulation from the hatch doors and seals.
142          That there was asbestos content in each of these components of the
        workplace, as described, at some times is undoubted. That there was a
        degree of shedding of dust and fragments from the roofs, of lagging from
        the pipes, and from fibrous insulations in the hatch doors and seals is also
        undoubted on the evidence. That each of these sources included an
        asbestos content and that workmen, including Mr Cotton, regularly had to
        sweep up and clean up these deposits is also clear.
143           It is also extremely probable, and I find, that as a result of this
        method of operation Mr Cotton was exposed to working in an
        environment where he almost certainly was breathing air which carried
        tiny fragments or filaments of asbestos which exposed him to the risk of
        developing asbestos lung disease. What is controversial, however, is how
        great, how long and how influential this exposure was because the case
        for the defendants is that, on any analysis, it was not great enough to
        justify any attribution to asbestos as a cause or contribution to the
        development of his lung cancer. For that reason, great attempts have been
        made by the third defendant to quantify the aggregate potential exposure
        of Mr Cotton to airborne asbestos and to demonstrate that, taken in
        conjunction with scientific and epidemiological studies, this is very much
        less than would justify a conclusion accepting its alleged causative effect.
144           The evidence of Mr Cotton about the nature and location of his
        employment with the third defendant is found in the statutory declaration
        of 17 July 2000 (Exhibit 1), in the evidence which he gave on oath in the
        Workcover hearing (Exhibit 2) and certain of his answers to
        interrogatories. In Exhibit 1 he said that:

              "In 1990 I was employed as a Bulka Bagger located in the
              section 2. This involved filling 2 tonne bags with pigment out
              of a big chute. When I commenced as a permanent worker I
              was employed as a shift worker process operator in section 3.
              This involved bagging the pigment, cleaning up the pigment,
              cleaning out the band drier room.


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              I was exposed to asbestos fibres whilst working in the band
              drier room in the period of my employment with Millennium
              Chemicals from 1990 to until it was removed.

              This exposure occurred when I was required to remove the band
              drier doors which were located in the band drier room. The
              band drier room is approximately 200 metres x 4 metres and
              about 3 metres high."

        And then, after detailing the nature of the doors on the band drier, the
        lagging which existed and other sources of asbestos, including lagging on
        the steam pipes, he mentioned a different hazard:
              "Another asbestos exposure occurred whilst KBE were
              removing the asbestos roof sheeting from area 500 in which I
              was working. The roof sheeting was removed whilst we were
              working below."

145           In his answer (response 10) to interrogatories delivered by the second
        defendant (Exhibit 3(D)), Mr Cotton described his duties at Millennium
        Inorganic Chemicals from 1990 onwards, distinguishing between the
        period before 1993 when he worked as a full-time casual employee and
        the following period when he worked as a permanent process operator or
        shift worker, but stating the work which he did under each classification
        was the same; namely, to bag the TiO 2 pigment, sweep the floor, drive
        forklifts, make up the chemicals and clean up in the BDR, including
        cleaning the band drier machine inside and out. He said that in the BDR
        his job involved sweeping, removing debris from the floor and cleaning
        trays on the band drier conveyor belt, to access which he had to move the
        doors or hatches which were lagged with asbestos in bad state of repair.
        He explained that when he was required to sweep up the BDR floor there
        were fragments of the lagging from the hatch doors and also from
        insulation on the pipes. He asserted that the lagging on the band drier and
        associated pipe work remained until it was removed in about 1995 and
        that his exposure to asbestos occurred from his regular work in the BDR.
        He added that he believed that in about the early 1990's he was also
        exposed to asbestos when contractors were engaged to remove asbestos
        cement roof sheeting from the building in which he worked and he
        recalled visible dust from the roof sheeting removal. Next, in response 11
        to the same interrogatories, he said that he believed that most of his
        exposure occurred in the BDR, an area in which he worked regularly
        throughout his employment and that this regular and frequent exposure in
        the BDR continued until the asbestos had been removed, according to his
        recollection not before 1995. He asserted that he had spent four to five

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        hours pulling trays from the band drier or doing BDR work some three
        times per week, although on other occasions he may only have been
        engaged in the BDR once a month. He also asserted that his exposure to
        asbestos from the removal of asbestos roof sheeting took place some time
        in the early 1990's.

146           In his evidence to the Workcover inquiry on 16 October 2000
        Mr Cotton said (Exhibit 2, p 16) that during the first 18 months of his
        employment at Australind he worked in the Raymond Mill area (section 2,
        as it was called) bagging 2 tonne bags of pigment. Asked about the type
        of construction, he said that the building was made of steel with sheets of
        asbestos sheeting, lots of lagging and lots of steel in section 1 where there
        were big round calsiners. He said that after the initial 18 months he was
        put off for a little while and then was taken back on and went into the
        Research and Development Department which was located in a tin and
        metal shed way over the other side of the plant (Exhibit 2, p 18) and that
        he worked at R & D for about three or four months. After that he went
        onto shift work in the production plant, bagging 25 kg bags, filling
        1 tonne and ½ tonne boulder bags, packaging ready for distribution and
        cleaning up everywhere and anywhere whenever there was a breakdown.
147           According to Mr Cotton, this cleaning up work included work in the
        band drier (Exhibit 2, p 20). He described the BDR as having lots of
        pipes in the roof, about 15, which were lagged with bits of lagging that
        used to hang off. He also described lagging hanging out of the stainless
        steel on the doors to the band drier. He described the lagging on the pipes
        and the insulation of the doors as being in poor condition and there being
        lagging on the floor which had to be swept up. According to Mr Cotton
        (Exhibit 22, p 27), there were pipes running along the top of the band
        drier, all covered with asbestos lagging that used to be hanging off and
        hanging everywhere with bits and pieces all over the place. He then
        described coming to work one day and finding that the whole BDR was
        sealed off with plastic tape while contractors were removing the asbestos
        lagging from pipes on top of the band drier roof. Mr Cotton said that he
        would be in the BDR cleaning up anywhere from five to eight hours at a
        time. At Exhibit 2, p 37, he described this work in the BDR as occurring
        many times when there was a breakdown or a grade change and that there
        was plenty of lagging on the floor when he was working there - "bits all
        over the place till about 1994". The broken lagging on the floor would be
        in all sizes, some pieces a foot long and six inches wide and smaller
        pieces. The lagging would be swept into a corner. During the asbestos
        removal programme in the BDR (which Cotton thought occurred
        somewhere around 1992/1993) he worked next door in the bagging room.

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        He described (Exhibit 2, p 42) working in the bagging shed when the roof
        was removed and seeing dust falling from the roof which "looked a
        whitey-grey colour". Asbestos sheets were being removed from the roof
        during this operation.
148           When asked to estimate the frequency of his labours in the BDR,
        Mr Cotton said that he commenced there in about 1992 and that he had
        been working in the BDR for about 12 months before the removal of the
        asbestos lagging from the pipes saying that he was there about 15 to 20
        times during that interval for about five to eight hours each always
        sweeping the floor when he finished and nearly always finding lagging on
        the floor when he did so. In cross-examination, he confirmed that he had
        been working in the BDR for about 12 months before the episode when it
        was sealed off with black plastic tape and warning signs while the
        asbestos removal crew worked inside. He put that episode as "roughly
        about 93 or 94" and it may well be the case that he is mistaken about that.
        The significant point, however, is that he was working in the BDR for
        about twelve months before the removal crews moved in, whenever that
        was.

149           After that asbestos removal programme Mr Cotton went back to
        work in the BDR on a regular basis doing the same work about 15 to 20
        times a year and doing other jobs around the plant. Of course, neither he
        nor any of the other workmen had been permitted inside the BDR while
        that removal process was occurring. During that removal programme he
        was working in the packing area which adjoined the BDR with a common
        wall but which was quite separate.
150          In cross-examination, Mr Cotton said that "area 500" was what was
        called the "packing end". There were three sections, 1, 2 and 3. Area 1
        was at the other end, later removed at the same time as the calsiners.
        Area 2 was the Raymond Mill's area where he first worked.

151          He denied (Exhibit 2, p 61) that there were any safety signs or
        warning signs in the BDR or elsewhere drawing attention to asbestos.
        During the removal process he was working in the packing area in the
        middle of the shed to one side, known as "area 500" and also in shed 4
        where they pick up the Bulka Bags. It was while he was working in the
        packing area that contractors were removing sheeting from the roof. The
        packing area was very big, "a fairly huge shed" - "bigger than the park
        across the road" - more than half an acre in area. He and other workmen
        were within the packing area as the roof was being removed and the roof
        over shed 4 was also removed over a period of about a week. The roof


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        workmen were not working directly above him but could easily be seen
        from where he and the other men were in the packing shed. He described
        the BDR as being extremely dusty with grey and white powder
        everywhere and after a day's work he would be covered with powder
        through his clothes and everything and the men would have to shower and
        take off their clothes at the end of the shift. He put the end of the asbestos
        removal programme at the time when the third defendant's contractors
        finished pulling the roof off which he thought would be some time in
        1996 or 1997. When it was suggested to him that he was only concerned
        with working in the BDR, he responded by saying that he referred to the
        BDR, the packing area and shed 4.

152           I take this evidence to mean that Mr Cotton was concerned about the
        potential exposure to asbestos while working with the third defendant, not
        only in the BDR but also while he was working in the packing area and in
        shed 4. In addition, the plaintiff's case asserts exposure to atmospheric
        asbestos before and after the asbestos removal programmes conducted in
        the BDR, as distinct from exposure during those removal programmes.
        Accordingly, air monitoring tests which relate only to the period when
        removal operations were being conducted do not address any presence or
        concentration of asbestos fibres for the other times when Mr Cotton
        claims he was exposed. The situation in relation to the removal of the
        asbestos roof sheeting is different, in this regard, because Mr Cotton was
        working in the packing shed while the asbestos roofs of that large building
        and the adjoining shed 4 were being removed and he claims to have been
        exposed to asbestos fibres during that removal process as well as to fibres
        emanating from the roof before then and, to that extent, air monitoring
        tests during the roof removal operations are of relevance.

153          As earlier stated, his sequence of work while with the third
        defendant, described by Mr Cotton, was that he was initially engaged as a
        casual packer in the Raymond Mill area and continued working there up
        until the time when he was retrenched in February 1991. On his
        re-engagement in October 1991 he spent three or four months in the
        R & D Department before being reclassified as a packer and then worked
        in the packing area with regular visits to the BDR. That pattern of work
        continued up until his diagnosis of cancer although, by May 2000, the
        asbestos removal programme had been completed
154         I see no reason not to accept the evidence given by Mr Cotton in the
        Workcover examination, or for that matter in his statutory declaration or
        answers to interrogatories, as being unreliable. It is true that in the
        Workcover proceedings he was not cross-examined on behalf of the first


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        or second defendants in the present action, but he was cross-examined by
        a representative of the third defendant although there were, of course, no
        issues of breach of duty involved in those proceedings in which statutory
        workers' compensation benefits were being sought. Nevertheless, the
        cross-examiner did not suggest to him that any of his evidence was false
        or mistaken or that any version or sequence of events other than the one
        advanced by Mr Cotton had occurred. So far as it is possible to tell from a
        mere transcript, Mr Cotton's answers were ample and responsive and were
        accepted as such by the third defendant's representative. I therefore
        regard his evidence as truthful.
155          The general tenor of Mr Cotton's evidence, without being precise, is
        that what are known as areas 1, 2 and 3 and the packing end were in close
        proximity to the BDR, although the BDR was closed off from them.
        Similarly, it appears from his evidence that his role as a shift work process
        operator, packer working in section 3 must have begun in January or
        February 1992 and that it was from then on that he began working
        regularly in the BDR. He said that this was about 12 months before the
        asbestos removal programme began in the BDR.

1. The workers at Australind
156           Mr Robert Colley was employed first as a packer and then as a mill
        operator by the third defendant at the Australind site from 12 January
        1989 to 30 October 1990. During this time he was working in the main
        factory area and, for the last 12 months of that period, as a mill operator
        side by side with Paul Cotton. He described Mr Cotton's duties as being a
        forklift operator bagging pigment, doing paperwork in the warehouse and
        said that he also w  orked in the BDR which was then still in the main
        factory building right alongside the mill (Exhibit 43, par 14). Mr Colley
        also said that while he was working in the main factory there were
        occasions when there would be men on the roof hosing down the asbestos
        cement sheeting with what he thought was water and that the men were
        wearing protective overalls, disposable face masks and gloves. He
        described the removalists as taking sheets off the roof, dropping them into
        a bin, covered on the inside and outside with black plastic and that while
        this was going on he, Paul Cotton and all the workers, continued to work
        in the general area of the main factory. He described noticing a very fine
        grey dust descending from the roof during these operations and
        distinguished this from the pigment itself which was very white. He and
        the other workmen constantly swept up the floors which were covered
        with the TiO 2 powder and the grey dust and they were working within a



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        25 metre radius of the area where the asbestos cement roofing sheeting
        was being removed.
157          In addition to the removal of the asbestos cement roofing sheeting, a
        dividing wall directly behind the mill where Mr Colley and Cotton were
        working was also made of asbestos cement sheeting and was also
        removed at some stage. Although Mr Colley did not work in the BDR
        Mr Colley said that he went in there on occasions and he also recalls
        seeing lagging hanging off parts of the band drier. He described it as
        being messy and in bad repair. He also recalled seeing pipe work in the
        BDR covered with asbestos lagging. He described the third defendant's
        operation as being a very large paint pigment factory which also produced
        sulphuric acid at that period. He said that the removal of asbestos cement
        sheeting from the roof in the main factory occurred during about the last
        two months before he left his employment which was in October 1990
        suggesting that the roof removal occurred in about September of that year.
        He said the asbestos cement sheeting appeared to be very old, was peeling
        and deteriorating. He was shown the illustrations of the pipe works and
        other apparatus within the BDR contained in the Matprolab report of
        March 1990, pp 5 - 11, Exhibit 45, and agreed that those illustrations
        represented the condition of the facilities during the time that he was
        working at the factory. He said that the heating pipes within the BDR
        were wrapped with insulation which had the appearance of matting, rather
        like underfelt. He said that the bandaging was coming off, that the hatch
        doors on the band drier were of pop-riveted tin with insulation beneath.
        He was not shaken in any of this evidence in the course of
        cross-examination.
158           Another former employee of the third defendant, Mr Christopher
        Edward Savage, gave evidence about the conditions at the Australind
        plant. He had worked at the site for 34 years and 8 months and had
        retired. My impression of him was that of an absolutely truthful, precise
        and reliable witness. He was the epitome of an intelligent, experienced,
        trustworthy senior tradesman. His employment began as a crane driver
        but he then became a maintenance service officer and he used to go
        through the BDR twice a day to grease the machinery bearings on the
        fans. He saw Mr Paul Cotton cleaning up in the BDR at different times.
        He knew that the lagging in the BDR contained asbestos because 30 years
        ago he had applied asbestos fibre lagging insulation himself in various
        parts of the building. He described the asbestos as coming in bags, being
        a blue fibre and being labelled as asbestos. It was kept in the lagging shed
        and he would mix the asbestos up with water and paste it over the pipes
        and then bandage it up. According to his recollection this occurred when

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        Laporte took over the plant in 1962 or 1963. That practice continued for
        about six years. The lagging shed was pulled down and the stored
        asbestos removed in about 1976.

159           Mr Savage described asbestos lagging being used over lead-lined
        pipes and plastic and steel pipes. According to Mr Savage there was
        asbestos lagging in the BDR, on all the heavy duty steam pipes, on the
        band drier itself and on the extractor fans on the top of the band drier.
        There was also asbestos lagging around the edges of the band drier doors
        themselves, some of which was damaged and which was just pushed back
        in again. He said that he saw Paul Cotton working in the BDR and
        removing the doors to the band drier to take them off and clean inside.
        According to Mr Savage, outside contractors repaired the asbestos lagging
        from time to time when it was damaged. Lagged piping ran along a brick
        wall on the left hand side of the band drier and on top of the band drier
        itself. Some of the piping was not in good condition and some was
        damaged. Sometimes the lagging would come down onto the ground and
        most times would be swept up. He recalled lagging on the inside of the
        hatch doors in the BDR which would sometimes fall onto the ground and
        the doors themselves would sometimes be falling off.
160           The exhaust fans had lagging on them as well and Mr Savage saw
        this during his duties of climbing up and greasing the fans. That lagging
        was not in good condition but the old lagging would just sit there until the
        fans were brought down for repair and re-lagging about twice a year. The
        lagging was taken off by the fitters in the workshop and was just picked
        up off the floor by shovel and by hand and put into a bag. Despite this
        process of re-lagging about twice a year, he estimated that there would
        still be about a third of the original lagging material still on the pipes.
        After some concern being expressed at safety and union meetings, the
        lagging was eventually removed from the BDR several years later. This
        was done with removalists putting the lagging in big skips with black
        plastic lining and it was mostly asbestos material so removed.

161          In cross-examination Mr Savage said that the contractor known as
        KBE was engaged to repair the lagging and that they came in regularly.
        He was asked if he was aware of a calcium silicate block being used to
        seal the lagging but he said that that was not known to him. In
        cross-examination he agreed that the removal of the lagging was done by
        the contractors in November 1991, but that there was more removal after
        1992. He maintained that much of the lagging had been removed and
        replaced with rock wool by 22 March 1995 and that it was pretty well
        correct to say that it had all been replaced by that date. The lagging on the


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        pipes was taken out in November 1991 and the rest by March 1992.
        However, the insulation on the band drier doors was mainly removed in
        the period 1994 to March 1995. Insulation on top of the band drier was
        taken out closer to 1995. He was asked whether there were warning signs
        about the presence of asbestos or signs on pipes bearing the word
        "asbestos", but he said that there were no such signs in the BDR but there
        were some such signs down in the boiler house but nowhere else.

162          According to Mr Savage the asbestos removal programme began in
        1990 and continued for several years. He was asked about an incident of
        asbestos exposure which occurred during the period 7 - 12 April 1995 and
        confirmed that this had occurred and that one of the men so exposed was
        Mr Cotton (see Exhibit 47 - the list of employees so affected, prepared for
        Mr Engebretsen - one of the third defendant's supervisors).
163           Another employee of the third defendant who worked at the
        Australind factory when Mr Cotton was employed there was Mr Noel
        Folbig. He began work for the third defendant on 17 October 1988 as a
        part-time electrician and was made full-time in 1990 or 1991 and, at the
        date of the trial was still employed by the third defendant. In May 2001
        he was an electrical instrument fitter doing electrical instrumentation work
        and was familiar with the BDR and surrounding areas. From the time of
        his first employment with Millennium he was a safety representative for
        about two and a half years and in that role attended Safety Committee
        meetings at which there was discussion about an asbestos removal
        programme. He remembered one such meeting where he discussed
        removal of asbestos from the roofs in the plant with the local DOSHWA
        (Department of Occupational Safety and Health of Western Australia) -
        Inspector Greg Baker. In about 1992, according to his recollection, the
        third defendant was planning to remove the asbestos and discussed this
        with the safety representatives at these meetings.

164          Mr Folbig went into the BDR about every three months for a regular
        overhaul or, on other occasions, when some electrical work needed to be
        done or an electrical fitting repaired. He described the BDR as a long
        room with a large slow steel conveyor upon which the pigment flowed.
        According to him it was a very hot environment and when the band drier
        was running and the fans going it was a very dusty and noisy place. Pipes
        came in from the northern end of the BDR where the main steam line runs
        in and pipes ran along the ground next to the band drier itself.
        Modifications took place in about 1995 or 1996 and most of the asbestos
        lagging was meant to have been taken out of the BDR at that time.
        Lagged steam pipes were removed during that period. However, there


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        was an incident after the asbestos removal programme. The band drier
        was started up and it "blew a lot of stuff out of the unit". A sample of the
        dust was taken to the lab and was confirmed to contain asbestos. All the
        men there at the time recorded their names on a document describing what
        happened as a permanent record. I find this to be a reference to the
        episode occurring from 7 - 12 April 1995 recorded in Exhibit 47.
165           Mr Folbig described the BDR as being in poor shape with lagging in
        poor condition during his earlier years there. He said that the lagging in
        the doors of the band drier was in bad condition and that each time one
        tried to take a fan out and put it back, the lagging would get squashed and
        break up. Lagging would hang out of the doors where the doors used to
        bolt up. There were old asbestos lagged pipes and the place was not
        sealed off. When he worked at the southern end of the BDR where the
        chain conveyors ran he noticed pieces of insulation on the floor as well as
        pigment and brown dust.
166          The Safety Committee meeting which he attended at which there was
        discussion about a proposed asbestos removal programme was the
        meeting of 15 January 1992 (the minutes are Exhibit 49). These recorded
        that there was still asbestos on the BDR pipes at that date and that,
        although some pipe work had been removed, it was felt that this was not
        enough as there was still a problem in that area. He attended another
        Safety Committee meeting on 11 March 1992, the minutes of which are
        Exhibit 80. These discussed guidelines for the removal of asbestos
        sheeting and the precautions which were then to be taken. He agreed that
        when this removal occurred measures were taken to separate the areas
        being worked on, that they were sealed off with plastic sheeting, and that
        ordinary employees were kept out while the lagging and insulation was
        removed. When the asbestos cement roof panels were removed the area
        below was cordoned off with coloured bunting or tape and air monitoring
        was conducted. The contractors for the removal of asbestos within the
        BDR were KBE and that work was done probably some time in 1992.

167           Another employee of the third defendant, Mr Mark Forrester, gave
        evidence. He began working at the Australind site on 23 March 1989 and
        at the time of the trial was still employed there. He knew Mr Paul Cotton
        who began working at the site about 18 months after Forrester himself
        did. They worked together on four or five jobs in the packing room, on a
        forklift job, bagging on the heads and bagging on the band drier. Both
        worked together in the BDR. Mr Forrester described the asbestos
        insulation existing on all the steam pipes in the BDR and he said that this
        was in bad condition with the lagging falling in pieces to the floor. The


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        hatch doors to the band drier itself had to be opened and the band drier
        scraped out on every grade change. The doors weighed about 30 kgs and
        were 1 to 1.2 metres wide with steam pipes inside and heavy insulation.
        According to Mr Forrester, when the asbestos roof was being removed
        work continued below, although not directly below. Paul Cotton was
        constantly cleaning and sweeping up and there was a constant presence of
        lagging on the floor. The environment was pretty dusty and dirty. He
        agreed that the removal of the asbestos in the BDR took place during
        November 1991 to March 1992 but, in retrospect, this must be regarded as
        confined to asbestos lagging rather than to the roof materials or the
        insulation in the doors.

168           A certificate of analysis dated 18 April 1995 (Exhibit 52) showed the
        results of testing of a sample taken from the band drier area. This
        confirmed that the sample contained asbestos, being both Chrysotile and
        Crocidolite asbestos. This is positive confirmation that asbestos within
                                                  ore
        the BDR contained Crocidolite, the m noxious blue asbestos earlier
        described by Mr Savage. I consider Mr Forrester to have been a careful,
        measured and precise witness who gave thoughtful and intelligent
        evidence with a good recollection of events. I found him to be truthful
        and frank. He did not recollect any tape marking off areas in the packing
        shed during the period of the asbestos cement sheeting removal from the
        overhead roof, but he did remember the occasion of the removal of
        insulation from the BDR when the whole door to that room was sealed
        off, the BDR was fully enclosed, when there was strict enforcement of an
        exclusion of entry of any personnel not involved in the operation, and that
        those who were admitted had heavy protective clothing. He accepted that
        the removal process of lagging in the BDR was between the period of
        November 1991 to March 1992.
169           Another former employee of the third defendant who had worked
        with Mr Paul Cotton was James Leonard Retter. According to his
        recollection the removal of lagging in the BDR occurred in about 1995.
        He began his employment with Millennium Inorganic Chemicals in about
        1986 and finished in about 2000. He worked on the same shift as Paul
        Cotton and saw the deceased work in the BDR. Mr Cotton then worked
        as an operator but was also required to clean in the BDR. According to
        Mr Retter insulation was present in the BDR, especially on the doors, and
        all the lagging inside the doors of the side of the band drier was visible.
        Piping running along the top of the band drier and along the wall had
        lagging. The doors or hatches to the band drier were filled with a fibrous
        material and the tin covering on the front was old and tended to peel off
        and expose the underlying fibres. According to Mr Retter, these doors

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        were about 20 or 30 years old and were in a bad state of repair.
        According to him, lagging on the pipes alongside the room appeared to be
        like a foamy substance and there were patches where it had broken down
        and broken off. In his view, the pipe lagging looked very old and was
        deteriorating. He saw broken lagging on the ground and whoever was
        sent in to clean up in the BDR had to sweep up the broken lagging. He
        did it many times and so did Mr Cotton. He also described the asbestos
        roof in the packing area being removed when he and Cotton worked there.
        He was one of the workmen who was subject to asbestos exposure during
        the incident in April 1995 and whose name is listed in Exhibit 47.
170           Another former employee of the third defendant was Milton
        Jonathon Mitchell Bidelle. At the date of trial he had worked for the third
        defendant for over 20 years from 9 March 1981. He worked in the
        bagging area (areas No 1 and 3) and also in the BDR. He used to control
        the band drier and used to clean in the BDR. He was on the same shift as
        Paul Cotton at some stage and worked together with him in the BDR.
        Mr Bidelle described Mr Cotton's role as being at the bagging end and
        doing general cleaning. Bidelle saw Cotton shovelling pigment into bags
        after having dragged it out of the band drier and also saw him put the
        doors back onto the band drier. He described this as a very dusty job.
        According to Mr Bidelle, there was a lot of lagged steam piping in the
        band drier area which was lagged with old asbestos which had been there
        for about 30 years. This lagging was dropping off in some areas. The
        hatch doors to the band drier which were removed for the cleaning were in
        a bad way. Sometimes the doors were split and the lagging would fall to
        the ground from them as well. This, and any other fallen lagging, would
        be swept up and shovelled into a bag. He thought the doors in the BDR
        were a problem because they fell apart (Exhibit 70). In cross-examination
        he said there were a lot of steam pipes in the BDR, some were elevated
        about 10 feet above the ground, others were closer to the ground. When
        asked about the damaged lagging, he said that it often remained in the
        damaged condition for ages without repair. I formed a good impression of
        Mr Bidelle as a truthful and reliable witness.

171          From 1969 to about 2000 Mr Robert Allan Elkington was a
        government inspector accredited under the Factories and Shops Act,
        which was replaced by the Occupational Health and Safety Act 1988
                                                       nd
        (WA). He was Chief Inspector of Factories a Shops and then Chief
        Inspector of the Workplace Branch and was involved in the first
        regulations dealing with occupational asbestos exposure in 1978. He
        continued to be involved in the revision of equivalent regulations and
        those now in force under the Occupational Safety and Health Regulations

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        1988. Sometime in the late 1980's, or early 1990's, he visited the
        SCM Chemicals' operation at Australind. On his first visit he noticed that
        lagging on the pipes had become very friable, because of the acid which
        had affected the pipes. He discussed with management a plan for
        substitution with a more acceptable system of lagging. Some years later
        he made a second visit and discussed with the safety officer at the time a
        draft plan to revise the work. He had been supplied with copies of
        photographs of the BDR taken by Matprolabs during its inspection in
        March 1990 (Exhibit 44) and, by reference to those photographs,
        confirmed that the illustrations of broken lagging which they depicted
        were representative of the condition of the pipes during his first visit.

172           Mr Elkington expressed the view that the lagging on the drier,
        depicted in Exhibit 44, photograph No 2, did not look in good condition
        and that if it contained asbestos he would be concerned about the
        exposure which it caused to people working in the vicinity. He described
        the insulation appearing in Exhibit 44, photograph No 3, as possibly
        containing asbestos and looking in very poor condition liberating fibres
        into the air. Mr Elkington added that for asbestos lagging of that period it
        was customary to have a hard coating of paint or sealant over the top of it,
        but that once that broke the underlying material released fibres which
        were frequently found on the floor or shelves in the vicinity. Anybody
        working in that vicinity could be exposed to breathing in such fibres. He
        went on to criticise the condition of the lagging on the electric motor
        (exhaust fan) in photograph No 4, pointing out its capacity to release
        fibres to the air. In his view, the photographs produced revealed that
        breakages to the outer crust of the lagging meant that any type of fibre in
        the interior would be released to the atmosphere. He mentioned this
        problem as arising not only with pipes but with joints and gaskets and that
        with an overhead pipe, if the casing comes away, whether a painted,
        sealed or metal casing, the insulation is revealed and becomes airborne.
        He added that once the lagging breaks away from the pipe, it falls out in
        lumps and a lot of small fibres would be released from these.
173          The real danger is in the microscopic fibres which are not visible and
        are smaller than those which occasionally show up, for example, in shafts
        of sunlight. Mr Elkington explained that if a worker trod on such broken
        lagging underfoot while involved in sweeping up pieces of it, those
        actions would release respirable fibres into the surrounding atmosphere.
        The first of his visits to the Millennium operation at Australind probably
        occurred before 1988 and the second, probably in early 1989. In
        cross-examination, it was suggested to him that if he was dissatisfied with
        the situation he could, and should, have initiated a prosecution.

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        Mr Elkington was not able to recall the exact details of his inspection, but
        pointed out that as deputy inspector he relied on the local representatives
        of the department to exercise powers to issue a prohibition or
        improvement notice if and when necessary and that his main priority was
        to secure improvement in working conditions through co-operation where
        possible. I do not regard this implied criticism of his conduct as in any
        way detracting from his reliability or frankness as an independent witness
        of truth.
174          On these issues the third defendant called its former maintenance
        supervisor at Australind, Mr Andrew Turk, who, since July 2004 had been
        operations manager at another different chemical plant. He had been
        maintenance supervisor at the third defendant's plant at Australind from
        1989 to 1996 and, during those years, was in charge of the asbestos
        removal programme. Mr Turk explained that during 1988 there was
        concern on the site expressed by employees over the presence of asbestos
        and that this arose from demolition then proposed for an old section of the
        plant which contained asbestos.
175           As a consequence of this and because of the realisation that there was
        asbestos within the workplace, the third defendant commissioned two
        surveys by a firm of materials protection engineers - "Matprolabs". The
        first of the resulting reports, is dated March 1990 (Exhibits 44,
        photographs and Exhibit 45, text) and relates only to the BDR. The
        second, dated August 1990 (Exhibit 113), relates to asbestos presence in
        sections 1, 2, 3 and 4 of the plant area. In his statement of evidence
        (Exhibit 221), Mr Turk said that these surveys identified that the lagging
        on several of the older steam pipes still in use did have some asbestos
        content in the black wrap around the fibreglass insulation. He said that
        this was not particularly hazardous because it was well encapsulated and
        less likely to become airborne. However, he acknowledged that "there
        were very few pipes with asbestos in the actual insulation" and said that
        by far the biggest scope of asbestos on site was the building sheeting.

176          According to Mr Turk, once the results of these surveys were known,
        pipes which were covered with material containing asbestos were clearly
        labelled with silver stickers bearing the words "Asbestos" in red and these
        were placed on items in the BDR - an example of such a sticker is
        Exhibit 232, later produced by Mr Engebretsen. Mr Turk said that when
        the survey identified sections of insulation which were in poor repair,
        these were temporarily patched up and made safe until it could be
        removed and that this work was done by licensed asbestos contractors.
        He said that he directed members of the third defendant's staff to seal any


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        sections of the asbestos cement sheeting around the plant which were
        broken as a precaution until it could be replaced. The work programme
        was spread over several years on a priority basis and, in order of priority,
        the hazards were:
              (1)      insulation;

              (2)      asbestos cement sheeting with which people may come
                       into contact; and

              (3)      the roofs.
        He described how an asbestos removal programme was publicised in
        advance to all personnel on site and how various asbestos removal
        contractors were used over the period. The main such contractor was
        KBE, but there were others as well. Mr Turk explained how the company
        instituted a monitoring programme before the start of the removal of the
        asbestos and that this involved testing monitors located around the whole
        of the Australind site, designed to identify the presence of any airborne
        asbestos. These test results were analysed by Matprolabs and reported on
        to the third defendant on a regular basis.
177          To Mr Turk's recollection, this monitoring programme lasted for
        several years before and during the asbestos removal programme and was
        said to determine whether or not any airborne asbestos level exceeded the
        then current DOHSWA standard of 0.1 fibre/ml of asbestos. He said (at
        pars 45 and 46 of Exhibit 221) that during the removal of the asbestos the
        third defendant's personnel were denied access to the removal area and,
        where possible, the plant was shut down but that on a few occasions this
        was not practical. In par 60 of Exhibit 221 Mr Turk set out a detailed
        description of the staging for removal of asbestos from the BDR and,
        essentially, this fell into four phases, namely:

                 (1)       Removal of asbestos lagging from three steam pipes and
                           from the fan housing. Quotes for this were sought in
                           September/October 1991 and according to Mr Turk about
                           50 per cent of that asbestos lagging had been removed
                           from the BDR by November 1991.
                 (2)       On 7 February 1992 a quote was obtained for the removal
                           of further asbestos from the BDR and the third defendant
                           gave instructions (Exhibit 221(E)) on 18 March 1992 for
                           that work to be done from 18 - 22 March 1992.




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                 (3)       Removal of asbestos tape from the band drier hatch doors
                           and roof and insulation on top of the band drier was carried
                           out by the contractors Bains Harding on 15 December
                           1994.
                 (4)       In March 1995 KBE Contracting removed asbestos wall
                           sheeting from the BDR and the adjoining DWF room.
178          Mr Turk maintained that all asbestos lagging and insulation in the
        BDR had gone by December 1994.                In cross-examination he
        acknowledged that he did not know the deceased Paul Cotton. He said
        that the doors to the band drier were the most serious areas of
        contamination. He visited the BDR once or twice a month and
        acknowledged that dust drifted down from the roof but he said that he did
        not ever see lagging on the floor of the BDR.
179          I am obliged to say, however, that in a number of respects I am
        unable to accept the reliability of Mr Turk's evidence. None of the actual
        workmen whose evidence I have already summarised, saw red asbestos
        signs on piping or elsewhere in the BDR and I see no reason why their
        testimony in this respect should be doubted. After all, the presence of
        absence of such labelling, is of very little moment in this case because,
        even if such labels were there, their presence did not diminish the hazard
        nor absolve the workers from the performance of any of their duties which
        have been described. There may have been such notices posted on some
        plant or apparatus elsewhere on the site, perhaps in the boiler room/power
        house as acknowledged by Mr Savage (see above), but I do not accept
        Mr Turk's evidence that they were conspicuous in the BDR or elsewhere
        where Mr Cotton and his colleagues worked.
180          Next, I do not accept Mr Turk's assertion that all the asbestos
        insulation and lagging in the BDR had been removed by December 1994.
        There is explicit confirmation that asbestos exposure occurred in the BDR
        in April 1995 to the consternation of the workforce. Furthermore, the
        evidence from Mr Turk that comparatively few of the pipes of the BDR
        were of the old lagged asbestos variety and that the only asbestos on
        others was contained in the sheet covering coated with tar is not consistent
        with the observations of the other workmen, nor with the Matprolab report
        which will be described in detail shortly. Nor is Mr Turk's assertion that
        the asbestos removal programme was effectively completed by December
        1994 consistent with the programming depicted in the third defendant's
        document prepared by him dated 25 August 1993 (Exhibit 257).




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181          Perhaps the most that can be said is that efforts were made to remove
        insulation containing asbestos by the end of 1994 and that asbestos
        sheeting (on walls or roofs) was programmed for removal over a 5 year
        period from 1994 to 1998 during which any particularly hazardous
        asbestos sheeting was to be sealed by some form of protective coating.
        The third defendant's own progressive maintenance reports (described in
        more detail later) contain many references to the presence of asbestos or
        to ongoing removal programmes after December 1994.
182          Because of these demonstrable contradictions of significant parts of
        the evidence given by Mr Turk, I can only treat his evidence as a whole
        with significant reserve and because of this, when any of his evidence
        conflicts with the testimony of workmen on the site or contemporary
        documents, I have concluded that it should be disregarded.
183          Generally speaking, from the contemporary documentary evidence,
        and the testimony of other witnesses, I have no doubt that the general
        condition of the lagging on the pipe work, fan exhaust systems, insulation
        in the band drier the state of asbestos was significantly worse than
        acknowledged by Mr Turk's statement.

2. The Matprolab Reports of March and August 1990
184          Perhaps the most telling and detailed contemporary description of the
        condition of the plant on the Australind site in 1990 is to be found in the
        two Matprolab reports already mentioned (Exhibits 44/45 and 113) and it
        is necessary to examine these in some detail. The introduction to
        Exhibits 44/45 describes that Matprolab was engaged to undertake a
        survey of various plant items in the band drier shed to identify asbestos
        materials. Matprolabs were to determine accurately the extent of the
        asbestos, take the samples of suspect material and have these analysed by
        a laboratory and to report. The investigation confirmed the presence of a
        variety of asbestos fibres in the BDR. The variety included Chrysotile
        (white asbestos); Amosite (brown or grey asbestos) and Crocidolite (blue
        asbestos). A qualitative estimate was given to the quantities of these
        fibres discovered and the categorisation adopted was:
              "A 'trace' - means much less than 1 per cent and denotes the
              presence of approximately 1-5 fibres in the sample examined.
              Minor - less than 20 per cent content.

              Major - greater than 20 per cent content."



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        All those estimates of percentage were by volume.
185           Of 17 samples taken from within the BDR, 14 were reported as
        positive for asbestos. 12 of these were reported as being "minor Amosite"
        - less than 20 per cent content. Two were reported as being "major
        Chrysotile", that is more than 20 per cent by volume. The report contains
        a series of six coloured photographs of the interior of the BDR illustrating
        areas sampled and observed or detected as asbestos locations. These
        photographs are those which have been said by other witnesses,
        Messrs Colley and Elkington to give an accurate depiction of the state of
        the works at the time those witnesses were working there or visiting that
        site.

186          Particular findings reported by the Matprolab investigation are now
        described:
              1.      Sample 1 - Minor Amosite was located in the pipe rack
                      running north-south on the eastern wall.
                      Sample of lagging material from the western pipe in the
                      rack. This is covered with cloth-like material and extends
                      approximately 55m along the eastern wall. The diameter
                      of the lagged pipe is approximately 200mm. The
                      cloth-like material is damaged in several places, exposing
                      the fibrous lagging material.
              2.      Sample 2 - Minor Amosite

                      Pipe rack running north-south on eastern wall.
                      Sample of lagging material from the middle pipe in the
                      rack. The lagged pipe has a diameter of approximately
                      200mm and extends approximately 55m along the eastern
                      wall. The lagging is covered with a cloth-like material,
                      however this is damaged in areas exposing the fibrous
                      lagging material.

              3.      Sample 3 - Minor Amosite
                      Pipe rack running north-south on eastern wall.

                      Sample of lagging material from the eastern pipe in the
                      pipe rack.    The lagged pipe has a diameter of
                      approximately 300mm and extends approximately 55m
                      along the eastern wall. The lagging covered with a


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                      cloth-like material, however, this is damaged in areas
                      exposing the fibrous lagging material.
              4.      Sample 4 - Major Chrysotile

                      Band dryer
                      Sample of hatch door lining material from east side of
                      dryer. The material is very friable and is coming away
                      from the door.

              5.      Sample No 5 - Synthetic mineral fibre
                      Band dryer

                      Sample of lagging material from the exhaust fan duct on
                      the east side of the dryer. The lagging material is sealed
                      with paint but the paint is damaged in several areas,
                      exposing the very friable lagging.
                      There are a total of two exhaust ducts on the dryer and
                      both contain the same lagging material as tested.
              6.      Sample No 6 - Minor Amosite

                      Band dryer
                      Sample of lagging material from the exhaust fan on top of
                      the dryer. The lagging material is sealed with paint,
                      however the paint is damaged in areas leaving the fibrous
                      lagging material exposed.
                      A total of two exhaust fans are situated in the band dryer
                      shed.
              7.      Sample No 7 - Minor Amosite

                      Band dryer
                      Sample of main steam pipe lagging material. Pipe
                      lagging extends approximately 35m along the west side
                      of the band dryer and is sealed with a cloth-like material.
                      The pipe diameter is approximately 300mm. The lagging
                      material is exposed in some areas and is very fibrous.
              8.      Sample No 8 - Minor Amosite


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                      Band dryer

                      Sample of small "off shoot" steam pipe lagging material.
                      The material is approximately one metre long and bends
                      around a corner on each offshoot. It is sealed with
                      material which has torn in several areas, exposing the
                      fibrous lagging. The diameter is approximately 250mm.
              9.      Sample No 9 - Minor Amosite

                      Band dryer
                      Sample of lagging material from steam pipes running
                      from the main horizontal line to the band dryer. The
                      lagging material is approximately 80mm in diameter and
                      extends approximately 600mm around an elbow. The
                      lagging material is sealed with calico cloth which is torn
                      in some areas, exposing the fibrous lagging material.

              10.     Sample No 10 - Minor Amosite
                      Band dryer

                      Sample of lagging material on southern section of main
                      steam pipe on the west side of the band dryer. The
                      lagging is approximately 80mm in diameter and extends
                      approximately 6m to the end of the pipe. The lagging is
                      sealed with calico cloth which is damaged in some areas
                      leaving fibrous lagging material exposed.

              11.     Sample No 11 - No asbestos detected.
                      Band dryer

                      Sample of cloth material sealing some of the lagged
                      steam pipes on the west side of the band dryer.
              12.     Sample No 12 - Major Chrysotile

                      Band dryer
                      Sample of lagging material from the long vertical section
                      of the steam pipes running from the main horizontal
                      steam line to the dryer. The lagging material is sealed
                      with a cloth-like material and has a diameter of


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                      approximately 70mm. Some damage in the form of torn
                      cloth was noticed, leaving the fibrous lagging material
                      exposed.

                      Some of the pipes mentioned in sample No 12 are lagged
                      with glass fibre.

              13.     Sample No 13 - Minor Amosite
                      East-west pipe rack on the south wall (continuation of
                      north-south rack).
                      Sample of lagging material from northern pipe in
                      east-west pipe rack. The lagging is approximately
                      200mm in diameter and extends approximately 8m along
                      the southern wall and outside. The lagging is sealed with
                      calico cloth which is damaged in areas leaving the fibrous
                      lagging exposed.

              14.     Sample No 14 - Synthetic mineral fibre
                      East-west pipe rack on southern wall.

                      Sample of lagging material from middle pipe. The
                      lagging is approximately 200mm in diameter and extends
                      approximately 8m along the southern wall. The lagging
                      is sealed with calico cloth which is damaged in areas
                      leaving the fibrous lagging exposed.
              15.     Sample No 15 - Minor Amosite

                      East-west pipe rack on southern wall.
                      Sample of lagging material from southern pipe. The
                      lagging is approximately 300mm in diameter and extends
                      approximately 8m along the southern wall and outside. It
                      is sealed with a cloth material which is torn in several
                      areas, exposing the fibrous lagging.
              16.     Sample No 16 - Minor Amosite

                      East-west pipe rack on southern wall.
                      Sample of lagging material from short middle pipe. The
                      lagging is approximately 300mm in diameter and extends


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                      approximately 4m along the southern wall. It is sealed
                      with calico cloth and has very little damage.
              17.     Sample No 17 - Minor Amosite

                      Finishing plant area (next to band dryer).
                      Sample of lagging material from vertical steam pipe
                      running up the north wall of the finishing plant. The
                      lagging is sealed with a calico cloth and very little
                      damage was noticed."
        I find this Matprolab report (Exhib it 44/45) to be objective and reliable
        and as providing substantial corroboration of the evidence of Mr Cotton
        and other former or present employees of the third defendant (excepting
        Mr Turk).
187           Of the second Matprolab report of August 1990 only some six from a
        total of 113 pages were tendered in evidence. However, that is sufficient
        to demonstrate that the report covered sections 1, 2, 3 and 4 of the plant
        (components of which have already been described in [      128] above) and
        that the purpose of this Matprolab survey was to audit the extent, location,
        composition and condition of asbestos cement sheeting and any insulation
        to lines which contain asbestos. Only the summary of the report was
        tendered but it confirms that asbestos materials had been identified.

188           The consultants reported that:
              "It was found that the asbestos was in one of four basic forms,
              either gasket material, woven tape lagging on pipe work,
              asbestos plaster lagging on pipe work or as asbestos cement
              products.
              These require different handling techniques and precautions.
              The safe handling of asbestos cement products is detailed in
              regulation 820 of the Occupational Health Safety & Welfare
              Regulations under DOHSWA Bulletin.

              As a general rule, asbestos incorporated into a stable (cement)
              matrix presents minimal risk. As this matrix breaks down the
              asbestos can become airborne and as such requires remedial
              action. Material in this form is called friable (fibre releasing).

              ...



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              In general, asbestos cement products at SCM were found to be
              structurally sound (no cracking) but physically soft and friable.
              It was found that some of the sheeting was very friable,
              particularly where direct chemical contact had occurred.
              ...

              Roof sheeting was found to be friable almost without exception.
              It was also found to be porous in many areas. This requires
              consolidation. An elastomeric coating may be required to seal
              leaks.

              ...
              Asbestos insulation on pipe work must ultimately be removed.
              Certainly the few pipes in section 1 insulated with asbestos
              must be removed prior to demolition. ...
              ...

              With respect to the rest of the plant surveyed it was generally
              found that pipe insulation was in poor condition and requires
              remedial action. It would therefore be recommended that a
              programme be instigated to remove the asbestos insulation.
              That which is in sound condition may be deferred but
              economics of scale may make this option less attractive.

              Repairs to insulation should only be considered temporary as
              removal will ultimately be required ... Precautions will need to
              be taken on pipe work with the appearance of being lagged with
              synthetic mineral fibre (glass wool, rock wool, etc) as there was
              evidence that previous asbestos removal has not always been
              thorough or to current standards."
189          Consequently, I accept that by August 1990 there was a general
        asbestos hazard in areas 1 to 4 of the defendant's plant. The pipe
        insulation was generally in poor condition, and even pipe work currently
        insulated with non-asbestos materials was suspect because of inadequate
        precautions taken when removing the original asbestos lagging. The
        asbestos cement roof sheeting throughout the areas was generally found to
        be friable and, therefore, prone to shedding asbestos cement dust. This
        obviously reflected the condition of the buildings which had been of
        concern to the workforce for quite some time in view of the complaints
        and agitations of the workforce which in 1988 had prompted this inquiry.


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        It also means that, notwithstanding the progressive removal of lagging
        containing asbestos from the pipes within the BDR in 1991/1992 and
        subsequent removal of asbestos insulation in the band drier doors and
        hatches in 1994/1995, there remained a constant potential hazard of
        asbestos exposure from the friable asbestos cement roofing.

190          It may be inferred that the third defendant did not adopt or follow the
        primary recommendations of Matprolab for the removal of the asbestos
        hazard. In Mr Turk's memorandum of 5 March 1991 (Exhibit 98), that is
        12 months after the first Matprolab report and six months after the second
        Matprolab report, Mr Turk was recommending that, rather than engage
        contractors to carry out the work, the third defendant should train up its
        own personnel to do the work because this would be considerably cheaper
        "though the work would probably take 2 - 3 years - rather than 3 - 6
        months". As it transpired, the removal programme lasted from about
        March 1991 until late 1997 or 1998, much longer than originally
        contemplated and, as it would seem, recommended by Matprolab.
        Throughout this period the risks of asbestos exposure to the workforce
        continued.

191          Mr Ian Derek Green was formerly a supervisor with KBE
        Contracting Pty Ltd, where he worked over the years from 1987 to 1998.
        He was called by the third defendant and gave evidence about working at
        the SCM site at Australind for KBE in relation to asbestos removal
        programmes. These resulted from discussions between himself on behalf
        of KBE and Messrs Andrew Turk and Mr Ross Engebretsen and others
        for SCM/Millennium. The work was done in accordance with the
        prevailing Code of Practice (Exhibit 230) and the third defendant's staff
        were not permitted to enter exclusion areas when asbestos removal was
        taking place. He described the removal of asbestos lagging from the BDR
        as taking place in four stages, all conducted during shut down
        maintenance periods when the band drier was not running.
192           Progress of the work was as follows:

                 1.        First Stage - Removal of calcium silicate block from steam
                           piping that surrounded the band drier room. The calcium
                           silicate block was an Amosite asbestos fibre product used
                           for pipe lagging or insulation. It came in a moulded shape
                           that surrounded the pipe and was then wrapped in
                           non-asbestos cloth material or in the case of the main
                           steam pipe it was coated in a black tar-like substance. In
                           Mr Green's recollection the black tar coating cloth was for


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                           the most part in reasonably good condition but he noticed a
                           few puncture holes and some chips on the outer coating of
                           various pipes but he did not see bits of asbestos lagging
                           falling or hanging from beneath the protective coatings.
                           (Mr Green's evidence that the material under the black
                           tar-like substance over the steam pipes was an Amosite
                           asbestos fibre product is inconsistent with Mr Turk's
                           explanation that the binding alone was asbestos and the
                           insulation beneath did not contain asbestos and, again, with
                           regard to this controversy, I reject the evidence of
                           Mr Turk.)
        Mr Green observed that the galvanised steel cladding on the calcium
        silicate blocks that surrounded the vertical pipes was in poor condition
        with joints split in areas and with the silicon block beneath visible through
        the outer non-asbestos cladding.
193           Next:

                 2.        Second Stage - This was the removal of asbestos seals,
                           gaskets and sheeting which did not require full isolation of
                           the working area. These were on the door and floor
                           gaskets of the band drier.
                 3.        Third Stage - This was asbestos removal performed by
                           Mr Green for the removal of redundant piping.
                 4.        Fourth Stage - This was the removal of asbestos sheeting
                           from roofing and walls on several different occasions.
194           Mr Green's evidence elaborated upon the methodology employed for
        each of these asbestos removal stages and their constituent procedures,
        ranging from full isolation of the working area to a lesser form of
        exclusion but, in each case, including the prohibition of having SCM
        employees in the near vicinity. He also explained how a programme of
        air monitoring was established and maintained during the asbestos
        removal operations. It is unnecessary to elaborate on his evidence in this
        regard because I am satisfied that, in relation to the more intensive and
        hazardous removal processes, namely the removal of asbestos lagging
        from piping, gaskets and exhaust systems, and the removal of asbestos
        insulation from the band drier doors, seals, hatches and gaskets,
        comprehensive isolation techniques were used and, of equal significance,
        that the work was completed quickly in short intervals each of a few days
        at the most. However, with regard to the removal of the asbestos cement
        sheeting on roofs or walls, the precautions were less intrusive and
        although the third defendant's employees were not permitted in the

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        immediate vicinity of the work site, I am satisfied that there was still
        scope for dust from the removal of overhead asbestos roof sheeting to
        float down onto areas in which employees were working, as described by
        Mr Colley who, with Mr Cotton, was working in the packing area for at
        least some of this time.

195           The Assistant Maintenance Superintendent of the third defendant's
        premises at Australind during the period March 1990 to June 1999 was
        Mr Ross Engebretsen who then went on to become the Construction
        Supervisor. It was his role to supervise the asbestos removal programme
        under responsibility delegated to him by Mr Andrew Turk. He gave
        evidence of his role in this regard in his written statement (Exhibit 234).
        At the date of the trial he was the Construction Supervisor for the third
        defendant and had been employed in that capacity since June 1999. He
        was the only maintenance supervisor involved in the asbestos programme
        from early 1992. He said that after the Matprolab's surveys of March and
        August 1990, signs indicating the presence of asbestos were attached to
        various areas of the plant, an example of which is the photograph in
        Exhibit 233. He said that the signs were subsequently removed as the
        asbestos was removed from the particular area and he recalls seeing such
        signs in the BDR in at least eight places which he lists in his statement
        (Exhibit 234). As previously noted none of the workmen who gave
        evidence, including workmen who had operated in the BDR, recalled
        seeing any such signs, although asked directly about them.
        Mr Engebretsen said they were there, has produced a photograph to
        illustrate at least one of them and said they were visible, but there is no
        detail given of the number of signs or their prominence. I can only
        conclude, therefore, that in the overall setting of the very large spaces and
        multiple pipe racks in the BDR that these were not conspicuous and were
        not noticed by the workmen during the relatively short duration in which
        they existed. However, as mentioned earlier, nothing turns on this
        because the signs were essentially identification labels rather than
        instructions prohibiting access or work in the nearby areas which
        continued unchanged.

196         Mr Engebretsen then described the sequence of the asbestos removal
        programme, as follows:

                 (1)       The first job was the removal of asbestos sheeting on the
                           surface treatments building in early 1991 - this is what is
                           referred to as the "old section 3".
        (The second Matprolab's report of August 1990 shows that section 3
        includes the Raymond Mills/crushing rolls area and calsiners, so these

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        were areas where Mr Cotton had been working during October 1991 to
        January 1993 (see Exhibit 235, p 3)).
                 (2)       The next sequence was removal of asbestos from the BDR
                           in late 1991 to early 1992 - according to Mr Engebretsen.
                           After an initial clean-up in the BDR involving sweeping
                           out all the dust and deposits with brooms and brushes and
                           then, but not before, isolating the BD area with black
                           plastic sheeting and excluding the workforce. Then, under
                           protected conditions, the KBE workmen removed asbestos
                           insulation from the saturated steam main at the north end,
                           the super heated steam main, the crossover, the headers,
                           the feeders, the condensate lines, the exhaust fan ducts and
                           the pipe work at the south end of the BDR. A further
                           clean-up was conducted by using a vacuum process before
                           ordinary operations resumed in early 1992.
        This implies that the BDR was sealed off, shut down and all the third
        defendant's personnel were excluded during the asbestos pipe lagging
        removal operations from late 1991 to early 1992. There is really no
        evidence to confirm that the BDR was shut down for so long or that,
        effectively, the production of TiO 2 was suspended for several months.
        This is inherently unlikely and it is more probable that the preparatory
        stages of work were carried out while the plant was still running and the
        shut down occurred for a week or so at the most in March 1992 (Exhibits
        265 and 221, Annexure E) Mr Engebretsen said (Exhibit 234, par 32) that
        the band drier was out of service during this time but, in the context, that
        observation must be confined to a period in which the BDR was sealed off
        with black plastic and all workers were excluded, rather than the initial
        cleaning and preparatory phase.
197          Not all the insulation in the BDR was removed during this process
        because there was some which did not contain asbestos. There has been
        no mention, however, of the reservation expressed by Matprolabs in
        Exhibit 113 of the need for precautions to be taken on pipe work which
        had the appearance of being lagged with non-asbestos material because of
        the signs that previous asbestos removal had not been thorough
        (Exhibit 113 at p 5). That report related to areas other than the BDR but
        there is no reason to suppose that the observation was any less applicable
        to pipes which had originally been lagged with asbestos in the BDR, as
        described by Mr Savage many years before, but where that lagging had
        been subsequently removed and covered with some non-asbestos bearing
        insulation.



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198          The KBE Contractors finished in the BDR room in March 1992 and,
        at that stage it was thought (wrongly as it transpired) that there was no
        other asbestos insulation or lagging remaining there. Later, however,
        asbestos tape sealing and insulation was found in the band drier hatch
        doors and floor panels during a maintenance activity in September 1996
        and replaced (Exhibit 315(8)).
199           Mr Engebretsen acknowledged that there was insulation between the
        front and back surfaces of the hatch doors to the band drier and that this
        was not tested for asbestos because it was fully encapsulated. According
        to his observation there was other insulating material on the outside of the
        hatch doors of a different kind enclosed by a light metal cladding pop
        riveted to the door. The cladding would often come undone as a result of
        vibration and the insulation would be exposed but this did not contain
        asbestos.

200          There was a further removal programme of asbestos products from
        the BDR in December 1994. This was to remove sealing tape from the
        band drier hatch doors and took about 10 to 14 days to complete
        (Exhibit 315(5)). The BDR was not shut down, nor were employees
        excluded, but the areas were marked off with tape and signposts
        preventing access to within 10 metres of the job.

201          The sixth stage of the process was removal of the asbestos cement
        sheeting from the band drier roof and other buildings, including the
        surface treatment building north, south, and internal walls and the band
        drier de-watering filter building. Quotes for this were received in
        February 1995 and KBE Contractors performed the work in March 1995.
        During this period the contractors also removed 35 metres of sealed
        asbestos insulation from the main steam line which ran from the main
        recovery area to the northern entrance to the BDR. During the roof
        removal the BDR was isolated and the interior was later cleaned by the
        contractors before the third defendant's staff were allowed to re-enter.
202           A later step was removal of insulation from the BDR which,
        according to Mr Engebretsen, was insulation material on top of the band
        drier itself which did not contain asbestos. It was replaced on two
        occasions because it had become heavily contaminated with pigment dust
        and was damaged. However, I consider that it should be inferred that if
        that insulation was contaminated with the pigment dust it was probably
        also contaminated by any other airborne materials which had been
        circulating within the BDR during the years in which it had existed.
        Consequently, if there was asbestos contamination within the BDR before


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        then, as plainly was the case, the probabilities are that the dusty deposits
        on this insulation also contained some of this contamination and that it
        could become airborne.

203           The next and seventh stage of asbestos removal was of the asbestos
        cladding or roof sheeting from the packing shed. This was done during
        the three week period during February and March 1996 and was preceded
        by notifications to the workforce by a written memorandum.

204          Steven Cotton was employed as a plant operator/packer between the
        period 1 - 10 March 1992 until the first indication of his cancer diagnosis
        appeared in January 2002 and, according to his evidence was working in
        the packing shed and, when required, in the BDR. This sequencing of the
        roof removals in the packing area therefore corresponds with his evidence
        that he was working in that area when the asbestos cement sheeting roof
        was removed.

205          Memoranda prepared by Mr Engebretsen at the time (Exhibit 234,
        Annexures A1 - A6) show that the third defendant's workforce was not
        excluded from the packing or palletising areas while this asbestos sheet
        programme was underway and that the w      orking area was not sealed off
        with black asbestos plastic as had been utilised when the lagging was
        being removed from the BDR in 1991/1992. These memoranda make
        reference to precautions being taken by the use of tarpaulins which had
        not proved very effective. They also reveal that areas were demarked by
        tape, which corresponds with the evidence of Messrs Cotton, Colley,
        Folbig, Forrester and Retter. They also record that workmen entering the
        areas were required to wear protective disposable clothing and rated face
        masks. Mr Cotton did not have protective clothing or face masks when he
        was working in the packing shed adjacent to, but outside, the demarked
        area, nor did Messrs Cotton, Colley, Folbig, Forrester and Retter. I
        conclude, therefore, that these precautions were limited and selective and
        that there were still workmen under the same roof and within sight of
        these asbestos removal processors while they were occurring.

206          The eighth stage of the process was the removal of the west wall of
        the BDR which occurred over a two-week period commencing 10 March
        1997.     Mr Engebretsen's memo of 5 March 1997 (Exhibit 234,
        Annexure B) reveals that not only was that being done, but asbestos
        sheeting was also being removed from the former Raymond Mill a       rea
        south wall simultaneously.




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207           It is clear from Mr Engebretsen's evidence, therefore, that there were
        asbestos removal operations being conducted at the third defendant's work
        site variously from early 1991 until February/March 1997, including the
        BDR, roof sheeting in the packing shed, walls and roof sheeting in the
        BDR, Raymond Mill and packing areas and that these operations were
        preceded by periods of sweeping and cleaning of deposited and
        accumulated dust in those areas. This programme accordingly took place
        in various stages and at intervals over that six year period all in, or nearby,
        places which Mr Cotton worked regularly or visited temporarily but for
        substantial periods.
208           In cross-examination Mr Engebretsen acknowledged that there was
        also removal of asbestos cement roof sheeting in 1998. In answer to
        questions by counsel for the plaintiff, Mr Engebretsen said that he had
        known Mr Paul Cotton when the latter was working at Australind and that
        he knew that he did cleaning work in the BDR. This involved lifting
        doors on the band drier machine, some of which were in bad repair.
        Mr Engebretsen agreed that pipes in the BDR had been lagged with
        asbestos until 1992 and that the men were involved in dry sweeping in the
        BDR before 1992 and that until then the pipe lagging was in a
        deteriorating condition. Mr Engebretsen said that he was not aware of
        asbestos lagging being deposited on the floor in the BDR. It emerged that
        Mr Engebretsen visited the BDR fairly regularly until 1999, that is, about
        four or five times a week. He maintained that he never saw asbestos
        lagging on the floor during that time. He described the seals on the doors
        to the hatches on the band drier and described them as approximately
        20 - 25 ml in width and generally in good condition but some were
        damaged. When asked about the insulation within the hatch doors,
        Mr Engebretsen said that some testing had been done and that insulation
        was found to have been fibreglass but it did not emerge whether that was
        the situation with all of the hatch doors.
209          I found Mr Engebretsen to be a careful and precise witness who was
        trying to be accurate and who gave evidence truthfully on matters within
        his direct knowledge. The principal controversy of fact emerging from
        his evidence is whether or not the lagging insulation or other asbestos
        products often fell onto the floor of the BDR and were later swept up by
        cleaning workmen. I accept his evidence that he did not see this but I
        infer that his visits to the BDR were relatively brief, concerned with
        maintenance activities and that there was unlikely to be any reason that
        would prompt his attention to this specific alleged feature.
        Notwithstanding his evidence about this, I accept the testimony of the
        deceased and the other workmen that deposits of broken lagging or

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        insulation or other fragments of asbestos frequently fell onto the floor and
        had to be swept up. This is consistent with the general description of the
        position contained in the Matprolab report (Exhibit 45/45).

210           Another former employee of the third defendant was Mr Patrick
        Charles Ligman who was employed by the third defendant from 1977
        until 2001 and worked as Day Supervisor from 22 July 1991 to 1 January
        1996, supervising the water treatment plant, the waste neutralisation plant,
        the boiler treatment plant and the work of the day crew. Paul Cotton was
        a member of his day crew at the time. These were general hands, usually
        classified as process operators and part of their role would be to perform
        relief shift work for long-term absentees and other shifts. Working on
        shrink-wrapping, forklift stacking and Bulka bagging all took place in the
        packing shed (Exhibit 236, par 18) and then a fork lift would be used to
        remove the Bulka bags from the packing shed to an adjacent warehouse
        shed. Additional daily tasks assigned included cleaning various areas of
        the plant, but mainly the packing shed.

211           Mr Ligman was also involved in the asbestos removal programme.
        He attended Safety Committee meetings, discussed the procedures to be
        followed and gave instructions to his crew to act in accordance with the
        sequencing which had been decided. Routinely there was a monthly Shift
        Safety Meeting at which each member of the day crew was required to
        attend where he was informed of imminent asbestos removal activities,
        areas that were to be cordoned off and areas from which the workforce
        were to be excluded. At these meetings members of the day crew,
        including Mr Cotton, were instructed that if they entered areas of asbestos
        removal they were to wear masks and disposable overalls. These areas
        were cordoned off with yellow warning tape or completely isolated with
        plastic sheeting, depending on the type of removal being conducted. The
        area or operation from which the staff were completely excluded was the
        removal of asbestos lagging and insulation from the pipes of the BDR.
        That is the only occasion described by Mr Ligman to which conditions of
        complete exclusion applied.
212          Mr Ligman said that the band drier was an old machine which would
        occasionally fail and require maintenance and when it was not operating
        properly or was shut down maintenance workers were required to fix the
        problems and that this occurred about once a month. Before this was
        done, a few members of the day crew were required to provide a general
        clean of the BDR and the choice of the crew men to do the work would
        depend on what other jobs were being done at the time.



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213          Mr Ligman said that when Mr Cotton was working as a Bulka bag
        operator filling bags or involved in shrink-wrapping, he was required to
        remain in the packing shed for the whole of the shift and was not required
        to go to the BDR. Similarly, when Mr Cotton was working as a
        packer No 4, this was a job which continuously required his attention
        throughout the shift and he was not obliged to go to the BDR. Similarly
        when he was working in the Raymond Mill and decommissioning the
        sulphate plant, it is unlikely that Mr Cotton would have spent much time
        in the BDR. However, when he was working as a packer No 5
        Mr Cotton's regular duties obliged him to be in the BDR intermittently
        throughout the day checking that the machine was running properly. This
        presence in the BDR was additional to visits to clean out the trays
        underneath the conveyor or to do cleaning work before a maintenance or
        repair operation. The frequency of attendance to the BDR for clean up
        operations was "a couple of times a month" - Exhibit 236, par 50. By
        reference to Exhibit 235 it is apparent that Mr Cotton was engaged as a
        plant operator - packer 5 over the period 26 May 1992 to 9 October 1995,
        except for the interruption to his employment from 28 January to
        11 February 1993 and for the period of six months spent as a plant
        operator in R & D from 11 February 1993 to 8 August 1993.

214           Mr Ligman also said that he used to walk through the BDR at least a
        couple of times a week, and sometimes daily, but had no recollection of
        pieces of insulation or lagging from the pipes there, or a nywhere else,
        falling onto the floor. He did say that there was sweeping and cleaning
        occurring in the packing shed every day but that this was not the case in
        the BDR, which was only swept clean by the day crew when men were
        scheduled to clean the band drier trays, or when the machine had broken
        down and maintenance was required. Taking this evidence in conjunction
        it would appear that, broadly speaking, for one reason or another,
        members of the day crew would be required to clean up in the BDR or
        clean out the trays about three times a month.

215           In cross-examination Mr Ligman said that Mr Cotton could be in the
        BDR for about four to eight hours at a time and that this would be, on
        average, once a month or so or, perhaps, 15 to 18 times a year. Naturally,
        these are retrospective estimates and must be regarded as approximations.
        Although not expressly stated, it is necessarily implicit in Mr Ligman's
        evidence that the sulphate plant, at which Mr Cotton was working during
        its decommissioning in January 1991, was a source of asbestos because of
        the presence of air monitoring devices during that operation - consistent
        with the arrangements for air monitoring which Mr Engebretsen had


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        described, and this was expressly acknowledged by him during his
        cross-examination.
216           Mr Ligman also visited the packing and warehouse areas but did not
        express any concern about an asbestos hazard there, but he mentioned that
        the packing area was a very white and dusty area as a result of the
        production of the TiO2. He also described labelling items identified as
        containing asbestos, including lagging on pipes, with red lettering on
        silver stickers. I accept that this was done but, again, there is no
        indication of the frequency, location or significance of these labels and,
        for reasons previously given, I do not consider that this issue has any real
        bearing on the case. At least I am satisfied that these notices did not come
        to the attention of, or affect the working practices of, the employees. In
        his statement (Exhibit 238(2)) Mr Foley conducted a review of the six
        photographs in the Matprolab report (Exhibits 44/45).

217           Further descriptions of the presence of asbestos at the Australind
        worksite was provided by Mr Paul Galen Foley in two statements -
        Exhibits 238(1) and (2). Mr Foley is an occupational hygienist, with
        qualifications in physics from WAIT (now Curtin University) and from
        Sydney University. He was employed with Matprolabs since 1988 and
        has a long experience in advising governments in relation to occupational
        health and safety with particular reference to the control of chemical,
        physical and biological hazards in the workplace. He examined the
        Matprolab's reports of March and August 1990 (Exhibits 44/45 and 113)
        and also attended at the SMC works at Australind on several occasions to
        observe the air monitoring work then being conducted. He explained how
        air monitoring was conducted at SCM Australind on roughly a monthly
        basis from about September 1989 until about July 1991, collecting about
        20 samples across the site per month. Air sampling devices (utilising the
        membrane filter method) were positioned around the site, their contents
        later collected and processed by Matprolabs by a properly certified
        analyst. That led to Matprolabs being commissioned to identify areas
        which were found and identified as containing asbestos. Mr Ligman was
        made aware that there were concerns about asbestos in the BDR. There
        were various pipes in that area. He visited the BDR and examined the
        situation and found that the lagging was made either of pre-cast plaster or
        fibreglass, covered with a non-asbestos calico wrap and then sealed with
        paint. The pre-cast plaster lagging was found to contain asbestos and this
        was also known as calcium silicate block. He confirmed that the presence
        of asbestos in the pre-cast plaster lagging was quite extensive. Mr Foley
        said that on the occasion of his four or five visits to the BDR between
        1990 and 1997 he did not see chunks of lagging on the floor and his

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        recollection is that the damage to the cloth surrounding the lagging in the
        BDR was isolated and not extensive.
3. Air monitoring
218           Mr Engebretsen also described how from 1990 onwards air testing or
        monitoring was done around the third defendant's site, mainly by the
        contractors carrying out the asbestos removal but also, on occasions, by
        SCM staff as well. This was done in accordance with then prevailing
        Work-Safe Code Practice. The air pumps used for this were brought to
        the site and the locations for the sampling pumps would be agreed and
        installed. Two pumps per work location per day was the norm. One
        would be located within the exclusion zone and another outside the
        exclusion zone, usually down wind. The contractor would collect the
        membrane filters from the pumps and send them to the laboratory for
        analysis. During the period of the monitoring the third defendant was
        alert to ensure compliance with the then DOSHWA Standard for
        maximum recommended exposure to asbestos of 0.1 fibres/ml and,
        according to Mr Engebretsen, all the certificates received from the
        programme of air monitoring showed maximum exposure levels less than
        this.
219           The routine practice was for Matprolabs to notify the third defendant
        if the air monitoring readings revealed more than 0.05 fibres/ml, that is
        half the DOSHWA safe working level but Mr Foley has no recollection of
        being aware of any such adverse readings for the BDR between 1988 and
        1985.

220          Part of the removal operations involved the decommissioning of the
        sulphate plant and air monitoring analysis was conducted during the
        period that this was occurring on 19 and 20 December 1990 and
        18 January 1991. Mr Cotton was involved in that decommissioning work.
        Mr Ligman explained that the air monitoring tests conducted on those
        days (except for one test which was rejected because the sample was said
        to be overloaded with dust) all revealed less than 0.01 fibres/ml. This
        occurred during the first of Mr Cotton's three periods of employment
        when he was classified as a plant operator - general cleaning (see
        Exhibit 235).
221          The progress of the asbestos removal programme at Australind can
        also be traced through the third defendant's periodic maintenance reports.
        Some of these are in evidence as Exhibit 353 - (1) to (8). These and
        extracts from other documentary evidence showing various steps in, or
        reports upon, the asbestos removal programme at Australind are

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        summarised in the Chronology which follows later in these reasons (at
        [234]). These materials show that the asbestos removal programme ran
        from late 1989 to at least 1997 and was conducted at various times at
        various places within the third defendant's large plant at Australind. So
        far as it is possible to say, the removal programme generally seems to
        have been planned to coincide with annual shut downs or other periods
        when the plant was not in operation and that, in between those breaks, the
        productive operations continued, notwithstanding knowledge that there
        was asbestos which eventually needed to be removed in many parts of the
        plant.
222           The Matprolab's reports, Exhibit 44 - 45 and Exhibit 113 (in its
        abbreviated form), tend to concentrate on the BDR and the packing areas
        where Mr Cotton was known to have worked from time to time, but it is
        clear that the extent of asbestos within the plant and the programme for its
        removal were, respectively, much more extensive and longer than these
        documents alone, the testimony of Mr Turk and many of the submissions
        for the third defendant, suggest. The only episode of complete sealing off
        and isolation of all employees during the asbestos removal programme
        appears to have been during the removal of the asbestos cladding from the
        pipes in the BDR. The evidence as to when this occurred is not precise
        but it seems to have been carried out in at least two stages, the first in
        about November 1991 and the second in about March 1992 on each
        occasion for several days at a time. During those two episodes the BDR
        was completely sealed off, isolated and protected by a process of
        depressurisation while only KBE Contractors wearing special protective
        clothing carried out the operations inside. The work was done according
        to then prevailing standards and the material was gathered up inside the
        BDR, put into containers which were later sealed and taken away under
        supervised conditions. No employees of the third defendant, nor in
        particular Mr Cotton, were within the building during these operations.
        Nevertheless, these necessary and extensive precautions were only in
        force during the actual removal of the asbestos lagging from the pipes.
        The operation was preceded by a process of sweeping clean the floors and
        fittings within the BDR and this was done by the third defendant's
        personnel before the precautions which I have described were in
        operation. It must follow, and I find indeed it is probable that, during this
        period any asbestos dust or fragments which had been deposited on the
        floor or other surfaces within the BDR, along with large quantities of TiO 2
        powder would have been swept up in a very dusty atmosphere and would
        have been circulating in the air that the men breathed.



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223           Indeed, I consider, and I find, that it is probable that whenever
        sweeping operations were conducted in the BDR before the removal of all
        the asbestos lagging from the pipes, the asbestos from the insulation on
        the band drier hatches, and the asbestos roof, that, to varying degrees, the
        dust which was agitated within that area contained quantities of asbestos.
        Obviously, the quantities are likely to have been small, but they cannot be
        regarded as insignificant because the very purpose of the asbestos removal
        programme was to eradicate the potential threat which this environment
        posed. Just how great or small was the degree of asbestos dust in the
        atmosphere in the BDR at any of these times is something which, in my
        view, it is impossible to determine with any precision. The consequence
        of this lack of known level of likely contamination is an important issue
        for further consideration.
4. Complaints about asbestos at Australind site
224          At the third defendant's work site there was a standing Safety
        Committee which included representatives of the employer, union
        representatives, engineering staff members and workmen. The minutes of
        the meetings of this committee reveal that the workforce had been
        concerned about the presence of asbestos at the work site over a long
        time. Selections of these minutes are in evidence and reveal:

        •     13 May 1987 - the question of asbestos fibre measurements was
              raised, with an explanation by J N Hardy along the lines of a Mach 2
              workshop safety meeting on 8.05.07. Measurements of all dust,
              fumes are part of an on-going programme. As part of an overall
              programme, an indication was given and the cost estimates were
              being obtained on replacement of asbestos containing sheet at the
              welding shop. (Exhibit 95(3))
        •     8 July 1987 - an individual report that asbestos had been found on
              the top of the band drier room (Exhibit 95(3)).
        •     12 August 1987 - another reference in similar terms (Exhibit 95(2)).
        •     9 September 1987 - a note that samples of lagging had been collected
              from on top of the band drier. Following analysis the area will be
              cleaned during a grade change. Analysis has indicated asbestos in
              two samples. Extraction be carried out at the next grade change and
              insulation sealed (Exhibit 95(1)).
        •     11 November 1987 - another reference in the same terms
              (Exhibit 95(2)).



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        •     23 August 1988 - a detailed memorandum was prepared by an officer
              of the third defendant dealing with complaints about asbestos at the
              Australind site during a then current chloride conversion project.
              This recorded that the original plant was built in the early 1960's and
              subsequently upgraded in the early 1970's and that many of the
              buildings are clad in asbestos based cement sheeting. It reported that
              a certified asbestos removal team undertook the removal of all
              asbestos based sheeting where building would have to be
              demolished, modified or tied into. However this left certain old
              buildings still clad in asbestos cement sheeting, some of which had
              been damaged.
225          On 29 July 1988 employee representatives on the Safety Committee
        affirmed their determination to be given a statement on the asbestos
        environment following which sheeting debris was to be cleaned up.
        Despite assurances about the safety of the site, all personnel from three
        named contractors rejected the employer's assurances and withdrew their
        labour until the site was completely clear of asbestos. This led to the
        employer approaching the Department of Occupational Health, Safety and
        Welfare (DOHSW) for a ruling on the safety environment of the site.
        When it was discovered that DOHSW did not have the resources to
        conduct such an investigation a consultant was suggested - Amdel Ltd.
226           Amdel was engaged and undertook air monitoring tests producing
        two reports dated 12 August and 16 August 1988 respectively. Among
        the samples taken and submitted for testing by Amdel was a sample taken
        near the band drier steam microniser. That was described as an area
        where asbestos based sheeting damage occurred before the then current
        project had commenced. In addition to the dust a number of fragments of
        asbestos based sheeting laying on the floor were included in the sample.
        The workforce went back to work on 11 August 1988 under conditions
        that a further clean-up at work would be done, broken edges of sheeting
        would be sealed and a supplementary safety induction held. However,
        after the return to work contract personnel again raised concerns about
        their working environment and in particular about being in close
        proximity to asbestos related materials (Exhibit 96).
227          Further records of complaints by the workforce at the third
        defendant's safety meetings can be found in Exhibit 97 of 29 July 1988
        including an item that asbestos cladding had been left laying about.




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5. Asbestos insulation removal
228          The Matprolab report to the third defendant of August 1990
        (Exhibit 113) dealt with the extent and condition of asbestos material in
        the plant at Australind (sections 1, 2, 3 and 4). This reported that:
              "It was found that the asbestos was in one of four basic forms,
              either gasket material, woven tape lagging on pipe work,
              asbestos plaster lagging on pipe work or as asbestos cement
              products."
        And that:
              "Roof sheeting was found to be friable almost without
              exception. It was also found to be porous in many areas. This
              requires consolidation. An elastomeric coating may be required
              to seal leaks."
        And that:
              "With respect to the rest of the plant surveyed it was generally
              found that pipe insulation was in poor condition and requires
              remedial action. It would therefore be recommended that a
              programme be instigated to remove the asbestos insulation.
              That which is in sound condition may be deferred but
              economics of scale may make this option less attractive.

              Repairs to insulation should only be considered temporary as
              removal will ultimately be required ...

              Precautions will need to be taken on pipe work with the
              appearance of being lagged with synthetic mineral fibre (glass
              wall, rock wall, etc) as there was evidence that previous
              asbestos removal has not always been thorough or to current
              standards."

229          The third defendant's officers prepared a memorandum seeking
        authorisation for the removal of all the asbestos insulation on the
        Australind site dated 5 March 1991 (Exhibit 98). This reported that many
        of the older pipes had been lagged with materials containing asbestos to a
        greater or lesser extent and referred to a survey of those carried out by
        Matprolabs - as consultant - to identify the asbestos material. After
        comparing costs of engaging specialist consultants with those of training
        the third defendant's own employees, it was recommended that the
        asbestos removal be done by an SCM removal crew.                     This


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        recommendation           came       from   Mr A D Turk,   the   maintenance
        superintendent.
230          However, it seems that this was not acted on and, instead, an
        independent contractor was engaged to perform the work. This was KBE
        Contracting Pty Ltd which had experience in asbestos removal among
        other industrial activities. That company submitted a quotation to the
        third defendant on 7 February 1992 to undertake asbestos removal in the
        BDR (Exhibit 99). It was to:
              "Remove all remaining asbestos insulation from the band dryer
              room including pipes, ducting and all loose lying asbestos
              visible on top of the band dryer. In addition vacuum off the
              mineral wall insulation around all penetrations, into the band
              dryer and generally clean the top of the band dryer and the
              whole of the room on completion of the removal to satisfy the
              DOHSW area inspector."
231          An Extraordinary Safety Committee Meeting of the third defendant's
        employees was held on 6 March 1992 to discuss the proposed removal of
        asbestos cement sheeting (Exhibit 111(1)), leading to the recommendation
        that certain guidelines be established and that they have DOHSW
        approval. It was noted at a meeting of the Safety Committee on 11 March
        1992 that there was asbestos in the BDR pipes still to be removed.
232          There was a report of the discovery and accidental disturbance of a
        quantity of asbestos tape in the band dryer area when installing band dryer
        recirculation fans on 31 October 1994 (Exhibit 10(1)). Analysis on
        10 November 1994 revealed that a sample of the band dryer sealing tape
        contained Chrysotile.
233           Again, an instance occurred on 26 April 1995 when redundant train
        lines were removed giving rise to the release of accumulated dust and
        pigment thought to include asbestos. The deceased, Mr Cotton, was one
        of those subject to this exposure (Exhibit 102). This has previously been
        referred to in the reference to Exhibit 47.

234           However, in the second half of 1995 there were still examples of
        asbestos contamination at the Australind work site. A sample was
        submitted for asbestos identification and microscopic examination on
        3 August 1995 (Exhibit 100) and was found to contain a mixture of
        Amosite asbestos and at least three additional types, namely Tremolite
        (calcium and magnesium silicate); Actinolite (calcium and magnesium
        silicate with various amounts of iron); and Chrysotile (hydrated

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        magnesium silicate). It seems that 10 samples were analysed by the
        laboratory, five of which were found to be Amosite and others
        Tremolite/Actinolite, Chrysotile and other forms not specifically
        identified.
235          The third defendant gave notice to its employees on 13 September
        1996 (Exhibit 108) that on 16 September 1996 KBE Contracting would be
        removing asbestos tape from the floor structure inside the south end of the
        band drier - a job expected to take 12 hours. The band drier area was to
        be demarked and access restricted.

6. Chronology of asbestos removal activities at Australind
236          It is now possible to list a selected chronology of the third
        defendant's asbestos removal activities at its plant at Australind.
        1989:
        19 June 1989 - Start of replacement of asbestos roof sheeting on main
        ablution building - duration three weeks (Exhibit 260).
        9 July 1989 - Asbestos sheeting on west wall of workshops to be coated
        with Bondcrete as a temporary measure (Exhibit 261).
        6 September 1989 - 12 July 1991 - Series of Matprolab reports showing
        sampling from (usually) 20 sites at Australind for asbestos air
        concentration all less than 0.01 fb/ml - Exhibit 247.

        1990:
        5 - 12 January 1990 - Report for air monitoring during asbestos removal -
        Exhibit 251.
        Late March 1990 - Asbestos sheeting removal programme for onsite water
        treatment - Exhibit 265(1), item 10.5.
        10 April 1990 - KBE Contractors Pty Ltd commenced removal of asbestos
        sheeting from west wall of the service treatment building (Exhibit 262).

        18 April 1990 - 14 May 1990 - Report for air monitoring during asbestos
        removal - Exhibit 251.

        5 May 1990 - Asbestos sheeting replacement on the west wall of the
        surface treatment building has nearly been completed. Contractors will
        then move onto the on site water treatment building.



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        Several trial sections of asbestos sheeting have been painted with
        Tangard. There have been some problems but generally the results look
        promising for providing a surface/sub-surface sealant for asbestos fibres -
        Exhibit 315(1).
        17 - 28 May 1990 - Report for air monitoring during asbestos removal -
        Exhibit 251.
        4 September 1990 - Trials of coatings for sealing asbestos sheeting have
        continued. Trials show that "Tangard" is a good sealant and primer on
        clean, worn sheets. However, where there is a layer of pigment on the
        sheets, the paint does not penetrate through the pigment - Exhibit 315(2).
        19 and 20 December 1990 - Decommissioning of sulphate plant - Paul
        Cotton working on crew.
        1991:
        18 January 1991 - Decommissioning of sulphate plant - Paul Cotton
        working on crew.
        Early 1991 - Removal of asbestos sheeting from surface treatment
        buildings (old section 3 - includes Raymond Mills) - Engebretsen.
        27 February 1991 - Asbestos lagging removal work presently being
        carried out in section 1 and 2 by KBE Contracting using a cold stripping
        process or piping removal intact - Minutes of Safety Committee Meeting
        27 February 1991 - Exhibit 265.
        11 September 1991 - Monthly air sampling for asbestos continued with
        usual results of less than 0.01 fibre/ml of air - Minutes of Safety
        Committee Meeting 11 September 1991 - Exhibit 265.

        September/October 1991 - Third defendant obtained quotes for the
        removal of asbestos lagging from three steam pipes and fan housing in the
        BDR.

        25 September 1991 - KBE Contracting Pty Ltd quote to remove asbestos
        from boiler room and band drier room (two weeks outage) - Exhibit 266.

        25 September 1991 - Fax transmission from KBE Contracting Pty Ltd to
        SCM Chemicals submitting a quote for removing remaining asbestos from
        the boiler house and, in relation to the BDR, to remove asbestos insulation
        from all pipes ducting and extraction fans, together with all loose lying
        mineral wall insulation on top of the band drier that is most likely to be


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        contaminated and for patching of damaged asbestos and other lagged
        pipes within the pipe racks and other areas of the plant.
        14 October 1991 - 9 March 1992 - Cotton employed in Raymond Mill
        (Exhibit 235).
        23 October 1991 - KBE Contracting Pty Ltd quote to remove asbestos
        insulation from steam line and BDR - Exhibit 267.
        23 October 1991 - Facsimile transmission from KBE Contracting Pty Ltd
        to third defendant containing a quote for specified work to be performed
        in the BDR, namely:

              "1.     Remove all asbestos insulation from the steam lines on
                      southern walls, together with the insulation and the first
                      bend of the duct work above the band drier. This also
                      includes the removal of the asbestos ... [illegible] the
                      steam line enters and all asbestos insulation ... [illegible]
                      area where it exists in the BDR."
        November 1991 - about 50 per cent of the asbestos lagging from steam
        pipes in the BDR removed.
        27 November 1991 - During annual shut down KBE Contractors removed
        all the asbestos lagged pipe work in the boiler house and approximately
        50 per cent of the asbestos lagging in the BDR (Exhibit 315(3)).

        Late 1991 - early 1992 - Removal of asbestos insulation from BDR -
        Engebretsen.

        1992:
        15 January 1992 - Safety Committee Meeting (Exhibit 49) - still asbestos
        on BDR pipes.
        7 February 1992 - third defendant obtains quote for the removal of further
        asbestos from the BDR.

        7 February 1992 - Quote KBE Contracting Pty Ltd to remove remaining
        asbestos insulation from BDR, including pipes, ducting and all loose lying
        asbestos visible on top of the band drier - Exhibit 268.
        12 February 1992 - Asbestos in BDR pipes still to be removed.

        Work expected to commence mid March 1992 (Minutes of Safety
        Committee Meeting 12 February 1992 - Exhibit 265).

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        March 1992 - Asbestos removal of lagging from pipes in BDR completed
        by KBE Contractors.
        3 March 1992 - 24 August 1992 - Series of laboratory results for airborne
        asbestos at plant all showing very low levels (Exhibit 249).
        18 March 1992 - Exhibit 221(E) - third defendant instructs contractor to
        remove further asbestos from BDR over period 18 - 22 March 1992.
        March and April 1992 - Guidelines for asbestos cement removal -
        Exhibit 265 (11 March 1992 and 15 April 1992).
        2 April 1992 - Third defendant's maintenance report of Mr A D Turk
        (Annexure "F" to Exhibit 221) which recorded that all remaining asbestos
        installation on the steam pipes in the BDR was removed. The badly
        corroded condensate lines were replaced.
        2 April 1992 - All remaining asbestos insulation on the steam pipes in
        BDR was removed (Exhibit 314(4)).

        15 July 1992 - Plans presented for removal of asbestos sheeting from the
        north wall of the microniser building to be commenced in near future.
        Minutes of Safety Committee Meeting - Exhibit 265.
        3 August 1992 - Asbestos sheeting removal work about to commence on
        north side of microniser building - Exhibit 272.
        3 August 1992 - GBR Construction will shortly be commencing work
        replacing the asbestos sheets on the north side of the microniser building -
        A Turk - Exhibit 272.

        1993:
        28 February 1993 - Test result of airborne asbestos concentration in
        workshop showing very low levels - Exhibit 249.
        1994:
        23 February - 27 February 1994 - Annual plant shutdown - asbestos roof
        sheeting to be removed and replaced on surface treatment building -
        Exhibit 272.

        15 June 1994 - Bains Harding to commence removal of asbestos lagging
        from a short section of steam piping outside the surface treatment control
        room - "the last section of asbestos insulation identified at Australind" -
        Exhibit 264.


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        16 June 1994 - 14 November 1994 - Air sample results from Australind
        production area - all very low levels of airborne asbestos (Exhibit 250).
        1 November 1994 - Asbestos safe working procedures being developed
        and are being discussed at the December departmental monthly Safety
        Committee Meeting - Minutes of Safety Committee Meeting
        14 December 1994 - Exhibit 265.
        1 December 1994 - Major maintenance work was done in the BDR with
        regard to the band drier circulating fans. During this operation it was
        found that the door sealing tapes were asbestos and a programme has been
        started to replace those tapes (Exhibit 315(5)).
        15 December 1994 - removal of asbestos tape from band drier doors and
        roof and insulation on top of band drier carried out by Bains Harding.
        Late 1994 - 10 to 14 day period of removal of asbestos containing sealing
        tape from band drier hatch doors.

        1995:
        5 January 1995 - Third defendant's maintenance report (Annexure "G" to
        Exhibit 221). This reported that one of the most significant major jobs
        undertaken during the period then under review was removal of asbestos
        sealing tape from the band drier but, at p 3, there is the reference that the
        sealing tape on most of the oven doors to the band drier was identified as
        asbestos. Contractors were employed to remove the tape from all
        accessible doors. About four remain which had been clearly marked with
        asbestos stickers (emphasis added).
        February 1995 - Quotes obtained for removal of asbestos sheeting from
        the roof of the BDR and other buildings.
        10 February 1995 - Quotation from KBE Contracting Pty Ltd, including
        work on band drier BWF building and band drier building roof -
        Exhibit 271.
        10 February 1995 - KBE Contracting submits quotes for surface treatment
        building south wall, north wall, internal wall, band drier DWF building
        roof and band drier building roof - Exhibit 271.

        2 March 1995 - KBE Contracting Pty Ltd quote for removal of three walls
        on the band drier DWF building, including asbestos removal -
        Exhibit 269.



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        March 1995 - KBE removed roof of BDR (and other areas).

        March 1995 - KBE Contracting removed asbestos wall sheeting from
        BDR and the DWF room.

        9 March 1995 - 18 April 1995 - Series of test results from (usually) three
        test sites for air contamination by asbestos at Australind - all showing
        very low levels - Exhibit 247.
        22 March 1995 - 3 April 1995 - Third defendant's sampling data results
        for airborne asbestos all showing levels less than 0.01 fb/ml -
        Exhibits 248(1) to (5).

        6 April 1995 - Third defendant's maintenance report which listed, among
        the most significant jobs recently carried out, the programmed
        infrastructure improvement work of replacement of asbestos sheeting in
        the band drier and surface treatment buildings and corrosion protection
        from the main north-south pipe rack nearing completion (Exhibit 315(6)).

        And, in the same report (at p 3):
              "Asbestos sheeting replacement:

              The programme replacement for the band drier building and
              service treatment building is progressing well and should be
              completed by early period 7."
        1 November 1995 - 7 November 1995 - Series of test results from
        (usually) three test sites for air contamination by asbestos at Australind -
        all showing very low levels - Exhibit 247.

        7 - 12 April 1995 - asbestos insulation found above band drier and
        accidentally cut by a workman. A number of employees exposed and
        samples taken which confirmed the presence of asbestos (see Exhibits 47).
        18 April 1995 - Certificate of analysis (Exhibit 52) identifies Chrysotile
        and Crocidolite in sample taken from BDR.

        1996:
        29 January 1996 - Memorandum concerning proposed contract for
        removal of asbestos sheeting from various areas, including No 3
        warehouse walls, palletiser building wall, palletiser/forklift traffic
        building, roof and wall - Exhibit 273.



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        29 January 1996 - KBE Contractors asked to quote for asbestos sheeting
        replacement in packing area - Exhibit 273 - work to be carried while plant
        is in operation and SCM personnel will require periodic access to work
        areas - work to be performed on:
              Accumulation conveyor building roof
              Palletiser building roof
              No 3 warehouse roof
              No 3 warehouse walls
              Palletiser building wall
              Accumulation conveyor building gutter - Exhibit 273.
        8 February 1996 - KBE Contracting replacing asbestos sheeting in
        palletiser area and all roofing in the centre shed over the next two or three
        weeks.
        22 February 1996 - KBE replacing asbestos wall sheeting throughout the
        packing area, initially in No 3 shed and then roof over palletising area
        26 February.

        28 February 1996 - 11 May 1996 - Series of test results from (usually)
        three test sites for air contamination by asbestos at Australind - all
        showing very low levels - Exhibit 247.
        February/March 1996 - Three week period - removal of asbestos cladding
        or roof sheeting from packing shed.
        For period 5 for the year 1996 contractors worked on asbestos sheeting
        replacement in the packing area - expected that work would be completed
        by early March 1996 - Exhibit 315(7).

        September 1996 - Asbestos tape and insulation found in the band drier
        hatch doors and removed during maintenance period.
        2 October 1996 - Installation of endless conveyors on band drier discharge
        and removal of asbestos from south end of the band drier - Exhibit 315(8).
        1997:
        10 March 1997 - For next two weeks - KBE Contracting replacing
        asbestos sheeting on band drier west wall in the former Raymond Mill
        area south wall - Exhibit 270.



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        10 March 1997 - 24 March 1997 - Removal of west wall of BDR.
        Mr Engebretsen's memo of 5 March 1997 (Exhibit 234, Annexure B)
        reveals that not only was that being done, but asbestos sheeting was also
        being removed from the former Raymond Mill area south wall
        simultaneously.

        10 March 1997 and next two weeks - Removal of asbestos cladding in
        band drier west wall and south wall of Raymond Mill building
        (Exhibit 275).
        10 March 1997 - KBE Contractors on site for next two weeks to remove
        asbestos cladding from band drier west wall from the super heater area,
        north to the wall which separates the band drier room from the Raymond
        Mill building and from the south wall of the Raymond Mill building:
              Entire BDR to be taped off during the day.
              Raymond Mill building will have the north end of the packing
              area taped off but this will not affect palletiser operators -
              Exhibit 275.

        11 March 1997 - 20 May 1997 - Series of test results from (usually) three
        test sites for air contamination by asbestos at Australind - all showing
        very low levels - Exhibit 247.
        26 August 1997 - Series of test results from (usually) three test sites for
        air contamination by asbestos at Australind - all showing very low levels -
        Exhibit 247.

        2000:
        22 June 2000 - Series of test results from (usually) three test sites for air
        contamination by asbestos at Australind - all showing very low levels -
        Exhibit 247.
Quantitative estimates of asbestos exposure
237          Because of the significance which epidemiologists attribute to the
        aggregate dose of asbestos fibres ingested by a worker over time
        (measured in fibre/ml years) great efforts were made by the parties to
        establish, essentially by processes of retrospective estimation, the
        aggregate exposure to asbestos fibres which Mr Cotton experienced
        during his employments with the first defendant and with the third
        defendant. Plainly, there are great difficulties in attempting accurate
        estimations. However, because of the impact of asbestos exposure on


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        workers and others worldwide in recent decades, an enormous amount of
        scientific research, investigation and sampling has been conducted in
        attempts to improve understanding of the threat of asbestos. This has
        been done both for preventative and safety reasons, on the one hand, and
        to aid diagnosis or to distinguish between serious pathologies in
        individual cases, which may, or may not, have been caused in whole or
        part by exposure to asbestos.

238          The relationships between various estimated levels of asbestos
        exposure over time and the development of one or more of various
        asbestos-linked diseases have been studied and reported upon by many
        specialist epidemiologists. Several very highly qualified and respected
        Australian epidemiologists experienced in this sphere have given evidence
        of their opinions about the sufficiency of time/dose exposure as a potential
        cause of lung cancer either alone or in combination with other potential
        carcinogens.
239           In contrast, the measurement or estimation of respirable asbestos
        fibres in a workplace is the particular province of occupational hygienists
        who, by a variety of measures, can sample, and then measure, the
        concentration of asbestos fibres in an area. They devise systems to
        conduct reliable sampling from representative places within any
        workforce and so build up a profile of airborne asbestos contamination, if
        it exists, over the period of sampling. From this, it can be extrapolated
        that if the conditions in the working environment were more or less the
        same before or after the period of scientific sampling then the
        concentrations of airborne asbestos particles could be expected to match
        those observed during the sampling period.
240          The method of sampling for airborne asbestos particles which was
        accepted as reasonably reliable in this trial is the membrane fitter method
        ("MFM"). This involves an air pump or sampler being placed in the area
        to be tested through which measured quantities of the ambient
        atmospheric air is passed. Within the pump are filters or membranes
        through which the atmospheric gas passes. The membranes capture
        airborne particles of dust or other substances, even of microscopic size,
        and retain them, so that at the end of the period of sampling, the
        membranes can be removed in a laboratory, examined under the
        microscope and the number of asbestos fibres (if any) located in areas of
        the membrane (divided for this purpose into very small grid squares) are
        counted and then, by a process of standardisation to ensure representative
        character of the results measured, a report is made of the number of fibres
        observed. By relating this to the quantity of air passing through the pump


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        in the given time, it becomes simply a matter of mathematics to provide a
        result of the number of fibres per millilitre of air in the environment
        during the time the sampling was conducted. This is reported as the
        number of fibres per millilitre of air - fb/mls.
241          It may be significant to note that this process provides a measure of
        airborne asbestos contamination which is not dependent upon the
        particular type of asbestos, or the extent of that asbestos which is found in
        the work source. In other words, at a factory involving work with
        asbestos cement pipes, whether the pipes contain 10 per cent, 20 per cent
        or 30 per cent of asbestos, or whether the asbestos is Chrysotile, Amosite,
        or Crocidolite or some other variety, will not alter the results of the
        airborne testing by the membrane filter method. The MFM simply
        provides a count of actual fibres detected in the atmosphere no matter
        what their source may be. It will often be possible, during the laboratory
        analysis of the products of the MFM, to identify the type or types of
        asbestos which became deposited on the filters, for example Chrysotile,
        Amosite or Crocidolite and that is often reported by the technicians
        together with the level of concentration found. However, the results of
        the MFM in a particular setting are not to be doubted only because of lack
        of knowledge or certainty about the quantity of asbestos or the types of
        asbestos which occur in the particular workplace.
242          As well as attempting to determine the concentration of asbestos
        fibres in the atmosphere in an individual workplace by this empirical
        method there are other ways of estimating the degree of exposure. There
        is much published literature about the level of asbestos fibre
        concentrations in the atmospheres of various workplaces which have been
        measured scientifically around the world. Thus, for example, there are
        papers dealing with typical atmospheric asbestos exposures in shipyards;
        in railway factories where brake linings are worked upon; in factories
        where asbestos cement materials are fabricated or assembled and so on.
        The occupational hygienists and epidemiologists draw upon this literature
        to make general estimates of the prevailing atmospheric concentration of
        asbestos fibres which could be expected to be found in a workplace
        performing comparable functions. This approach also has been attempted
        in the present case.

243           Finally, with particular regard to the asbestos exposure to which
        Mr Cotton may have been subject in South Australia, tests have been done
        at the initiation of the second defendant about the levels of contamination
        which could be expected from processes of working in the open when
        asbestos cement water pipes are being laid. These two studies - the


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        Amdel Report and the WAIT AID Report - are relied on by the first and
        second defendants in this action. It is necessary, therefore, to review the
        evidence which attempts to estimate, in this quantitative manner, the
        aggregate asbestos dose or doses to which Mr Cotton may have been
        exposed during these two periods of his employment.

1. The WAIT AID Study
244           The report on the exposure of water pipe workers to asbestos dust
        over an eight hour day undertaken for James Hardie & Coy Pty Ltd by
        WAIT AID Ltd dated 5 October 1983 is in evidence as Exhibit 153(4)
        (relied on as part of the evidence of Mrs Janet Sowden) and, again, as
        Exhibits 175 and 287. In the latter half of 1983 James Hardie & Coy Pty
        Ltd was evidently concerned about potential occupational risks to workers
        engaged in laying asbestos cement water pipes and therefore
        commissioned a series of tests to establish the levels of potential asbestos
        exposures for such workers in the field.
245           The consulting firm WAIT AID Ltd, then associated with the
        Western Australian Institute of Technology (now Curtin University), was
        engaged to conduct the tests and did so under the supervision of officers
        of the Department of Environment and Health of Western Australia. The
        results of the tests were analysed by the State Government Chemical
        Laboratories and the report was distributed, by the second defendant, to
        the Premier of Western Australia, the State Minister for Industrial
        Relations and to the Ministerial Advisor on Industrial Relations as well as
        to various James Hardie staff (see Exhibit 153(3)). The reports were
        completed by Dr J Spickett and Dr M Nedved and the tests took place in
        what was then a new suburban subdivision for a future housing estate at
        Ballajura - a Perth suburb. There, three contractors were engaged in
        installing mains water pipe using James Hardie asbestos cement pipes.
        Air samples were taken by samplers prepared by the second defendant,
        collected on membrane filters, the contents of which were eventually
        taken to the Government Chemical Laboratory for analysis.

246           The reports observed that the dust from the pipes was only noticed
        during the machining of the cut pipe ends and that no other operation
        produced noticeable dust. Most of the day's work involved laying of the
        pipes, some time was spent bringing pipes to the trench. About one hour
        was spent performing three cuts on pipes and subsequent machining. The
        total machining time was about 30 minutes. It was also observed that dust
        from the machining of the cut pipe ends could be reduced considerably if
        the pipe end was kept wet during the machining process. During the


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        period of the test the contractors worked laying 200 mm class "D"
        asbestos cement pipes in a trench approximately 1.5 m deep. A total of 35
        lengths of pipe was laid with two hydrant take-offs fitted and two
        15 degree cast irons bends. The pipe laying team confirmed this was
        representative of a normal working day. Sampling included a membrane
        filter pump being placed close to the cutting area of the pipe during an
        eight and a half minute interval when the pipe was cut with the Wheeler
        pipe cutter and again when a contractor was cutting a pipe with a hammer
        and chisel. Three membrane filter pumps were used and each conducted
        six sampling tests at, respectively, 7.15 am, 9.50 am, 12.30 pm, 1.05 pm,
        4.10 pm and 4.55 pm on the one day when the weather was fine and calm.

247          All of the tests conducted showed results of less than 0.1 fibres per
        ml of asbestos. The evidence does not disclose what type of asbestos
        fibre was in the particular pipes and it seems that only cutting involving
        the Wheeler cutter and a hammer and chisel were tested and that there was
        no sampling of machining or rasping of concrete pipe ends conducted,
        although Dr Nedved appears to have observed that the practice of using a
        field lathe (manual) was seen to produce visible dust and swarf
        (Exhibit 153(4)).
248           Mr J Lawless, an Industrial Hygiene Officer at James Hardie was
        involved in observing and reporting on these tests. Neither Dr Spickett
        nor Dr Nedved, nor any other officer of WAIT AID Ltd involved in this
        testing, was called to give evidence. In his evidence Mr Lawless
        confirmed that this WAIT AID Report had been commissioned by him at
        the direction of James Hardie & Coy Ltd. In his evidence, Mr Lawless
        said that the pipes involved in that testing contained Amosite and
        Chrysotile, but no power tools were used in the test but the workmen did
        use a manual field lathe.
249          The first and second defendants rely upon the WAIT AID tests
        results to submit that the levels of asbestos exposure which may have
        been experienced by Mr Cotton when working in Adelaide for the EWSD
        were probably comparable and revealed very low levels of exposure to
        asbestos - levels below the then accepted tolerable norm of 1 fb/ml which
        was the accepted hallmark of the NHRMC at the time.
250          I have considerable reservations in accepting the WAIT AID Reports
        as being indicative of working conditions experienced by Mr Cotton in
        Adelaide from March 1976 until October 1978 because the tests do not
        indicate that they were conducted during periods when rasping and filing
        of the edges of cut pipe was being undertaken. Another significant


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        difference is that the AC pipe then in use by the contractors participating
        in the test did not contain any component of Crocidolite, whereas the
        evidence is that there was Crocidolite in the AC pipes in use in Adelaide.
        Other evidence suggests that Crocidolite is considerably more noxious
        than Amosite or Chrysotile. Nevertheless, the WAIT AID tests do
        provide a basis for the first and second defendants' submissions that work
        involving the cutting of AC pipes in the open with Wheeler pipe cutters
        only produces a very low level of airborne asbestos fibre contamination.
2. The Amdel Report
251           This report is also in evidence several times - as Exhibit 153(6),
        being part of the evidence of Mrs Janet Sowden, and again as Exhibit 174
        and as Exhibit 286 (with some variations). Amdel is the trade name of an
        industrial scientific and laboratory service conducted by the Australian
        Mineral Development Laboratories and this report of 18 June 1984
        resulted from its engagement by the Queensland Workers' Health Centre
        ("QWHC") to oversee and monitor a trial pipe laying programme being
        carried out by James Hardie & Coy Pty Ltd near Brisbane at its Meeandah
        plant. The purpose of the study was to assess the workers' exposure to
        any airborne asbestos dust generated during the preparation, cutting,
        trimming and installation of a typical building site drainage system and
        was designed to duplicate a typical pipe laying operation on a building
        site on two consecutive days using the two cutting methods approved and
        recommended by the manufacturer. Officers of both James Hardie and
        Amdel were involved in setting up and conducting tests and commenting
        upon the results. Testing of airborne asbestos was conducted by the then
        current membrane filter method approved by the NHMRC (Membrane
        Filter Method for estimating airborne asbestos dust - National Health and
        Medical Research Council - October 1976).
252           In the Amdel tests the cutter of the AC pipe used on the first day was
        a Wheeler cutter. On the second day a 240 VAC Makita electric saw
        fitted with a water lubricated diamond cutting disc was used for all cuts.
        Clean up of the cut pipe sections was carried out using a low cost rasp
        fitted with a disposable blade and a soaked water absorbent sponge.

253          All the sample results obtained indicated an operating exposure
        lower than the then current NHRMC recommended threshold limit value
        for Chrysotile of 1 fb/ml - in fact the results were less than 0.1 fb/ml, that
        is one-tenth of the then current recommended threshold. All the results
        for cutting using the Wheeler Pipe Cutter, followed by trimming with a
        manual lathe and dampened sponge, were low and observers noted that


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        this process generated few particles and few airborne particles. By
        contrast, the cutting with the Makita electric powered diamond cutter drill
        produced a substantial amount of fine wet waste material and, at the end
        of the equivalent day's pipe cutting and laying, operators using this
        process had notable signs of fine AC abrasion waste on their trousers.
        The conclusions and recommendations of the exercise included the
        following:

              "1.     Providing the methods used in these tests are followed,
                      the risk of operator exposure to airborne asbestos dust at
                      the current NH & MRC recommended threshold limit
                      value for Chrysotile (1 fibre/ml) is slight.

              2.      The Wheeler-cutter system for cutting asbestos cement
                      pipe is preferred."
        Exhibits 153(6) and 174 each contain a series of photographs showing the
        pipes, equipment and methods used in the cutting process which was
        tested.
254           Again, there are some differences between the process involved
        when Mr Cotton was employed by the second defendant in Adelaide and
        the operations tested by Amdel in Brisbane in 1984. Firstly, the
        appearance is that the pipes used in the process at Brisbane for the Amdel
        testing contained only Chrysotile for there is no report revealing any
        Amosite or Crocidolite being detected. Secondly, the manual rasping of
        the cut ends of the pipe which was observed and tested (not specifically
        addressed in the WAIT AID Report) involved the use of a particular rasp
        and a damp sponge - presumably because of the then known risk of
        airborne fibre generation from dry manual rasping. No such precaution
        was followed by the first defendant at the time Mr Cotton was employed
        in Adelaide and it is, therefore, likely that asbestos fibre generation from
        that process during his employment was greater than detected in the
        Amdel testing. Again, however, the Amdel Report does provide a basis
        for the first and second defendants' submission that the likely exposure to
        asbestos fibres from working and cutting with asbestos cement water pipe
        in the field was relatively low.

3. The A/C Pipe Producers Association Report
255          The second defendant also tendered a copy of the report prepared for
        the Asbestos Cement Pipe Producers Association of Arlington, Virginia,
        prepared by Equitable Environmental Health Inc of Berkeley, California,
        dated 15 December 1977, being a report of dust exposures during the


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        cutting and machining of asbestos cement pipe (Exhibit 155). This is a
        supplementary report to an earlier submission to the A/C Pipe Producers
        Association of the USA prepared in March 1977 providing quantitative
        data on dust exposures during field operations in which sewer and
        pressure pipe was subjected to a number of typical field cutting and
        machining operations.       It included a report of airborne fibre
        concentrations associated with unloading pressure pipe at a work site,
        laying the pipe in a trench, cutting operations with a manual saw, snap
        cutting equipment and with a wet abrasive disc. It also scrutinised
        machining operations, including cutting and machining with a powered
        tool, a tapering tool, hole cutting, tapping operations and coupling
                                    n
        removal. The test results i clude a series of published tables showing
        levels of exposure for various operations, including short-term peak
        exposures.

256          Within the summary and conclusions of the report can be found the
        observation that potential asbestos exposures during most operations were
        well below current occupational health standards, but that one tool, the
        abrasive disc saw, resulted in unacceptably high concentrations of fibres.
        In addition, short-term concentrations of total dust suggested that if
        crystalline silica content was high permissible levels might be exceeded.
        A further finding was that:
              "All operations that were studied produced airborne
              concentrations of asbestos far below the current short term
              OSHA standard of 10 fibre/ml (5<µm in length) and none
              would have exceeded a time-weighted average of 2 fibre/mls or
              even 0.5 fibre/mls if continued for a full working day except for
              (1) the abrasive disc saw and (2) some operations with the Doty
              tool when used dry."
257          The tests conducted and reported upon by the A/C Pipe Producers
        Association of the USA appear to me to be more comprehensive and
        representative than either of the tests conducted by WAIT AID or Amdel
        and, significantly, they recognised the phenomenon of peak exposure
        loads during intensive parts of the daily operation. Again, however, they
        do not report upon the type of asbestos fibres in the sources, or in the air
        samples, but the overall tenor of the report, in common with the Amdel
        and WAIT AID reports is that airborne asbestos contamination from these
        type of operations was regarded as being low, although not as low as that
        reported by Amdel or by WAIT AID.




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4. The James Hardie Asbestos Cement Cutting Tool Study of February
            1980
258          The second defendant also tendered (as Exhibit 176) portions of an
        Asbestos Cement Cutting Tool Study undertaken for James Hardie by
        P A King in February 1980. This report was commissioned to study the
        concentrations of asbestos fibre dust generated from a variety of manual,
        machine and other processes conducted on James Hardie products,
        including a variety of asbestos cement, corrugated sheets, building boards,
        pipes and other products in different working situations. It included a
        study of working with AC pipe with a variety of cutting tools including
        the Wheeler hydraulic pipe cutter and using manual field lathes.
        Quantitative results are tabulated in Table VII at p 57 in Exhibit 176 and
        show that the mean results for fibre/ml concentrations for the various
        works range from 0.3 fibre/mls to 1.4 fibre/mls with standard deviations
        varying from 0.11 to 0.35 and (at p 70). The results, when dealing with
        pressure pipes, were said to be that the mean fibre counts of the four tests
        undertaken fell between 1 and 1.5 fibres/ml for tests using the Wheeler
        pipe cutter, a Trepanning unit, a manual field lathe and a motorised field
        lathe. The reporter observed that it might be necessary to limit the work
        rates of those tools to allow fibre counts of less than 0.5 fibre/ml to be
        generated in confined areas.
259           Again, there must be some doubt about the comparability of these
        tests and findings with other reported test results relied upon by the first
        and second defendants and the conditions experienced by Mr Cotton when
        working for the first defendant in Adelaide. Generally speaking, however,
        these results are more consistent with the American A/C Pipe Producers'
        Reports which have been described and show results higher
        (approximately by a factor of 10) than those reported upon by WAIT AID
        and by Amdel. Again, however, the general tenor of the report is that
        airborne concentrations of asbestos fibres from the processing of AC pipe
        in the open by the methods likely to have been followed when Mr Cotton
        was employed in Adelaide are relatively low.
5. Ontario Royal Commission Report
260          Another similar study is the report of the Royal Commission on
        Health and Safety Arising from the Use of Asbestos in Ontario, delivered
        in 1984 (Exhibit 177). This shows (in Table 10.4) exposure levels in
        construction work for the various processes using asbestos cement sheet
        and pipes, including United Kingdom data and other reported data for the
        compression shearing of pipe. This data shows levels slightly higher than


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        those reported on in the other studies discussed so far, but still
        comparatively low.
6. Japanese Study of 1993
261          A Japanese study estimating asbestos exposure among workers
        repairing asbestos cement pipes used for conduits was the subject of a
        published extract in the Japanese Journal of Independent Health 1993
        (Exhibit 193) which was tendered by the third defendant. This reported
        upon repair operations conducted in water mains constructed of asbestos
        cement pipe containing 15 - 20 per cent Chrysotile or Crocidolite where
        workers use high speed disc cutters to replace the new conduit. The
        operations studied appear to be materially different to those experienced
        by Mr Cotton because the high speed power cutting tools were used in
        confined areas, although the operations were of short duration - about five
        minutes each. It was reported that the concentration of asbestos fibres
        ranged from 48 to 175 fibres/ml (92 fibres/ml on average) inside the hole
        and 1.7 to 15 fibres/ml outside the hole. The overall conclusion was that
        these workers had a risk of developing asbestos-related diseases,
        including lung cancer, through their exposure. In my view the Japanese
        study reported on a level of exposure to asbestos contamination
        appreciably greater than that probably experienced by Mr Cotton.

The occupational hygienists
1. Mr M H Kottek
262           As part of the preparation for trial the solicitors for the plaintiff
        sought an opinion about the likely extent of Mr Cotton's exposure to
        asbestos from Mr Michael Harvey Kottek, an occupational and
        environmental health consultant - in response to a report of expert
        evidence from the second defendant's witness Mrs Janet Sowden. The
        letter of instructions to Mr Kottek, detailing the history of Mr Cotton's
        potential exposure to asbestos, the details of his diagnosis and reports on
        his medical treatment are to be found in Exhibit 73. I am satisfied that the
        record provided to Mr Kottek is substantially correct.

263          Because of his wife's employment in Scotland, Mr Kottek gave
        evidence in this trial by a video link connection from Care Hall at the
        University of Dundee in Scotland. He has a Degree of BSc (Honours)
        from Melbourne University in 1987, a Graduate Diploma of Occupational
        Environmental Health from Monash University in 1997 and a Masters
        Degree of Science from Melbourne University in 1993 and Bachelor of
        Laws (Honours) from University of Melbourne in 2003. He has had


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        letters which he has co-authored published in the American Journal of
        Industrial Medicine relating to asbestos and cancer and is a member of a
        number of international societies concerned with industrial hygiene and
        occupational hygiene or epidemiology. He has studied and advised on
        asbestos removal operations in compliance with risk controls and has been
        engaged as a private consultant in this field since 1999. The substance of
        his evidence is to be found in his statement Exhibit 71 and the published
        articles or references upon which he relied, numbering 64 in total,
        comprise Exhibits 72(1) to (64).

264           Mr Kottek's report (Exhibit 71) begins with a lengthy review of the
        literature dealing with the hazards of asbestos exposure dating from the
        1898 Annual Report of the British Chief Inspector of Factories and
        Workshops which was published in 1900. He deals with a series of
        articles published in the 1930's concerning the hazards of working with
        asbestos, and a series of other similar articles. He observed that, in 1961,
        there was an article published in the "Archives of Pathology" by Hueper,
        noting that asbestos was recognised as causing lung cancer. He pointed to
        a further series of articles and an international conference in 1965 noting
        that asbestos exposure was associated with lung cancer and diffuse
        mesothelioma. These establish, and indeed it is not contested by any of
        the defendants, that exposure to asbestos is potentially harmful and was
        known to be associated with fatal lung disease long before Mr Cotton
        began his employment with the first defendant in South Australia in 1975.
265          Turning to his expression of opinion about the likely exposure of
        Mr Cotton to asbestos, Mr Kottek refers to measurements of asbestos
        contained in James Hardie documents referred to by Mrs Sowden as
        involving work in 1983 - 1984. That, therefore, is a reference to A/C pipe
        containing only Chrysotile which Mr Kottek expected would emit less
        dust than pipes containing Amosite and Chrysotile used by Mr Cotton at
        the EWSD in Adelaide. With regard to the work done in Adelaide
        described by Mr Cotton, Mr Kottek expressed the following opinions of
        special note:
              •       Holding an AC pipe while it was being cut with an angle
                      grinder would almost inevitably have exposed Mr Cotton
                      to in excess of 50 fibre/mls for the duration of the
                      operation.
              •       The manufacturer of the pipe should have been aware that
                      the then applicable 4 fibre/ml standard was based on
                      protection against asbestosis and, when Mr Cotton was


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                      working for EWSD it was not known if there was a level
                      of exposure free from lung cancer risk.
              •       The manufacturer should have been aware of reports i    n
                      the medical literature that the risk of lung cancer among
                      asbestos workers was very much greater for smokers.

              •       It is very difficult to estimate Mr Cotton's exposure to
                      asbestos at Australind while in the employ of the third
                      defendant. This could plausibly range from trivial to
                      moderately intense.

266         Dealing with Mr Cotton's exposure to asbestos fibres at Australind,
        Mr Kottek said:

              -       The contribution from the roof removal operation is
                      unlikely to have been significant although he would not
                      exclude that incident completely. The reports in the
                      literature and Mr Kottek's own testing beneath the
                      removal of many asbestos cement roofs show that the
                      results of exposure from such operations is very low.
                      Nevertheless, sweeping up the floor upon which dust
                      from the roof had gathered may have temporarily
                      increased the amount of airborne asbestos dust.

              -       The main sources of Mr Cotton's exposure appear to have
                      been when he or others dry swept the band drier room
                      floor.
        With regard to this potential source of exposure, Mr Kottek wrote
        (Exhibit 71, p 9 - 10):
              "Without knowing the amount of lagging debris present it is
              hard to estimate an airborne fibre level, but a few observations
              can be made. The first is that dry loose mixtures containing
              more than 0.001% asbestos can give rise to dangerous levels of
              airborne asbestos fibre when disturbed.
              ...

              However, I am confident that at least 20 fibre/mls of airborne
              dust was generated by the sweeping ... This makes 5 fibre/mls
              as a relatively conservative estimate of Mr Cotton's airborne
              asbestos exposure during the sweeping of dust that contained
              asbestos debris. Five fibre/mls is also a reasonable estimate of

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              the airborne fibre levels which may have been generated when
              the band drier doors with loose insulation were being
              manipulated. I have no information on how long or frequently
              Mr Cotton carried out such works, but I shall assume it was for
              1½ hours a day. This leads to a minimum estimate of
              Mr Cotton's time weighted average daily exposure of
              0.9 fibre/ml.

              ...
              I stress that this is quite a speculative estimate, the actual
              airborne fibre levels will have been heavily dependent on the
              amount of debris actually swept up, as well as whether it was
              pipe insulation debris or band drier door debris ...
              If this exposure estimate is correct then Mr Cotton would have
              exceeded the occupational exposure limit for mixed asbestos
              dusts of 0.1 fibre/mls. ...
              One could estimate [that] Mr Cotton's cumulative asbestos
              exposure at [Australind] is 4.5 fibre/ml years. This is based on
              5 years exposure at 0.9 fibre/mls."

267           Mr Kottek then went on to address issues raised by Mrs Sowden's
        report about the continuing controversy over whether asbestosis is a
        prerequisite for being exposed to an increased risk of lung cancer from
        asbestos exposure. Mr Kottek observed that the literature supports the
        view that it is quite clear that people exposed to asbestos can be at
        increased risk of lung cancer even without the presence of asbestosis on
        an X-ray and referred to the Consensus Report for the Helsinki Criteria
        that, while the presence of asbestosis may contribute some additional risk
        of lung cancer for cumulative asbestos exposures below 25 fibre/mls
        years, there is still some level of increased risk of lung cancer. He then
        addressed the literature which, generally speaking, establishes a view that
        the interaction between the increased risk of lung cancer caused by
        smoking and asbestos exposure interact in a multiplicative fashion. He
        described the controversies which existed in the literature about this
        matter and concluded:

              "In the interim it is quite clear that the two agents interact in
              some synergistic manner (certainly the increase in risk caused
              by each agent [is] not merely added together), the precise
              mechanism of interaction and the correct mathematical function
              representing the interaction remains to be determined."

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268          Exhibit 194 is a selection of the written evidence submitted to the
        UK Advisory Committee on Asbestos in 1976 - 1977 and was tendered by
        counsel for the second defendant. It includes a passage dealing with the
        installation of asbestos cement pipes which is to the effect that the
        handling of such pipes and the use of hand tools do not normally give rise
                                                        our
        to dust levels over 2 fb/mls averaged over a f hour working period.
        However, tests have shown that machine sawing outdoors using dry
        portable disc cutters do give counts between 5 and 35 fb/mls over short
        periods. Similarly, Exhibit 195, being an extract from the British
        Department of Employment: "Probable Asbestos Dust Concentrations for
        Construction Processes", put forward tables considered as representative
        of dust concentrations for various works involving asbestos. For
        demolition involving de-lagging, carried out dry without the use of water
        sprays, the table showed the concentrations were likely to be over
        20 fb/ml. For the use of asbestos/cement sheeted pipes, hand sawing can
        give rise to concentrations of 2 - 4 fb/ml and machine sawing, without
        effective exhaust ventilation, with a circular saw would give rise to
        10 - 20 fb/ml. These independent sources provide, in my view, further
        grounds for preferring the estimation of dust concentrations propounded
        by Mr Kottek and the rejection of the much lower levels of concentration
        propounded by Mrs Sowden.
269           Mr Kottek concluded by stating that, in his opinion, Mr Cotton was
        exposed to asbestos while working with both the first defendant and the
        third defendant and that the magnitude of his exposure was such that he
        would have faced at least some increase (certainly more than minimal) in
        the risk of lung cancer over or above that which he would have faced from
        smoking alone.       In the course of his oral evidence, Mr Kottek
        acknowledged that in the course of Mr Cotton's two sequences of
        employment he probably had an irregular and erratic exposure to asbestos
        which varied from day to day and pointed out that there was a potential
        for uncontrolled exposure to asbestos.

270          Mr Kottek was cross-examined by counsel for the second defendant
        with a view to establishing that his original training and qualification was
        in botany and that only his part-time two year course leading to his
        Diploma of Occupational and Environmental Health was a qualification in
        occupational hygiene. An attempt was made in cross-examination to
        suggest that tests which Mr Kottek carried out in measuring asbestos
        concentration in the atmosphere were not peer reviewed or subject to
        NATA approvals, in contrast to methods followed by Mrs Sowden.
        Mr Kottek acknowledged that his tests had not been subject to general
        scientific scrutiny, but I do not have any reservations about his objectivity,

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        or acquaintance with the professional discipline for this or any other
        reason.
271           Mr Kottek impressed me as an honest and well-informed consultant
        in the field of industrial safety with special interest in asbestos exposure.
        He did not claim or pretend to have professional medical or higher
        scientific qualifications or experience of the hazards of asbestos but he has
        made a special study of literature and his evidence and opinions appeared
        to me to be well-balanced and fair. He accepted Mrs Sowden's report as
        being quite sound and accepted her figures as reasonable estimates for
        Mr Cotton's exposure to asbestos. When asked about his estimate of
        exposure to 50 fibre/mls of asbestos Mr Kottek acknowledged that that
        was not drawn from the literature, was his estimate of peak exposure and
        that the daily time average would therefore be less.
272           With respect to the WAIT AID results, Mr Kottek said the
        conclusion that the level of asbestos exposure was less than 0.1 fibre/ml
        was an observation below the accuracy of the measuring equipment
        available at the time. He acknowledged that in the late 1970's in South
        Australia the standard tolerable asbestos exposure level promulgated by
        the NH & MRC in 1975 Guide was a time-weighted average of
        4 fibres/ml.

273          Mr Kottek did not himself make a formal estimate of the risk facing
        Mr Cotton and said that it was not possible to do so from the data
        available. When asked in cross-examination by counsel for the third
        defendant about the basis for his calculation for the aggregate exposure to
        asbestos while working at Australind, Mr Kottek said that he had assumed
        five years of exposure based on a working week of five days, 48 weeks
        per year. He was content to assume a peak exposure of 5 fibre/mls to
        10 fibre/mls which he regarded as significant. That was higher than the
        figure adopted by Mrs Sowden but, in his view, her calculation was an
        underestimate.
274          In my view, Mr Kottek was well justified in declining to accept,
        directly, any measured level of asbestos exposure by extrapolation from
        the WAIT AID tests or from the literature when it came to estimating the
        degree of exposure to which Mr Cotton was subjected to during either of
        his two periods of employment. There is very considerable force in
        Mr Kottek's view that it is impossible, on the limited data, to make
        accurate or precise estimates about the level of exposure. However,
        Mr Kottek indicated that the exposure levels were relatively low but
        potentially above the then recommended limit of 0.1 fibre/ml. His


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        estimates as to the aggregate exposure over time are only estimates, and
        from the manner in which he gave his evidence, I am satisfied that he
        would accept that wide range of variations for any such estimate would be
        necessary. Rather, I consider that he preferred, and I accept, the more
        qualitative opinion that Mr Cotton was subject, during both periods of
        employment, to low levels of asbestos exposure which, nevertheless, were
        entirely capable of contributing to the development of lung cancer in
        conjunction with his history of smoking.
2. Professor de Klerk
275          The plaintiff also called Professor Nicholas de Klerk, a consultant
        epidemiologist and biostatistician, who is the head biostatistician and
        epidemiologist at the Telethon Institute for Child Research in Western
        Australia. Professor de Klerk holds degrees of Bachelor of Science
        (Physics) from Imperial College of London, a Master of Science degree
        from the University of Sussex in Statistics and the degree of Doctor of
        Philosophy from the University of Western Australia in 1989. He
        maintains the Mesothelioma Register in Western Australia and lectures
        nationally and internationally to a number of bodies, including to the
        members of the Royal Australasian College of Physicians on lung cancer
        due to industrial exposure. He has published many articles dealing with
        asbestos-related disease and has a special interest in the pathology of lung
        tumours. He is undertaking the ongoing study of the epidemiology
        associated with the Wittenoom Cohort - that is the study of the pathology
        and morbidity of persons exposed to asbestos at the operations of the blue
        asbestos mines at Wittenoom Gorge in this State.
276           From the materials supplied to him, Professor de Klerk assumed that
        Mr Cotton had approximately one hour per day exposure to cutting
        asbestos pipes for two years and also worked in the residual dust in the
        soil (Exhibit 74(1)). He also assumed that Mr Cotton had some bystander
        exposure for the last 10 years doing various operations in an area that now
        appears to have been fairly heavily contaminated with all kinds of
        asbestos used particularly in the insulation of the various machinery at
        Millennium Inorganic Chemicals. He said:

              "While a long 'latent' period between exposure and disease is
              accepted for mesothelioma, such a period is not defined for the
              association between lung cancer and asbestos exposure. It is
              also accepted that asbestos acts as a 'promoter' in the causation
              of lung cancer, that is, it acts at a late stage of the disease (Day
              and Brown, 1980), and thus theoretically could act almost


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              immediately, certainly within a year or [two]. Work with the
              Wittenoom Cohort has indicated no latent period for increase in
              risk of lung cancer (de Klerk et al, 1991), thus all of the five
              years of exposure at Millennium when asbestos was present can
              be considered as contributing to causation of the disease."

277          Professor de Klerk referred to a pooled analysis of many studies
        estimating the relative risk of lung cancer from smoking between 15 to 24
        cigarettes a day and, taking Mr Cotton's daily consumption of cigarettes at
        15 a day, he assigned a relative risk of lung cancer due to smoking alone
        as being 7.7. With regard to the estimated level of asbestos exposure from
        both sources, Professor de Klerk wrote (Exhibit 74(2)):

              "Likely levels of exposure are hard to assess but sawing of
              asbestos cement pipes has been estimated to produce 10 - 20
              f/ml (Brown, 1981). The residual exposure would have been
              much less, say 0.1 f/ml. His exposure to insulation would have
              been slight ... would have been at the heavy end of exposure in
              contaminated buildings ie 2 - 5 f/ml (Brown, 1981), say an
              average of 2 f/ml of mixed exposure. Thus his asbestos
              exposure could be set at 5.2 f/ml year working for the Water
              Supply and 10 f/ml year at Millennium.

              The type of asbestos in the pipes is likely to have been of mixed
              type and therefore increases in relative risk for exposure to
              mixed types, of 0.01 - 0.05 per f/ml year are appropriate, say
              0.02 (Doll and Peto, 1985). It can also be assumed that a
              multiplicative relationship between asbestos exposure and
              smoking on risk of lung cancer holds.
              Using these assumptions and the results already cited gives the
              following relative risks:
                 Relative risk from smoking = 7.7

                 Relative risk from exposure to asbestos = 1.3
              Therefore:

                 Probability that lung cancer due to smoking = 0.87
                 Probability that lung cancer due to asbestos = 0.23

                 Probability that lung cancer due to smoking and asbestos
                 together in combination = 0.20

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                 Probability that lung cancer due to smoking only = 0.67

                 Probability that lung cancer due to asbestos only = 0.03
                 Probability that lung cancer due to neither smoking nor
                 asbestos = 0.10."
278          Professor de Klerk adopted a risk co-efficient of 0.02, that is
        2 per cent for each fibre/ml year of exposure.
279           To the uninitiated these figures may appear to suggest that the
        greater probabilities, that is more probable than not, were of the lung
        cancer being due to smoking alone, but Professor de Klerk explained that
        was not their meaning. Each of the calculations was an independent
        calculation dealing only with the single factor producing the lung cancer,
        regardless of all other factors, or a combination of two factors, to the
        exclusion of all others. The calculation is to take the relative risk (of the
        isolated agent) to deduct from that the base figure 1.0, indicating the
        background relative risk and to divide that sum by the relative risk due to
        that agent so, when doing the calculation for the probability of lung cancer
        being due to smoking alone, with a relative risk of 7.7, the calculation
        becomes:

                                            7.7 - 1/7.7 = 0.87
        And, when dealing with the probability due to exposure to asbestos alone
        where the relative risk is assessed at 1.3, the calculation becomes:
                                            1.3 - 1/1.3 = 0.23

        Because of the synergistic or multiplicative effect of smoking and
        exposure to asbestos, the combined effect is to multiply the two
        proportions, that is:
                                            0.87 x 0.23 = 0.20
        And, in each case, the product gives the probability of the enhancement
        over the unitary background risk (of 1) of the assumed factor or
        combination of facts contributing to the lung cancer. On the above figures
        the product of 0.23 represents an indicator that, in addition to the
        background level assumed at the unitary 1, there is a 0.23 factor - making
        a total of 1.23, that the tumour is due to the combined effect of smoking
        and asbestos exposure. It is also necessary, in considering Professor
        de Klerk's ratios, to realise that every calculation of probability will be



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        less than 1, because that is the limit to which the product approaches, but
        can never reach, because of the formula RR - 1/RR.
280          Another way of expressing the product is that a risk co-efficient of
        0.23 constitutes a 23 per cent risk above the normal background risk of
        the pathology being due to the combination of the nominated carcinogens.

281           In cross-examination, Professor de Klerk stressed that care should be
        taken in attempting the estimates of cumulative dosages and that attempts
        at precision are not all that valuable. These are only estimates.
282          In cross-examination by counsel for the third defendant, Professor
        de Klerk carried out a number of calculations of the risk co-efficient of the
        lung cancer being due to asbestos alone for different levels of exposure
        for different periods, with the following results:
              (a)     2 fb/mls for a period of 1 year to 2 years. This produces a
                      risk co-efficient of 0.04 above the background relative
                      risk so the probability calculation is 1.04 - 1/1.04 = 0.038
                      or 3.8 per cent.

              (b)     Similarly, 0.5 fb/mls for 5 years = 2.5 fb/ml years
                      2.5 x 0.2 = 0.05 a relative risk of 1.05, so the probability
                      becomes 1.05 - 1/1.05 = 0.476 = 4.7 per cent.
              (c)     1.5 fb/mls for 5 years is equivalent to 7.5 fb/ml years, so
                      7.5 x 0.02 = 0.15, relative risk is 1.15, the probability
                      calculation is 1.15 - 1/1.15 = 0.1304 = 13 per cent.

283          He was asked, in cross-examination by counsel for the second
        defendant, to assign attributable fractions for the two separate periods of
        occupational exposure in South Australia and at Australind. Professor
        de Klerk did this and the exercise led him to opine that the probability that
        the lung cancer was due to smoking was 0.87, and the probability that it
        was due to asbestos inhaled in South Australia was 0.09, and that the
        probability that it was due to the two factors combined was 0.08.

284          However, taken in the light of all the evidence, and especially under
        cover of Professor de Klerk's own warnings, these mathematical
        calculations of relative risk, probability and combined probabilities, seem
        to be of very limited validity and guidance, not merely for large
        populations but more so in individual cases. Hesitancy in using these
        mathematical methods is due to the large degree of approximation in the
        base data itself, and the lack of any demonstrated or agreed mathematical
        function to reflect the interactions of more than one potential carcinogen.

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        In my view all that the evidence permits is that the combination of two
        carcinogens operating together is far more potent than the sum of their
        individual effects. Not only is the precise interrelationship unknown, and
        therefore immeasurable, but the contributions of the single carcinogens
        for any individual are also, at best, only approximate. In my view, the
        evidence establishes that only very limited regard can be had to these
        mathematical manipulations and that they can be no more than a guide
        and, even to that extent, they require a great deal of reserve in their use or
        application.

3. Mrs Janet Sowden
285           The occupational hygienist called by the second defendant was
        Mrs Janet Melville Sowden, whose curriculum vitae is listed in
        Exhibit 151. She holds the degree of Bachelor of Science from
        Melbourne University, is a full member of the Australian Institute of
        Occupational Hygienists, a fellow of that Institute and a certified
        occupational hygienist. She began her career as a scientific officer in the
        Pathology Department of the Bendigo Base Hospital and then, after a
        period at home, became a research assistant in the Biochemistry
        Department of Monash University, a scientific officer in the Industrial
        Hygiene Division of the Department of Health of Victoria with a special
        role in asbestos diseases, after which she had many different positions as a
        scientific officer in government dealing with asbestos. Since 1995 she has
        been a private consultant. Mrs Sowden's extensive CV lists her academic
        appointments, professional registration approvals and service on
        committees with special interest in occupational hygiene and asbestos
        working groups. She has written published papers on the membrane filter
        method of sampling for asbestos and other subjects. She is well known
        and respected in the scientific disciplines associated with the study and
        effects of occupational asbestos exposure.

286           Mrs Sowden has produced four separate reports which have gone
        into evidence as Exhibits 152(1) to (4), as expressions of her expert
        opinion on this case prepared for the solicitors for the second defendant.
        In the first of these Mrs Sowden commences by commenting on the
        difficulty of making retrospective assessments of occupational asbestos
        exposure simply by inference but, she observes, for all their weaknesses,
        retrospective exposure assessments are important tools in epidemiology.
287          Mrs Sowden has never taken any measurements of asbestos exposure
        during the laying of AC pipes but has other experience in asbestos cement
        products which she says can be extrapolated to that situation. In her other


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        works in this area most of her measurements showed exposures to be less
        than 1 fb/ml, although occasional very high short-term exposures of up to
        60 fb/mls occurred in factory situations. She observed that measurements
        taken during brief periods of high exposure - short-term measurements -
        may be valuable for control purposes but are not useful for assessing
        exposures to substances such as asbestos where the pathological effect is
        the result of accumulation in the body over a long period. On those
        assumptions Mrs Sowden's observations are no doubt apt, but it remains
        the fact that there is controversy about the effect of asbestos exposure and
        that, Professor de Klerk and others do not accept that asbestos related lung
        cancer is due to a long accumulation of asbestos exposure but, instead,
        maintain that short-term exposures, without accumulation, can be
        significant.
288          Mrs Sowden then had regard to a series of studies reporting on fibre
        levels generated during work with asbestos cement pipes, including the
        Kumagai article (see [261] above), the UK Advisory Committee on
        Asbestos Report, James Hardie Pty Ltd Internal AC Cutting Tools Studies
        by P A King (see [258] - [259] above) and the USA Asbestos Cement
        Pipe Producers Association Report of 1997 ([255] - [257] above). After
        considering those sources and the description given to her of Mr Cotton's
        employment with the EWSD of South Australia, she made the following
        assumptions about Mr Cotton's asbestos exposure:

              "•      He did not use powered cutting tools for the routine
                      cutting of asbestos cement pipes;

              •       The pipes that he used were predominantly high-pressure
                      thick-walled pipes;
              •       He spent 10 - 20 minutes 3 - 4 times per day cutting and
                      rasping the pipes within the trench during which time his
                      exposure was 20 times greater than that measured in the
                      open air by the A/C Pipe Producers Association, ie
                      20 x 0.22 fibres/ml;

              •       The remainder of his day was spent laying the pipes
                      within the trench, during which time his exposure was
                      similar to that measured by the A/C Pipe Producers
                      Association, ie 0.02 fibres/ml;

              •       He was exposed as a bystander to dust arising from the
                      use of an angle grinder on asbestos cement pipes in the
                      open air on four occasions, each lasting about five

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                      minutes. The asbestos level generated in the breathing
                      zone of the operator was similar to that reported for
                      cutting with a circular saw, ie 20 fibres/ml. Mr Cotton
                      was exposed to some fraction of this amount depending
                      on his distance away from the operator; I will assume that
                      he was within 3 metres of the cutting operation and
                      inhaled 1/3rd of the source concentration, ie 6.7 fibre/ml.

                      Mr Cotton's average daily exposure over the period
                      1975 - 1978 (said to be two years by Prof Musk) was
                      thus:
                               (80 x 20 x 0.22) + (400 x 0.02) fibres per ml

                                                    480
                                       = 0.78 fibres/ml." (after rounding)
        She estimated that his cumulative exposure from this source was 1.6 fb/ml
        years. Mrs Sowden also assumed that any additional exposure from the
        presence of in situ asbestos insulation at Millennium Chemicals would
        only be trivial and, therefore, did not include it in her calculations.
289           In commenting on the potential causative effect of her estimated
        asbestos exposure for Mr Cotton, Mrs Sowden mentioned that there still
        remains controversy over whether, in the absence of smoking, asbestos
        exposure at levels insufficient to cause asbestosis increases the risk of
        lung cancer; and, secondly, if asbestosis is a necessary pre-condition for
        the causation of asbestos-induced lung cancer, whether the proximate
        cause is asbestos per se or the fibrotic process. She then referred to
        published literature on those issues and said that most risk models
        developed for the purpose of setting exposure standards assumed a linear
        relationship between lung cancer risk and exposure and intensity and
        exposure duration, with no threshold. She added, however, that this
        model (involving no safe threshold) is probably reasonably accurate at
        high dose levels, but that its use for predicting risk at low exposure levels,
        for which no data are available, has been severely criticised.

290          Mrs Sowden then referred to two major reports which had concluded
        that clinically detectable asbestosis will not occur when cumulative
        asbestos exposure is below 25 fb/ml years. Because she calculated
        Mr Cotton's asbestos exposure as being about 1.6 fb/ml years she then
        reached the conclusion (on the basis of the earlier reports) that his
        exposure could not give rise to clinically detectable asbestosis but she


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        added a caveat that this was subject to the possibility of better evidence
        becoming available. This reservation is simply a step in Mrs Sowden's
        reasoning because, of course, there is no diagnosis of asbestosis for
        Mr Cotton, nor any histological, radiographic or other evidence of any
        form of fibrotic asbestos lung disease.

291          Moving onto the risk of lung cancer from asbestos exposure,
        Mrs Sowden wrote that despite the most common assumption of a
        no-threshold model for asbestos-related lung cancer, the commentators
        "appear to agree" that a sub-asbestosis exposure (ie less that 25 fb/ml
        years) involves either a non-existent risk of developing lung cancer or a
        risk so small as to be indistinguishable from the background incidence.
        For this conclusion, she relies upon the Helsinki Protocols but, as will be
        discussed later, those protocols, even if they are regarded as being
        applicable to cases of lung cancer due to occupational exposure (as to
        which there is considerable controversy with notable consultants,
        including Professors Musk and de Klerk rejecting that approach), the
        Helsinki document does not appear to support that conclusion. It
        acknowledges (Exhibits 55 and 188, at p 314) that small exposures to
        asbestos are known to cause lung cancer and on a reading of the document
        as a whole I am not satisfied that it advances or supports the argument that
        an exposure of 25 fb/ml years is a prerequisite for an attribution of
        asbestos-induced lung cancer, as distinct from an attribution of asbestosis.
        Mrs Sowden concludes her first report by observing that Mr Cotton's
        cumulative exposure was certainly well below 25 fb/ml years.

292          Turning to Mr Cotton's "27 year smoking history, alone"
        Mrs Sowden said that this appeared to be a more credible source of his
        condition than his asbestos exposure. It is to be noted, however, that
        Mrs Sowden's extensive academic qualifications and experience do not
        include any detailed studies of the effects of smoking, either alone or in
        combination with asbestos, whether as a sole or synergistic cause with
        another carcinogen in the development of lung cancer. She does not have
        formal qualifications in medicine or in epidemiology which are fields of
        knowledge which, on all the evidence in this case, have an important
        bearing on whether or not any such ultimate conclusion should be
        reached.

293          In her second report (Exhibit 152(2)), Mrs Sowden responded to
        information submitted to her by the solicitors for the second defendant
        recording time-weighted average asbestos exposure of persons cutting and
        laying pipes under Australian field conditions. Included in these were the
        WAIT AID and Amdel reports (Exhibits 153(4) and 153(6) - discussed at


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        [244] and [251], and following, above. As earlier noted, these recorded
        that the time-weighted average asbestos exposure for this type of work
        was less than 0.15 fb/ml and Mrs Sowden took them as being
        representative of Mr Cotton's exposure over the 1975/1998 period.
        Recalculating the exposures on this basis led her to conclude that
        Mr Cotton's cumulative asbestos exposure was less than 0.2 fb/ml years
        and to repeat the opinion expressed in her first report that such an
        exposure would not make any material contribution to Mr Cotton's lung
        cancer risk. However, I am not prepared to accept either the WAIT AID
        Report or the Amdel Report as being a reliable indication that the
        exposure to which Mr Cotton was subject while working in Adelaide was
        as low as 0.1 fb/ml. Those figures are more than one order of magnitude
        less than exposures reported elsewhere, in the international studies and in
        the assumptions of Mr Kottek and estimated in the first report of
        Mrs Sowden. I therefore reject this lower estimation and quantification of
        the cumulative exposure to asbestos by Mrs Sowden in Exhibit 152(2).

294           A third report was prepared by Mrs Sowden, dated 8 February 2001
        (Exhibit 152(3)), after the second defendant's solicitors had submitted to
        her a statement of the evidence of Mr Mark Campbell of the South
        Australian Water Service (see [108] - [110] above). However,
        Mrs Sowden expressed reservations about short-term subjective estimates
        of the nature of work done involving asbestos products and expressed a
        preference to rely upon whole day measurements such as contained in the
        WAIT AID Report. On that basis, she did not rely upon Mr Campbell's
        information except to observe that it added weight to her earlier
        conclusion that Mr Cotton's asbestos exposure as a pipe layer would have
        been very small. She adhered to her second estimate of cumulative
        exposure, namely, less than 0.2 fb/ml years. As mentioned in discussing
        Exhibit 152(2), I do not accept that conclusion and regard Mrs Sowden's
        first estimate of 1.6 fb/ml years as representing her own opinion based
        upon a study of the literature and general experience, uninfluenced by the
        WAIT AID Report.
295           Finally, Mrs Sowden produced a fourth report (Exhibit 152(4)) dated
        1 July 2001 after having been provided with copies of the plaintiff's
        reports from Professor K Wan and from Professor Nicholas de Klerk.
        Mrs Sowden was, with all respect, very dismissive of Professor Wan's
        opinion because, in her view, it ignored what she took to be a fundamental
        relationship, namely that the cumulative dose of asbestos over time is
        determinative of its potential for harm. This is another example of her
        commitment to the view that a minimum aggregate of cumulative
        exposure to asbestos, which she claims is the test adopted by the Helsinki

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        Protocols of 25 fb/ml years, is essential before an attribution of
        asbestos-induced lung disease can be made, including lung cancer, in the
        absence of a confirmed histological or radiographic diagnosis. She again
        referred to the fact that most dose response models for asbestos-related
        lung cancer assumed there is no threshold, but she did not adopt that
                                                                        ore
        thesis because of her view that cigarette smoking is a far m potent
        cause. Again, with respect, I consider that in this regard Mrs Sowden is
        venturing an opinion beyond the area of her expertise. She is a very
        highly qualified and experienced occupational hygienist but she does not
        have medical or research qualifications to venture opinions which would
        dismiss the potential effect of low dose asbestos exposure, either alone or
        in combination with cigarette smoking, as a potential cause of lung
        cancer.
296           Mrs Sowden also rejected Professor Wan's exposure assessments, not
        only during Mr Cotton's employment in Adelaide but also at Millennium
        Chemicals - an area which she had not previously addressed in any of her
        first three reports. The sources of the information given to Mrs Sowden
        about the levels of exposure to asbestos by Mr Cotton at Australind are
        not identified and, in view of the extensive and evolving evidence about
        this which was adduced at this trial, and which I have already examined, it
        seems most unlikely that she received a full or adequate description of
        this. I am not prepared, therefore, to accept any of Mrs Sowden's
        observations about the actual or potential exposure to asbestos
        experienced by Mr Cotton when he was working at Australind. Nor,
        despite her criticism of his views, can I regard Mrs Sowden's rejection of
        the opinions expressed by Professor Wan as carrying any weight. The
        issue raised by Professor Wan of the potential contribution towards lung
        cancer of low dose or occasional exposure to asbestos does arise in this
        case but, in my view, it can only be determined upon the basis of the
        medical and epidemiological expert evidence bearing on those issues.
297          Mrs Sowden also criticised Prof de Klerk's report, observing that she
        believed that he had also overestimated Mr Cotton's exposure. Again,
        however, she showed a preference for the WAIT AID reported results as a
        more reliable indication of the type of exposure, but I am not prepared to
        accept that view. Finally, Mrs Sowden again rejected a conclusion by
        Professor de Klerk that exposure to asbestos contributed to Mr Cotton's
        lung cancer by reference to her interpretation of the Helsinki Protocols
        which, controversially, she asserted required a minimum cumulative dose
        exposure of 25 fb/ml years before an attribution of asbestos-induced lung
        cancer could be made. Again, despite persistent efforts by the defendants
        in this action to establish that proposition I do not consider that that is

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        what the Helsinki Protocols themselves promote or, that even if it were,
        that the figure is an irreducible minimum either generally or in any given
        case. As will be seen later, the defendants' attempts to clothe the 25 fb/ml
        year figure as a universal parameter for a diagnosis of lung cancer is
        unwarranted on the basis of the Helsinki Protocol itself, it is contrary to
        the preponderance of the scientific literature, and is in my view repugnant
        to proper scientific scepticism about accepting absolute assertions.

298          In cross-examination Mrs Sowden said that, to her knowledge as
        advisor on asbestos working standards in Victoria and elsewhere, there
        was no other asbestos cement pipe manufacturer in Australia other than
        James Hardie & Coy Ltd after 1976 - except for one manufacturer in
        Tasmania.
299           In cross-examination by counsel for the third defendant, Mrs Sowden
        said that, to her knowledge, the calcium silicate asbestos lagging at
        Australind contained about 15 per cent asbestos. However, it was evident
        that she had never been to that factory or analysed the asbestos lagging on
        the pipe work system and therefore the source of her belief about this,
        necessarily hearsay, does not emerge. As, in Exhibit 152(1), Mrs Sowden
        disclaimed any detailed knowledge of the conditions under which Mr
        Cotton worked at Millennium Inorganic Chemicals, I do not see how any
        reliance can be placed upon this statement of the asbestos content of that
        lagging.

4. Mr Geoffrey Pickford
300           The second defendant also adduced evidence from another
        occupational hygienist, Mr Geoffrey Claude Pickford. At the time of the
        trial he was conducting business as an occupational hygiene consultant
        under the name "Pickford Consulting", and had been involved in studying
        and advising on the effects of asbestos since 1959. He had a long
        employment with CSR Ltd in its engineering and production projects and
        its building materials research laboratories, then with Wunderlich Ltd as
        an environmental control officer and from 1977 until 1988 as an industrial
        hygiene engineer and advisor to James Hardie Industries Ltd. He holds
        the degrees of Bachelor of Engineering in Mechanical Engineering from
        the University of New South Wales in 1963, a Master of Engineering
        Science from the University of New South Wales in 1972 and since 1984
        has been a certified industrial hygienist to the American Board of
        Industrial Hygiene Standards. He is one of only 15 fellows of the
        Australian Institute of Occupational Hygienists and has made a long study
        of the testing for airborne asbestos. He contributed, as a technical


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        secretary, to the NH & MRC Working Group for the establishment of
        standards for the airborne asbestos dust membrane filter method. His
        report (Exhibit 220) is directed to an estimation of Mr Cotton's likely
        exposure to airborne asbestos fibres whilst working with asbestos cement
        pipes in Adelaide for the three year period from 1975 to 1978.

301          Essentially, Mr Pickford's opinion is that the best estimate of
        Mr Cotton's exposure to asbestos during the asbestos cement pipe laying
        work in Adelaide is a cumulative dose of 0.09 fb/ml years. As this is so
        much less than the 25 fb/ml years (Helsinki criteria), Mr Pickford is of the
        opinion that Mr Cotton's dose is insignificantly small and indicates that
        his airborne asbestos exposure as a pipe layer would not contribute to his
        lung cancer. Generally speaking, Mr Pickford's opinion is prone to the
        same criticisms which I consider deprive the second, third and fourth
        reports of Mrs Sowden of persuasive effect (Exhibits 152(2) to (4)).
        These are that Mr Pickford:
              •       treats the Helsinki criteria of 25 fb/ml years exposure to
                      asbestos as a minimum exposure for attribution of
                      asbestos-induced lung cancer, either alone or in
                      combination with smoking;
              •       accepts the Amdel Report as establishing that the use of
                      the Wheeler cutter on asbestos pipes results in exposure
                      of less than 0.1 fb/ml on an open field work site;

              •       also accepts the WAIT AID Report as establishing that
                      working with asbestos cement pipes on an open field site
                      using the Wheeler cutter results in an exposure of less
                      than 0.1 fb/ml of air;
              •       interprets the James Hardie Asbestos Cement Cutting
                      Tool Cutting Study by Mr P A King (Exhibit 176,
                      [258] - [259] above) which revealed an average personal
                      airborne asbestos fibre concentration of 1.1 fb/ml when
                      working with a manual lathe as unrepresentative of
                      typical field use in the open air; and
              •       rejected the Ontario Royal Commission Report of 1984
                      (Exhibit 177, [258] above) findings of airborne asbestos
                      fibre concentration based on UK data and USA data as
                      being unrepresentative because they involved continuous
                      asbestos cutting operations without interruption.


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        Mr Pickford did not discuss the effect of peak short-term loads.
302          Mr Pickford then went on to estimate Mr Cotton's possible airborne
        asbestos dose by reference to the exposure of the standards reported in the
        Amdel Report (Exhibits 153(6); 174 and 286) and, by a process of
        reasoning, set out in Exhibit 220 which involved diminutions in those
        figures for various reasons, came up with a final total laying dose of
        0.9 fb/ml years. This compares with 1.6 fb/ml years in Mrs Sowden's first
        report (Exhibit 152(1)) and 0.2 fb/ml years in Mrs Sowden's subsequent
        reports.

303           While I do accept that Mr Cotton's aggregate exposure to asbestos
        while working with the second defendant's products in Adelaide for the
        first defendant was a lot less than 25 fb/ml years, I consider that
        Mr Pickford's conclusions are gross underestimates and are based on the
        WAIT AID and Amdel reports which I have already concluded are not
        reliable representations of that level of exposure - indeed, varying from
        other international studies of comparable activities by more than one order
        of magnitude. I am therefore not able to accept Mr Pickford's quantitative
        opinion about the aggregate exposure to asbestos experienced by
        Mr Cotton. I note that he did not attempt to make any estimate of
        Mr Cotton's exposure to asbestos while working with Millennium
        Inorganic Chemicals.
5. Mr Paul Foley
304          The third defendant also adduced evidence from expert occupational
        hygienists. The first of these was Paul Galen Foley. Reference has
        already been made to Mr Foley's evidence when conducting studies at the
        Australind plant (see [217] above). However, his evidence also extended
        to quantitative assessments of likely exposure. His curriculum vitae is set
        out in Exhibit 237 and his statement of evidence is to be found in
        Exhibits 238(1) and 238(2).

305           Mr Foley's role in advising upon and observing the progress of the
        asbestos removal programme from the third defendant's premises at
        Australind has already been described. For present purposes, the
        significant aspects of his evidence are that from about September 1989
        until about July 1991 he was involved in the air monitoring for asbestos
        which was conducted at SCM Australind on a monthly basis involving the
        collection of 20 samples across the site per month. The results of those
        samples were analysed by NATA certified analysts named on the
        respective test certificates. It was as a result of the 1990 test reports that
        Matprolabs were commissioned to develop the procedure for undertaking


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        removal of asbestos or effecting repairs in sections 1, 2, 3 and 4 of the
        site. Mr Foley explained how Matprolabs was asked by the third
        defendant to conduct further air monitoring and did so between 1988 and
        1995 in the BDR and at other areas of concern at the plant.
306           The system of sampling was that if any test result showed a reading
        of 0.05 fb/ml (ie half the then current Worksafe level of 0.10 fb/ml)
        Matprolabs was to notify the client. Mr Foley was responsible for
        reporting on the information to the client but has no recollection of any
        adverse air sampling readings or of advising the third defendant of any
        such adverse results between 1988 and 1995. An example of these test
        reports is provided by Exhibit 240, showing the results for 16 out of the
        20 samples taken on 11 June 1991 (the other four samples being rejected
        for technical reasons). The set of 51 of these sample reports is found in
        Exhibits 247(1) to (51) showing the results of sampling conducted at
        various dates between 16 June 1988 and 22 June 2000. Within that series
        of exhibits is a document dated 6 September 1989 which shows the
        sampling locations of the 20 membrane filter pumps at that date. None of
        them was then in the BDR or in the packing areas. Another description of
        the sampling locations is found in the document dated 9 November 1989,
        but again none was in the BDR or packing areas. The same observations
        can be made in respect of the location of the sampling pumps on
        5 December 1989, 5 March 1990, 20 April 1990, 18 May 1990, 15 June
        1990, 17 September 1990, 15 October 1990, 20 November 1990,
        20 December 1990, 15 March 1991 and 18 April 1991.

307           This pattern of reporting on the analysis of 20 samples from various
        locations in the third defendant's premises appears to have occurred over
        the period from early September 1989, at regular intervals, but to have
        ceased on about 16 July 1991. From then on there is a gap in the
        certificates of analysis and a new series of analysis certificates
        commences on 9 March 1995 which runs at intervals of only a day or a
        few days between samples until 18 April 1995, with another interruption
        before a further series of certificates of samples covering the period from
        about 2 November 1995 to 7 November 1995, followed by yet another
        series commencing on 27 February 1996 to 11 May 1996, with further
        sample results on 11 March 1997 to 26 August 1997 and a final certificate
        on 22 June 2000.
308          These second and subsequent series of air analysis reports all differ
        from the first. The first series reported on the results from 20 sampling
        locations. The second and subsequent series reported mostly only on
        three samples for each test, but occasionally four and sometimes two or


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        only one and from different locations. The second series of such samples
        (the March 1995 series) included samples from the BDR, in each case
        reporting that the fb/ml count was less than 0.01, but the sampling was not
        continuous within the BDR. Further results of tests of samples from the
        BDR were conducted in May 1996 to March 1997, but it is quite evident
        that the pattern of sampling had changed and was less extensive.
309          No explanation of this variation in membrane filter sampling and
        analysis emerged at the trial, but one can well infer that the earlier more
        numerous series of samples were collected and tested during the period
        when Matprolabs was conducting its initial evaluation of the premises and
        was recommending a planned programme of asbestos removal. I
        appreciate that the pattern of sampling from 20 locations continued after
        the second Matprolab report of August 1990 (Exhibit 113), but the major
        work of removing lagging from the BDR (by then a recognised source of
        asbestos) was not commenced until October or November 1991.
310           The pattern of sampling revealed by the second and subsequent
        series of analysis reports strongly suggests that this was sampling
        conducted in areas where contractors were actually removing asbestos,
        rather than an overall continuous planned estimation of airborne asbestos
        risks within the plant as a whole. There is no doubt that this system of air
        sampling was extensive and that it indicated that the airborne asbestos
        concentration at the areas sampled was low, and below the norms
        accepted for industry at the time. However, because of the nature and
        location of the sampling, it does not reveal the conditions in the BDR at
        the time Mr Cotton was working there and does not reveal anything about
        potential peak loads of airborne asbestos during operations such as
        sweeping up or cleaning in the BDR or, for that matter, in the packing
        sheds at the time of the removal of the asbestos cement roof sheeting.
        Nevertheless, it does show that during the periods when it was conducted
        and in other areas of the plant, the general level of airborne asbestos
        contamination was very low.

311          Exhibits 248(1) to (5) comprise a series of eight of the third
        defendant's industrial hygiene sample data sheets in respect of air samples
        which were taken on the dates nominated during the asbestos removal
        operations at the Australind site. These eight certificates relate to samples
        taken on 22 March 1995 - (4), 24 March 1995 - (2), and 3 April
        1995 - (2). The data sheets comprising Exhibits 248(1),(5) all show
        readings for asbestos fibres per ml of less than 0.01. Although the
        locations from which each sample was taken were described, the
        descriptions are not informative to the uninitiated but none makes specific


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        reference to the BDR or to the packing areas. Exhibit 249 is a series of
        industrial hygiene reports of analysis for asbestos from airborne sampling
        conducted over the period 3 March 1992 to 24 August 1992 and for two
        test results in different parts of the plant on 24 February 1993. Mostly,
        these are 0.01 fb/ml or thereabouts but there are three test results in
        August 1992 ranging from 1 fb/ml to 6 fb/ml which apparently come from
        the analysis laboratory area of the plant. Nothing in those sample results
        alters the general impression that, when and where tested, the analysis
        results revealed the very low levels of airborne asbestos. The same can be
        said of air samples taken over the period 16 June 1994 to 14 November
        1994, reported in Exhibit 250.

312           There is also a series of air monitoring certificates in evidence
        comprising Exhibits 251(1)-(6), 252(1)-(8), 253(1)-(4) showing the results
        of airborne asbestos monitoring conducted by other consultants for the
        Australind worksite, apparently during asbestos removal operations. All
        of these showed concentrations in fibres per ml of less than 0.01 and they
        reported on samples taken on: 4 January 1990, 14 - 28 May 1990, from
        19 February 1991, early August 1991, 8 November 1991, 9 and 18 March
        1992 and from 23 - 24 February 1994 (Exhibit 253(1)-(4)). Exhibit 254
        comprises a series of graphs tendered by the third defendant showing the
        levels of airborne asbestos fibres in various parts of the operation over the
        period 1991 to 1996. These graphs include the BDR and the packing area
        and show levels ranging from the undetected to a maximum of 0.01 fb/ml
        at times when the TLV (threshold limit value) was 1.0 fb/ml. The source
        of the sampling and the certificates of analysis for samples apparently
        taken within the BDR and the packing areas for these periods are not
        evident.

6. Mr Alan John Rogers
313          The third defendant called another occupational hygienist, Mr Alan
        Rogers, who also is highly qualified and has written extensively in the
        professional literature on asbestos and industrial lung disease. He is a
        fellow of the Australian Institute of Occupational Hygienists and holds the
        degrees of Bachelor of Science (UNSW), Master of Science (University
        of London) and Master of Science (UNSW), all degrees with a special
        interest in applied chemistry, occupational hygiene and environmental
        chemistry. He has lectured extensively in occupational health at the
        Faculty of Medicine at the University of Sydney and for the National
        Occupational Health and Safety Commission ("NOHSC"). He has held
        senior positions within the NOHSC and from 1993 to 1996, and was the
        head of the Occupational Hygiene Unit and Principal Research Scientist at


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        the NOHSC. Since 1996 he has been director of his own company which
        provides consultancy services for occupational health and safety. His
        very extensive curriculum vitae (Exhibit 243) reveals professional
        experience in the United Kingdom, United States, Canada, New Zealand
        and many other countries. He has been a member of, or chairman of,
        important professional associations and committees. He has been
        involved in extensive research concerning the composition of mainstream
        cigarette smoke and filtering methods. He has written on mesothelioma,
        and industrial lung disease with a special emphasis on the effects of
        asbestos.
314          He was engaged in June 2005 by the solicitors for the third defendant
        to advise on the plaintiff's allegations of asbestos exposure of her husband
        as a potential cause of his fatal lung cancer. The background information
        provided to him is set out in Exhibit 244 which contains a summary of the
        anticipated evidence of workers at Adelaide and in Australind concerning
        the working conditions and potential asbestos exposures. As a result, he
        prepared two detailed reports setting out his opinions with regard to this
        case which are, respectively, Exhibit 245 (which contains a series of
        calculations which, during his oral evidence, he corrected at p 13) and
        Exhibit 246. In these Mr Rogers sets out the results of his examination of
        the published literature and his appreciation of contemporaneous scientific
        opinion about the hazards of asbestos exposure during the two periods of
        Mr Cotton's employment now under notice; his opinions in relation to the
        potential effects of exposure to the levels of asbestos in those working
        places as far as these could then be ascertained and, in Exhibit 246 in
        particular, his opinion about the importance of the concept of "latency"
        with respect to the development of asbestos-related lung disease.

315           It is convenient to begin the analysis of Mr Rogers' evidence by
        identifying the concluding opinions which his analysis produced. These
        are that:
              (a)     Mr Cotton's alleged exposure to asbestos dust while
                      working in Adelaide and at Australind was infrequent and
                      slight in comparison to traditional primary asbestos
                      workers. He estimated that Mr Cotton's combined
                      employment period accumulative of asbestos exposure
                      was very low at 0.136 fibre/ml years or less.
              (b)     This asbestos exposure resulted in a relative risk of lung
                      cancer of 1.0026 which is much less than the value of 2.0
                      required for reasonable attribution (50 per cent chance


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                      that the asbestos exposure caused the lung cancer,
                      50 per cent chance due to smoking or other causes).
              (c)     Mr Cotton's long-term tobacco smoking history was the
                      major risk contributor (RR 15.5 contributing to
                      93.6 per cent of total risk) to the development of his lung
                      cancer.
              (d)     Mr Cotton's alleged asbestos exposure was only a very
                      minor     contributor      (RR 1.0026     contributing    to
                      0.02 per cent of total risk) to the development of his lung
                      cancer.
              (e)     The contribution from smoking is so overwhelming that
                      even assuming the multiplicative effect on different
                      scenarios of cumulative asbestos exposure, there is little
                      change in the relative proportion of 93.6 per cent of
                      Mr Cotton's lung cancer risk arising from the effects of
                      smoking.

              (f)     The extremely low level theoretical risk associated with
                      the alleged exposure at Australind is unlikely to have
                      been expressed due to the short latency period of only
                      eight years which is well below the value observed in
                      asbestos workers.
316          Mr Rogers' estimation of Mr Cotton's cumulative asbestos exposure
        while working for the South Australian Water Corporation was reached
        by the calculation of:

              2.5 years x 50 per cent (half the time involved in handling,
              laying and fitting pipe ends into couplings and cutting or
              rasping pipe) x 0.1 fibres/ml = less than 0.13 fibre/ml years.

317           In selecting these factors for the calculation Mr Rogers took the
        fibre/ml count of 0.1 fibre/mls because of his belief in the comparability
        of the WAIT AID Report study (Exhibit 153(4)) and the Amdel Report
        (Exhibit 153(6)) which each reported exposure of less than 0.1 fibre/ml
        from the activities there studied. However, Mr Rogers did make reference
        to the Japanese study, Kumagai and Others (Exhibit 193) and the James
        Hardie Tool Cutting Study and Field Studies (Exhibit 176) which showed
        exposure levels of approximately 1.4 fibres/ml and 2.0 fibres/ml
        respectively, but evidently rejected these in the light of the WAIT AID
        and Amdel studies. For reasons given earlier, I am not satisfied that the


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        WAIT AID and Amdel studies are representative of the working
        conditions experienced by Mr Cotton in Adelaide and, as it seems to me,
        the general literature is a better indication of the concentrations to which
        Mr Cotton may have been exposed. Previously I have mentioned that
        those other studies suggest an increase of at least one order of magnitude
        for the estimated air concentrations (ie multiplied by 10), but in reality the
        difference is a factor of 14 to 20 which, if applied directly to Mr Rogers'
        calculation would produce a cumulative exposure while working with the
        first defendant of 2.6 fibre/ml years if Mr Rogers' other assumptions were
        to be retained.
318           It is sufficient for me to observe that I am not satisfied that
        Mr Rogers' estimate of 0.13 fibre/ml years is reliable and, like
        Mrs Sowden's, it involves a calculation which is well towards the lower
        end of a broad distribution of potential possibilities. Using the James
        Hardie Tools Study results, the level of exposure would be more and
        could be 20 times greater. However, at 2.6 fibre/ml years, that is still
        relatively low but it is more in accordance with the estimations of
        Mr Kottek.

319           The calculation which Mr Rogers conducted to estimate Mr Cotton's
        cumulative exposure to asbestos while working with the third defendant
        produced a figure of 0.006 fibre/ml years which is, plainly, extremely low.
        However, his calculation was based on the assumption that the only
        detectable level of asbestos exposure experienced by Mr Cotton was that
        which came from the Chrysotile tape door seals on the band drier when
        opened and closed and this could only have occurred during 10 per cent of
        the time during which he worked in the BDR which, in turn, was assumed
        to be 15 to 20 times over a 12 month period each of 5 to 8 hours.
        Mr Rogers expressly excluded potential exposures to asbestos cement
        roofing and other asbestos materials and from the insulated steam pipes on
        the basis that such would not be detectable. He paid no regard to the
        evidence that there was fibrous materials on the BDR floor from falling
        lagging which was regularly swept up, exposing Mr Cotton to elevated
        exposures of asbestos in peak loads. For these reasons, therefore, I
        consider that Mr Rogers' estimate of 0.006 fibre/ml years for cumulative
        exposure at Australind is quite unrepresentative of the probabilities and is
        outside the lower end of any probable cumulative exposure distribution
        scale.

320          Mr Rogers then turned to the criteria to be adopted for an attribution
        of asbestos exposure as a cause of lung cancer. Referring to the Helsinki
        Protocols, which he described as "a conservative approach [which] selects


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        the highest risk for the basis of determination", a cumulative exposure of
        25 fibre/ml years is used to predict a two-fold increase in lung cancer risk
        - that is, rendering it more probable that a cancer sufferer with that degree
        of cumulative exposure would have had his/her cancer caused by the
        asbestos exposure rather than the inescapable general hazards faced by
        members of the non-exposed community. He also made reference to the
        AWARD criteria, repeating his reliance on the 25 fibre/ml year
        cumulative exposure value and observed that it was accepted that the risk
        from Chrysotile exposure was generally less, but that for exposures to a
        mixture of amphibole and Chrysotile, the cumulative exposure leading to
        a doubling of the risk will be dependent on the proportion of the types in
        the mixture. Adopting the aggregate exposure figure which he had
        calculated (which I have rejected), Mr Rogers considered that the
        exposure of Mr Cotton to less than 0.136 fibre/ml years in total was very
        far short of the 25 fibre/ml years of cumulative standard which those
        criteria promoted. He added that there was a view developing that the
        Helsinki criteria were too low and that a more likely value required for
        doubling of lung cancer risk is 100 to 200 fibre/ml years for many
        industries.
321           Turning to a different approach, Mr Rogers then addressed the
        estimation of Mr Cotton's specific dose of asbestos exposure by reference
        to epidemiological studies reporting specific industry dose responses. In
        doing so he observed that the overall lung cancer risk depends on a
        combination of factors such as the cumulative exposure, type of asbestos,
        stage of the asbestos processing and the type of product being
        manufactured. He wrote that for Chrysotile exposure, the best estimate
        should be an increase in risk of 0.1 per cent per fibre/ml year, but for
        amphiboles the increase in risk should be regarded as 5 per cent per
        fibre/ml year. For mixed asbestos exposures the mean estimate for mixed
        asbestos fibre types is 0.32 per cent fibre/ml year and that for an overall
        risk for a mixture of 96 per cent Chrysotile with a risk of 0.1 and
        4 per cent amphibole with a risk of 5.1, the combined risk would be
        0.3 per cent per fibre/ml year. And, drawing on published studies,
        Mr Rogers adopted a factor of 2 per cent increase in risk per fibre/ml year
        for exposure at the South Australian Water Corporation and 0.1 per cent
        increase in risk per fibre/ml year for exposure at Millennium Inorganic
        Chemicals (on the basis that the exposure there was solely to Chrysotile -
        which the direct evidence shows is a false assumption), thus producing an
        overall RR of less than 1.002606 compared with the normal population of
        1.0. This led to his conclusion that the RR was so far less than the value



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        of 2.0 deemed necessary for reasonable attribution under the Helsinki
        Protocol, that any causal relationship should be rejected.
322           An analysis of Mr Cotton's reported smoking history of 15 cigarettes
        per day for 26 or 27 years was then undertaken by Mr Rogers who
        calculated that the deceased had a history of 19.5 to 20.5 pack years of
        smoking with no cessation prior to the date of his diagnosis. He observed
        that the commonly reported relative risk of male smokers is 15, versus
        non-smoking non-asbestos workers, based on a British study (Doll and
        Peto: "1994 British Medical Journal"). According to a subsequent
        European study, the RR of lung cancer for long-term male smokers is 23.9
        (for all histological types), (Simonato: (2001) "International Journal of
        Cancer"). Mr Rogers selected a relative risk for Mr Cotton of lung cancer
        for all histological types of about 15.5. Applying the formula of
        (RR - 1)/RR = 15.5 - 1/15.5 that produced a probability quotient of
        93.6 per cent. Mr Rogers' description of this was that if Mr Cotton had
        not been exposed to asbestos then (non-asbestos) background factors
        (such as air pollution, radiation, passive smoking, chemicals, diet etc)
        contributed to the remaining 6.4 per cent of the risk.

323          Turning then to the question of the probability that Mr Cotton's lung
        cancer resulted from the alleged asbestos exposure and/or smoking,
        Mr Rogers undertook a more complicated calculation. He criticised both
        the additive and the multiplicative models for the combined effect of such
        carcinogens but, nevertheless, calculated the chances on the basis of a
        purely multiplicative model revealing the following components:

              Background risk                           6.44 per cent
              Due to smoking (alone)                   93.31 per cent
              Due to asbestos (alone)                   0.02 per cent
              Synergistic effect (asbestos/smoking)     0.24 per cent
                                                      100.00 per cent

        He undertook a further subdivision of the risks based on the multiplicative
        effect to reach his final conclusions of the risk and proportion due to
        asbestos and smoking as:
              Background risk                           6.44 per cent
              Risk due to smoking                      93.55 per cent
              Risk due to asbestos                      0.02 per cent



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        This led Mr Rogers to his conclusion that Mr Cotton's long-term tobacco
        smoking was the major risk contributor (RR 15.5 contributing to
        93.6 per cent of total risk) to the development of his lung cancer. The
        alleged asbestos exposure during his two major periods of employment
        would have resulted in a near multiplicative effect, but the contribution of
        asbestos to the multiplicative value amounted to only 0.02 per cent of the
        overall lung cancer risk.
324          Mr Rogers was cross-examined about these calculations which
        caused him to make some minor corrections to p 13 of Exhibit 245, but
        which have already been accommodated in the figures which I have just
        set out. However, one feature of these attempts at estimation which
        Mr Rogers did not appear to me to explain persuasively is the distinction
        which he maintained between the risk due to smoking and the risk due to
        asbestos in situations where it is widely recognised that the two
        carcinogens in combination are more potent than either acting alone.
        Mr Rogers recognised this phenomenon and asserted that he had
        addressed it by adopting the synergistic or multiplicative model but, in his
        mathematical conclusions, only a very small chance is attributed to the
        synergistic effect of the two carcinogens - only 0.24 per cent when, on the
        hypothesis adopted, the instance of cancer due to a combination of
        asbestos exposure and smoking, among people exposed to asbestos, must
        be greater than the incidence attributable to smoking alone, or at least
        involve an earlier onset. It follows, in my respectful opinion, that there
        must be an unspecified fallacy in these calculations which failed to report
        the chance of developing lung cancer from a combined exposure to
        tobacco and asbestos.
325          The approach adopted by Mr Rogers, while cogent on the
        mathematical assumptions which he has adopted, advances three
        categories of lung cancer, the first exposure to smoking alone, the second
        exposure to asbestos alone, and the third, exposure to both carcinogens.
        Such categorisations will be justifiable for a population at large, but when
        one is dealing with a population of lung cancer sufferers who have been
        exposed both to asbestos and to smoking, I am not persuaded that such
        divisions can or should be maintained. What Mr Rogers' calculations do
        not appear to address is the issue, crucial in this case, of what proportion
        of lung cancer sufferers, who have both a long-term smoking history and
        an exposure to asbestos, can it be said that smoking is the sole material
        cause of the pathology.
326          Next, Mr Rogers relied on the concept of latency as rendering it very
        unlikely that any exposure to asbestos while in the employ of the third


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        defendant caused Mr Cotton's lung cancer. His explanation of the
        significance of latency was developed considerably in his second report
        (Exhibit 246). Simply stated, latency is a reference to the period or lag
        time between a patient's first exposure to asbestos and the development of
        the disease to the point of diagnosis. The underlying premise is that the
        initial exposure is not causative of the cancer but, rather, the accumulation
        of a dose of the carcinogen during the first few years after exposure
        provides a likelihood of the development of the disease. Mr Rogers drew
        on a number of studies dealing with mesothelioma and said that with lung
        cancer a similar latency effect is observed with actual or potential
        carcinogens. The literature which Mr Rogers cited suggests that, with
        persons having a history of exposure to asbestos, there were no, or very
        few, cancer deaths for people with a latency period of 10 years or less and
        that only about 7.4 per cent of lung cancer deaths occurred after a latency
        of between 10 and 20 years.
327           Applying these figures to the history of Mr Cotton's employment was
        said to show that his first exposure to asbestos while employed with the
        first defendant occurred 25 years before his death, but his first exposure to
        asbestos in the employment of the third defendant occurred eight years
        before his death. This led Mr Rogers to the conclusion that it was very
        unlikely that the eight year latency period applicable for employment at
        Australind would express itself as an observable lung cancer risk.
        However, again, with all respect to him, I consider that Mr Rogers is
        attempting to make distinctions in Mr Cotton's history which the literature
        which he cited does not address. The fact of the matter is that Mr Cotton
        had some exposure to asbestos during the period 1976 to 1978, followed
        by a second period of exposure from 1991 to 2000. To apply the theory
        of latency only to the second period of exposure with a view to rejecting it
        as any potential contributor to his known lung cancer, is to ignore the
        possibility of a combination of effect with the earlier period of exposure.
        Nothing Mr Rogers said or wrote justifies such an approach and he did not
        cite any studies supporting his reliance on the latency period for lung
        cancer sufferers who had been exposed to asbestos on two or more
        separate series of occasions, each quite some time apart.
328          I find it even more difficult to adopt the principle underlying
        Mr Rogers' calculations in this regard in the light of the other expert
        medical evidence that the current state of scientific knowledge does not
        explain, at a cellular level, how or when such cancers develop and
        acknowledge that this pathogenesis is not presently understood. Hence,
        there is a variety of opinion among the medical consultants and in the
        general literature over whether or not asbestos is a "sole carcinogen" or

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        merely a "promoter" which accelerates or triggers the development of
        cancer after a process of cell mutation which is incompletely understood.
        While it is acknowledged that the risk of lung cancer due to asbestos is
        dose related, in the sense that the higher the cumulative dose the higher
        the risk of developing the disease, that does not mean either that a
        minimum cumulative exposure is accepted as being necessary before there
        is development of cellular change which leads to much later emergence of
        cancer or, for that matter, that exposure to asbestos after the initial
        mutations and the incomplete development of the disease does not itself
        cause or enhance the development of the disease. Without knowing how
        the cancer develops in this way, it is not obvious how the assumptions
        underlying Mr Rogers' reasoning can be accepted.
329           For these reasons, therefore, I consider that Mr Rogers' estimation of
        Mr Cotton's cumulative exposure to asbestos are significantly understated
        and that his probable cumulative exposure was greater than Mr Rogers
        described. The figures he a    dopted for airborne asbestos concentrations
        experienced by Mr Cotton were far too low. One cannot say exactly how
        far they were off but it must have been by more than one order of
        magnitude at least. Similarly, I am not persuaded that the shorter period
        of latency associated with exposure to asbestos at Australind means that
        this can or should be excluded as a contributing cause to Mr Cotton's lung
        cancer. Nevertheless, in a general way, I accept the thesis of Mr Rogers
        that, in comparison with many of the studied cohorts and for people
        working in an asbestos exposed environment for long periods,
        Mr Cotton's cumulative exposure was comparatively low and much lower
        than the 25 fibre/ml years criteria referred to in the Helsinki Protocols or
        by the Australian AWARD criteria.

330         I deal elsewhere in these reasons with Mr Rogers' evidence
        concerning the available knowledge of the occupational risks of asbestos
        from 1975 onwards.
331           A feature of Mr Rogers' testimony when giving his evidence was just
        how emphatic he was about the mathematical models which he employed
        and the criteria which he adopted for measuring the probabilities. In
        many ways he gave the appearance of an enthusiastic proponent of a
        mathematical thesis which could reduce imponderables to measured order.
        I have no doubt about his wide experience and learning but, in the light of
        the medical evidence and the disparity of views which exist in the
        literature, I consider that Mr Rogers exemplified a confidence in his
        conclusions which other related disciplines do not espouse.



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Results of Attempts at Quantitative Assessment of Asbestos Exposure
332          It is now necessary to attempt to draw together the threads of the
        evidence from the occupational hygienists and their efforts to measure
        quantitatively the probable cumulative exposure of Mr Cotton to asbestos
        in his two relevant periods of employment. In my view this evidence
        supports, at a general level, a finding that Mr Cotton's exposure to
        asbestos while working for the first defendant was intermittent and that
        there were only limited occasions each day when he was likely to have
        been exposed to peak doses of asbestos dust. I do not think it can be
        doubted that exposure to respirable asbestos fibres occurred through that
        employment in this way but, in aggregate, over the two and a half year
        period of his employment the exposure is likely to have been relatively
        low. I find it most invidious to attempt any quantitative assessment but I
        consider if this is to be done the result is bound to be much closer to
        Mr Kottek's estimates than those of Mrs Sowden, Mr Pickford or
        Mr Rogers.

333          To the extent that it may be significant, I am satisfied that the
        probabilities are overwhelming that it was significantly less than the
        25 fibre/ml years to which so much significance has been given by the
        defendants. In making that finding, I also find that during both periods of
        employment, that is at Adelaide and at Australind, there were almost
        certainly repeated periods of peak exposure, perhaps of relatively short
        duration. These occurred when Mr Cotton was working with, or close to,
        other workers rasping the ends of concrete pipes, or standing in proximity
        to a powered abrasive cutting device and, at Australind, when he was
        required to sweep up dust and debris from the floor of the BDR or to
        sweep or clean other areas of the premises where it is probable, that
        asbestos dust and fibres were included among the TiO 2 dust and other
        debris. Just how great those intermittent periods of peak exposure and
        what effect they had cannot be precisely measured, but I am satisfied that
        such patterns of exposure did occur.

Specialist medical opinion - clinical and epidemiological
334          This long recitation of the evidence and the attempts at qualitative
        and quantitative estimation of Mr Cotton's occupational exposure to
        asbestos sets the stage for the evaluation of the specialist medical opinion
        bearing on diagnosis and causation in this case.
335          The sources of this evidence are both clinical and epidemiological. It
        has been amplified by the tender of a very large quantity of published
        scientific literature dealing with asbestos lung disease, other cancers,

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        causation, epidemiology and criteria for attribution of asbestos-related
        lung cancers. That literature is too copious to be incorporated specifically
        in these reasons, but it is nevertheless evidence before the court which
        must be considered. Largely it bears on attempts made by the medical
        and scientific communities to understand and evaluate asbestos lung
        disease and the extent of hazards due to various degrees and types of
        exposure to asbestos products, either alone or in combination with other
        carcinogens. It is so extensive and specialised that its selection and
        evaluation calls for expert knowledge and experience and, in this case,
        that comes from those witnesses whose oral evidence has addressed these
        issues and, to greater or lesser extent, quoted or considered the literature.
        The literature is also significant in evaluating the reliance to be placed on
        the opinions and contentions of the various expert witnesses and, indeed
        for that matter, the submissions by counsel. The literature is, in addition,
        primary evidence of the contemporary states of understanding, or lack of
        understanding, or of controversy concerning all these issues which, as I
        must, I have considered. The references to this literature and its actual or
        potential significance are discussed later in these reasons under the
        heading "Scientific Literature" and the overall conclusions from which are
        set out later. In this section of these reasons, however, I deal with the
        consultant medical evidence on these issues as given by witnesses at the
        trial.

1. Professor A W Musk, AM
336          The role of Professor Musk in the evaluation of Mr Cotton's case and
        his prognosis has already been described, but the plaintiff relies on
        Professor Musk's very extensive knowledge and experience of lung
        disease, and in particular asbestos-related lung disease, to support her
        submission that Mr Cotton's two periods of occupational exposure to
        asbestos made a material contribution to the development of that disease.
        Professor Musk is a leading Australian and international authority on
        respiratory medicine and in particular an asbestos-related lung disease.
        He is a consultant to many organisations in relation to asbestos diseases,
        he is a referee on submissions dealing with lung disease for the Medical
        Journal of Australia and other highly reputed medical journals, he has had
        over 210 of his publications published in scientific journals dealing with
        asbestos and smoking and has made more than 250 presentations to
        scientific societies on these subjects. He has received a public honour for
        his contribution to the study of dust diseases in Australia, has treated
        thousands of patients with asbestos lung disease and continues his
        scientific studies and research in these areas.



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337          Professor Musk's description of Mr Cotton's history and diagnosis is
        contained in his report of 16 June 2000 (Exhibit 56) and, for present
        purposes, the material section of that reads:

              "Mr Cotton has a history of exposure to asbestos and has been a
              cigarette smoker. He has now developed non small cell
              bronchogenic carcinoma. It is my opinion that his relative risk
              of developing lung cancer as a smoker would have been about
              20 and that his relative risk of developing lung cancer from his
              asbestos exposure as described would have been about 1.1 - 1.2.
              Both agents would have acted independently of each other, ie
              his risk of lung cancer from asbestos exposure would have
              multiplied that of his risk from smoking."
        In the course of his oral evidence Professor Musk said that, in his view,
        asbestos was a "complete carcinogen" and not merely an initiator. He
        described how, in Australia, cigarette smoking was the major cause of
        lung cancer but that not all heavy smokers contracted lung cancer and that
        the incidence of the development of that disease for those people was
        about 5 per cent, but that continuation of smoking would inevitably lead
        to the development of lung cancer if the patient did not first succumb to
        other illnesses. He explained that the same phenomenon occurred with
        continued asbestos exposure. In his view there were not many cases of
        lung cancer for people aged younger than 50 years and that most cases
        were people in their sixties. Professor Musk produced a graph
        (Exhibit 54) showing the incidence and mortality from lung cancer
        according to age and, whereas the earliest incidence in mortality
        appearing from the graph was at about the age of 25 years, the incidence
        of mortality for people in the 40 - 44 age group was less than 10 deaths
        per 100,000 population on the logarithmic graph depicted. This is to be
        contrasted with a figure of something in the order of over 150 deaths per
        100,000 population for the 60 to 64-year-old cohort of males - much more
        than a tenfold increase.
338          Professor Musk found no abnormality on his physical examination of
        Mr Cotton and, apart from his history of smoking and exposure to
        asbestos, can suggest no other potential cause for his cancer.
339           With regard to the effect of exposure to asbestos Professor Musk said
        that, in his opinion, there was no safe level of exposure. Nevertheless,
        Professor Musk agreed that it was generally accepted that the
        development of asbestos lung disease was dose responsive, but said that if
        there was a known carcinogen such as asbestos present in the patient's
        history one should not exclude that as a potential cause. In his view the

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        absence of pleural plaques from any report of Mr Cotton's radiology
        examinations does not exclude adverse effects of exposure to asbestos. In
        Professor Musk's opinion, the causal criteria for lung cancer are generally
        agreed among medical scientists but there remains a difference of opinion
        as to the level at which the presence of those carcinogens become
        influential or causative. He specifically rejected the suggestion that
        cumulative dose of asbestos is an appropriate measure in the
        determination of the causative effect of that carcinogen. Specifically, he
        rejected the thesis that lung cancer due to asbestos must necessarily be
        associated with asbestosis in order for such an attribution to be made.
        This view promoted by Professor Hans Weill (Exhibit 290 is one of
        Professor Weill's publications but this was not specifically put to
        Professor Musk) to the effect that the causal attribution of asbestos for a
        particular lung cancer should not be made in the absence of asbestosis or
        other asbestos lung disease, which was earlier prevalent among medical
        scientists, has fewer adherents in modern times.

340          In cross-examination Professor Musk was asked about the
        epidemiological approach that for a person with lung cancer the RR of the
        effect of his or her asbestos exposure should be 2 or more before it
        becomes more probable than not that this particular case was attributable
        to asbestos. Professor Musk agreed with that as a general proposition and
        for a general randomised population of lung cancer sufferers, but he
        emphasised that the toxic effects varied among different types of asbestos
        and that the amphiboles (Crocidolite and Amosite) are more toxic than the
        serpentinites, such as Chrysotile, although he added a warning that the
        potentially more toxic effect of the amphiboles is less clear in cases of
        lung cancer than the corresponding noxious effects of asbestos types with
        respect to mesothelioma. In his view it was common for estimations of
        cumulative exposure by a patient to asbestos to be u   nderestimated and
        often by orders of magnitude.
341          Again, in cross-examination, Professor Musk was asked about the
        Helsinki Protocol and the criteria which it promoted for the diagnosis of
        mesothelioma, asbestosis and lung cancer. He agreed that, for lung
        cancers due to asbestos, the increase in relative risk was of the order of
        0.5 per cent to 4 per cent for each fibre/ml year and therefore could be
        regarded as doubling after 25 to 200 fibre/ml years. However, he did not
        agree that the same approach should be taken in relation to cases of lung
        cancer not associated with asbestosis. He repeated his opinion that in
        Mr Cotton's case his RR with respect to smoking was 20 (that is, he had
        20 times the risk of developing lung cancer than a non-smoker) and that
        with respect to asbestos, his relative risk was in the range of 1.10 to 1.20

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        (that is, that he had a 10 to 20 per cent increased risk of developing lung
        cancer than a person not exposed to asbestos). In his view, the overall
                              n
        risk for Mr Cotton i developing lung cancer from the combination of
        these causes was arrived at by multiplying those risks (20 x 1.10 or
        20 x 1.20) producing a figure of 22 or 24 or, in other words, an increased
        risk of developing lung cancer due to asbestos alone of 10 to 20 per cent.
        Professor Musk offered the opinion that he would apportion that elevation
        of risk to be in the range of 3 to 8 per cent due to the exposure in South
        Australia and in the order of 7 to 12 per cent for the exposure at
        Australind.
342          Furthermore, Professor Musk agreed that Mr Cotton's life expectancy
        would have been diminished in any event because of his history of
        smoking and that with this and his chronic bronchitis he could be
        expected to have a reduction of five years or more in life expectancy when
        compared to an ordinary man of his age and that he could well have been
        incapacitated before the age of 65 years.

343           In the course of cross-examining Professor Musk, counsel for the
        third defendant put to him a series of published articles from the scientific
        literature (Exhibits 140(1) - (7)) containing analyses of various studies of
        the mortality of insulation workers with varying degrees of asbestos
        exposure and the onset of lung cancer; the relationship of mortality to
        measures of environmental asbestos pollution; an analysis of mortality
        among Chrysotile workers; and a further study in relation to a cohort
        exposed to Amosite. These articles were published during the periods
        1979 - 1982, 1985, 1993 and 1998. The point put by the cross-examiner,
        in various ways, to Professor Musk based on these articles was that this
        literature supported a view that there was a significant lag-time or latency
        associated with the development of lung cancer after the date of first
        exposure to asbestos fibres and that there was a normal type distribution
        of this latency in the number of cases studied but that, commonly, the
        mean period was 20 years or more, leading to the suggestion that it was
        improbable that any exposure by Mr Cotton to asbestos at Australind
        caused or contributed to his fatal lung cancer. Professor Musk did not
        dispute this pattern of distribution for periods of latency but pointed out
        that the reported literature included cases of asbestos-related lung cancer
        with significantly shorter latency periods than those at or near the mean
        figures, and that this was typical of any distribution which could be
        expected to range over a broad spectrum. In Mr Cotton's case his initial
        exposure to asbestos at Adelaide was about 25 years before the diagnosis
        of his lung cancer and first exposure at Australind was about nine years


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        before. Either of those figures alone, but more so in combination, was
        consistent with the history of Mr Cotton's disease.
344          Considerable caution must be exercised when attempting to
        transpose from a general medical or epidemiological study, opinions or
        conclusions to an individual case. This is evident from a further article
        from the literature put to Professor Musk by counsel for the third
        defendant, the article by Dr Hauptmann and others (Exhibit 141)
        discussing the exposure time response relationship between asbestos
        exposure and the development of lung cancer. That article, dealing
        chiefly with different mathematical models of estimating aggregate
        exposure over time, included the observation that despite the numerous
        studies which had been carried out to evaluate the association between
        lung cancer and occupational asbestos exposure, the effects of timing of
        exposure had not been analysed thoroughly. Writing in 2002, these
        authors concluded that, in contrast to previous indications, the risk of lung
        cancer increases soon after asbestos exposure with its maximum effect
        from 10 to 15 years after the exposure was received. Consequently, this
        attempt to suggest that Dr Musk's opinion that Mr Cotton's exposure to
        asbestos was a contributory cause to his fatal lung disease should be
        rejected because of alleged insufficient period of latency, simply failed.

345          In my view, Professor Musk provided a persuasive and convincing
        opinion for his proposition that in Mr Cotton's case the reported exposure
        to occupational asbestos on two occasions increased his risk of developing
        lung cancer due to that carcinogen by something in the order of 10 to
        20 per cent and that this probably interacted with a much higher risk of
        developing the disease because of his history of smoking to produce a
        combined fatal effect.

2. Professor K Wan
346          The opinion that Mr Cotton's exposure to asbestos contributed to the
        development of his lung cancer was also supported by Professor
        Kah Wan, who is a consultant in occupational medicine, a former chief
        occupational health physician at the Health Department of Western
        Australia (1980 - 1985) and Chairman of the Industrial Diseases Medical
        Panel. Professor Wan is a member of the Royal College of Physicians,
        having earlier graduated MBBS at the University of Singapore in 1969.
        He has worked as a physician in hospitals in Malaysia, in the United
        Kingdom, in Australia and the United of America and he was adjunct
        professor in occupational health at Edith Cowen and Curtin University of
        Western Australia.


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347           Professor Wan prepared a report on 12 April 2001 (Exhibit 58) on
        Mr Cotton's case at the request of the President of the Asbestos Diseases
        Society of Australia Inc, having been provided with Mr Cotton's
        employment history, reports from Dr Kendall (Exhibits 67 and 69), a
        Medical Panel determination that Mr Cotton had lung cancer, the report of
        16 June 2000 of Professor Musk (Exhibit 56) and other documents there
        listed. The substance of Professor Wan's opinion (from Exhibit 58) can
        be summarised in the following way:
              •       Mr Cotton's occupational exposure to asbestos in
                      Adelaide and at Australind is capable of causing his lung
                      cancer but it is more likely that he inhaled more Amosite
                      asbestos in the BDR room in the third defendant's
                      employment than from sawing asbestos cement pipes in
                      South Australia.

              •       Amosite has a higher carcinogenic potential than
                      Chrysotile which is more often used in asbestos cement
                      pipes. As exposure is a combination of this potential,
                      intensity and duration, his exposure in the BDR at
                      Australind was to Amosite which is likely to have been a
                      greater and longer exposure than in South Australia.

              •       All the asbestos minerals (Chrysotile and the amphiboles)
                      may cause asbestosis, lung cancer and benign pleural
                      diseases but only the amphiboles appear to be related to
                      the production of malignant mesothelioma ... All types of
                      asbestos appear capable of causing lung cancer and all
                      histological types of lung cancer are increased in
                      incidence in asbestos-exposed individuals.

              •       The amount of airborne asbestos fibre inhaled and the
                      duration of exposure make independent contributions to
                      the risk of development of lung cancer. Smoking greatly
                      increases that risk. If the relative risk of developing
                      cancer for members of the general population is
                      expressed as 1, then that of smokers is up to 10 times as
                      great. Exposure to asbestos alone over many years in the
                      absence of smoking might marginally increase the
                      relative risk, but where such asbestos exposure is
                      combined with cigarette smoking, the risk could be
                      extraordinarily changed so that the relative risk of the
                      combined exposure may approach 100 times that in the


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                      general population. The exact relationship is uncertain
                      but is certainly far greater than merely an additive risk.
              •       Although a level of exposure below which an increased
                      risk of lung cancer would not occur is not known, it is
                      known that exposure sufficient to cause asbestosis
                      increases the risk of lung cancer. According to the
                      Helsinki Criteria established by the International Expert
                      Meeting on Asbestos, Asbestosis and Cancer in 1997,
                      four histological types (squamous, adeno, large cell and
                      small cell carcinoma) can be related to asbestos. The
                      histological type of lung cancer and its anatomic location
                      (central or peripheral, upper lobe versus lower lobe) are
                      of no significant value in deciding whether or not an
                      individual lung cancer is attributable to asbestos. Clinical
                      signs and symptoms of asbestos related cancer do not
                      differ from those of lung cancer of other causes. In some
                      circumstances of extremely high asbestos exposure, a
                      2 fold risk of lung cancer can be achieved with exposure
                      of less than 1 year.
        In this report Professor Wan was asked for his opinion, in light of the fact
        there was both Chrysotile and Amosite in the BDR, whether the inhalation
        of Amosite fibres increased the risk of Mr Cotton's lung cancer. His
        answer was:
              "Yes, the inhalation of asbestos fibres such as amosite increased
              the risk of lung cancer developing in Mr Cotton. The relative
              risk of lung cancer is estimated to increase 0.5 - 4% for each
              fibre per cubic centimetre per year (fibre years) of cumulative
              exposure. A cumulative exposure of 25 fibre years is estimated
              to increase the risk of lung cancer 2 fold. Clinical cases of
              asbestosis may occur at comparable cumulative exposures. The
              likelihood that asbestos exposure has made a substantial
              contribution increases when the exposure increases.
              Cumulative exposure, on a probability basis, should thus be
              considered the main criterion for the attribution of a substantial
              contribution by asbestos to lung cancer risk. Heavy exposure,
              in the absence of radiologically diagnosed asbestosis, is
              sufficient to increase the risk of lung cancer. Cumulative
              exposures below 25 fibre ml years also are associated with an
              increased risk of lung cancer, but to a lesser extent. The
              presence of asbestosis is an indicator of high exposure. Results


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              of air monitoring of such processes reported in the book
              'Engineering Aspects of Asbestos Dust Control' by Rajhans
              (1982) [show] Mr Cotton's work with cement pipes in South
              Australia could have exposed him to 5 - 15 airborne respirable
              asbestos fibres per cubic centimetre and his exposure in the
              band drier room in Millennium Chemicals could be up to 10
              fibres per cubic centimetre. Based on 10 fibre/cc and 8 years
              exposure, the cumulative exposure for Mr Cotton would be 80
              fibre years. The relative risk increase would be 40% - 320%.

              Mr Cotton was exposed to asbestos 25 years ago in 1975 when
              he worked with asbestos pipes in South Australia and later in
              1990 which is about 10 years ago to friable asbestos cladding
              during his work in the band drier of Millennium Chemicals.
              His lag time from first exposure to development of lung cancer
              is 25 years and therefore is more than the minimum lag time of
              10 years required to attribute the lung cancer to asbestos in the
                                                                  h
              Helsinki Criteria. The New Zealand Report of t e Asbestos
              Advisory Committee to the Minister of Labour 1991 states that
              the relative risk of smoking and cancer combined is 8.2 - 52.2."
        and then Professor Wan went on to point out the very large number of
        respirable fibres involved in an exposure standard of 1 fibre/ml of air in a
        7½ hour working day, observing that these calculations did not take into
        account fibres smaller than 5 microns in length or others of small diameter
        unable to be seen under phase contrast with an optical microscope and, if
        fibres of such sub-microscopic dimensions were taken into account, the
        quantity of inhaled fibres would be vastly greater.
348           In cross-examination Professor Wan was asked whether or not he
        accepted that the risk or hazard of asbestos lung cancer was relative to
        dose. His response was that, generally it is, in the sense that the higher
        the dose the higher the risk, but he pointed out that it was not entirely
        relative to dose and that the risk exposure relationship was non-linear and
        pointed to recommendation 10 of the 1991 report of the Asbestos
        Advisory Committee to the Minister of Labour (Exhibit 60, p 21) which
        recognises a greater potential effect from superfine fibres.
349          Professor Wan was cross-examined about his assumption that
        Mr Cotton's asbestos exposure while working on cement pipes in South
        Australia could have involved up to 10 fibres/ml and his reliance upon the
        work by Rajhans (supra) for that conclusion. The relevant passages in the
        work by Rajhans and Bragg were tendered (Exhib it 59) which, at 68 and
        following, describe the dust emissions when working with asbestos in

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        mining or milling, including scraping and shovelling. At 84 of that same
        exhibit there is a table describing typical exposures to be expected in
        normal machine operations, including hand sawing, machine sawing with
        a jigsaw or circular saw. The typical exposures for hand sawing were
        2 - 4 fibres/ml, for machine sawing with a jigsaw 2 - 10 fibres/ml and for
        machine sawing with a circular saw 10 - 20 fibre/mls. It was therefore
        suggested to Professor Wan that his assumption of 10 fibre/mls exposure
        constantly during the cement laying processes in Adelaide may be an
        overestimate and, in my view, there is some force in that suggestion.
        However, Professor Wan was disinclined to place great reliance on
        precise numerical estimates of the extent of fibre exposure, no doubt
        recognising the great limitations of such attempts, and also because of his
        earlier statement that any such respirations are likely to be accompanied,
        to a great extent, by sub-microscopic fibres which cannot be measured by
        current methods. In a supplementary exhibit (59(2)), being a further
        extract from Rajhans and Bragg at 88 and 89, there is a discussion about
        asbestos exposure in houses, offices and other buildings. The authors
        made reference to a work which measured asbestos dust concentrations in
        a group of storehouses insulated with sprayed Crocidolite and Amosite.
        Those results showed the range of concentrations varying from
        0.26 - 11.89 fibres/cc.    They concluded that the concentrations of
        Crocidolite and Amosite dust that may occur when unsealed sprayed
        insulation of fallen asbestos debris is disturbed are likely to be in excess
        of the threshold levels. This is especially so for Crocidolite if the
        threshold level is to be held below 0.2 fibres/cc.
350          Counsel for the second defendant also suggested to Professor Wan,
        in cross-examination, that the contemporary tolerable standard for
        asbestos exposure in 1994 and the years following was 4 fibres/ml or less
        and that this was the recommendation of the National Health and Medical
        Research Council publication "Atmospheric Contaminants", published by
        the Australian Department of Health. Professor Wan agreed that this was
        so and an extract from that publication (Exhibit 61) was tendered.
        However, it is also important to note the qualifications appearing at p 2 of
        the report to the effect that the data on which the standards are based are
        seldom accurate enough to warrant dispute about slight deviations
        (plus/minus 20 per cent) from the values listed. It is in the spirit of these
        standards that wanton exposure to airborne chemicals be avoided:
        enlightened Industrial Hygiene maintains exposures well below the
        standard rather than at the standard. Among the special features which the
        NH & MRC identified for noting was (Exhibit 61, p 2, par (4)):



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              "Mixtures of contaminants pose special problems of
              interpretation for which no simple hard and fast rule can [be]
              given. The physiologic effects of two or more substances
              inhaled together may be exerted independently, additively, -
              more than - additively, or antagonistically, and specific
              consideration has to be given to each type of mixture
              encountered. The literature on the subject should be consulted."

        The specific reference to asbestos in Exhibit 61 is found at p 12, par (2),
        dealing with Chrysotile and Amosite asbestos. The recommendation is
        that "the long-term average fibre concentration of the air breathed by the
        worker should not exceed four fibres per cubic centimetre of air, as
        measured by the membrane filter method of the British Occupational
        Hygiene Society, or by any other method proven equivalent to this
        method".
351           Professor Wan's reference to the probability that breathing air with
        asbestos fibres is likely to involve inspiring large quantities of
        sub-microscopic sized asbestos is confirmed by the work "Asbestos:
        Medical and Legal Aspects", by B I Castleman, an extract of which is in
        evidence as Exhibit 62. At 261 there is a passage to the effect that
        1 fibre/ml is equivalent to 1,000,000 fibres per cubic metre of air and that
        in the course of an eight hour work day a worker would breathe in at least
        five cubic metres of air, perhaps much more for heavy work. So, the
        author explained, someone exposed to the OSHA limit of 2 fibres/ml is
        breathing in over 10,000,000 microscopic asbestos fibres per day. This
        does not take into account those fibres smaller than 5 microns in length
        and those which are 5 or more microns long but too small in diameter
        (0.1 micron or less) to be seen under phase contrast with an optical
        microscope, and that even an exposure of 0.1 fibre/mls equates to an
        inhalation burden of over 50,000,000 total fibres per day, for sedentary
        work. It is hardly surprising, therefore, that Professor Wan, and, for that
        matter Professor Musk, appear to show some reserve about the magnitude
        of the significance which their cross-examiners were suggesting should be
        given to the fibre/ml estimates being discussed for these working
        environments.
3. Dr James Leigh
352          The next witness for the plaintiff was Dr James Leigh, a very highly
        qualified and senior occupational physician. Dr Leigh holds the higher
        degrees of Doctor of Medicine and Doctor of Philosophy, Master of Arts
        and Master of Science from Sydney University, is a fellow of the
        Australian Faculty of Occupational Medicine, a fellow of the Royal

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        Australasian College of Physicians and is a consultant in respiratory
        medicine at St George Hospital, Sydney. He advises as a consultant to the
        Health Commission of New South Wales, the Joint Coal Board of New
        South Wales, he is head of the Epidemiology Department and head of the
        Epidemiology Unit of the Mesothelioma Register. Among other
        responsibilities, he is consultant on asbestos issues to the Department of
        Defence, to the governments of the Commonwealth, of New South Wales
        and of the ACT. He is a referee for many professional medical journals
        and has published 76 articles on lung disease which have been subject to
        peer review. At the request of the solicitors for the plaintiff, Dr Leigh
        prepared a detailed report dated 27 July 2001 which is in evidence as
        Exhibit 63.
353          Dr Leigh's ultimate opinion can be shortly stated. His opinion is that
        asbestos exposure and smoking together caused Mr Cotton's lung cancer
        and that there is a clear dose response relationship for lung cancer and
        asbestos with no threshold for mixed fibre type exposure. On an
        apportionment model he attributes the fraction of causation due to
        asbestos as between 2 per cent and 20 per cent.

354           In his report, Dr Leigh draws attention to the variations in the
        estimates of Mr Cotton's cumulative asbestos exposure. He observes that
        the estimates range from 0.2 - 15 fibre/ml years and says that he does not
        wish to speculate further. With regard to latency, he says that it is more
        likely that the earlier exposures were causative as latency less than 10
        years is relatively uncommon but that all exposures add cumulatively to
        the risk. With regard to causation, Dr Leigh refers to a number of
        published papers which he co-authored dealing directly with the issues
        arising and points out that Mrs Sowden did not refer to any of those
        reviews and that other leading authors present quite different views to
        those given by the references cited by Mrs Sowden. Significantly,
        Dr Leigh wrote:
              "Asbestos exposure and tobacco smoking interact
              multiplicatively to cause lung cancer ... All types of asbestos
              can cause lung cancer. All tumour cell types have been
              associated with asbestos, and tumours may appear in any lung
              site. It is my opinion on the balance of probabilities that
              asbestosis is not a necessary prerequisite for attributing lung
              cancer to asbestos in an asbestos exposed smoker. A recent
              review article promoting the opposite case has been strongly
              criticised by the editors of the journal in which it was published



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              who concluded that asbestosis is not a necessary prerequisite for
              asbestos related lung cancer ...
              Even though Mr Cotton was a smoker, the asbestos exposure
              would have been a significant independent risk factor and
              would also have had a synergistic effect with tobacco in causing
              the lung cancer and thus made a material contribution to
              causation. Such synergism is well accepted."

        And, after identifying other applicable scientific literature and the
        physiological and carcinogenic effects of tobacco and asbestos, he went
        on to say:
              "While the precise mechanism of interaction between asbestos
              and tobacco smoke in causing lung cancer is not known, it is not
              possible in my view to separate their effects in the individual
              case when both have acted and it is thus more probable than not,
              that in this situation, the lung cancer was the singular result of
              the two factors acting together. It is however true that exposure
              to either factor alone is capable of causing lung cancer."
        Then Dr Leigh addressed the epidemiological approach which took
        25 fibre/ml years as a diagnostic indicator, and said that a cumulative
        exposure of 25 fibre/ml years associated with the first signs of clinical
        asbestosis and was also the level accepted as being associated with an
        approximate doubling of lung cancer for mixed fibre type exposures, but
        pointed out that there is a further additive increase by a factor of 1.5 for
        workers in Amosite factories and that Professor de Klerk put the
        multiplicative increase in relative risk for Amosite at 1.25 so that, on
        those models, an exposure of 25 fibre/ml years would have a relative risk
        of greater than 2.
355           He made reference to developments in the research and to a more
        recent large case study in Sweden which concluded that the co-efficient
        for the increase in lung cancer risk was 0.14 fibre/ml year, giving a
        relative risk of 4.5 for a 25 fibre/ml year - that is, that there would be a
        doubling in the relative risk at a significantly lower cumulative exposure.
        He observed that there was no threshold for lung cancer caused by
        amphibole types.
356          With reference to the epidemiological approach of demanding a RR
        of 2 or greater before attributing asbestos as the cause of lung cancer,
        Dr Leigh explained the mathematics but then said that there had been
        persistent criticism of this approach and that it is now thought that the


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        attributable fraction in the exposed may often underestimate the
        probability of causation pointing out that, in the case of some
        occupational lung cancers, a relative risk of 1.1 (rather than 2) equating to
        an attributable fraction of 9 per cent has been accepted as indication of a
        material contribution to causation rather than being "the cause" (see
        Exhibit 63, p 5).      He also pointed out that there is a risk, in
        epidemiological studies, of unknown confounders in the studies distorting
        the results, emphasising that much depended on the quality of the
        epidemiological study design, implying a reservation about the acceptance
        of a number of studies published. Dr Leigh then went on to address
        specifically Mr Cotton's case and took an estimate of cumulative asbestos
        exposure of about 8 fibre/ml years together with a conservative additive
        risk co-efficient of 0.02 per fibre year mils to give an approximate
        16 per cent increase of risk - that is, an increase of relative risk from
        1 to 1.16.
357           Next, Dr Leigh explained how it was possible to apportion the
        attribution of cause to smoking and asbestos under a variety of
        mathematical risk models which were explained in the literature he
        identified. Assuming a smoking history of 15 cigarettes a day for 27
        years, he attributed a RR to tobacco of 8 and with the deduced RR of 1.16
        for asbestos, the approximate apportionment causation to asbestos was in
        the range of 2 to 12 per cent, but depending upon the model used.

358           In cross-examination, Dr Leigh was asked whether he accepted the
        25 fibre/ml year cumulative dose as propounded by the Helsinki Protocol
        and by the AWARD Criteria as applicable to cases with alleged
        asbestos-induced lung cancer. He agreed that those figures were chosen
        for lung cancers but said that in his view it was doubtful if they applied in
        common law jurisdictions where the issue was whether or not a material
        contribution had been made by the carcinogen to the development of the
        disease.
359          In cross-examination, Dr Leigh was asked whether he had seen the
        reports prepared by Professor Berry containing evidence to be adduced on
        behalf of the second defendant (later admitted into evidence as
        Exhibits 145(1) - (3)), but he said that he had only been given copies the
        previous day. Later, Dr Leigh said of Professor Berry's a    pportionment
        opinions, that they had been based on the latter's apportionment modelling
        but they did not represent his own opinion. His own method of
        apportionment was to use three models (Chase model; Cox model and a
        Norwegian model (Exhibit 63, see t/s 630)) to produce the range of
        figures which he had advanced, namely, 2 to 20 per cent.


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360           I accept Dr Leigh as an eminently qualified and experienced expert
        in this field and I must say that I consider there is much to be said for his
        approach of taking, if only as an estimate, a cumulative asbestos exposure
        of something in the order of 8 fibre/ml years and concluding that this
        represents an increase in the relative risk from 1 to 1.16 or a 16 per cent
        increase in the risk. This is within the range of 1.10 to 1.20 propounded
        by Professor Musk (Exhibit 56, p 2) and is also consistent with the
        opinions of Professor Wan and Professor de Klerk, all of whom appear to
        me to be, justifiably and prudently, aware of the uncertainties and
        limitations of attempts at precise quantitative analysis.
4. Dr Peter Kendall
361          The role of Dr Peter Kendall FRACP, consultant physician in
        respiratory medicine, in the examination of Mr Cotton before his death
        and reporting to the solicitors for the second and third defendants, has
        already been described. In the reports which he prepared (Exhibits 67 and
        69), Dr Kendall also touched upon issues of causation and the relative
        roles of asbestos and tobacco smoking in the development of this cancer.
        To the solicitors for the second defendant he wrote, on 13 October 2000
        (Exhibit 69, p 2), saying that the effect of the two carcinogens was not a
        simple problem and that he was unable to say whether or not the lung
        cancer was due to smoking or inhalation of asbestos products or to some
        other cause, but that he believed it was a combination of all three,
        remarking that his total intake of cigarettes was rather small and that
        physicians do see people with lung cancer from very small amounts of
        asbestos exposure. He added that Mr Cotton's asbestos exposure certainly
        had given rise to an increased risk of developing lung cancer and that he
        considered that the lung cancer was partly attributable to that factor.
        Similar answers were given in his report (Exhibit 67) to the solicitors for
        the third defendant which included the observation that, in Dr Kendall's
        opinion, lung cancer can be caused by exposure to asbestos in the absence
        of asbestosis or asbestos related pleural plaques - which supports the same
        view expressed by Professor Musk and by Dr Leigh and by Professor
        Wan and Professor de Klerk, all of whom disagree, on this issue, with
        Professor Berry and Professor Fox. Nothing in the cross-examination of
        Dr Kendall produced, or in my view warranted, any review of the
        opinions which he expressed.
5. Professor Geoffrey Berry
362          On these issues of alleged causation and apportionment, the second
        defendant adduced evidence from Professor Geoffrey Berry an eminent
        epidemiologist and biostatistician from the University of Sydney.

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        Professor Berry's reports became Exhibits 145(1) - (3), subject to the
        exclusion of a small quantity of content of Exhibits 145(1) and 145(3) due
        to objections by counsel for the plaintiff which I upheld. Professor Berry
        is Emeritus Professor in the School of Public Health at the University of
        Sydney and continues his work as a research epidemiologist and
        biostatistician through his own consultancy business. He has degrees in
        Mathematics and Mathematical Statistics from the University of
        Cambridge, including a Doctorate of Philosophy. He is a chartered
        statistician of the Royal Statistical Society and an Honorary Fellow of the
        Australian Faculty of Occupational Medicine. He has a long and
        important career in those disciplines holding many external appointments
        of considerable responsibility and importance, as well as being the author
        of many professional publications and papers which are listed in his
        curriculum vitae (Exhibit 144). It is to be noted that he has no
        professional medical qualifications, but I have no doubt that his
        knowledge and experience in his field of biomedical statistics renders him
        a very highly qualified expert. I found him to be very balanced, modest
        and careful in giving his evidence and ready to accept qualification if
        thought necessary, besides being extremely technically competent. His
        opinions on the issues in this case merit great attention and respect.

363           Professor Berry's professional life has been spent largely as a
        biostatistician and epidemiologist working in the area of the health
        hazards of asbestos exposure after a long history of statistical studies of
        industrial lung diseases. For 16 years he was a biostatistician on the
        British Medical Research Council and Pneumoconiosis Unit. Then he
        served as Associate Professor of Biostatistics at the University of Sydney
        and then as Professor in Epidemiology and Biostatistics in the Department
        of Public Health at the University of Sydney since 1988 until 1999 before
        taking up a part-time chair and acting as an independent consultant. He
        has written and published widely in the field, including as co-author or the
        work "Statistical Methods in Medical Research", Blackwell Oxford,
        3rd ed, 2001.
364          Professor Berry helpfully isolated the factors and methodology of
        attempting to attribute a likelihood to a known carcinogen producing lung
        cancer in a given patient in his report (Exhibit 145(1)), at p 2, where he
        wrote:
              "Relative risk

              It is impossible to state the cause of a condition, such as lung
              cancer, in an individual with certainty. This is because there are


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              a variety of possible causes, and also cases for which no
              particular cause is known. For example cases occur in life-long
              non-smokers who have not been exposed to dusts or fibres;
              these cases are sometimes referred to as background cases.
              However, from epidemiological studies that have been
              conducted on groups of people, and analysed using statistical
              methods, it is possible to obtain information on the risk of
              exposures to various agents.
              Risk is usually expressed in terms of the measure relative risk
              (RR). This is defined as The ratio of the risk of disease or death
              among the exposed to the risk among the unexposed. As an
              example it has been estimated that the relative risk in smokers
              compared with non-smokers is 15. Another example is that the
              relative risk of lung cancer due to asbestos exposure in a
              particular factory in London was estimated as 3. These are both
              average values and further analysis shows that the relative risk
              due to smoking depends on the amount smoked, and that due to
              asbestos exposure on the extent and intensity of that exposure.
              That is, for an agent that increases the cancer risk, higher
              exposures increase the risk more than low exposures.

              Another measure used is attributable fraction among the
              exposed. This is defined as (RR - 1)/RR, so that a relative risk
              of 15 gives an attributable fraction of 14/15 = 0.93 or 93%. An
              interpretation of this figure is that 93% of the lung cancers in
              smokers are attributable to smoking (and 7% are background
              cases). Note that a relative risk of 1 indicates no excess risk, so
              that a relative risk of 15 may be divided into 1 (background) +
              14 (excess). Thus, for an individual smoker who develops lung
              cancer, although it is not certain that the lung cancer was caused
              by smoking, one can say that the probability that it was due to
              smoking is 93%.

              A relative risk of 2 gives an attributable fraction of 50%. That
              is, it is equally likely that the condition was due to the exposure
              or not. For relative risks higher than 2 then the exposure is the
              more likely cause, and for relative risk less than 2 the exposure
              is the less likely cause."
        On the basis of the information supplied to him (Professor Musk's report
        (Exhibit 56) and Mrs Sowden's reports (Exhibits 152(1) to (3)), Professor
        Berry assumed that Mr Cotton had smoked 15 cigarettes per day from the


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        age of 16 (1972) up to April 2000. From this, he concluded that
        Mr Cotton's risk of lung cancer due to smoking was increased by about
        15 times (using the "15 to 24 cigarettes a day" category). That is, that his
        RR for developing lung cancer due to his history of smoking was 15.
365           With regard to the aggregate asbestos exposure for Mr Cotton,
        Professor Berry was more guarded. In his initial report (Exhibit 145(1))
        he confined his attention to this subject to potential exposure during the
        period of Mr Cotton's employment with the first defendant in Adelaide.
        Later, in Exhibits 145(2) and (3), Professor Berry explained that he had at
        first ignored any exposure at Millennium Chemicals on the grounds that
        the latency period after the first exposure there, until discovery of the
        disease, was only 10 years or less but, after considering the views of
        Professor de Klerk, said that this initial assessment "was perhaps too
        stringent", acknowledging that the period of latency in the literature is
        usually taken as the period from first exposure until death caused by the
        lung cancer whereas, in Mr Cotton's case, his diagnosis was a little short
        of two years from his death, meaning that the latency period for exposure
        at Australind could have been up to 12 years and, accordingly, should be
        taken into account. I am satisfied that this is a proper approach by
        Professor Berry and that, in addition to the acknowledged variability in
        latency periods referred to by Professor Musk, Dr Kendall, Professor
        de Klerk and Dr Leigh, Mr Cotton's period of latency in association with
        his exposure to asbestos at Australind was probably closer to 12 years
        than the shorter periods of 10 years or less postulated by others.

366          However, according to Professor Berry, the period of latency does
        not constitute the only uncertainty or difficulty in estimating the risks due
        to asbestos exposure. The risk varies between different industries and
        different types of asbestos. The risk due to exposure varies between
        different industries working with the same form of asbestos - Chrysotile -
        as between textile workers and others exposed to commercial Chrysotile.
        According to the literature most of those exposed to asbestos have been
        exposed to amphibole asbestos (Crocidolite and/or Amosite) as well as to
        Chrysotile and mixtures containing amphobiles have a higher risk than
        does pure commercial Chrysotile exposure. Professor Berry then referred
        to the Helsinki Protocol which concluded that:

              "A cumulative exposure of 25 fibre-years is estimated to
              increase the risk of lung cancer twofold."

        but observed that this figure was taken from one end of a range of
        estimated potential risk increments so that it could not therefore be
        appropriate for all conditions of exposure but that, in his view, it was a

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        reasonable figure to use for exposure to asbestos which was
        predominantly amphibole (Crocidolite and Amosite) asbestos. He thought
        Mr Cotton's exposure was not predominantly to amphibole and may have
        been intermediate between Chrysotile exposure and Crocidolite exposure
        and in that case a doubling of the lung cancer risk would not be expected
        to occur until a cumulative exposure of 50 fb/ml years, but he nevertheless
        proceeded with calculations based on an assumed doubling of risk
        exposure after 25 fb/ml years.
367           In Professor Berry's first report (Exhibit 145(1)) he took the
        estimates of exposure from Mrs Sowden's report, namely 1.6 fb/ml years
        (Exhibit 152(1)), revised to less than 0.2 fb/ml years (Exhibit 152(2)) -
        figures which I have already decided should be rejected as substantial
        underestimates. On those figures, on the basis of calculations set out at
        p 4 of Exhibit 145(1) Professor Berry calculated that an exposure of
        1.6 fb/ml years corresponded to a relative risk of 1.06 and that an
        exposure of 0.2 fb/ml years resulted in a relative risk of 1.008. At first he
        adopted the lower and revised estimate of Mrs Sowden which produced
        the risk estimate of 1.008 which is, of course, less than 1.01 and said:

              "Then the attributable fraction is less than 1%. To put this
              another way, if there were 100 (actually 125) men with lung
              cancer, all of whom had exposure to asbestos similar to that
              experienced by Mr Cotton, and similar smoking habits, then for
              one of these men the exposure to asbestos would have been the
              cause and for the other 124 the lung cancer would have been
              due to other causes (mostly smoking)."
        Professor Berry then went on to calculate the combined effect of asbestos
        exposure and smoking and then attempted to attribute mathematical
        probabilities to each of those causes, a combination of them, and to
        background risk. It is unnecessary for me to set out the details of his first
        calculations (Exhibit 145(1), p 4) because they were based upon
        Mrs Sowden's lower revised estimate of asbestos fibres in the working
        environment in Adelaide which I have rejected.
368          Later, however, in Exhibit 145(2), Professor Berry re-does these
        calculations based on Professor de Klerk's estimate of 5.2 fb/ml years for
        exposure in Adelaide between 1975 and 1978 and 10 fb/ml years at
        Millennium Chemicals. Where Professor de Klerk used 5 fb/ml years in
        his calculations for exposure at Millennium Chemicals, Professor Berry
        voiced some reservation or surprise about some of the assumptions made
        by Professor de Klerk, for example, the selection of a value as high as
        2 fb/mls exposure due to the presence of asbestos in lagging in a building


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        and his assumption that asbestos acts in a late stage of the lung cancer
        process, but he nevertheless acknowledged that Professor de Klerk and
        himself were in reasonable agreement upon the overall approach and
        calculations. Professor Berry also concluded that Professor de Klerk's
        resort to the meta-analysis of the effects of smoking was probably better
        than taking the value from a single study. I conclude from this that, in the
        end, Professor Berry accepted that it was appropriate, as Professor
        de Klerk had done, to bring to account the potential effects of asbestos
        exposure while Mr Cotton was working at Millennium (which had been
        ignored by Mrs Sowden) and to utilise higher concentration levels for
        exposure during the employment in Adelaide than had been adopted by
        Mrs Sowden (which were, as previously explained, taken from the WAIT
        AID and Amdel studies - which I do not accept as representative of the
        conditions under which Mr Cotton was working).

369           In his third report (Exhibit 145(3)) Professor Berry also addresses
        and analyses the report of Dr James Leigh (27 July 2001, Exhibit 63). He
        accepted Dr Leigh's RR for lung cancer due to smoking as 8 (significantly
        lower than other figures including his own attributed figure of 15 -
        Exhibit 145(1)). He also accepted Dr Leigh's adoption of an exposure of
        about 8 fb/ml years, the figure also adopted by Professor de Klerk. On
        that basis he then addressed the combined effect of asbestos exposure and
        smoking in Exhibit 145(3), p 2, as follows:

              "As discussed in my report of 18 January 2001, it is possible to
              subdivide Mr Cotton's risk of lung cancer into components
              representing the percentage contributions of the different risks.
              The total relative risk, relative to a non-smoker unexposed to
              asbestos, is 8 x 1.16 = 9.28 (taking RR = 8 for smoking and
              1.16 for asbestos exposure). Without ambiguity the following
              subdivision of the total risk applies:

                      (a)       due to smoking alone - 75%
                      (b)       due to asbestos alone - 2%

                      (c)       due to smoking-asbestos combination - 12%
                      (d)       background risk - 11%

              A problem is how to subdivide component (c), due to the
              combined effect, into allocations for asbestos and smoking. In
              one sense it is impossible to do this since, by definition, it is that
              part of the combined effect which cannot be separated out into


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              the separate effects (a) and (b). If it is required to divide the
              interaction into separate effects for the purpose of attribution
              then, as discussed in my report of 18 January [Exhibit 145(1)],
              methods have been proposed for doing this. Dr Leigh also
              discusses this at the foot of page 6 of his report [Exhibit 63].

              If the combined part (c) is distributed to the two causes
              proportionally to their respective excesses (a) and (b), then the
              attribution to asbestos exposure is 2%, since most of the
              combined effect is allocated to smoking because of the much
              higher risk due to smoking compared with the asbestos
              exposure.

              If all of the combined effect is allocated to the asbestos
              exposure then the attribution is 14%. Dr Leigh gives a range
              from 2 to 12% for the apportionment of damages to asbestos. I
              obtain a very similar range 2 to 14%."
        For Dr Leigh's estimate see Exhibit 63 and [356] to [357] above.
370           I was greatly impressed by the independence and objectivity of
        Professor Berry, and his readiness to concede the legitimacy of the
        assumptions and factors identified by Professor de Klerk. I have already
        explained why I consider the estimates of asbestos concentration in the
        working environment in Adelaide deduced by Mrs Sowden are more than
        an order of magnitude less than the probabilities derived from the
        literature. The approximate congruence of the views of Professor
        de Klerk, Dr Leigh and Professor Berry lead me to the conclusion that,
        subject to all the limitations (and there are many of them) about the
        accuracy and reliability of statistically based estimates of risk in this field,
        particularly where asbestos air concentrations are being estimated
        retrospectively, the elevated risk above the background levels experienced
        by Mr Cotton was in the order of 2 per cent to 14 per cent.

371           It is significant that Professor Berry accepted (Exhibit 145(2), p 3)
        that if Mr Cotton's exposure to asbestos at Australind is to be regarded as
                                                   h
        a contribution to his lung cancer risk, t en his total excess risk due to
        asbestos is a consequence of Mr Cotton's exposure both when working for
        the State of South Australia as a pipe layer and when working for
        Millennium Chemicals. In his view, the excess could be subdivided
        between the two periods of employment in proportion to the exposure at
        each. Professor Berry wrote that:




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              "For example, using Professor de Klerk's figures of 5 fibre/ml
              years as a pipe layer and 10 fibre/ml years at Millennium
              Chemicals then one third of the asbestos components of risk
              would be attributed to work as a pipe layer and two thirds to
              work at Millennium Chemicals."

372           Inherent in these approaches and calculations, as acknowledged by
        Professor Berry, is the assumption that there is a linear relationship
        between elevated risk to lung cancer due to asbestos exposure, and the
        cumulative dosage expressed in fb/ml years. Whether such a thesis can be
        supported, and if so whether only over a limited range or ranges near the
        critical figure of 25 fb/ml years as adopted by the Helsinki Protocols,
        seems to be very much an open question. In particular, whether a reduced
        elevated risk, based on the assumed linear relationship, for low levels of
        asbestos exposure, or low cumulative levels which nevertheless involve
        high but short-lived peak levels of exposure, remains a controversy which
        this data does not answer. Furthermore, in the absence of any
        acknowledged scientific or medical explanation of a clinical pathogenesis
        of asbestos-induced lung cancer it seems, with respect, impossible to
        maintain that such a linear relationship exists over all ranges of exposure.
373           This is a convenient point to deal specifically with one area of the
        statistical evidence concerning the interaction of elevated risks of
        exposure to smoking, on the one hand, and of exposure to asbestos on the
        other when acting in a "synergistic" or "multiplicative" or "non-additive"
        way which, when the two carcinogenic factors are present, enhance the
        effect of each other. This was of concern to me during the course of the
        trial and I raised this question with Professor de Klerk (t/s 786 - 792),
        again with Professor Berry (t/s 1024 - 1029) and, finally, with Professor
        Fox (t/s 1376 - 1378) and it has to deal with the statistical method of
        measuring the combined effect of multiple causes, each capable of
        producing a particular phenomenon.
374           In the end I consider these experts accepted that the methodology to
        be adopted varied, depending upon whether the separate causes
        potentially acting in combination were entirely independent of each other
        in effect, or whether, as seems to have been generally acknowledged in
        this case, the separate causes potentially acting in combination were
        non-independent in the sense that the effect of each was greater in the
        presence of the other. All the epidemiological and statistical experts
        accepted that the correct methodology to move from an elevated relative
        risk to the probability that that relative risk caused the phenomenon (in
        Professor Berry's language to the "attributable fraction among the


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        exposed" (Exhibit 145(1), p 2) is by the application of the formula
        (RR - 1)/RR. No matter what value is selected for RR the application of
        the formula will, of necessity, always produce a figure of less than 1. This
        is to be expected because no matter how high the RR may be, there
        always remains a possibility (progressively a smaller one) that the
        phenomenon may be due to some other factor and, hence, the calculation
        may approach, but never arrive at, the figure of 1.0 (ie 100 per cent).
        However, when in a case such as the present, where one is identifying two
        potential carcinogens to both of which the deceased is known to have
        been exposed (here tobacco and asbestos) and one calculates the RR for
        each and converts that to the probability of cause being due to that
        carcinogen alone, each resultant probability figure will necessarily be less
        than one. It is the next step which is, to say the least, enigmatic. In order
        to estimate the combined or "multiplicative" effect of the two carcinogens
        acting together, a number of the experts, specifically Professor de Klerk,
        Mrs Sowden and Mr Kottek, have multiplied those two factors (each
        being less than one) together. The inescapable result is that the
        "synergistic" or "multiplicative" effect is lower than the probability of
        either the more potent or the less potent factor alone. Thus, in the present
        case, if the risk of the probability that smoking caused Mr Cotton's lung
        cancer is 80 per cent (ie 0.80) and the probability that asbestos caused the
        disease is 16 per cent (0.16) then, on this methodology, the combined
        effect is 0.80 x 0.16 = 0.128 or 12.8 per cent - markedly lower than the
        probability that either of the carcinogens alone caused the disease. In the
        passages in the transcript, to which I have just referred, each of the three
        experts accepted that this runs counter to the qualitative evidence that the
        combined effect of smoking and asbestos exposure as a potential cause of
        lung cancer is greater than the effect of either carcinogen acting alone but
        explained, nevertheless, that it was correct statistically because the
        calculation addressed the three potential possibilities, namely:
              a. - probability that cancer was due to smoking alone;

              b. - probability that smoking was due to asbestos alone;
              c. - probability that cancer was due to combined effect of
                   smoking and asbestos
        but by a method which excluded from categories (a) and (b), in this
        trilogy of categories, cancers which could be attributed to the combination
        of the two carcinogens and the exclusion of either alone.
375         This accounts for the low figures attributed to the smoking/asbestos
        combination in Professor Berry's reports (Exhibit 145(1), p 4, and 145(3),

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        p 2) as well as to the correspondingly apparently incongruous figures in
        the calculations of Mrs Sowden (Exhibit 152(4)) and Professor de Klerk
        (Exhibit 74(1) at p 2 and Exhibit 74(2) at p 2). On this being pointed out
        to them, the three epidemiologists and statisticians, Professor de Klerk,
        Professor Berry and Professor Fox, acknowledged that it was due to a
        methodology appropriate for treating either carcinogen as an independent
        cause of cancer, even in the presence of the other. So Professor de Klerk
        acknowledged (t/s 788):
              " ... but if you are looking at it as a proportion of getting the
              disease altogether, it's always going to be slightly more, than the
              two of them combined ... "

        and then he went on to add (at t/s 789) that the assumption that the
        attributable risk is the same as the probability of causation is questionable,
        especially in the light of the work of Greenland in the article published in
        the American Journal of Public Health in August 1999 - Exhibit 76.
376           Professor Berry acknowledged that there was a difference in the
        approach to the estimation of the combined effect of probabilities
        depending upon whether each was conditional or unconditional
        (t/s 1027 - 1028) in a manner which meant that, when there were two
        causes acting in combination, the effect of which was to e     nhance one
        another, the combined effect of the two operating together would
        necessarily be greater than the effect of one operating alone.

377          This is of significance because it reveals that the epidemiological
        approach and the statistical analysis favoured by the defendants postulate
        the combined effect of unrelated and independent causes whereas, in this
        case, there is no issue but that the combined effect of the carcinogens of
        smoking and asbestos exposure is to increase the effect of each other. In
        my view, Professor Berry has come closest to dealing with the difficulties
        associated with this phenomenon in his report (Exhibit 145(1)) at p 4 - 5).
        His analysis there deals with relative risks and levels of asbestos
        contamination based on Mrs Sowden's low estimates which I have
        rejected but, he applies the same analysis, in a truncated but readily
        comprehensible form, to the higher risk levels derived from the de Klerk
        analysis in Exhibit 145(3) at p 2.
378          This statistical approach, correct mathematically when it is realised
        precisely what the calculations are intended to reflect, postulates that in a
        given category of persons with lung cancer who have been exposed both
        to smoking and to asbestos there exist, and it is possible to compute the
        probabilities, of three sub-categories, namely:

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              (i)     those whose cancer is due entirely to smoking;

              (ii)    those whose cancer is due entirely to asbestos;
              (iii)   those whose cancer is solely due to a combination of
                      smoking and asbestos.
379           No one disputes the legitimacy of the mathematical process as a
        consequence of the identification of the different relative risks and the
        consequent attributable risks for each carcinogen, but the result, appealing
        as it may be as a symmetrical mathematical exercise in probability, is
        inconsistent with the undisputed clinical and epidemiological evidence
        that, a population which is exposed to both asbestos and to smoking has
        an appreciably greater frequency of lung cancers than to either a
        population exposed only to smoking or a population exposed only to
        asbestos. That qualitative evidence, and indeed all the clinical medical
        evidence bearing upon the effects of these two carcinogens in
        combination, is to the effect that the two combine to give a greater risk,
        and therefore frequency of cases, of lung cancer than either alone.

380           That evidence does not support the conclusion, implicit in these
        statistical results, and in the defendants' submissions that it is possible to
        say, that in a population of lung cancer sufferers who have been exposed
        to both smoking and to asbestos, there is only this measurable minority
        whose disease can be attributed to the combination of the two carcinogens
        acting simultaneously and that the greater proportions of those groups
        have had their cancers caused either solely by smoking or solely by
        asbestos. I therefore regard it as a major, and significant, fallacy in this
        litigation for the defendants to be contending that these mathematical
        results (correct for the precise application to which they must be limited)
        mean or support a conclusion that in cases of lung cancer with combined
        exposure to smoking and asbestos, it is only members of the smallest
        category of that group who have had their cancers caused by the
        combined effect of both carcinogens. This fallacy is due, as both
        Professor de Klerk and Professor Berry accepted, to failing to recognise
        that the mathematical models which their proponents adopted are only
        appropriate for the combined effect of independent causative agents acting
        simultaneously but not for dependent or related causes acting in
        combination.

381          This conclusion allows one to approach closer to the essential legal
        (as opposed to mathematical) question of causation in this case, namely
        whether Mr Cotton's exposure to asbestos, taken in combination with his


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        long history of smoking, made a material contribution towards the
        development of his lung cancer. It is here that the conclusions of
        Professors de Klerk and Berry, that Mr Cotton's elevated risk of
        developing cancer due to asbestos in the presence of a long history of
        smoking is of the order of 2 per cent to 16 per cent as the best
        approximation possible, demand evaluation.
382           Significantly, this is quite a different question from enquiring
        whether Mr Cotton's exposure to asbestos in this case can be shown to
        result in an increase of relative risk to two or more and whether or not
        such a conclusion would follow, if at all, only by demonstrating a
        cumulative asbestos exposure of 25 fb/ml years. This is because those
        questions and formulae deal with the presence or influence of asbestos
        alone as the sole potential carcinogen to which the imputed attribution
        may, or may not, be made. To my mind, if an attribution to asbestos alone
        can be made for a lung cancer where there is 25 fb/ml years cumulative
        exposure to asbestos (or, if the higher threshold of 50 fb/ml years is to be
        taken, then of that higher level of exposure, is to be made), then it must
        necessarily follow from all the other evidence that if the victim with that
        degree of asbestos exposure is also a chronic smoker, then the
        probabilities of his or her cancer having been caused and contributed by
        the two carcinogens acting in combination must have passed the
        50 per cent point at a figure below the nominated threshold for asbestos
        alone, whether that be 25 or 50 fb/ml years. The defendants submitted
        that this was not a correct process of reasoning and that the conclusion
        was excluded by the Helsinki Protocol and by the AWARD Criteria but,
        for reasons which will become apparent when I consider those in more
        detail, I do not accept that that criticism supports that argument and that,
        instead, the proposition as enunciated must stand. Again, however, it is a
        very difficult question to convert this qualitative conclusion to an
        applicable quantitative application but it is necessary that that be
        addressed when dealing with the plaintiff's case to establish causation as it
        is known and understood at law.
383           The processes of formulating a figure for relative risk, or incremental
        relative risk due to increasing asbestos fibre air concentrations, and the
        subsequent processes of converting the relevant risk to an "attributable
        fraction among the exposed", or a chance of a member of a disease group
        having his or her disease caused by the exposure to the carcinogen
        postulated are, clearly, entirely mathematical. This presupposes that the
        assumed relationships are symmetrical and, on the formula employed,
        constant - at least over the range of figures being analysed. This is
        apparent from the premise that the relative risk of developing lung disease

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        (in this case cancer) due to asbestos exposure increases by 0.5 per cent to
        4.0 per cent for each fb/ml year of cumulative exposure (the Helsinki
        Protocol) or for whatever other incremental risk per fb/ml year is adopted.
        This assumes a linear constant relationship for all such levels of exposure
        from the very small to the very heavy. Similarly, the conversion of the
        relative risk to an attributable risk factor or chance relies on the
        application of the formula (RR - 1)/RR = attributable fraction. This, too,
        involves a symmetrical and constant form of mathematical relationship for
        all levels of RR from the very small to the very great. This relationship
        will not be linear but, rather, will describe a curve of steadily diminishing
        gradient, approaching but not reaching the limiting value of 1.0 for all
        ranges of RR. If the underlying assumptions about this symmetry of the
        relationships and their constancy are accepted then the statistical methods
        can certainly be helpful, but the evidence in this case does not establish
        that the relationships are indeed symmetrical or constant over all ranges of
        the chosen variables.

384           There are other criticisms of this mathematical approach to deducing
        whether or not elevations in the relative risk due to exposure to asbestos
        need to reach an attributable factor of two or more, before a probability of
        causation can be attributed. These are found in more sophisticated
        mathematical terms in the article by Dr Greenland in the American
        Journal of Public Health (1999) (Exhibit 76), which cites (footnotes 1 - 9)
        a series of other published articles making similar criticisms.
        Dr Greenland's principal points are, first, that the probability of causation
        cannot be computed solely from the relative risk, particularly when
        exposure accelerates the time of disease occurrence the standard
        epidemiologic estimates of probability of causation will tend to
        underestimate that probability. The second tenet in his criticism is that the
        exposure dose at which the probability of causation exceeds 50 per cent
        may fall well below the "doubling dose". It seems to me that there is
        much force in these criticisms and that Dr Greenland's thesis provides
        another reason to look with reserve at these mathematical analyses and to
        treat them as guides rather than as determinative tests.

385           The formulae are no doubt useful, and widely employed, in relation
        to a series of people with known measurable exposures who have been
        traditionally found to be associated with greater incidence of the disease
        among asbestos workers such as, for example, the Helsinki Protocol and
        the AWARD Criteria, but whether the same relationships hold good for
        lower levels of exposure, perhaps with intermittent high short-term peak
        doses, does not appear to be known, or at least if known well understood
        or accepted. This much is clear from the language of the Helsinki

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        Consensus Statement itself. Therefore, while the epidemiological and
        statistical relationships which have been so extensively deployed in this
        case may represent the best method of quantitative analysis presently
        available for the estimation of increased risk due to asbestos exposure, the
        absence of an adequate scientific understanding of the pathogenesis of the
        disease of asbestos-induced lung cancer, necessarily means that there are
        many assumptions, express and tacit, in the use of such a mathematical
        model and that care and judgment needs to be exercised in its application.
386          I certainly reject any implicit assumption that the statistical methods
        should be employed blindly in a case such as this and, in particular, I
        reject any notion that, on the figures adopted by the statistic ians and
        epidemiologists in this case and the formulae by which they have been
        apportioned, the question of whether or not a causal attribution to asbestos
        exposure for an individual case of lung cancer can be made will depend
        entirely upon whether or not the RR is shown to have reached a figure of
        2.0 or more.

387          Not only do I consider that these observations have application to
        this methodology generally but, in my view, they have greater application
        to the present case where the deceased was clearly exposed to potential
        carcinogens, smoking and asbestos, which are known to interact in a
        manner which mutually amplifies the effect of each and, again, where the
        pathological reason for that amplification effect is not fully understood.
        In a case like this, while the statistical and epidemiological evidence is
        unquestionably important and significant, I take the view that it needs to
        be taken into account in conjunction with other known evidence and that,
        in the end, the attribution, or non-attribution, of a causal effect requires a
        large degree of judgment to be exercised in conjunction with the
        mathematical approach which I have described. In other words, I am not
        persuaded that one can or should simply pick up a calculator and perform
        the iterations described by Professor Berry, Dr Leigh, Professor Fox or
        Mrs Sowden and Mr Rogers to provide the answer in any given case.

388          For an example of the variability, and subjectivity, of the
        mathematical analysis it is unnecessary to go further than to the assumed
        incremental increase of between 0.5 per cent to 4 per cent for each
        additional fb/ml year identified in the Helsinki Protocol. Professor Berry
        identified this in Exhibit 145(1) and then questioned the adoption, as the
        incremental component, of the figure at the top end of the range for
        exposure to amphibole asbestos, leading him to observe, in his oral
        evidence, that a suitable incremental figure for asbestos containing



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        10 per cent Chrysotile, 2 per cent Amosite and 88 per cent cement would
        be about 1.2 per cent per fb/ml year.
389          In the course of his cross-examination Professor Berry accepted that
        asbestos was a "complete" carcinogen and not merely a promoter.
6. Professor R M Fox
390           The second defendant also called Professor Richard Mark Fox, a
        clinical haematologist and medical oncologist and director of the
        Department of Clinical Haematology and Medical Oncology at the Royal
        Melbourne Hospital and the University of Melbourne. Professor Fox has
        a very extensive and distinguished career as a physician and researcher in
        the field of medical oncology. As well as holding primary degrees in
        medicine and surgery, he holds the degree of Doctor of Philosophy from
        the University of Sydney and attained his fellowship of the Royal
        Australasian College of Physicians in 1974. He has undertaken research
        and taught in haematology and oncology in the United Kingdom and in
        Australia and in the Republic of China. He is an honorary professorial
        research fellow at the Walter and Eliza Hall Institute for Medical
        Research in Melbourne. His extensive career in medical research,
        teaching and publishing is set out in his curriculum vitae (Exhibit 223).
        Professor Fox is, without doubt, a very eminent and experienced specialist
        in the field of cancer treatment and research. He was engaged by the
        solicitors for the second defendant in March 2001 (Exhibit 228) to advise
        on Mr Cotton's case.
391          In his first report (Exhibit 224(1)) dated 14 August 2001, Professor
        Fox addresses Mr Cotton's case on the basis of the information derived
        from Professor Musk's report (Exhibit 56) and descriptions of the
        CT scan. For Professor Fox it was significant that there was no evidence
        to suggest interstitial fibrosis, nor any sign of pleural plaques. He also
        expressed some concern that the CT scan findings were not entirely
        consistent with a non small cell lung cancer and suggested the possible
        co-incidence of another tumour, for example a malignant lymphoma, to
        explain the splenomegally and extensive lymph node involvement.
        Professor Fox also appears to have deduced or assumed that Mr Cotton
        was suffering from emphysema, presumably because of his history of
        smoker's cough and sputum production described by Professor Musk and
        by Drs Kendall and Mincham. In this respect, however, it is important to
        note that both Professor Musk and Dr Kendall each gave evidence that
        Mr Cotton's lung function was not impaired, that he showed that he did
        not exhibit breathlessness and, in Dr Kendall's case, that he did not have


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        any chronic obstructive airways disease (COAD). In his second report
        (Exhibit 224(2) Professor Fox enlarged on this by observing that
        extensive splenomegally and abdominal retroperitoneal lymphadenopathy
        is not commonly found in primary squamous cell lung cancers, although it
        is possible, but it is also a characteristic of a lymphoma. He stated,
        however, that he believed that Mr Cotton's lung cancer was in fact a
        primary lung cancer of squamous cell nature. Despite this reservation, no
        other consultant has suggested, nor has any of the defendants submitted,
        that Mr Cotton's death was the result of the operation of two unrelated
        cancers operating simultaneously or sequentially and, therefore, I do not
        pursue this hypothesis any further.

392           Like Professor Berry (in his first report - Exhibit 145(1)), Professor
        Fox rejected the potentiality of any exposure to asbestos by Mr Cotton at
        Australind as causing or contributing to his lung cancer because of a short
        latency period of 10 years and also because it was thought to be minimal.
        His opinion, therefore, proceeded on the footing that the only exposure to
        asbestos which might potentially cause or contribute to the lung cancer
        was Mr Cotton's employment with the first defendant in Adelaide working
        with asbestos cement pipes. Professor Fox rejected this as a tenable
        hypothesis and expressed the opinion that Mr Cotton's lung cancer was
        totally explained by his smoking habit. In his first report (Exhibit 224(1)),
        Professor Fox did not expressly address or consider the possibility that an
        interaction between smoking and asbestos exposure may have
        cumulatively caused this lung cancer, confining his attention to the
        separate potential roles of those two carcinogens alone.
393           In relation to the potential role of Mr Cotton's asbestos exposure
        while working in Adelaide, Professor Fox drew attention to the Helsinki
        Protocol but pointed out that those criteria were not representative of the
        whole of medical opinion because they ignored those who propounded the
        view that lung cancer should not be attributed to asbestos unless the
        established asbestos exposure was sufficient to cause asbestosis and that
        asbestosis, that is interstitial fibrosis, was actually present. He also
        criticised the Helsinki report because of its failure to consider the
        increased risk for those associated with emphysema. Whatever the force
        of that criticism may be generally, and it was not pursued in this case,
        there does not seem to be an established basis for assigning Mr Cotton to
        the category of those whose illnesses included emphysema, in the absence
        of any clinical finding that emphysema was a material factor in his
        presentation.




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394          Professor Fox then made reference to a study by Professor Roggli
        (Exhibit 203) who demonstrated an increase in asbestos fibre load in those
        with interstitial fibrosis of the order of 30 times those with pleural plaques
        and 300 times those without plaques. On this basis he pointed out that in
        Mr Cotton's case there had been no finding of interstitial fibrosis, nor any
        finding of pleural plaques, and that this consigned Mr Cotton's case to the
        low end of asbestos fibre load exposure, quite insufficient to cause
        asbestosis and, therefore, by employment of the Helsinki Protocol,
        insufficient to justify an attribution of causal effect between asbestos
        exposure and his lung cancer. He went on to observe that the general
        view is that pleural plaques in the absence of asbestosis do not represent
        an increased risk for the development of lung cancer and, therefore,
        because of the inference that Mr Cotton's exposure was insufficient to
        produce asbestosis, his lung cancer could not be attributed to asbestos
        either.
395           It is apparent from this approach that Professor Fox is not only a
        critic of the Helsinki Protocol, because of his view that it ignores a
        volume of medical opinion which holds to the view that the presence of
        asbestosis is necessary before an attribution of asbestos exposure can be
        made as a cause for a case of lung cancer in the patient, but also because
        of his view that, without pleural plaques, there could be no attribution of
        asbestos as the cause of an individual case of lung cancer. As already
        noted, Professor Fox excluded the potential asbestos exposure at
        Australind as a contributor to Mr Cotton's lung cancer because of his
        opinion that the latency period was too short - a view which, unlike
        Professor Berry, he was not prepared to revise.                     In his
        examination-in-chief, Professor Fox maintained that the necessary latency
        period, which he saw as being at least 10 years, related to the period from
        the first exposure to asbestos until the date of diagnosis - another
        departure from the approach taken by Professor Berry. Further, as also
        already noted, Professor Fox did not, in Exhibit 224(1) address the
        potentiality of a combination of effect of smoking and asbestos exposure
        acting together.

396           In his oral evidence Professor Fox made clear his opinion that, for
        lung cancer due to asbestos, the disease is dose related and that the dose
        relationship is the same as that necessary to produce asbestosis.
397           In giving his oral evidence Professor Fox was asked to consider
        Mr Cotton's potential exposure to asbestos at Australind and on the basis
        that it included Amosite and Chrysotile. It was put to him that Mr Cotton
        had probably worked in the BDR some 15 to 20 times at periods of five to


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        eight hours each. He calculated that this was a maximum of 160 hours
        exposure in the BDR which was equivalent to four normal working
        weeks. Even on the assumption that Mr Cotton had spent all that time
        sweeping up dust from the floor which included asbestos, Professor Fox
        regarded that as a trivial amount of exposure. In his view it might be
        sufficient to cause mesothelioma but not lung cancer.
398           In cross-examination it emerged that it was Professor Fox who had
        recommended the engagement of Mrs Sowden as a consultant
        occupational hygienist. It also became apparent that, despite his
        professional knowledge and acquaintanceship with Professor Musk and
        his regard for Professor Musk's high reputation, he disagreed with
        Professor Musk's opinions in this case. In particular, Professor Fox
        expressed the view that the multiple agents or carcinogens in this case
        were smoking and asbestos acting independently. Counsel for the second
        defendant tendered Exhibit 209 - which is a duplicate of Exhibit 72(61) -
        (a study by Liddell and Armstrong in 2001) as supporting the view that
        the relationship of cigarette smoking and Chrysotile exposure in effect
        was not multiplicative and that the two agents acted independently.
        Nevertheless, that conclusion appears to run counter to the general pattern
        of opinion on that subject and was not maintained by Professor Fox in
        cross-examination. As none of the other expert witnesses propounded that
        theory, I am not prepared to accept it in this case. He placed great
        reliance on the paper by Sir Richard Doll and Professor Richard Peto
        (Exhibit 179) relating to the long study of mortality due to smoking in
        Britain. It is to be noted, however, that in this paper (at 309 BMJ, p 208)
        there are observations that in most of the causal associations, including
        exposure to asbestos, smoking seems to act synergistically and, in all the
        listed causes of death, including the figures cited for lung cancer, shown
        in Table VII, the death rates for current cigarette smokers are very much
        greater.
399           Further, in the course of his cross-examination, Professor Fox was
        quite emphatic in stating that he adhered to the view that there needs to be
        asbestosis present before a lung cancer could be attributed to asbestos
        exposure and he cited a report of the Royal Commission of the Canadian
        Province of Ontario (Exhibit 200) as supporting a dose response
        relationship between a  sbestos exposure and asbestosis, of an essentially
        linear relationship between cumulative dose and mortality and as
        supporting his view that a causal connection between asbestos exposure
        and lung cancer requires a similar degree of cumulative exposure as for
        asbestosis - but the graphs depicted in that exhibit (p 279) appear to show
        a non-linear relationship.

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400           In cross-examination Professor Fox said that Mr Cotton did not
        exhibit any greater than normal susceptibility to cancer because of his
        parents' history (including death from cancer), but he rejected the
        observation of Professor Musk that 43 years was a young age for a man to
        develop lung cancer in Australia, pointing out that the age distribution
        follows the pattern of a normal curve starting from men in their 30's and
        that all that could be said was that Mr Cotton was at the lower end of the
        recognised age group for the development of the disease.
401          On the issue of whether or not smoking and asbestos exposure in
        combination have a synergistic or multiplicative effect, Professor Fox said
        that there was an assumption that the effect was a mixture of
        multiplicative and additive but that in the present case the fundamental
        issue was that because Mr Cotton appeared to have a very low asbestos
        fibre count, the far greater risk of cancer due to his smoking was not
        materially affected or altered by such a low risk associated with the
        second carcinogen. He put his position clearly at t/s 1378:

              "I think the issue is not really relevant in this because the factor
              that you have to multiply with is so extremely low that it
              becomes irrelevant because the level of fibre exposure and the
              duration is so low, that you have nothing to multiply with."

402           This observation was made with reference to the need, in Professor
        Fox's opinion, to show an intensity of asbestos exposure of at least
        25 fb/ml years to get to a level of a twofold risk, and that Mr Cotton's
        exposure was so far short of that that consideration of a multiplicative
        versus additive effect would have no significant consequence on the
        attribution of cause. In the end it became clear that Professor Fox
        required the attainment of the Helsinki criteria as an indispensable
        minimum for the attribution of asbestos as a causal effect for Mr Cotton's
        lung cancer.

403           Despite his impressive credentials, I am not prepared to accept,
        without qualification, the opinions advanced by Professor Fox. My first
        reason for this reserve is that he clearly places himself among the
        supporters of that group of specialists who maintain that the presence of
        interstitial fibrosis, that is asbestosis, must exist before an attribution to
        asbestos can be made in any particular case of lung cancer. Professor
        Musk, Dr Kendall, Professor Berry, Dr Leigh, Professor Wan and
        Professor de Klerk all rejected that view and gave cogent reasons for their
        opinions that the preponderant modern view is to the contrary.



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404          Second, Professor Fox rejected any possible effect of asbestos
        exposure at Australind as contributing to Mr Cotton's lung cancer
        because, in his view, the period of latency was insufficient. Not only did
        Professor Berry take a different view of the measurement of the period of
        latency, but he, and the other consultants including Professor Musk,
        Dr Kendall and Dr Leigh, adopted the view that the earlier exposure at
        Adelaide could operate in conjunction with the later exposure at
        Australind in combination to produce a carcinogenic effect and that such a
        result would be consistent with current k     nowledge and opinions about
        latency. Thirdly, Professor Fox rejected any significant effect or
        combination between asbestos exposure and smoking on the basis that the
        asbestos exposure was so minor that even if it were to be allowed to have
        a multiplicative effect on the risk of contracting cancer from smoking, that
        resultant effect would be so small as to be negligible. With all respect to
        him, I find the opinions of Professor Musk, Professor Wan, Dr Kendall,
        Professor de Klerk and Professor Berry to the effect that the consequences
        of Mr Cotton's occupational exposure to asbestos increased his risk of
        contracting that disease by something of the order of 2 per cent to
        20 per cent which, taken in conjunction with the enhancing carcinogenic
        effect of his smoking, provides a good explanation for his fatal tumour.

405           Finally, Professor Fox's view that degrees of exposure to asbestos
        fibres, in descending orders of magnitude, are associated with those with
        interstitial fibrosis (asbestosis), those with pleural plaques and those
        without any such features in the ratio of 300 is to 30 is to 1, appears to me
        to be no more than a variant on the proposition that either the presence of
        asbestosis, or the demonstration of a level of cumulative exposure to
        asbestos fibres sufficient to justify a diagnosis of asbestosis, is an essential
        prerequisite in order to attribute any particular lung cancer to asbestos
        exposure.

Conclusions
406          From this evidence I consider that the plaintiff has demonstrated that
        Mr Cotton was exposed to ambient asbestos fibres during the period of his
        employment with the first defendant in Adelaide and again during the
        period of his employment with the third defendant at Australind. The
        quantification of the cumulative exposure to asbestos during these periods
        of employment is fraught with difficulty, approximation and, at the
        extremes, speculation. However, there is little doubt in my mind that
        while Mr Cotton was working for the first defendant in Adelaide laying
        cement asbestos water pipes he was, on repeated occasions, subjected to a
        series of peak exposures to asbestos cement dust which were relatively


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        short and transient but which occurred two or three times each working
        day for periods of something in the order of half an hour or more and, that
        at other times when working with the asbestos cement pipes, there was
        probably a significantly lower level of background exposure to asbestos
        fibres, but greater than occurs in a workplace where asbestos is neither
        used nor present.
407          Similarly, I consider that the evidence reveals to a high degree of
        persuasion that, when Mr Cotton was working in the employ of the third
        defendant at Australind he was, at various places in the workplace, but
        especially in the packing sheds and in the BDR, exposed to transient
        levels of asbestos some of which are likely to have been quite high during
        sweeping up operations. Other exposure while employed with the third
        defendant was probably experienced by Mr Cotton during the removal of
        asbestos roof sheeting in the vicinity of the packing areas and adjacent
        buildings, including the extensions to the BDR. This is likely to have
        been a lower level of exposure but not insignificant.

408           Once more, estimations of a quantitative figure for cumulative
        asbestos exposure at Australind and at Adelaide must be taken with a
        great deal of reserve and care. I am not prepared to accept either the
        Amdel study or the WAIT AID study, Exhibits 153(6) and 153(4),
        advanced by the second defendant as reasonably indicative of the levels of
        exposure when working with cement pipe in Adelaide. That also leads me
        to reject the Sowden and Rogers' estimations of asbestos air concentration
        in that working environment.

409          Equally, I am not persuaded that the membrane filter test results
        produced by the third defendant are indicative of the levels of exposure to
        which Mr Cotton was subject. My reasons for this have been set out more
        fully above but, in the main, those results are derived from air sampling
        conducted when the asbestos removal operations were in train at
        Australind and in places other than in the BDR. There are some test
        results relating to concentrations in the BDR, but they are few in number
        and in proportion so there does not appear to me to be any basis to
        conclude that they are in any way indicative of the type of peak loads
        which occurred during sweeping up of dust, fragments of lagging and
        other deposits on the BDR floor which Mr Cotton was required to do. My
        view is that the most indicative and reliable opinions about the degree of
        asbestos concentration in the air in these two working environments
        comes from Mr Kottek and Professor de Klerk and that the calculations
        based on those by Professor Musk, Dr Leigh and Professor Berry lead to
        the conclusion that that aggregate exposure did elevate Mr Cotton's risk of


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        contracting lung cancer and that the elevation of that risk is something in
        the order of 2 per cent to 20 per cent above the background risk, having
        regard to the influence of asbestos alone. The probabilities are that the
        range is 10 per cent to 20 per cent or a little more. When combined with
        Mr Cotton's history of smoking, all the evidence, except that of Professor
        Fox, is to the effect that the combined effect of the two carcinogens would
        necessarily be greater than the effect of either one alone and that this
        "synergy" allows a multiplicative effect to be given to the mathematical
        estimations of chance, always bearing in mind the limitations and
        approximations of those mathematical models.
410           In concluding that the estimates of Professors Musk, de Klerk and
        Berry and Dr Leigh to the effect that the risk of contracting lung cancer
        was increased by Mr Cotton's periods of exposure to asbestos by
                                 o
        something of the order t 2 per cent to 20 per cent, does not mean that I
        regard that range as precise or inflexible. At best, I regard it as an
        approximation well capable of increase. Nevertheless, I am satisfied that,
        in comparison with many of the studies of asbestos-induced lung disease
        including lung cancer, which have been cited in the literature tendered in
        this case, Mr Cotton's cumulative exposure was well towards the low end
        encountered in industry among those who developed asbestos-related lung
        diseases (excluding mesothelioma).
411           While deploring the contentions of several of the witnesses,
        particularly the occupational hygienists, when suggesting precision in
        their estimation of asbestos air concentrations and increases in relative
        risk in this case, I am nevertheless satisfied that that area of evidence does
        establish that Mr Cotton's exposure was probably, indeed almost certainly,
        less than the 25 fb/ml years threshold promoted by the Helsinki Protocols
        and the Australian AWARD study. In making this criticism of some of
        the evidence of the occupational hygienists, I wish to make it clear that I
        do not doubt the integrity, the learning or the experience of any of those
        individual witnesses but, rather, I have concluded that their conscientious
        quest for precision and symmetry in their attempts at quantification go
        further than available learning, limits in the methodologies and the many
        variables for attempts at retrospective estimation can justifiably assert.
412          What then can be made of this conclusion that, as a result of both
        occupational exposures to asbestos, Mr Cotton had an increased risk of
        developing lung cancer something of the order of 10 per cent to
        20 per cent in circumstances where that risk was operating as the
        combination of asbestos and the other carcinogen, tobacco smoke, which
        he was inhaling and where a fatal lung tumour developed, the cause of


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        which is consistent with both carcinogens acting in combination or with
        the effects of tobacco smoke acting alone?
Scientific literature
413           The primary evidence upon which I must rely on in this case comes
        from the witnesses and their individual reports upon which they have been
        examined and cross-examined. However, by consent, a large quantity of
        medical literature bearing upon the pathogenesis of lung cancer,
        asbestos-induced lung disease and associated epidemiological studies has
        been introduced which I must notice and examine. It is not practicable to
        deal with all the literature to which I have been referred, although I have
        examined it, and any such attempt would be unnecessary in light of the
        explanations given by the witnesses of the principles involved.
        Nevertheless, there are some areas of controversy in this case, particularly
        the significance of the Helsinki Protocols and the AWARD Criteria; the
        issue of whether or not an attribution to asbestos can be made in cases of
        lung cancer not involving asbestosis or cumulative exposure to asbestos
        justifying a diagnosis of asbestosis; the use of the mathematical formula
        and modelling to determine relative risks and attributable risk factor; and
        at what point a doubling of the relative risk can be established. In
        particular, there is the issue about the nature and degree of interaction
        between two carcinogens, smoking and asbestos, operating in
        combination.

414          It is with those particular controversies in mind that I have selected
        the following evidence from the literature for special mention.

415          In Exhibit 182 ("Asbestos Facts on Health of Exposure to Asbestos"
        by Doll and Peto) there is a discussion of the dose response relationship
        with regard to asbestos and cancer and the authors make the point that the
        problems are in many respects different in cases of lung cancer to those
        experienced in analysing cases of asbestosis. The authors assume a direct
        proportionality between increase in risk and intensity of exposure (ie a
        linear relationship) which they say is consistent with available data, but
        they go on to observe that there are examples of both upward and
        downward curvature in dose response for other carcinogens and that the
        assumption of dose-linearity, although scientifically plausible, is not
        demonstrably correct. They also appear to reject the postulate that
        asbestos-induced lung cancer is associated with degrees of exposure
        potentially necessary to cause asbestosis and have said that this idea
        originated in the days before the discovery of DNA when there was a
        different, and now discarded, theory about the operation of carcinogenesis


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        at the cellular level. In my view this study supports the views of Professor
        Musk on these issues and tells against the opposing views of Professor
        Fox.

416           Exhibit 189 is a publication by Hodgson and Darnton: "The
        Quantitative Risks of Mesothelioma and Lung Cancer in Relation to
        Asbestos Exposure" published in 2000, resulting from studies conducted
        in the United Kingdom. It estimated quantitative exposure risks for
        various lung diseases and for various types of asbestos exposure and
        concluded that, for the risk of mesothelioma, the exposure specific risk
        was in the ratio of 1 is to 100 is to 500 for Chrysotile, Amosite and
        Crocidolite, respectively. However, for lung cancer the conclusions were
        less clear cut. Exposures to Crocidolite or Amosite revealed similar
        exposure risk levels (around 5 per cent excess lung cancers per fib/ml
        year), but Chrysotile exposures showed a less consistent picture. Dealing
        with exposures to mixed asbestos fibres, the authors suggested that a best
        estimate lung cancer risk for Chrysotile alone would be 0.1 per cent, with
        the highest reasonable estimate of 0.5 per cent. The risk differential
        between Chrysotile and the two amphibole fibres for lung cancer was thus
        between 1 is to 10 and 1 is to 50. Further, these authors reported that an
        examination of the interstudy dose response relationships for the
        amphibole fibres suggested a non-linear relationship for all three cancer
        end points (including lung cancer). The risk for peritoneal mesothelioma
        is proportional to the square of cumulative exposure, lung cancer risk lies
        between a linear and square relationship and pleural mesothelioma seems
        to rise less than linearly with cumulative dose. The authors concluded
        that although these non-linear relationships provide a best fit to the data,
        statistical and other uncertainties mean that a linear relationship remains
        arguable for pleural and lung tumours (but not for peritoneal tumours).
417           Despite the acceptance by these authors of the legitimacy of an
        assumed linear relationship for statistical purposes, the observation that
        with lung cancer the risk lies between a linear and square (exponential)
        relationship would appear to mean that there is even more cause to
        entertain reserve about precise or automatic application of the
        mathematical modelling favoured by Professors Berry and Fox. At 582 of
        Exhibit 189 those authors observed that the data which they studied
        suggest that the relation between lung cancer and cumulative exposure
        may be concave - that is, that the excess lung cancer risk is proportional to
        a power greater than 1 of cumulative exposure. This is yet another reason
        to exercise caution and reserve about the automatic or necessary
        application of the applicable risk factor produced by the employment of
        formulae favoured by the epidemiologists and statisticians in this case.

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418           Vainio and Baffetta: "Mechanisms of the Combined Effect of
        Asbestos on Smoking in the Etiology of Lung Cancer" (1994),
        Scandinavian Journal Work Environ Health, vol 20. This article
        contained a detailed discussion of the complex, but incompletely
        understood, interaction between smoking and asbestos exposure in the
        development of lung cancer. The pattern revealed by epidemiological
        studies was variable, ranging from supra-multiplicative to less than
        additive. It was thought this may reflect the fact that both asbestos and
        smoking are complex carcinogens which can affect more than one stage of
        lung carcinogenesis. The joint effect of two such agents will depend on
        the relative magnitude of the effects at each stage. Both tobacco smoke
        and asbestos fibres can be genotoxic and cytotoxic and cause proliferative
        lesions in the lung. Chronic inflammation of the lungs can release various
        cytokines and growth factors which may provide a selective growth
        advantage to mutated cells. Speaking of the reliability of these statistical
        studies (at 236), the authors wrote that the measures of interaction are
        very imprecise as the small numbers of lung cancers among non-smokers
        exposed to the two risk factors strongly reduce the statistical power. The
        relationship ranged from additive interaction (Canada - Chrysotile), to
        multiplicative, to more than multiplicative (for Australian underground
        Crocidolite miners).
419           I conclude that the interaction of the two carcinogens is not
        completely understood, but the mathematical function of the relationship
        is variable depending upon degrees of exposure, types of asbestos, and
        stages of progress of the multi-stage disease. This study does not support
        a conclusion that a simple mathematical model (either multiplicative or
        additive) can be applied to all cases involving the interaction of the two
        carcinogens and shows that the relationship may change having regard to
        the factors identified (Exhibit 190).

420          Berry, Newhouse and Antonis: "Combined Effect of Asbestos and
        Smoking on Mortality from Lung Cancer and Mesothelioma in Factory
        Workers" (1985), 42 British Journal of Industrial Medicine - 12
        (Exhibit 191). This article noted that there was no significant association
        between smoking and deaths due to mesothelioma - presumably because
        the cause of mesothelioma can be attributed solely to the action of
        asbestos on lung tissue. The authors reviewed data from several studies
        which show that the relative risk of contracting lung cancer due to
        asbestos was highest for those who had never smoked, but the authors
        express some uncertainty about the accuracy of the degree of difference
        revealed by the studies, but conclude that the combined estimate was that
        the relative risk of lung cancer due to asbestos was 1.8 times greater in

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        non-smokers than in smokers. But the authors observe, despite those
        figures, they would not claim that it is established that non-smokers have
        a higher relative risk due to asbestos than smokers. They concluded that
        in absolute terms the smokers had the higher risk of dying of lung cancer
        as a result of their extra risk due to asbestos exposure because the base
        risk is much higher due to smoking.
421           Exhibit 192, Chase and Others: "Evaluation for Compensation of
        Asbestos-exposed Individuals" (1985), vol 27, Journal of Occupational
        Medicine 189. These authors begin by recognising that the instance of
        lung cancer in the cigarette smoking population occupationally exposed to
        asbestos is inordinately high. However, not all lung cancers among
        asbestos-exposed persons are necessarily related to asbestos. Although it
        is difficult to determine unequivocally whether a particular cancer is or is
        not related to asbestos exposure, some cancers are definitely more likely
        than others to be related to asbestos exposure - so that for a person with
        lung cancer exposed to a large dose of asbestos, the disease is more apt to
        be related to the exposure than one in a subject with less exposure. The
        authors then go on to develop a multi disciplinary approach for identifying
        or apportioning the role asbestos might have played in the development of
        the lung cancer in a smoker. In doing so, they recognise that lung cancer
        develops in the multi-stage sequence and they distinguish between two
        major sequential stages - initiation and promotion. They treat asbestos as
        a classic promoting agent rather than an initiating agent, and also rather
        than being a complete carcinogen but, again, they exclude mesothelioma
        from this categorisation because, for that type of lesion, the extent of the
        asbestos exposure is of such a magnitude that it is customary to assign the
        entire risk to the asbestos exposure.

422           In the present case both Professor Musk and Professor Berry said,
        that in their view, asbestos was a complete carcinogen and did not act
        solely as a promoter. The only witness in this case who appeared to be of
        the opinion that asbestos acted as a promoter for lung cancer was
        Professor de Klerk but, as explained elsewhere, his remarks in this regard
        were made specifically with reference to the significance of latency and
        exposure of Mr Cotton at Australind. However, it is difficult to see how
        much can turn on this scientific controversy in the present case.
        Nevertheless, the paper is of potential significance because of its
        discussion of the mathematical treatment of the determination of relative
        risk of lung cancer from smoking (p 192) and from asbestos, smoking and
        other causes (p 193). The paper shows that there are four variables which
        must be taken into account in the mathematical model for determining the
        risk of developing lung cancer due only to smoking and more variables

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        still in any mathematical model dealing with a person who is both a
        smoker and exposed to asbestos. The mathematical models developed are
        more complicated than the formulae propounded and applied by the
        occupational hygienists and epidemiologists in this case and suggest that
                                                   i
        the relationship is more variable than the l near relationship which those
        witnesses postulated.
423           Exhibit 197, Egilman: "Lung Cancer in Asbestos Exposure:
        Asbestosis is Not Necessary" (1996), vol 30, American Journal of
        Industrial Medicine 398. This study addressed the question of whether
        lung cancer can be attributed to asbestos exposure in the absence of
        asbestosis.     After analysing contemporary epidemiological and
        pathological studies, and the basic scientific controversy, the author
        concluded that the assertion that asbestosis must be present in order to
        attribute a lung cancer to asbestos exposure does not meet accepted
        standards for establishing causation. He concluded that lung cancers can
        occur as a result of asbestos exposure in the absence of clinical or
        histologic asbestosis. The author joins with another commentator in
        observing that the debate (about the need for asbestosis) has been
        motivated more by litigation than by medical evidence. In accepting that
        exposure to asbestos can, and in certain cases does, cause lung cancer
        without any pleural fibrosis or histological signs of asbestos presence or
        damage the authors acknowledged that asbestos exposure is recognised as
        having multiple health effects and that asbestos exposure alone can
        produce lung cancer. They did not attempt, however, to present
        guidelines to address the secondary question of whether asbestos could be
        said to have caused lung cancer in the case of any particular patient.
424          This study supports the approaches taken by Professor Musk, by
        Dr Kendall, by Professor de Klerk and by Professor Berry and is
        inconsistent with the opinion, on this issue, of Professor Fox. It provides
        additional grounds for my conclusion to decline to accept Professor Fox's
        opinion on this particular topic.

425          Churg: "Asbestos Related Disease in the Workplace and the
        Environment: Controversial Issues" (Exhibit 198). Writing in 1993,
        Dr Churg undertakes a review of the literature and the epidemiological
        studies relating to the controversial question of whether or not asbestos
        exposure, in the absence of asbestosis, can cause or contribute to the cause
        of lung cancer. His conclusion, which supports the opinion of Professor
        Fox, is that there is strong epidemiologic and pathologic evidence that the
        only association of asbestos exposure and lung cancer is the association of
        asbestosis and lung cancer, so that a lung cancer should only be attributed


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        to asbestos exposure when asbestosis is present on clinical or pathological
        grounds (Exhibit 198, p 172). In the course of his article Dr Churg refers
        (at 58) to numerous epidemiologic studies which have made it clear that
        the development of asbestosis requires what would now be judged high
        exposure to asbestos. It has been estimated that a minimal exposure of
        25 fb/ml years is necessary to find any evidence of asbestosis. Thus,
        asbestosis is usually encountered in workers with many years of high
        exposure; for example, asbestos miners and millers, asbestos textile
                                                                        n
        workers and asbestos insulators. But asbestosis can also be i duced by
        relatively brief, extremely high, exposure and this phenomenon is seen in
        workers who worked inside ships under construction or refit during World
        War II where exposures reached levels of hundreds of fibres per ml.
        Dr Churg also observed that there is considerable evidence that cigarette
        smoking increases the attack rate and/or progression rate of asbestosis,
        although not every study comes to this conclusion.
426           As indicated, I am persuaded that this opinion about the necessity for
        the presence of asbestosis before a diagnosis of asbestos induced lung
        cancer can be made, is a view which does not represent the prevailing
        opinion of contemporary experts in this area, although it continues to have
        supporters. Therefore, while I do not accept this approach to the present
        case, Dr Churg's writing is nevertheless revealing because it shows that
        the quantitative assessment of 25 fb/ml years cumulative exposure to
        asbestos is closely associated with the accepted epidemiological studies
        about the level of exposure likely to produce asbestosis - very heavy
        levels of cumulative exposure. If the necessity for asbestosis to be present
        before lung cancer can be regarded as asbestos induced is rejected, then
        the selection of the 25 fb/ml year cumulative exposure as a prerequisite
        for an attribution of asbestos as the cause of a lung cancer (without
        asbestosis) is undermined. The question which must be asked is: Is the
        same degree of asbestos exposure needed to produce asbestosis (a high
        level) necessarily at the same degree of exposure necessary to provide an
        explanation for the development of lung cancer in the absence of
        asbestosis, and, if so, why? This question seems to be significant in the
        present litigation but it is not addressed, let alone answered, by this
        particularly research.

427           Exhibit 201 is a presentation by Dr Julian Peto to the Australian
        Institute of Occupational Hygienists in Canberra in 1998 about problems
        arising in relationships of dose response and risk assessment in
        occupational epidemiology with specific reference to smoking and cancer
        (Exhibit 201).     No particular conclusions about the quantitative
        relationship between asbestos exposure and/or smoking history are

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        propounded which are likely to lead to a resolution of any of the
        controversies in this case. Nevertheless, the paper contains a number of
        emphatic and salutary warnings about indiscriminate adoption or
        application of many of the statistical and epidemiological models which
        have been the subject of evidence in this trial. Dr Peto made the
        following points:
              •       Any analysis based on measures of a cumulative dose
                      such as working level months for radon or pack-years for
                      smoking entails a very strong scientific assumption which
                      is often wrong. The same may be true of analyses based
                      on relative or absolute risk. It is often not clear what
                      measure of dose or response is appropriate, and the wrong
                      choice can lead to very wrong conclusions.
              •       The second type of error is purely statistical. Both
                      exposure and response are usually measured inaccurately,
                      and these errors have important effects which can be
                      adjusted for but are almost never considered even by
                      statisticians.

              •       The third problem relates to exposure data which is so
                      unreliable that any attempt to calculate the risk per unit
                      exposure from them leads to virtually meaningless
                      conclusions. Dr Peto believes that certain uses of
                      asbestos may fall into this category. There is simply no
                      solution to this.

428           In his discussion of lung cancer incidence in relation to smoking,
        Dr Peto refers to, and illustrates, a series of graphical depictions of the
        relationships which are plotted on logarithmic scales, so that the power
        scales produce parallel straight lines both with slopes equal to four. These
        curves or lines may, to an uncritical observer, therefore appear to be
        linear, but that is only because they are plotted on a logarithmic basis
        which reveals that the true nature of the mathematic relationship is much
        more complicated and is, in fact, exponential. Whether the same is true
        for quantitative analysis of the effects of asbestos exposure is not stated,
        apart from the generality of Dr Peto's warnings about the methodologies.
429          This paper, in my view, supports the general conclusion that the
        cause and effect relationship, if any, and the significance of differing
        degrees of exposure upon risk are far more complicated than the linear



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        mathematical models propounded by the occupational hygienists in this
        case.
430           The study by Liddell and Armstrong (Exhibit 209):                "The
        Combination of Effects on Lung Cancer of Cigarette Smoking and
        Exposure in Quebec Chrysotile Miners and Millers" (2001), addressed the
        relationship between asbestos exposure and lung cancer for smokers and
        non-smokers and those who had, or who had not had, long-term exposure
        to Chrysotile in their occupations. Significant statistical differences
        between the groups were identified and the study then addressed the
        additive and the multiplicative models of the combined effect of the risks
        from the two carcinogens. Both linear and log-linear models were used
        but the additive model was found to fit best. The multiplicative models
        were found to fit better if a factor was introduced to imply less than a
        direct multiplicative relationship. Their conclusion was that the refutation
        of the multiplicative hypothesis by these data reinforce its inapplicability
        in general; but the additive hypothesis is not generally applicable either
        and there seems to be no good reason to believe that the interactions
        conform to any simple theory.

431           It seems important to treat this study as being confined to the effects
        of Chrysotile because of other literature and opinions which accept that
        the influence of the amphiboles is much greater in its toxicity. The study
        appears to be consistent with the study of Professor Berry and others set
        out in [420] above, but it is evident that the author's studies consider that
        caution should be exercised in drawing implications or applications.
        Much seems to depend upon the type of asbestos and the levels of doses
        which suggest that simple linear relationships which do not have regard to
        those factors, or the stage in process of the development of the disease,
        may not give a complete explanation.
432           Exhibit 214 is an article by Koskinen and others: "Different
        Measures of Asbestos Exposure in Estimating Risk of Lung Cancer and
        Mesothelioma Among Construction Workers", and is published in the
        American Journal of Occupational and Environmental Medicine (vol 44,
        December 2002). It involves a study of workers exposed to asbestos in
        Finland over the period 1990 - 2000 with a multivariate analysis of
        cumulative exposure levels. The principal finding was that the risk of
        total cancer and of lung cancer among this group of male construction
        workers was similar to that of the general male population but that their
        risk of mesothelioma was significantly increased. The group included a
        large component of smokers but their representation was similar to that
        reported in a random sample of the general population at the same time


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        and so it was thought that the differences in smoking habits did not bias
        the results significantly. Those with lung fibrosis (asbestosis) were
        identified as having a 1.9 fold risk of lung cancer in comparison with
        those without such changes, whereas the risk of lung cancer among those
        with pleural plaques was only slightly increased. These authors
        determined the incidence rate ratios or relative risks (RR) of lung cancer
        using a log-linear model (Exhibit 214, p 1192), but the grouping of
        subjects according to cumulative exposure was not by any process of
        individual quantitative analysis or clinical measurement but, rather,
        simply by occupational activity multiplied by an exposure weighting
        factor (Exhibit 214, p 1192, Table 1). It was pointed out that it was
        difficult for construction workers themselves to know and recognise all
        their past exposures and even for an experienced industrial hygienist to
        assess exactly the cumulative exposure of a construction worker. It was
        for this reason that general occupational activity risk factors were utilised
        for the groupings.

433          While this study reveals that workers with occupational exposure to
        asbestos had only a relatively low increased risk of contracting lung
        cancer, standardised incident ratio (SIR) of 1.1, for a group of workers
        including smokers, it is nonetheless evident that a correlation between a
        higher incidence of lung cancer, for such workers, does exist. The fact
        that the authors deliberately rejected attempts at calculating individual
        past cumulative exposure levels or elevated risks because of
        shortcomings, difficulties and inaccuracies in such estimates, even for
        industrial hygienists, is notable.
434           A study by Simonato and others: "Lung Cancer in Cigarette
        Smoking in Europe, an Update on Risk Estimates and an Assessment of
        Inter-country Heterogeneity" (2001) - Exhibit 215, describes a large
        multicentric study of lung cancer conducted in several geographical areas
        of Europe in relation to the connection between smoking and lung cancer.
        The study found a higher than expected proportion of all lung cancers as
        being attributable to smoking, but recognised that other risk factors in the
        various occupational settings could have contributed to the variability of
        the results. Among a large number of known occupational carcinogens
        which increased the risk of developing lung cancer was asbestos.
        Otherwise, however, this study does not appear to contribute to a
        resolution of the principal issues in this case or of the suitability of the
        epidemiological or statistical methods for determining cumulative
        exposure levels.




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435           Exhibit 282 is an extract from the publication "Asbestos Related
        Malignancy" edited by Antman and others, published in 1986. It
        comprises ch 3 by J C McDonald and A D McDonald entitled
        "Epidemiology of Asbestos Related Lung Cancer" and was tendered by
        the third defendant. It deals with all forms of asbestos related cancer,
        including mesothelioma, and, therefore, must be examined carefully in the
        present case to identify those features of the lung cancer, as presented in
        Mr Cotton's case, that is, no mesothelioma. The opinions contained in
        this publication are relied upon heavily by the third defendant and, for that
        reason and because of their overall importance, are discussed fully
        elsewhere in these reasons for decision. In this setting it is sufficient to
        note that the general conclusion is that, on the present state of scientific
        knowledge, it is likely to be a long time before attributability to asbestos
        exposure in a given case of lung cancer could ever be made.

436           A number of important propositions emerge from the McDonald text.
        First, it is clear that there were strong grounds for suspecting that
        asbestos-caused lung cancer before the first major epidemiological studies
        were published in 1955 (see the article by Knox, Doll and Hill -
        Exhibit 301). Second, from 1964 on, the association between asbestos
        exposure and lung cancer was no longer in doubt and, by the end of the
        1970's, even the most stringent requirements for evidence on cause and
        effect had been satisfied. Despite this progress and certainty at the macro
        or public health level there remained, at the time of writing, basic
        questions which could not be answered with certainty because:

              •       Cases of lung cancer attributable wholly or in part to
                      asbestos cannot be distinguished clinically or
                      pathologically from those that are not. Attribution can
                      only be assessed in terms of probability from their
                      epidemiologic characteristics.

              •       Three important epidemiologic facets of the disease -
                      exposure response, fibre type, and industrial process -
                      form an interrelated web that has yet to be wholly
                      disentangled.

              •       The quantitative and qualitative definitions of exposure
                      during the relevant time, ie 20 to 50 or so years earlier,
                      can only be guessed; fibres present in the lung at autopsy
                      or biopsy may or may not reflect past patterns of
                      exposure in fibre type distribution or physical character.



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              •       Cigarette smoking is a powerful co-factor, and
                      unidentified carcinogens could well be, but reliable
                      quantitative and qualitative information on these and
                      asbestos exposure at the same time is almost impossible
                      to obtain.

              •       The statistical interpretation of cohort studies depends
                      always on the bases of comparison - the reference
                      populations. The degree of comparability is always
                      uncertain and can lead to substantial over-or-under
                      estimation of excess mortality in any given situation.
        The authors of the McDonald article observed (Exhibit 282, p 63) that in
        one of the cohort studies it was found that the standardised mortality rate
        for exposed workers was also inflated by an unexplained excess of lung
        cancer in men with very short low exposures. But no explanation for this
        was given or offered.
437          In their work the McDonalds (Exhibit 282, p 65 and following)
        identify and review a series of studies of the risk of lung cancer in relation
        to measured exposure to asbestos. They observed that in all of those
        studies length of exposure was established fairly accurately but
        environmental dust concentrations, particularly at times in the past, which
        mattered most, were often little more than informed guesses and that their
        conversion to an equivalent in fibre concentrations introduced a serious
        uncertainty. I have considerable sympathy with these researchers and
        commentators because it is only too evident that these problems have
        beset the attempts to estimate the concentrations of dust exposure in these
        two workplaces of Mr Cotton and the consequent attempts at estimating
        his cumulative dose or load of asbestos in fibre ml years.

438           The McDonalds also showed that there were equivocal results from
        the epidemiological studies about the effect of the combination of
        smoking and asbestos exposure, but explained that this is likely to be due
        to the selection of the groups studied which, because they were largely
        male industrial workers, included very high proportions of smokers so
        rendering difficult adequate statistical analysis of the effect of such
        exposure upon non-smokers. After reviewing the literature the authors
        agreed with the conclusion of Berry et al (Lancet (1972) - footnote 7 to
        Exhibit 282) that the simple multiplicative hypothesis of the effect of
        relative risks due to each of those carcinogens should not be rejected. It is
        apparent from Exhibit 144 (p 7, par 23) that the co-author of the Lancet
        article is the same person as Professor Berry who gave evidence in the
        course of this trial and whose testimony I have already discussed.

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439           These authors observed that since there is no clinical or pathologic
        method by which asbestos-related cancers can be distinguished from the
        rest, some epidemiologic ingenuity is required to arrive at any estimate.
        Studies conducted in the United States up to 1985 implied that about
        7 per cent of lung cancer deaths in American men in 1985 will probably
        have resulted from occupational asbestos exposure and that subsequent
        detailed predictions of future mortality rates may tend to be too low when
        it comes to asbestos-induced lung cancer. These authors then say
        (Exhibit 282, p 74):

              "In none of the 22 exposure-response data sets represented in
              Figure 3-1 is a straight line the only or necessarily the best
              relationship, and in none does the arbitrary line of best fit pass
              through the origin. Epidemiology being an imprecise science,
              this is no surprise; indeed it is remarkable that the lines fit and
              converge as well as they do. To get over this problem it has
              become customary to present the relationships in terms of
              relative risk ... The investigators who have carried out these
              studies, however, are well aware of their limitations and have
              serious reservations about the use of their data to predict risk
              under circumstances that depart very far from those they
              studied. A few of the more important reasons for this are as
              follows:

                   1.        Duration and intensity of exposure are dealt with as
                             if they were interchangeable, which can only be
                             approximately true even when applied within quite
                             narrow limits.
                   2.        The straight lines are largely attributable to duration
                             of employment rather than intensity of exposure, yet
                             it is in relation to the latter that we want to
                             generalise.
                   3.        In all 11 studies, the exposure estimates were subject
                             to considerable error, the effect of which would be
                             to smooth curves and obscure thresholds ... "

440          The McDonalds then go on to warn of the dangers of extrapolating
        beyond this data in order to quantify exposure levels, at low doses of
        exposure. They conclude by emphasising the prominence of the role of
        tobacco in lung cancer, both in relation to its individual effect and its
        effect combined with another carcinogen, but also in relation to the


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        history and methodology of the epidemiology that first led to the
        recognition of the carcinogenic effect of industrial asbestos exposure.
441           In an article published in 1998 by Stayner and others (Exhibit 302)
        the authors evaluated various models to estimate the risk of mortality from
        lung cancer and asbestosis after exposure to Chrysotile. They discovered
        that the exposure response relationship for lung cancer seemed to be linear
        on a multiplicative scale and that this was consistent with previous
        analyses for lung cancer and exposure to asbestos. They found no
        significant evidence for a threshold in models of either the lung cancer or
        asbestosis and they concluded that the risk estimates for lung cancer
        derived from their analysis were higher than those derived from other
        populations.
442           The United Kingdom Advisory Committee on Asbestos reported in
        1979 and part of that report is Exhibit 303 tendered by the third defendant.
        As set out in par 86 of that report, it was said that the available
        measurements of dose and response were subject to considerable error and
        uncertainty and that one of the most important sources of uncertainty was
        the problem of dust estimation. The introduction of the membrane filter
        sampling method in 1970 and after led to the detection of much higher
        concentrations of dust particles, so that reported dust concentrations
        before 1970 might be only a half or a quarter of that detected by the
        modern methodology - a factor which needs to be accommodated when
        interpreting earlier studies. At par 96 the authors' report concluded that
        for lung cancer the available data in man, all of which are derived from an
        industry, show an increase in risk with increasing dose of dust and the
        authors found that no evidence within the range of dust levels studied for
        a threshold of dose below which there is no evidence of risk. Different
        relationships were evident for exposure to Chrysotile as opposed to
        Amosite, but no information was available about dose response
        relationship to workers exposed exclusively or predominantly to
        Crocidolite. This study concluded that exposure to asbestos dust probably
        increases the risk of lung cancer in man irrespective of smoking but much
        more in the presence of smoking than in its absence. The two factors
        (tobacco and asbestos) act synergistically but the exact relationship is
        uncertain and may be less than multiplicative.

443           This is further confirmation of the uncertainty of the strictly
        quantitative methods in analysis and their reliability, but it does show an
        accepted synergy between the effects of tobacco and asbestos exposure in
        combination. It provides little encouragement for the defendants' position
        that, in a significant number of lung cancer cases where the patient was


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        subject to such a dual exposure, the asbestos exposure had no or no
        material effect in the development or progress of the disease.
444          In a further publication: "Asbestos: The Control Limit for
        Asbestos", Exhibit 304, produced by Mr Rogers, the authors essentially
        confirmed the findings and conclusions of the British Advisory
        Committee (just described) and observed that the quantitative data from
        which a dose-response relationship for asbestos exposure resulting in lung
        cancer relate only to Chrysotile and that for Amocite and Crocidolite no
        quantitative data from which the shape of the dose-response relationship
        could be deduced were available (Exhibit 304, p 9, par 57). At par 65 of
        the same exhibit the authors report that their review of many studies
        discloses that linear dose relationships provide a satisfactory description
        of the association between mortality from lung cancer and cumulative
        dose of asbestos, and that the concept of a linear relationship now seems
        to be generally accepted but not without reservations (see, for example,
        Peto; Selikoff and McDonald). With regard to the combined effect of
        cigarette smoking and asbestos, the authors say (par 81) that the latest
        evidence on this synergism suggests that a relationship may be
        intermediate between additive and multiplicative (citing Berry, 1980, and
        Selikoff and others), leading to an expression of caution about the use of
        many of the published dose-response curves because so few of the studies
        accommodated smoking habits. The graphs at p 22 of that exhibit show
        markedly different cumulative dose/mortality relationships, depending
        upon whether the exposure was to Amosite or Chrysotile.

445          Exhibit 304 includes a supplementary publication by Doll and Peto:
        "Asbestos - Effects on Health of Exposure to Asbestos" (1985). On the
        nature of the relationship for the interaction of cigarette smoking and
        asbestos exposure, those authors conclude (at p 36) that the effect is in
        fact close to being exactly multiplicative. But this study again stressed
        problems associated with the reliability of the data and the deduction and
        comparison of cumulative dose estimates and, furthermore, it appears to
        have been predominantly concerned with exposure to Chrysotile alone.
446          Exhibit 306, the Parliamentary Report of the Inquiry Into Asbestos
        Issues as Wittenoom (1992), and Exhibit 307, a letter from Mr A Rogers
        to the Journal published by the British Occupational Hygiene Society in
        2001, need only be noted briefly as the first deals mainly, the second
        entirely, with mesothelioma and the Wittenoom Cohort. The features
        worthy of note from these writings are the problems experienced in
        obtaining accurate data about asbestos air fibre concentrations and in
        calculating cumulative dose, whether at any particular time or as part of a


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        Public Health survey to allow safer occupational health precautions to be
        prescribed. A theme emerging from the Parliamentary Report was that
        the many attempts at detailed air sampling studies conducted at
        Wittenoom by various authorities over the years have given little useful
        information about asbestos dust air concentrations due, presumably, to the
        variability and transience of exposures due to location, weather,
        concentration of asbestos waste and many other factors. The conclusion
        of the Parliamentary Committee was that, despite many submissions
        urging it to recommend threshold or acceptable standards for air particle
        concentration, this could not be done and should not be attempted.
447           Exhibit 301 is an extract from publications by the Finnish Institute of
        Occupational Health at an international expert meeting dealing with
        asbestos, asbestosis and cancer and contains extracts from a work of
        Dr Paul de Vuyst of the University of Brussels entitled "Guidelines for the
        Attribution of Lung Cancer to asbestos". At page 93 of that exhibit,
        dealing with attributions for lung cancer, the author describes the
        European trend to attribute asbestos as a cause of lung cancer in the
        absence of radiological signs of fibrosis. In other words, he describes the
        departure from the earlier view (still presently espoused by Professor Fox
        in this case) that asbestosis is an essential diagnostic sign before an
        attribution of cause can be made to asbestos for an accompanying lung
        cancer. In describing that European trend, Dr de Vuyst draws attention to
        the fact that the epidemiological studies showing an increased risk for
        lung cancer in such cases show an RR lower than 2, that is that the
        attribution has been made notwithstanding that the studies do not show a
        doubling of the expected cases.
448          In the survey of the literature which has been tendered in this case I
        have largely, but not entirely, excluded from express mention publications
        dealing solely, or principally, with the incidence of mesothelioma, the
        results of the Australian Mesothelioma Surveillance Programme and
        epidemiological studies dealing with mesothelioma and associated risk
        levels. The reason for this is that Mr Cotton clearly did not have
        mesothelioma and that, unlike patients with lung cancer who have
        smoked, it seems to be generally recognised that the risk of developing
        mesothelioma is unrelated to smoking levels and that quite different levels
        of asbestos exposure and/or cumulative dose apply in the case of
        mesotheliomas. This is simply another way of saying that a diagnosis of
        mesothelioma is, in itself, indicative of asbestos being the cause.




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The Helsinki Protocol and the AWARD Criteria
449           Frequent reference was made during the course of the evidence to the
        supposed consensus, among asbestos disease and cancer experts and
        epidemiologists, that a minimum cumulative exposure of 25 fb/ml years
        was necessary before it could be postulated that a lung cancer in any
        particular patient was more probably due to his or her history of asbestos
        exposure, than to other general or background factors. This "doubling of
        the risk" was said to be regarded by epidemiologists as essential before an
        attribution could be made in any particular case that a lung cancer was due
        to asbestos exposure. It is of significant importance, therefore, to examine
        the so-called Helsinki Protocol and the AWARD Criteria in order to
        evaluate their significance and then to turn to the manner in which those
        reports have been dealt with by the qualified experts who gave evidence at
        this trial.

450           The Helsinki Criteria (Exhibits 55, 188 and 309) emerged from the
        International Expert Meeting on Asbestos, Asbestosis and Cancer held in
        Helsinki in January 1997. It is to be noted that a large quantity of
        significant research and analysis of asbestos-related diseases has
        originated in Finland because of a high prevalence of such disorders in
        that country deriving from industrial work with asbestos there over many
        years. The meeting was attended by 19 participants from eight countries
        which did not produce asbestos. The two Chairmen were Professor
        D W Hendersen of Flinders Medical Centre in Australia and Professor
        Jorma Rantanen of the Finnish Institute of Occupational Health. The
        group was a multi-disciplinary gathering of pathologists, radiologists,
        occupational and pulmonary physicians, epidemiologists, toxicologists,
        industrial hygienists and clinical laboratory scientists specialising in tissue
        fibre analysis.
451           It is significant to note other evidence at this trial which explained
        that in a number of continental European countries there are public health
        or welfare systems which purport to classify and compensate asbestos
        disease victims by a number of processes which seek, as objectively as
        possible, to assess the significance of past asbestos exposure. Many of
        these systems adopt, or refer to, various quantitative methods in order to
        allow their various national systems to be applied to the large number of
        cases requiring attention. Such systems exist in Germany and Holland,
        among other places (see Exhibit 217, p 449). In the Helsinki Consensus
        Report the meeting concluded that a cumulative fibre dose as expressed in
        fibre years per cubic centimetre (millilitre) is an important parameter of
        asbestos exposure. The Helsinki document then addressed various forms


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        of asbestos disease, in particular, asbestosis; pleural disorders;
        mesothelioma and lung cancer. With reference to mesothelioma, it
        concluded that smoking has no influence on the risk of developing that
        disease (Exhibit 309, p 313).
452           With regard to lung cancer, the Helsinki Protocol noted that all four
        major histological types of cancer (squamous, adeno -, large - , cell and
        small - cell carcinoma) can be related to asbestos. Also, that the
        histological type of lung cancer and its anatomic location (central or
        peripheral, upper lobe versus lower lobe) are of no significant value in
        deciding whether or not an individual lung cancer is attributable to
        asbestos. The report records that, as examples, "one year of heavy
        exposure (eg manufacture of asbestos products, asbestos spraying,
        insulation work with asbestos materials, demolition of old buildings) or
        5 - 10 years of moderate exposure (eg construction, shipbuilding) may
        increase the lung cancer risk 2-fold or more and that in some
        circumstances of extremely high asbestos exposure the 2-fold risk of lung
        cancer can be achieved with exposure of less than one year".
453           Importantly, in the present case, the authors of the Helsinki Protocol
        turned to a quantitative analysis of the conditions appropriate for an
        attribution to asbestos being the cause of a lung cancer, saying:

              "The relative risk of lung cancer is estimated to increase
              0.5 - 4% for each fibre per cubic centimetre per year
              (fibre-years) of cumulative exposure. With the use of the upper
              boundary of this range, a cumulative exposure of 25 fibre-years
              is estimated to increase the risk of cancer 2-fold. Clinical cases
              of asbestosis may occur at comparable cumulative exposures.
              A 2-fold risk of lung cancer is related to retained fibre levels of
              2,000,000 Amphibole fibres (greater than 5<µm) per gram of
              dry lung tissue or 5,000,000 Amphibole fibres (greater than
              1<µm) per gram of dry lung tissue.               This lung fibre
              concentration is approximately equal to 5,000 to 15,000
              asbestos bodies per gram of dry tissue, or 5 to 15 asbestos
              bodies per millilitre of bronchoalveolar lavage fluid. When
              asbestos body concentrations are less than 10,000 asbestos
              bodies per gram of dry tissue, electron microscopic fibre
              analyses are recommended."




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        Then, after discussing the less toxic effects of Chrysotile fibres, and the
        corresponding need for higher concentrations of that form of asbestos
        exposure, the authors said:
              "The likelihood that asbestos exposure has made a substantial
              contribution increases when the exposure increases.
              Cumulative exposure, on a probability basis, should thus be
              considered the main criterion for the attribution of a substantial
              contribution by asbestos to lung cancer risk. For example,
              relative risk is roughly doubled for cohorts exposed to asbestos
              fibres at a cumulative exposure of 25 fibre-years or with an
              equivalent occupational history, at which level asbestosis may
              or may not be present or detectable. Heavy exposure, in the
              absence of radiologically diagnosed asbestosis, is sufficient to
              increase the risk of lung cancer. Cumulative exposures below
              25 fibre-years are also associated with an increased risk of lung
              cancer, but to a less extent."

        And then, further, the paper states:
              "A minimum lag time of 10 years from the first asbestos
              exposure is required to attribute the lung cancer to asbestos.
              Not all exposure criteria need to be fulfilled for the purposes of
              attribution. For example, the following can be considered:
              (i)     significant occupational exposure history with low fibre
                      burdens (eg, long exposure to chrysotile and long lag time
                      between the end of exposure and mineralogical analysis);
                      and
              (ii)    high fibre counts in lung or broncho lavage fluid with an
                      uncertain history or without long-term duration (short
                      exposures can be very intense).
              At very low levels of asbestos exposure the risk of lung cancer
              appears to be undetectably low.
              Although tobacco smoking affects the total lung cancer risk,
              this effect does not detract from the risk of lung cancer
              attributable to asbestos exposure. No attempt has been made in
              this report to apportion the relative contributions of asbestos
              exposure and tobacco smoking."




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454          On the basis of the Helsinki Protocol, the defendants each submitted
        that an attribution to asbestos exposure should not be made as materially
        contributing to Mr Cotton's lung cancer unless his total cumulative
        exposure could be established to be 25 fb/ml years or more and that there
        has been a lag time of 10 or more years since his first exposure. They
        further submit that these criteria need to be satisfied regardless of whether
        or not his smoking habit is regarded as a major or contributing cause of
        his disease.
455           Some of the defendants' submissions, certainly those which contend
        that the presence of asbestosis is an essential component of the diagnostic
        tests that a lung cancer is due to asbestos exposure, equate, or at least
        approximate, the cumulative asbestos exposure dose of the patient
        recognised as sufficient to cause asbestosis with that required for lung
        cancer, although the Helsinki Protocol does not specifically state that.
        Indeed, that consensus statement observes that asbestosis is generally
        associated with relatively high exposure levels, subject to the qualification
        that low levels of cumulative exposure may produce interstitial fibrosis at
        a level not detectable by many of the radiographic or tomographic
        techniques employed.
456          Generally speaking, the defendants' submissions ignore the
        acknowledgement in the Helsinki Protocols themselves that cumulative
        exposures below 25 fibre years are also associated with an increased risk
        of lung cancer and that not all the exposure criteria need to be fulfilled for
        the purposes of attribution. When it is recognised that the Helsinki
        Protocols were an attempt to meet diagnostic criteria at an
        epidemiological, that is macro, level and that they specifically
        acknowledged that in certain cases of low exposure enhanced risk to lung
        cancer did occur, one should be disinclined to conclude that, if an
        individual case failed to meet the express quantitative tests formulated by
        that document, any prospect of a causal link between the asbestos
        exposure and the lung carcinoma is negatived. I am satisfied that this is
        not the express or implied meaning of this important statement.
Adelaide Workshop on Asbestos-Related Diseases (AWARD Criteria)
457          This document (Exhibit 217 and also Exhibit 288) is the Australian
        sequel to the Helsinki Protocol. It has been published in the Journal of
        Occupational Health and Safety for Australia and New Zealand (2002),
        vol 18, at 443 - 452, and is the product of a meeting of a group of 15
        participants (comprising epidemiologists, industrial hygienists,
        oncologists, pathologists, physicians, radiologists and scientists who are


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        currently active in this field) who met in Adelaide in October 2000. The
        purpose of the meeting was to analyse current thinking, identify issues
        and seek agreement for a document relating to Australian circumstances
        based on the prevailing scientific evidence on asbestos-related diseases in
        Australia. In the introduction to the document the authors remarked that
        attribution of lung cancer to asbestos exposure (with the associated legal
        claims for compensation) was also an area of increasing concern as are
        compensation payments for asbestos-related lung cancer and that the
        definitions of criteria for the assessment of asbestos-related diseases had
        been the subject of some controversy. The authors also wrote:
              "That the risk of lung cancer associated with exposure to
              asbestos is limited to asbestosis has been contentious - due, in
              part, to the imprecision of the various diagnostic modalities
              (whether clinical, radiological or pathological)."

458          This paper then addressed eight specific pathologies associated with
        asbestos exposure, including asbestosis, malignant mesothelioma and lung
        cancer. Importantly, in relation to the latter disease, the authors wrote
        (Exhibit 217, at 446):

              "The majority of evidence and the prevailing expert view is that
              attribution of lung cancer to asbestos does not require the
              presence of asbestosis; instead, the evidence indicates that it is
              the cumulative dose of inhaled asbestos that is the main
              determining factor for attribution of lung cancer to asbestos by
              way of a significant contribution (usually in combination with
              tobacco smoke)."
459          Then, turning to the criteria for lung cancer attribution at 448, the
        authors wrote:

              "A cumulative exposure to asbestos of 25 fibres/ml - years is
              generally associated with approximately a doubling of the risk
              of lung cancer (in both smokers and non-smokers), although
              this cumulative exposure may produce greater or lesser relative
              risk depending on variations in industry and fibre types."
        And, later, at 449:
              "A cumulative exposure of 25 fibres/ml - years also delineates
              exposure of a character and magnitude sufficient to induce
              clinical/radiological asbestosis in some individuals so exposed."



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460           The AWARD statement concludes with an explanation that there is
        no accurate estimate of the extent of occupational cancers (except for
        mesotheliomas) in Australia and that the accumulation of further
        information on the asbestos fibre burden in the lung in different disease
        settings and exposure conditions will be especially important for applying
        the Helsinki Protocols to Australian conditions with greater accuracy.
461           Clearly, therefore, it emerges from the AWARD Criteria that the
        25 fibre/ml - year cumulative exposure is a relatively high level of
        exposure and comparable with the extent of exposure expected to produce
        detectible signs of asbestosis. It would seem to follow, therefore, that
        despite the universally conceded proposition that there is no minimum
        exposure threshold for asbestos which can be considered safe, or free
        from risk of the development of mesothelioma or lung cancer, the
        25 fibre/ml - year test for attribution is a species of threshold for the
        attribution of the cause of lung cancer and, despite its utility, does not
        recognise the accepted potential for lower doses of cumulative exposure
        to cause the disease. It is not surprising, therefore, that the eminent
        specialists who gave evidence in the course of this trial displayed varying
        attitudes of acceptance or reliance to the Helsinki Protocols, insofar as the
        latter was suggested to be an unambiguous hallmark which must be
        satisfied for the attribution of a particular lung cancer to asbestos
        exposure.

462           Professor Musk agreed that the Helsinki Protocol was a product of
        the opinion of those attending the conference of the point at which the risk
        of asbestos exposure causing lung cancer approximately doubled the
        background risk. He did not attribute this conclusion, or the purpose of
        the Helsinki Conference, only to the designation of compensation criteria
        but, rather, accepted it as an attempt to formulate an international
        consensus about the point at which an attribution could be made in the
        absence of other clearly diagnostic signs.               In response to
        cross-examination by counsel for the second defendant, he accepted that
        the 25 fb/ml year figure was based on acceptance of a 4 per cent relative
        increase in lung cancer for each fb/ml year of cumulative exposure, that
        is, at the top end of the 0.5 - 4 per cent range and, accordingly, that the
        assumed level of exposure was likely to be too high, and hence the
        adopted cumulative exposure level in fb/ml years too low, for many cases.
        Nevertheless, he asserted, that 25 fb/ml years seems to be a reasonable
        figure which fitted most of the observations. He was not asked, and did
        not say, whether the cumulative exposure figure adopted should be
        regarded as smaller or greater for a patient with a history of chronic
        smoking.

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463          Professor Wan, when asked specifically whether the 25 fb/ml year
        figure for cumulative asbestos exposure should be regarded as greater or
        less for a lung patient victim who was a chronic smoker, said (t/s 552),
        that it would be many times less than the 25 years because of the
        synergistic affect that asbestos has with smoking, a point which he
        confirmed at t/s 554.         When challenged on this very point in
        cross-examination by the second defendant, Professor Wan pointed to the
        Helsinki document (Exhibit 310, p 314) which, as already noted, stated
        expressly that no attempt had been made to apportion the relative
        contributions of asbestos exposure and tobacco smoking, therefore
        revealing his reasoning to be that if 25 fb/ml years cumulative exposure
        was sufficient to justify the attribution of a cancer to asbestos exposure for
        a non-smoker, it must necessarily be the case that a lower degree of
        cumulative exposure would suffice for a chronic smoker whose habit has
        had a synergistic or potentiating effect on the asbestos carcinogen.
464          Doctor Leigh also discussed the Helsinki Protocol in detail. When
        speaking of the 25 fb/ml years cumulative exposure figure he said,
        apropos the Helsinki Protocol:

              "They are intended as guidelines for essentially statutory
              compensation schemes to give a socially equitable number of
              asbestos related lung cancers compensated in relation to
              mesotheliomas in the same populations. They started in
              Germany and then they adopted it in European countries. Their
              application to common law I don't think was actually envisaged
              by the writers of the Helsinki and AWARD Criteria. I think
              they were essentially geared to giving guidance to statutory
              compensation rather than dealing with causation in the
              individual common law situation."
465          On the applicability of the Helsinki/AWARD Criteria for smokers
        Dr Leigh said that the AWARD Criteria expressly mentioned smokers,
        indicating that the quantitative test for cumulative exposure was
        applicable to both smokers and non-smokers and he implied that the same
        approach was evident in the Helsinki Criteria - however, in the light of the
        express terms of the Helsinki Criteria, as noted by Professor Wan, this is
        certainly open to doubt at the very least.            He was asked in
        cross-examination about the studies which suggested that the risk of
        contracting lung cancer through asbestos exposure was greater for
        non-smokers than for smokers and he acknowledged that this was the
        case, although pointed out that this was an oddity in the statistics and
        explained that, in absolute terms, the person who was exposed to asbestos


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        and was also a heavy smoker had a far higher absolute risk of developing
        a carcinoma of the lung. However, Dr Leigh went on to observe that,
        because of the interactive effects between smoking and asbestos exposure,
        some allowance should be made for the combination of the factors and
        that, in the case of a heavy smoker, you would need less asbestos acting
        with it to cause the cancer, and that this phenomenon is not reflected by
        the adoption of the 25 fb/ml year criteria of the Helsinki Criteria - t/s 629.

466           It is evident that Dr Leigh's explanation of this had already been set
        out in Exhibit 63, as follows:

              "Asbestos may cause chronic inflammatory changes which
              release cytokines including growth factors providing a selective
              advantage for cells which have undergone cancerous mutation
              into carcinogens in tobacco smoke or due to asbestos itself.
              Recent animal studies have directly shown interaction between
              known lung carcinogens and asbestos in causing lung cancer.
              While the precise mechanism of interaction between asbestos
              and tobacco smoke causing lung cancer is not known it is not
              possible, in my view, to separate their effects in the individual
              case when both have acted and it is thus more probable than not
              in this situation that the lung cancer was the singular result of
              the two factors acting together."
        From this I take Dr Leigh to mean that, if it were possible specifically to
        identify the cumulative dose of asbestos exposure, which would double
        the background risk of the development of lung cancer then, that figure
        would need to be adjusted further according to whether the exposed
        person was a smoker or a non-smoker. If he were a smoker then the total
        cumulative exposure of asbestos acting in combination with his smoking
        sufficient to double the background risk of developing lung cancer would
        be smaller.
467          However, there is no escape from the reality that there is no actual
        precision possible in any of these calculations or estimates and that the
        selection by the authors of the Helsinki Protocols that a fb/ml year of
        exposure may increase the risk of developing lung cancer over a range
        from anything between 0.05 per cent to 4 per cent, is itself a choice of a
        broad spectrum accommodating a multiplicity of cases so that,
        consequently, it is not possible to say whether or not it includes smokers
        although, quite possibly, it does. These questions which, no doubt were
        appealing to those analysts with enthusiasm for mathematical modelling,
        leading to quantitative analysis, did not seem to have great appeal to
        Dr Leigh or to the other expert witnesses such as Professor Musk,

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        Dr Kendall, Professor Wan and Professor de Klerk who, undoubtedly,
        were fully aware of the limitations of such attempts at precision.
468           On the use and application of the statistics adopted in the Helsinki
        Protocols, Professor Berry agreed that the risk co-efficient of 4 per cent
        per fb/ml year might be appropriate for pure amphibole exposure and said
        that the lower end of the range of 0.5 per cent corresponded to Chrysotile.
        In his view, a risk co-efficient for a mixture of amphibole and Chrysotile
        asbestos would be somewhere in between. He acknowledged that
        adopting, as the Helsinki Committee had adopted, a risk co-efficient of the
        upper edge of the range was not good statistical practice unless a reason
        existed for supposing that the situation corresponded to the level adopted.
        When asked whether the choice of a cumulative exposure figure for lung
        cancer (25 fb/ml years) was the same or approximate to other asbestos
        lung diseases, Professor Berry explained that the relative risk of lung
        cancer due to asbestos increases with the years of exposure.
        Mesothelioma, by constrast, is a particular case because of its rarity and
        because it is known to be induced by quite a low exposure when a
        definitive diagnosis is possible. Whereas, in cases of lung cancer, the
        condition is far more common and it is necessary to select a quantitative
        level at which the many cases of lung cancer, which have nothing to do
        with exposure to asbestos, can be excluded. With regard to the interaction
        of asbestos exposure and smoking in workers who had developed lung
        cancer, Professor Berry confirmed that a study which he had conducted
        had revealed that the relative risk for non-smokers developing lung cancer
        due to asbestos was different to the relative risk of smokers developing
        cancer but, nevertheless, in absolute terms smokers have a much higher
        risk.

469          Apart from explaining the history of various epidemiological studies
        which had produced various risk co-efficients for the development of lung
        cancer from asbestos exposure and which had preceded the Helsinki
        Protocols, Mrs Janet Sowden accepted that many of the controversies
        concerning the significance of the Helsinki Protocols for the present case
        were outside her field.

470           Consistently with his major premise that the presence of asbestosis is
        essential for a diagnosis which attributes any lung cancer to asbestos
        exposure, Professor Fox criticised the Helsinki Protocols which suggested
        that this was not necessary. In his view, the Helsinki Meeting was not
        representative of the body of scientists who had studied and written on
        this phenomenon, because adherents to the "asbestosis essential" school of
        thought had not been invited to the meeting. He made the point, however,


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        which has already been noted as an implication from the Helsinki
        Protocols, that the authors had suggested that for a cancer attribution to be
        made to asbestos exposure, the workers should have a history of
        inhalation of the quantity of asbestos fibre equivalent to that required to
        cause interstitial fibrosis.

471           Indeed, there appears to be no escape from the recognition that, in
        this respect, there is an apparent inconsistency in the Helsinki statement.
        Professor Fox was of the opinion that a 25 fb/ml year exposure to asbestos
        was insufficient to make an attribution to asbestos for a case of lung
        cancer. In his view there was a biological explanation that the cellular
        changes associated with pulmonary fibrosis, whether idiopathic or due to
        asbestosis, as triggering the cytokines and growth factors which may set
        off a secondary malignancy which, in turn, suggested that such a process
        required for its initiation the same or similar degree of influence upon the
        lung by the foreign body, before it would take effect. This, in turn, led
        him to the view that Mr Cotton would not have had a duration or intensity
        of exposure to asbestos which would have been equivalent to induce
        interstitial fibrosis - a variation on the "asbestosis is essential" thesis. It is
        obvious that Professor Fox accepts and regards as essential the factors
        which lead him to the conclusion that the existence of asbestosis, or
        cumulative exposure to asbestos equivalent to that regarded as sufficient
        to cause asbestosis. In his opinion these are essential factors for any
        diagnosis attributing a lung cancer to asbestos exposure, but, clearly, his is
        the minority opinion on this issue in this case and, I am satisfied, also in
        the contemporary literature. Most significantly, his view is not espoused
        by the authors of the Helsinki Statement or of the AWARD Criteria and,
        on the preponderance evidence in this case, I should reject that view in
        favour of "the prevailing expert view is that attribution of lung cancer to
        asbestos does not require the presence of asbestosis ... " (Exhibit 217,
        p 446).
472           Mr Rogers, the third defendant's Occupational Hygienist, was also
        asked about the Helsinki Protocol and criticised it for adopting the
        25 fb/ml years as the point at which a doubling of the background risk for
        lung cancer occurred as a result of that degree of occupational asbestos
        exposure. He went so far as saying that "the [Helsinki] process was done
        very sloppily and very shoddily and that it took basic epidemiological
        concepts and trivialised them". His further criticism was that the Helsinki
        process adopted a hard and fast rule of attributing a lung cancer to
        asbestos exposure in cases of 25 fb/ml years or more. The point of his
        criticism was that there would be many cases, in which a doubling of the
        risk would not occur until a significantly higher cumulative exposure dose

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        had been reached, as he made no concessions to the possibility of a risk
        doubling at a lower level. For reasons earlier stated, my impression was
        that, extremely learned and proficient though he was in his awareness and
        application of the epidemiological studies relating to asbestos exposure,
        Mr Rogers was most inclined to adopt models of mathematical precision
        without regard to the limitations of the source data and to extrapolate from
        them to a wider degree than is convincing, or even plausible.

473           The most detailed account of Mr Rogers' evaluation and criticism of
        the Helsinki Protocols is contained in the report which he himself
        conducted for the Dust Diseases Board of New South Wales in November
        2001 (Exhibit 208). As set out in the Executive Summary to that report,
        Mr Rogers advances a major criticism of the Helsinki Protocols as being
        that many of the conclusions contained in the criteria were not adequately
        supported by references found in the associated technical papers presented
        at the meeting and were not reflective of previously reported international
        research outcomes. He propounds a value of 100 - 200 fb/ml years
        presented by other UK asbestos textiles industry research as a more
        applicable value and also criticises the selection of the 90th percentile
        exposure data as giving a distorted value two to three times higher than
        the average exposure values used in published epidemiological studies.
        He argues that in cases with low asbestos exposure the contribution of
        tobacco smoking to lung cancer is a very high proportion of the risk and
        as such its effect needs to be added to the attribution equation. At p 67 he
        asserts that research conducted in New South Wales means that risks
        prediction using the odds ratio method reporting in the Helsinki Protocols
        are not applicable to the Australian population. The burden of his report
        culminates in Mr Rogers' recommendations that the Dust Diseases
        Tribunal of New South Wales should establish its own criteria of
        cumulative asbestos dust exposure for attribution to lung cancer and other
        cases in Australia and that the criteria so to be set should be much higher
        than adopted by the Helsinki Protocols (and it would follow by the
        AWARD Criteria).
474          One cannot but be impressed by the extent of the examination of the
        international literature and by the elaborate statistical methodology used
        in the attempt to deduce symmetries and patterns from the data but, as I
        have already indicated, this approach reveals an optimistic confidence in:
        the reliability of the data; the sampling systems on which it depends; and
        the comparability of the data in various published reports - all of which
        are subject to express reservations in the literature which has been
        examined so far in this case. Mr Rogers' qualifications are extensive
        (Exhibit 243), but they are in the fields of chemistry, occupational hygiene

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        and environmental chemistry rather than in fields of medicine, physiology
        or in the specialties of respiratory disease and carcinoma in which the
        consultant physicians such as Professor Musk and Dr Kendall are highly
        qualified. This may well account for Mr Rogers' confidence in the
        statistical process but it is a confidence which is not shared by those who
        have the responsibility for the clinical management and treatment of
        patients, nor of those epidemiologists with higher medical qualifications
        who have written on these topics in the scientific literature and the
        epidemiologists who have given evidence in these proceedings.

475           The real flaw, as it appears to me with respect, in these highly
        developed statistical models for attribution is that the underlying
        pathogenesis of asbestos-induced lung cancer is not understood and,
        therefore, there must be uncertainty whether the assumptions, both
        express and tacit, in the mathematical modelling really reflect the
        variables and dynamics of the onset and development of the disease. I am
        satisfied that the physicians and doctors with specialist medical
        qualifications, together with the general body of scientific writing, adopt,
        with justification, a far greater reserve about close reliance on these forms
        of mathematical modelling.
476          Nevertheless, Mr Rogers' criticism of the arbitrariness of the
        25 fb/ml years of cumulative exposure to asbestos adopted by the Helsinki
        Protocols may be well justified although, if it is arbitrary, any ensuing
        error is capable of taking effect in the opposite direction as well -
        notwithstanding the selection of the 4 per cent incremental risk for
        cumulative fb/ml years having been taken from the top of the range of the
        epidemiological studies.
477           I am satisfied that the Helsinki Protocols, and for that matter the
        AWARD Criteria, represent a considered and careful estimate from
        experts in the field about criteria which may be adopted, at an
        epidemiological level, for the attribution of lung cancers to asbestos
        exposure. However, I cannot accept, that they were ever intended to
        mean, that the criteria would be determinative in every individual case or,
        for that matter, that in an individual case a reliable history could be
        assembled to reveal whether an individual with lung cancer had, or had
        not, experienced a cumulative exposure to asbestos of 25 fb/ml years. No
        reading of the scientific literature produced in this case, nor consideration
        of the expert testimony, could possibly justify a conclusion that 25 fb/ml
        years of exposure is a thin bright line which distinguishes between those
        lung cancers which are due to occupational exposure and those which are
        not. The conclusions are no doubt very important and significant for


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        epidemiological and public health reasons and may be as reliable a guide
        as present scientific knowledge can deliver, when dealing with large
        groups. But, in the individual case the limitations are only too apparent.

478          The literature recognises, and I am persuaded, that there are certainly
        cases of asbestos-induced lung cancer occurring with lower cumulative
        doses than espoused by the defendants in this case and with other
        unrepresentative features. This much is expressly acknowledged by the
        Helsinki Protocols paper itself. Whether or not Mr Cotton's case is one of
        those cannot be answered by concluding that a confident attribution of
        cause cannot be laid at the door of asbestos without higher levels of
        cumulative exposure.

Other literature
479          A further example of the reserve which needs to be exercised before
        developing any one general or mathematical model for the interaction
        between asbestos exposure and the development of cancer is provided by
        Exhibit 141, an article produced by Professor Musk by Hauptmann and
        others:      "The Exposure - Time - Response Relationship Between
        Occupational Asbestos Exposure and Lung Cancer in Two German
        Case-control Studies". This was published in the American Journal of
        Industrial Medicine in 2002 and it makes the point that the effects of
        timing of exposure to asbestos and the development of lung cancer have
        not been analysed thoroughly in many of the numerous studies which had
        been performed to evaluate the association. Using a system designed to
        take into effect not only the duration of exposure to asbestos but,
        variability of the exposure level and the effects of cessation of exposure,
        the authors reported (at p 93):
              " ... An individual's lung cancer risk following an exposure to
              asbestos increases for 5 - 15 years after exposure, then declines,
              with exposures experienced 12 years before the index date
              having the greatest effect on risk."
        And then (at p 96):
              "There was a 2.4-fold increase of risk for subjects having
              worked for eight or more years in a job with potential asbestos
              exposure compared to never-exposed ...
              ...

              Under the model, there is a shorter latency period than
              previously assumed, especially for high intensity of exposure."

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        The ultimate conclusion of this analysis was that, in contrast to previous
        indications, the risk of lung cancer increases soon after asbestos exposure
        with its maximum effect from 10 to 15 years after the exposure was
        experienced.
480           Exhibit 158 contains a selection of papers given at a seminar in Perth
        in 1988 dealing with occupational cancer. At p 53, and following, is a
        paper by Dr E M Rathus: "The Terrifying Triad - Tobacco, Toil and
        Tumours", which reviews the association between asbestos exposure and
        lung cancer. At p 57, the author observed that the ratio of deaths for
        persons who were asbestos workers and who smoked was anything
        between 5 to 12 times greater than cancer deaths without that exposure.
        This led to the observation that smoking asbestos workers are 5 to 12
        times more likely to develop lung cancer than asbestos workers who do
        not smoke and that asbestos workers who smoke are 92 times more likely
        to die of lung cancer than men who neither smoke nor work with asbestos.
Knowledge of the hazards of asbestos - scientific literature relied upon by
            Dr James Leigh
481           In addition to the oral evidence which he gave at trial and set out in
        his report (Exhibit 64), Dr James Leigh produced a series of articles which
        were referred to in his report (Exhibit 64) bearing on the available
        scientific information from time to time which addressed the health
        hazards of asbestos, including, in particular, the occupational hazards of
        exposure to asbestos in industry. There are 45 such articles in all,
        comprising Exhibit 64(1) - (45) which are numbered sequentially in the
        index to those two volumes of materials which were received into
        evidence. It is unnecessary for me to deal with each of these articles in
        turn and some general observations will be made instead.

482          The publications date from 1900 to 1968 and all substantially
        precede the periods when Mr Cotton was working for either of the first or
        third defendants in this action. They include publications in the United
        Kingdom, the United States, Australia and elsewhere and constitute a
        clear demonstration that the hazards of working with asbestos were
        well-known to the scientific community, and to various national, state and
        occupational authorities concerned with the safety and wellbeing of
        employees.

483          Fibrosis of the lungs caused by exposure to asbestos dust was a
        recognised occupational hazard, at the latest, by 1907. Pulmonary
        asbestosis was discussed widely from 1927 onwards and was the subject
        of a report to the Legislative Assembly of New South Wales by the


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        Director of Public Health of that State in 1927. The risk of asbestos lung
        disease from working in industry involving cutting and abrasion of
        asbestos sheets and similar products was the subject of a report by His
        Majesty's Stationery Office in London in 1930. The risk of pulmonary
        asbestos as a disabling condition and being capable of causing death was
        discussed widely in the literature during the 1920's and 1930's, and was
        the subject of a major study and report of the United States Treasury
        Department in 1938. In July 1953 there was an article published in the
        Lancet by Dr A I G McLaughlin MD FRACP, Her Majesty's Medical
        Inspector of Factories which associated industrial exposure to asbestos
        dust with lung cancer. Writing in 1955 in the AMA Archives of Industrial
        Health, the same Dr McLaughlin referred to cases of asbestosis appearing
        in workers who do asbestos lagging of pipes and boilers.
484          A pulmonary carcinoma in a man with asbestos lung fibrosis was the
        subject of an article by Dr K M Lynch in the American Journal of Cancer,
        vol 24, published in 1935. The connection between asbestos exposure and
        pulmonary carcinoma was also advanced by Dr W C Hueper in 1942 in an
        American publication "Occupational Tumours and Allied Diseases".
        Association between industrial exposure to asbestos and pulmonary
        cancer was described by Dr G C Smith in the Medical Journal of Australia
        in November 1950.
485          A major article concluding that lung cancer is a specific industrial
        hazard of certain asbestos workers was published by Sir Richard Doll in
        the British Journal of Industrial Medicine in 1955. There are many
        subsequent references to this article and there appears to be every reason
        to observe that from then on the association between asbestos exposure
        and pulmonary cancer became established. Dr S R Gloyne, a London
        pathologist, was writing to similar effect in 1951 although the cancers he
        discussed were attributed to pneumoconiosis of all forms, including that
        induced by asbestos exposure. An association between asbestos exposure
        and lung cancer was the subject of a note in a German medical publication
        in 1943. The connection between asbestos exposure and diffuse pleural
        mesothelioma was reported in 1960 in an article by Dr J C Wagner and
        others published in the British Journal of Industrial Medicine and this
        evoked support by a letter to the British Medical Journal published in
        November 1962. A similar association between asbestos and malignant
        lung disease appeared in the British Medical Journal in July 1964.

486          In an important article by Dr I J Selikoff and others of New York:
        "Asbestos Exposure and Neoplasia", published in April 1964 an
        association between asbestos exposure and carcinoma of the lung was


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        clearly stated. The authors reported that industrial exposure to asbestos
        by insulation workers resulted in a marked increase in the incidence of
        cancer of the lung, approximately six to seven times the expected
        incidence. The group studied by Selikoff and others consisted of men
        with only intermittent exposure to materials containing limited amounts
        (often 2 per cent to 20 per cent) of asbestos under working conditions
        varying from very dusty, as in extracting old insulation in closed quarters,
        to those with little dust exposure, as in building construction in the open
        air. Incidentally, these authors also reported elevated death rates for other
        forms of cancer (the stomach, colon and/or rectum) for members of the
        exposed workforce. The Selikoff publication remarked that pulmonary
        carcinoma had been observed in the earlier studies of asbestosis and
        association between the two conditions was first suggested by Lynch and
        Smith in 1935 and they referred to striking data to this effect being
        presented by the Chief Inspector of Factories of Great Britain in 1955
        leading to the Doll Report, already mentioned, being published later that
        year.
487          Consequently, it can be seen that the risk of developing the incurable
        condition of lung cancer, inevitably, with fatal results, was known and
        recognised from the mid-1950's and concern for industrial safety and
        adequate preventative conditions then became obvious and continued to
        be a matter of major concern for public health authorities and industrial
        bodies. For a number of years after the middle 1950's there continued to
        be an association in the scientific literature between asbestos-induced lung
        cancer and asbestosis which, doubtless, accounts for the remaining
        controversy over whether or not a diagnosis of asbestos-induced lung
        cancer should be made in the absence of demonstrated asbestosis.
        However, as Professor Musk, Professor de Klerk and Professor Berry,
        among others, have said, the preponderant modern view is that
        asbestos-induced lung cancer may occur in the absence of asbestosis.
The scientific literature relied upon by Mr Kottek
488          The occupational hygienist, Mr Michael Kottek, who estimated the
        asbestos dust concentrations and cumulative exposure to which Mr Cotton
        was exposed, also produced a large volume of scientific literature upon
        which he had drawn for the opinions and conclusions which he expressed.
        This literature is all collected as Exhibit 72 and extends to two lever arch
        volumes containing 64 separate publications. These date from 1898 to
        2001 and, at the broad level, it can be said that they trace the early
        recognition of the incidence of disease and morbidity associated with
        occupational exposure to asbestos; the attempts to analyse and quantify


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        the effects of this risk; the types of pathologies which progressively came
        to be associated with such exposure; more recent controversies about
        asbestos dust exposure levels which are hazardous; and associations
        between asbestos exposure and smoking jointly. Again it is unnecessary
        to examine all of this literature closely but s  ome facets of it should be
        noted.
489           In the written substance of evidence which he tendered in this case
        (Exhibit 71), Mr Michael Kottek made reference to many articles in the
        published literature dealing with the hazards of asbestos exposure and, in
        footnotes to his written statement made specific reference to many of
        these. During the course of his oral evidence, counsel for the plaintiff
        tendered, through Mr Kottek, two volumes of written materials taken from
        the literature, Government reports and similar publications.            As
        mentioned, the articles comprise Exhibit 72(1) to (64). They cover the
        period from 1898 until 2001 with many of the articles being written or
        published from the late 1930's onwards. They include some of the
        literature which was also included in the exhibits produced and tendered
        by Dr Leigh (Exhibit 64, which I have already more extensively
        reviewed). Publications in this category include some of the seminal
        writings on this subject, including publications by Dr McLaughlin,
        Professor Sir Richard Doll, contributions from Dr J C McNulty of
        Western Australia, publications by Dr Selikoff and others and, of course,
        the Helsinki Protocol. I have had regard to all of these publications but I
        do not propose to examine them individually because of their extent, but I
        will make specific reference to certain of them. Before doing so, some
        general observations are necessary.
490           The scientific literature of the 20th century acknowledges that, for a
        long time in the past, there had been noticed a higher degree of illness and
        death associated with persons working with or in the vicinity of asbestos.
        Some countries in the world, notably Turkey, where there were large
        asbestos deposits in use over the centuries, displayed this pattern. The
        writings in the early part of the 20th century pointed out the risk of illness
        and incapacity through exposure to work in asbestos mines or workplaces
        with, what was then, a well recognised general occupational health
        problem of silicosis. Asbestos was included among the many other
        minerals which were known to cause occupational silicosis. As the
        literature progressed there became frequent references to asbestos
        becoming associated with pneumoniconiosis and, not surprisingly during
        the period when the disease was prevalent worldwide, with tuberculosis.




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491          The link between asbestos and a causal contribution to carcinoma of
        the lung began to receive attention in the 1930's and, as already noted,
        appears to have become well accepted after the Doll article of 1955
        (Exhibit 72(28)). The association between asbestos, and what was then
        known as silicosis or pneumoniconiosis, continued to be the subject of
        many writings as well as the link with lung cancer. Next came the
        recognition that asbestos was a potent cause of the pleural lung cancer
        specifically known as mesothelioma. Much writing continued about the
        association between asbestos and mesothelioma and associated subjects,
        but the link with lung cancer and its effect received increasing attention in
        the professional literature from the 1960's onwards.

492          This background is important because it establishes that, regardless
        of the uncertainties which may remain about the exact processes of
        pathogenesis which may lead to an asbestos induced lung cancer; the
        degree of exposure likely to produce such a disease; or accepted criteria
        for attribution of such a cause; there has been a worldwide recognition,
        since the mid 1950's that asbestos exposure can lead to the development
        of this fatal and incurable disease. It has also been known, and for much
        longer, that exposure to asbestos in the working environment can produce
        other serious illnesses and disability.

493          It is perhaps also important to mention that mesothelioma and cancer
        of the lung are not the only cancers which have been linked with asbestos
        exposure and that the reports include references to cancer of the
        oesophagus, cancer of the liver, cancer of the stomach and of the
        duodenum and of other organs. Whatever may be the incidence of
        carcinoma of the lung due to asbestos exposure, it is only one of the
        manifestations of very serious illness and incapacity which may result
        from exposure to asbestos. In other words, asbestos is, and for a long time
        has known to be, a dangerous product which produces, illnesses with very
        serious, including fatal, consequences. Even if the risk from exposure
        may be slight in certain situations, or the effects imperceptible and of long
        delayed onset, the risks have been known and documented and have
        received attention in the professional literature for a very long time.
        Correspondingly, these risks have been known to industry, governments,
        manufacturers and employers for a long time as well and this knowledge
        and the need to exercise reasonable care for the health and safety of
        workers generates a proportional obligation upon those who produce,
        manufacture, distribute or work with asbestos or asbestos products.
494          A convenient history of the occupational risks of asbestos over time,
        and in many parts of the world, can be found in Exhibit 72(18) an extract


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        from the publication from the International Labour Office in Geneva in
        1938 and this included a proposal, not then full demonstrated, that
        asbestos exposure could produce a carcinoma of the lung (pp 9 - 10). In
        his publication "Carcinogens in the Human Environment" in "Archives of
        Pathology" (1961), Dr W C Hueper (Exhibit 72(34)) acknowledged that
        asbestos was a recognised cause of lung cancer but listed, among the
        exposure stigmata chronic fibrosing pneumonia (asbestosis) and asbestos
        bodies in the sputum and asbestos warts of the skin on the fingers - a
        demonstration of the early view that asbestosis was an accompanying
        diagnostic symptom. It must be noted that there was no suggestion, in this
        case, that asbestos-induced lung cancer cannot, or does not, often
        accompany asbestosis and, indeed, with the high degree of cumulative
        exposure thought to be necessary to produce asbestosis that is entirely
        unremarkable. The pertinent issue, as it has emerged in this case, is that
        the preponderant modern view is that lung cancer due to asbestos can
        emerge without accompanying asbestosis and, by implication, that the
        cumulative dose required to cause this may be less than that usually seen
        with cases of asbestosis.

495          I turn now to deal specifically with a small selection of the
        publications produced by Mr Kottek forming parts of Exhibit 72.
        Exhibit 72(35) is a contribution to the Medical Journal of Australia in
        1962 by Dr J C McNulty, then chest physician at the Kalgoorlie District
        Hospital in this State who reported what was believed to be the first case
        of pleural mesothelioma reported in an asbestos worker outside South
        Africa. The patient was a miner who had also been employed as a mill
        worker in an asbestos mine from 1948 to 1950 who suffered from
        asbestosis and silicosis after two years' work in a blue asbestos mill 10
        years before.
496           In 1965 two researchers at the Queen's University at Belfast in
        Northern Ireland, Elmes and Wade, wrote a paper "Relationship Between
        Exposure to Asbestos and Pleural Malignancy in Belfast"
        (Exhibit 72(37)), which, while dealing principally with mesothelioma,
        also concluded that among asbestos workers carcinoma of the lung is at
        least as frequent a cause of death as mesothelioma. Again, Exhibit 72(38)
        is an extract from the "Reports and Recommendations of the Working
        Group on Asbestos and Cancer" published by the International Union
        Against Cancer in 1965. This paper contains references, at p 7, 10 - 11,
        that carcinoma of the lung has been shown to be associated with exposure
        to asbestos dust and is not limited to exposure to any one type of asbestos
        fibre. This report was formally adopted by the UICC in its report in 1965
        (Exhibit 72(40)), later published in the Canadian Medical Association

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        Journal as Exhibit 72(41). Writing in 1966, in a post-graduate medical
        journal, Dr P C Elmes said (Exhibit 72(45)), at p 730, that cancer of the
        lung appears to occur in workers exposed to any type of asbestos fibre but
        that statistics were then very fragmentary and that, having regard to the
        industrial conditions of the day, this risk of cancer of the lung amongst
        workers exposed to factory conditions before any effort of dust
        suppression had been estimated at 15 times that expected. Dr Elmes also
        wrote (at p 634) that "such forms of lung carcinoma appear to be common
        in patients whose exposure to the dust was insufficiently long or intense to
        cause crippling fibrosis [sic - asbestosis]".
497          Exhibit 72(47) is an extract from the "Hygiene Standards for
        Chrysotile Asbestos Dust" published by the British Occupational Hygiene
        Society in 1968. At p 11 of that publication it is reported that it is
        generally recognised that there is, in addition to the risk of asbestosis, also
        a significant risk of lung cancer associated with asbestosis but that it was
        then not possible to specify an air concentration which is known will be
        free of risk in this respect.
498           Also in 1968, Dr Selikoff and others, writing in the Journal of the
        American Medical Association (Exhibit 72(48)) under the heading
        "Asbestos Exposure, Smoking, and Neoplasia", found that asbestos
        insulation workers, as a group, have a high risk of dying of bronchogenic
        carcinoma - about seven or eight times expected - and that calculations
        suggested that asbestos workers who smoke have about 92 times the risk
        of dying of bronchogenic carcinoma than men who neither work with
        asbestos nor smoke cigarettes. An earlier article of Dr Selikoff's bearing
        this title has been examined earlier in these reasons.
499          Writing in the annals of occupational hygiene in 1970, an officer of
        the Factory Inspectorate Department of Employment in London, S Luxon
        (Exhibit 72(52)) discussed the then new asbestos regulations which came
        into effect in May 1970 and propounded that attempts to control asbestos
        dust should aim for a level of 2 fb/ml and 0.1 mg per ml for Chrysotile
        asbestos and spoke of the new methods of atmospheric testing then
        introduced, as proposed by the British Occupational Hygiene Society in
        1968. However, he wrote that despite the adoption of those long-term
        average air concentrations, one should not ignore entirely peak
        concentrations and that in his view it seemed reasonable to accept that a
        concentration of, say, 12 fb/ml should not be exceeded during any period
        of 10 minutes. He went on to write:




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              "It must be remembered that we are using the fibre count not as
              an absolute measure of concentration but rather as a
              conveniently measurable parameter to indicate the total asbestos
              in the air. The work leading to the formulation of the BOHS
              Standard referred to above related to conditions in the textile
              industry and not enough information is yet available on the
              relationship between mass of asbestos and fibre counts in other
              industries. To further complicate the problem, it is not known
              what fibre sizes are biologically active and, even if this were
              known, appropriate elutriation (ie the rejection of material not
              biologically active) would be very difficult with a fibrous
              material such as asbestos. We ourselves are making both fibre
              counts and total mass determinations by X-ray diffraction
              analysis in industries, such as the motor industry, where
              degradation of the fibres may occur, resulting in a substantial
              change in size distribution."

500           These observations are another salutary reminder about the
        limitations of attempts to measure the concentration of asbestos in the air
        by quantitative methods, including the membrane filter method. In this
        regard it is pertinent to recall the evidence of Professor Wan to the effect
        that many small submicroscopic particles of asbestos can be expected in
        an environment where there is ambient asbestos dust in the air and that
        such extremely small particles could be expected to be undetected by the
        membrane filter method of sampling, either because even if caught on the
        filter the particles are too small to be seen on the process of microscopy
        utilised for the evaluation of that test (as exposed to more powerful
        electron microscopy undertaken in the course of more intensive research)
        or simply pass through the filter membrane. It follows, therefore, that
        informed scientists and observers realised that the results of sampling
        under the membrane filter method are incapable of revealing the full
        extent of potentially harmful fibres in the air being sampled.

501          Writing in the Medical Journal of Australia in 1972, Dr Robert
        Barnes of the Workers' Compensation (Dust Diseases) Board in Sydney
        (Exhib it 72(54)) confirmed that there had then been a long known
        association between asbestos and bronchogenic cancer of the lung,
        whereas the association between asbestos and mesothelioma was a more
        recent observation, being first described in 1960 by Wagner and others.

502          Exhibit 72(56) is an extract from an article by S K Brown, writing in
        the American Industrial Hygiene Association Journal in 1987, concerning
        asbestos exposure during renovation and demolition of asbestos cement


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        clad buildings and also reporting upon the problem of asbestos as a cancer
        producing agent as studied by the International Agency for Research in
        Cancer (part of the WHO). Quoting from a then recent International
        Symposium on that subject, the author referred to a statement that one
        extremely important fact which emerged from the meeting was the
        infinitely greater danger from exposure to asbestos dust faced by heavy
        smokers and that "whilst even for non-smokers asbestos dust presented a
        risk of lung cancer, for heavy smokers in the asbestos industry the
        combination was quite disastrous".

503           Mr Kottek included in his materials an article by Dr Finkelstein
        (Exhibit 72(59)) published in 1997, to the effect that radiographic
        asbestosis is not a prerequisite for asbestos associated lung cancer in
        Ontario asbestos cement workers, another rejection of the thesis that
        attribution to asbestos should not be made in a case of lung cancer unless
        accompanied by asbestosis. Exhibit 72(61) is a publication in the Annals
        of Occupational Hygiene published in Great Britain in 2001 by
        F D K Liddell of the Department of Epidemiology and Biostatistics of
        McGill University, Montreal (also in evidence as Exhibit 209). This
        addressed the tenability of the multiplicative theory of the interaction of
        the risks of asbestos exposure and chronic smoking. Liddell was critical
        of the multiplicative theory and, while acknowledging (p 355) that it was
        still accepted by perhaps the majority of workers in the field, said that it
        did not account for the phenomena of the results from the Cohort Studies,
        being prized because of its relative simplicity "more parsimonious in
        parameters". He attributed the variations of the errors which he criticised
        to the inevitable imprecision adopted by writers in the RAE - Relative
        Asbestos Effect. Although Liddell termed the multiplicative hypothesis
        untenable he did report that the relative risk of lung cancer from asbestos
        exposure is about twice as high in non-smokers as in smokers and that the
        best estimate of RAE was 2.04 with a 95 per cent confidence interval over
        the range 1.28 to 3.25. That would tend to suggest a much greater
        incidence of risk than offered by the opinions of Professors Musk,
        Professor Wan or Professors Leigh and Berry.

504          In direct contradistinction to the conclusions of Liddell is the report
        of P N Lee (Exhibit 72(62)) in 2001 dealing with the relation between
        exposure to asbestos and smoking jointly and the risk of lung cancer. He
        concluded that there was no overall departure from the multiplicative
        model so that the proportional increase in risk of lung cancer with
        exposure to asbestos being estimated at 0.90 times higher in smokers than
        non-smokers which, notwithstanding the preference espoused from the
        multiplicative model, still leaves the increased risk near to a factor of 2.

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        Resort to far more sophisticated mathematical models for measuring the
        interaction of the risks between exposure to asbestos and cancer can be
        seen in Exhibit 72(64), by an epidemiological statistician,
        Dr Van der Linder and others from Germany, but the results seem
        inconclusive for any application to the present litigation.

Further Conclusions
505           Mr Cotton was plainly exposed to airborne asbestos while working
        with the first defendant in Adelaide and again when working with the
        third defendant in Australind. During both periods of employment the
        level of exposure was variable and intermittent, but the probabilities are
        that during each period of employment there were repeated short-term
        intervals of significant exposure to asbestos dust. The most obvious are
        when rasping the cut ends of asbestos cement pipes while working at
        Adelaide, and the relatively few occasions when Mr Cotton was working
        in proximity with a power cutting tool used on the AC pipes. However,
        for the duration of his work with AC pipes there is likely to have been a
        higher than normal exposure to asbestos fibre although, by the standards
        of intensive asbestos use, relatively low. That occurred during a period of
        about two years from early 1976 to late 1978 which was more than 20
        years before the diagnosis of his lung cancer in February 2000.

506          The second period of occupational asbestos exposure occurred at the
        Australind factory from about early 1991 to the date of diagnosis in
        February 2000, although the probabilities are that, because of the asbestos
        removal programme, in cumulative terms, the larger part of that exposure
        occurred between 1991 and late 1997, or thereabouts. Again, the level of
        exposure was variable and intermittent, being probably at its greatest
        while working on sweeping operations in the BDR and in the packing
        room, although there is likely to have been variable levels of asbestos
        throughout the Australind site, particularly during the various removal
        operations, the most significant of which for Mr Cotton seems to have
        been the asbestos sheet removal from the roof in the area of the packing
        sheds and buildings adjacent to the BDR.
507          The composition of the cement asbestos pipes supplied by the second
        defendant and used by the first defendant in the operations in Adelaide
        were such that something in the order of 15 - 20 per cent of the content of
        the pipe was mixed asbestos. The composition of this asbestos was, it
        seems, largely Chrysotile but, significantly, there was also Amosite and
        some Crocidolite, the latter two types being the more noxious (and dusty)
        amphibole asbestos.


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508          The composition of the asbestos present at the third defendant's
        premises at Australind is less certain. The main sources were the asbestos
        lagging surrounding the heating pipes in the BDR; the asbestos insulation
        in the doors and door seals to the hatches on the band drier; and the
        asbestos in the roof sheeting and wall cladding to the various units in the
        factory. The only indication of the content of these asbestos sources
        comes from Matprolab's reports (Exhibits 45 and 113) and the laboratory
        analysis reports which derive from that investigation. These reveal that,
        mostly, the detected asbestos was largely Chrysotile but some Amosite
        and Crocidolite was reported, particularly in the lagging and insulation.
        There was probably Crocidolite in the insulating lagging on the heating
        pipes.
509          It follows from this, and I find, that the asbestos to whic h Mr Cotton
        was exposed while working with the first defendant in Adelaide was a
        mixture of Chrysotile and Amosite with some Crocidolite, but that the
        comparative proportions of the two varieties cannot be ascertained with
        any acceptable degree of confidence. Similarly, I am satisfied that the
        probabilities are, and I find, that the asbestos to which Mr Cotton was
        exposed while working at Australind was of different varieties and that
        the different sources of asbestos within the BDR collectively included
        Chrysotile, Amosite and some Crocidolite, whereas the asbestos dust
        either deposited on floors or surfaces in the packing areas where he
        worked, or dislodged into the surrounding atmosphere during the roof
        removal operations was, predominantly, Chrysotile.

510           For reasons set out when dealing with the evidence of the various
        occupational hygienists, I consider that the most probable total exposure
        to asbestos from these combined sources is the degree estimated by
        Mr Kottek and also by Professor de Klerk, that is, something in the
        vicinity of 5 to 10 fb/ml years, although every consideration demonstrates
        that this is an approximation and that the actual degree of cumulative
        exposure (if that were ever capable of precise identification) could be
        larger or smaller but of about the same order of magnitude. Although, for
        reasons already given, I deprecate the attempts to fix upon any precise
        figure for cumulative exposure, I am nevertheless satisfied that the total
        cumulative exposure in Mr Cotton's case was less than the 25 fb/ml years,
        mentioned in the Helsinki Protocol, the AWARD Criteria and which is the
        hallmark propounded by the defendants' epidemiologists and hygienists.
        Just how much less than 25 fb/ml years cannot be said but, in my view, it
        is likely to be well less than that figure for I do not envisage the upper
        bounds of Mr Kottek's or Professor de Klerk's estimates as coming within
        striking distance of that alleged hallmark.

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511           This has led me to adopt the opinions of Professor Musk, Dr Kendall,
        Dr Leigh and Professor Berry that, insofar as it may be significant, the
        relative risk of Mr Cotton developing lung cancer due to this asbestos
        exposure was in the order of 1.1 to 1.2, that is, some 10 to 20 per cent
        above the standard background risk.

512           The next and difficult step in this process is to consider whether or
        not the evidence establishes that Mr Cotton's exposure to asbestos
        materially contributed to the development of his lung disease
        notwithstanding that, as I have indicated, it is probably clearly less than
        25 fb/ml years of cumulative exposure which the defendants maintain is
        an essential prerequisite to any such attribution. There are several major
        areas of controversy bearing on the answer to this question. I turn first to
        the issue of latency. The exposure to asbestos in Adelaide was, as already
        stated, a little over 20 years before the diagnosis of the lung tumour and,
        leaving aside the significance of the long subsequent interruption to the
        periods of continuous asbestos exposure, this is well within the accepted
        knowledge about periods of latency from first exposure to development of
        the disease. The period of first exposure at Australind to diagnosis is
        approximately eight to nine years or, adopting Professor Berry's approach,
        about ten to eleven years from first exposure until death. If this was the
        only period of asbestos exposure it would be at the lower end of the
        generally recognised necessary periods of latency for any attribution to be
        made, but it is not so short as to exclude, or even to discourage, such an
        attribution.

513           More importantly, in my view, there were two periods of exposure,
        the second capable of combining with or adding to the effect of the first. I
        accept the opinion of Professor Musk that discrete periods of exposure to
        asbestos, even if separated in time, are capable in combination of causing
        or contributing to the cause or progress of the disease. This too, I am
        satisfied, is the opinion of Professor de Klerk. This opinion appears to me
        to be consistent with the literature of this topic which I have examined and
        I accept it. Accordingly, the periods of exposure to asbestos experienced
        by Mr Cotton are, in my view, capable, either alone, or more probably in
        combination, of causing or contributing to the development of his disease.
514          In my view, this question of whether Mr Cotton's exposures to
        asbestos made a material contribution to the development of his fatal lung
        cancer cannot and should not be isolated from the evidence that
        Mr Cotton was a chronic smoker.




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515          I am satisfied that the best estimate which can be made of
        Mr Cotton's history of smoking is that he smoked approximately half a
        pack of cigarettes a day from the age of 17 or 18 until the diagnosis of his
        cancer in February 2000. This is equivalent to about 18 to 20 pack years
        of smoking which is not unduly heavy. His relative risk of developing
        lung cancer due to that smoking has been placed at factors of 20 by
        Professor Musk and 8 by Dr Leigh with other estimates in between those
        figures. Again, precision is impossible but it seems to me probable that
        the relative risk of developing lung cancer due to smoking alone is
        somewhere in the range of 15 - Professor Berry's figure.
516           All the evidence is that the risk of a person developing lung cancer
        from exposure to both asbestos and tobacco smoking is more than additive
        and that many commentators and studies adopt the multiplicative nature
        of the interaction of the risks attributable to each carcinogen alone. There
        is controversy in the scientific literature as to whether or not the
        relationship is truly multiplicative, or is less than multiplicative but more
        than additive, or there is some different form of exponential relationship
        between the two. No exact mathematical function fits precisely all the
        data but the consensus of expert opinion is to the effect that a
        multiplicative relationship gives the best fit but that the utilisation of this
        or any other formulation of the interaction must accommodate the
        uncertainties and asymmetries apparent from the data. Therefore, while I
        shall adopt the multiplicative description of the relationship, I
        acknowledge that this is not a completely precise description and that any
        mathematical products relating from its employment need to be assessed
        in the light of that knowledge.
517          Above, I recorded the evidence and calculations for witnesses Musk,
        de Klerk, Leigh and Berry on the mathematical attempts to calculate a
        figure for the combined e  ffect of the elevated risks of developing lung
        cancer arising from exposure to asbestos and tobacco for Mr Cotton.
        These efforts applied the formula of arriving at attributable chance by the
        calculation (RR - 1)/RR which, as I described in that earlier discussion,
        will always produce a product which is less than one so that, accordingly,
        when two such attributable chances (each less than one) are multiplied
        together, the ensuing product will always be less than either of the
        individual attributable chances. As Professors Leigh and Berry each
        acknowledged, this is a mathematical approach appropriate only for
        calculation of the effects of independent causes, rather than
        interdependent causes which have a synergistic effect such as occurs with
        exposure to tobacco and asbestos together. The employment of such a
        method in the present case, therefore, involves a mathematical fallacy if

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        the product were to be treated as measuring the combined chance of
        developing a lung cancer as the result of exposure to both asbestos and
        tobacco. The synergistic nature of the relationship, and the evidence of
        the statisticians Dr Leigh and Professor Berry on this issue, demonstrates
        clearly that the chance of developing lung cancer from exposure to both
        asbestos and tobacco must be greater than the chance of developing
        asbestos from exposure to either carcinogen alone.

518          This has led me to reject the calculations of attributable chance
        formulated by Mrs Sowden, Mr Rogers and, in this respect, Professor
        de Klerk and, instead, to select an attributable chance greater than either
        one alone. However, for the reasons already given, I have extreme doubts
        about the reliability of this procedure when it comes to being applied to an
        individual case such as Mr Cotton's, because retrospective assessments of
        dust concentrations in the air, the assumptions about the average
        long-term level of dust exposure which do not accommodate short-term
        peak exposures, and the linear assumptions about the rise in relative risk
        being constant for all levels of exposure over all periods of time are very
        questionable according to the literature. Indeed, the writings and opinions
        which I have examined acknowledge the potential toxic effect of asbestos
        even at low doses (including the Helsinki Protocol); they acknowledge
        that short-term peak doses less than the long-term average, especially if
        they exceed more than 10 fb/ml may be very harmful; and they show that
        the assumption that this linear relationship of risk to cumulative exposure
        is unaffected by tobacco smoking does not fit the data.

519           Consequently, to employ mathematical methodologies which apply,
        as if they were constant and unvarying symmetrical functions, a series of
        such imperfect approximations can only result in the factor of error,
        inherent in each one of them, becoming aggravated by the factors of error
        in the second, third and fourth assumed relationships. So a mathematical
        product which involves a function of them all will have a much higher
        degree of error than any one alone. These shortcomings may not be so
        important, or potentially misleading, in studies involving large numbers of
        cases, because the pattern which emerges from the study of very large
        numbers will be more clearly defined and discernable than studies of
        small numbers. But to apply this methodology to a single case leaves no
        room at all for the corrective factors which are present in the larger
        studies. For this reason, I am driven to the conclusion that one cannot do
        better than take the considered estimates of Professor Musk and Dr Leigh
        that Mr Cotton's increased risk of developing lung cancer due to his
        exposure to these two carcinogens is in the region of 1.10 to 1.20, that is
        some 10 per cent to 20 per cent above the background level. Professor

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        Berry put the increased risk at between 2 per cent and 16 per cent which is
        also consistent with those other estimates.
520           Nevertheless, the defendants seize even upon this figure as being
        very far less than sufficient to show a probability that Mr Cotton's lung
        cancer was due in part to his asbestos exposure. Reduced to essentials,
        the defendants' submissions are that, even taking these figures, this only
        means that the chance of Mr Cotton's lung cancer being due to asbestos
        was, at best, somewhere between one in five and one in 10. This means,
        they submit, that the court should approach the case on the basis that he is
        one of a group of people with lung cancer, with no individual pathologic
        diagnostic signs and, therefore, the chance of him being the one in five, or
        the one in 10, whose cancer was, to a material degree, due to asbestos
        exposure is clearly less than 50 per cent and that, therefore, his claim must
        fail.

521          However, I am not satisfied that this is a proper, or even an
        acceptable process of reasoning. Any group of people with lung cancer
        which has been selected randomly in the community will, if the group is
        large enough, include people whose lung cancer is due to smoking; is due
        to asbestos exposure; is due to other unrelated carcinogens (such as
        exposure to radiation or to non-asbestos carcinogenic chemicals) and there
        will also be those whose genetic profile has condemned them to the
        development of this disease.

522           There is no reason to suppose that Mr Cotton is simply a randomly
        selected member of a group with such a wide spread of potential inducing
        causes for his lung cancer. His case was carefully investigated by the
        doctors and physicians who were responsible for his diagnosis and
        treatment from 2000 to 2002. Detailed histories of his family medical
        background, his individual medical history and his work history were
        taken. These are sufficient to exclude, and it has not been suggested
        otherwise in this case, that his lung cancer might have been caused by
        exposure to radiation or to other non-asbestos carcinogenic chemicals.
        Similarly, his family medical history has been studied and, despite the fact
        that two grandparents on his maternal side died of different varieties of
        cancer (Exhibit 57), the evidence of Professor Musk and Dr Kendall was
        that Mr Cotton was not genetically predisposed to develop this lung
        cancer.
523          In fact it was common ground throughout the trial that the only
        carcinogens likely to have played a part in the development of
        Mr Cotton's cancer are tobacco and asbestos. Consequently, of that


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        assumed random sample of people with lung cancer from all possible
        causes, Mr Cotton falls into that portion of the group whose cancers were
        caused either by asbestos or by smoking or by the interaction of both
        carcinogens. This therefore disposes of the defendants' submissions that,
        at the highest, Mr Cotton's chance of being a person whose lung cancer
        was caused or contributed to by asbestos was somewhere between one in
        five and one in seven.

524           In my view, the evidence drives one inevitably to the position where
        it is necessary to ask whether the plaintiff has proved that it is more
        probable than not that he is within the second or third category of the
        tripartite group which I now describe. This group is a random selection of
        persons who have lung cancer and of whom it can be said that their cancer
        is due to one or other of the carcinogens tobacco or asbestos or to a
        combination of those two. For persons who have lung cancer and have
        had a history of exposure to both carcinogens there will, presumably, be
        persons whose lung cancer is due solely to the effects of tobacco. There
        will be those whose cancer is due solely to the effects of asbestos.
        Importantly, there will be those whose cancer is due to the combined
        effect of asbestos and tobacco so long as the contribution towards that
        result caused by asbestos can be regarded as being material. If it is more
        probable than not that Mr Cotton's case fits into either the second or the
        third of these categories, that is that his cancer was solely caused by
        asbestos or was caused by the combined effect of smoking and asbestos,
        then the plaintiff will have succeeded in proving causation at law
        sufficient to demonstrate an actionable claim for damages. However, if
        the plaintiff cannot prove that it is more probable than not that
        Mr Cotton's smoking was not caused solely by smoking, her claim will
        fail.
525           Conspicuously absent from the evidence, and from the submissions
        of the defendants, was any body of professional opinion or literature
        which allows one to segregate, in a quantitative fashion, those with lung
        cancer exposed to both asbestos and tobacco, in a way which could lead to
        a conclusion, or even a probability, that asbestos played no material part
        in that individual's carcinoma. In my view, the burden of all the evidence
        is in the opposite direction, namely that, in combination, the carcinogens
        tobacco and asbestos are interactive and synergistic, each enhancing the
        effects of the other. Similarly, the established preponderance of opinion
        that there is no safe threshold of exposure to asbestos precludes a finding
        in this particular case, that from the point of view of potential contribution
        to the development of the cancer, the extent of Mr Cotton's asbestos
        exposure was insignificant.

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526           Because of the view in the Helsinki Protocol and the AWARD
        Criteria that the figure of 25 fb/ml years is necessary for an attribution of
        lung cancer to asbestos exposure, while at the same time recognising that
        that degree of exposure is typical of the exposure which will usually
        produce asbestosis, I do not consider that that figure can be applied as a
        minimum exposure threshold essential before an attribution to asbestos
        exposure as the cause for an individual case of lung cancer can be made.
        The Helsinki Protocol acknowledges that asbestos exposure can occur at
        lower or shorter levels of cumulative exposure. The evidence is that the
        extent of exposure associated with the development of asbestosis is a high
        or heavy level of exposure. The modern prevailing view, which I accept,
        is that asbestos-induced lung cancer can, and does, appear in the absence
        of asbestosis. In those circumstances to insist on the 25 fb/ml year level
        of cumulative exposure as indispensable for an attribution to asbestos as
        the cause of lung cancer, even if the methods of quantitative analysis were
        far more reliable than the literature reveals them to be, is simply
        untenable.
527          In this case the only evidence from a suitably qualified expert to the
        effect that Mr Cotton's degree of cumulative exposure to asbestos was so
        negligible that it could make no material contribution to the development
        of his lung cancer was from Professor Fox. However, I have, despite my
        high respect for him, rejected this opinion because of Professor Fox's
        adherence to the view that the presence of asbestosis is an indispensable
        diagnostic accompaniment for an attribution of asbestos-induced lung
        cancer. In any event he regards the 25 fb/ml year cumulative exposure
        adopted by the Helsinki Protocol and by the AWARD Criteria as much
        too low. Professor Fox also has assumed that Mr Cotton's cumulative
        exposure to asbestos was very much lower (by more than an order of
        magnitude) than I have concluded the evidence establishes. Putting
        Professor Fox's evidence aside, therefore, the remaining expert evidence
        and the literature is to the effect that in most, but not all, cases of dual
        exposure to these two carcinogens asbestos combines to aggravate the
        effects of tobacco. That is certainly the opinion of Professors Musk, Wan
        and de Klerk, Dr Kendall, Dr Leigh and Professor Berry and it is entirely
        consistent with all that is known of this case.

528          Other factors which tend to suggest that Mr Cotton's case is not
        simply one otherwise featureless example of a patient with lung cancer
        chosen at random from the general population are: that he was unusually
        young to present with lung cancer due solely to smoking (not outside the
        lower end of the curve of distribution of such cases arranged with respect
        to age onset, but well towards the lower end of the tail of that distribution

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        - see Exhibit 54), and that the very experienced clinicians, Professor Musk
        and Dr Kendall who examined him shortly after his diagnosis and advised
        on his case, being fully conversant with the possibilities and uncertainties,
        nevertheless expressed as their professional opinion their individual views
        that Mr Cotton's asbestos exposure made a material contribution to the
        development of his carcinoma.
529           Returning to the categorisation of patients with lung cancer who have
        been exposed to both asbestos and to tobacco, the evidence satisfies me
        that a very large proportion of that category of cases are those whose
        cancer is due, in a material way, to the interaction of both carcinogens. In
        other words, of that one category, the evidence leads me to the conclusion
        that those whose cancers are due to asbestos alone, or to smoking alone,
        form smaller proportions of that group, with the first sub-group (cancer
        due to asbestos alone) probably being very small. In this case I think the
        conclusion is unavoidable that Mr Cotton falls into that subdivision of this
        category comprising patients whose cancers have been caused, to a
        material degree, by the interaction of both smoking and asbestos
        exposure. I am satisfied that it cannot be said, with any acceptable degree
        of confidence, that his case falls into the category of those patients whose
        cancer has been caused by asbestos alone, but if it did it would mean that
        causation had affirmatively been proved. As I am satisfied that of those
        patients with lung cancer who have been exposed to asbestos and who
        have a history of smoking, the largest proportion have their cancers
        caused by the interaction of the two carcinogens, it follows that it is more
        probable than not that Mr Cotton's case is within that sub-group. It is not
        necessary for the plaintiff to establish that Mr Cotton's exposure to
        asbestos was the sole, or even the dominant cause of his lung cancer, so
        long as it materially contributed to the development of that disease this is
        sufficient in law to establish causation. This is what I consider the
        evidence demonstrates in this case.
530           It is well known that the concepts of "cause" and "causation" can
        mean many things in different disciplines: in philosophy, in science, in
        common human practice, and at law. There are many authorities which
        distinguish between the concept of cause, in the law, and in other
        provinces of life in such a way that make it unmistakeable that the law's
        concept of material cause, differs markedly from the idea of scientific
        cause - Goodwin v Nominal Defendant (1979) 54 ALJR 84; Hole v
        Hocking [1962] SASR 128 and Clarke v Chandler Clay Pty Ltd (1984)
        A Tort Rep 80-631; (1984) Rosenberg v Percival [2001] HCA 18; (2001)
        205 CLR 434 per Gummow J at 460; March v Stramare (E & M H) Pty
        Ltd (1991) 171 CLR 506. While a court will, generally, attempt to follow

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        science in cases of uncertainty - Paris v Matkovich, unreported; FCt SCt
        of WA; Library No 980614; 27 October 1998 - the necessity to preserve
        the legal understanding of cause must be maintained and the exercise must
        not become converted to an adoption and application of scientific theories
        of causation or higher levels of proof.

531           This provides another reason for scrutiny of the Helsinki Protocols
        and the AWARD Criteria because both are silent when it comes to
        defining the concept of "cause" which is being applied for the attribution
        under examination. No mention is made in either of those papers about
        attribution when there exist two or more potential concurrent causes for
        the pathology; nor do the papers recognise the concept of a material
        contribution being made whether by way of complementation or
        aggravation of another single more significant cause. To a very large
        degree both the Helsinki Protocol and the AWARD Criteria appear to
        pursue the essential minimum diagnostic requirements for an attribution to
        a single factor as the sole, or at least dominant, cause for the condition.
        To this extent they embark on a quest, and so necessarily suggest
        standards, more demanding than necessary to identify a factor which
        makes a material, that is not an insignificant, contribution to the
        development of the disease notwithstanding that its role may be less than
        some other more potent concurrent cause. Resort to the Helsinki Protocol
        and the AWARD Criteria in cases such as this, while, perhaps
        understandable from a scientific view, nevertheless involves a tacit, but
        major, alteration to the established rules of legal causation.

532           The quest for the sole or dominant cause which these criteria imply
        similarly fails to reveal whether the degree of persuasion which is
        sufficient to establish the putative attribution of cause is, as the law
        requires on the balance of probabilities, or is some higher scientific
        standard of proof. There are some signs that those criteria may be
        satisfied on the balance of probabilities arising from the fact that the
        attribution of cause would be made if the RR exceeds 2.0 but, even if that
        is so, this cannot be assumed for other elements in the criteria, such as the
        premise that the RR increases by 4 per cent for each fb/ml year of
        exposure; or because of the assumption that a similar cumulative exposure
        dose for lung cancer as is observed in cases of asbestosis is required for
        such an attribution. These premises or components of the criteria adopted
        by the Helsinki Protocol and by the AWARD Criteria are not readily
        transparent and, therefore, cannot safely be assumed to reflect the
        components of the legal tests for causation of damage.




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533          A particularly telling refutation of the thesis that an attribution to
        asbestos as a cause of an individual lung cancer should not be made in the
        absence of interstitial fibrosis, and hence of Professor Fox's views on this
        subject, is the AWARD Criteria, upon which, for other reasons, the
        defendants place so much reliance. At 446 of Exhibit 207, the AWARD
        Criteria, there appears a passage recording that the majority of evidence
        and the prevailing expert view is that attribution of lung cancer to asbestos
        does not require the presence of asbestosis. Instead, the evidence
        indicates that it is the cumulative dose of inhaled asbestos that is the main
        determining factor for attribution of lung cancer to asbestos by way of a
        significant contribution (usually in combination with tobacco smoke).

Liability for negligence, breach of contract or breach of statutory duty
534          By her statement of claim, the plaintiff alleges that there were
        implied terms in Mr Cotton's contract of employment with the first
        defendant that the first defendant would take all reasonable care:
              (a)     not to expose him to a risk of damage or injury at which it
                      knew or ought to have known;
              (b)     not to expose him to any substance or material which was
                      known, or should have been known, or was suspected, to
                      be dangerous, without warning and appropriate protective
                      treatment;
              (c)     to warn and provide information to him about the hazards
                      of asbestos so that Mr Cotton could use his own
                      commonsense in terms of assisting with his own
                      protection;
              (d)     to provide him and his fellow employees with instructions
                      as to methods for minimisation of dust, including
                      instructions as to damping down methods;
              (e)     to provide regular air monitoring to ensure compliance
                      with standards;
              (f)     to provide appropriate dust masks as well as training in
                      the use of masks and supervision of the wearing of such
                      masks;

              (g)     to comply with industrial health and safety and welfare
                      legislation and regulations, in particular reg 39 of the


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                      South Australian Industrial Safety Code Regulations
                      (statement of claim par 7).
535          By its defence, the first defendant admits that it was under a duty to
        take reasonable care for Mr Cotton's safety while he was engaged in
        carrying out his work with the Engineering and Water Supply Department
        between 4 September 1975 and 2 October 1978 but otherwise does not
        admit the allegations relating to the existence of a contractual or tortious
        duty of care and specifically does not admit any of the allegations relating
        to the existence or content of the alleged implied terms of the contract of
        employment (defence, par 4).
536          By par 12 of the statement of claim the plaintiff alleges that, in the
        light of the facts pleaded in par 11 (broadly speaking, the widespread
        knowledge by then that asbestos was a dangerous hazard), the first
        defendant was under a duty to its employee to take reasonable care to
        avoid unnecessary risk of injury, to provide proper supervision of the
        work, to provide appropriate respiratory protection, to provide pipes
        which did not contain asbestos in substitution for asbestos cement pipes,
        to comply with industrial health and safety and welfare legislation and
        regulations, in particular with reg 39 of the South Australian Industrial
        Safety Code Regulations, to take such other measures as were necessary to
        guard Mr Cotton against inhalation of asbestos dust and fibre, to provide a
        safe system of work and to warn the deceased of the necessity to avoid the
        inhalation of asbestos fibre and dust.
537           Regulation 39 of the Industrial Safety Code Regulations 1975 (SA)
        was made under the Industrial Safety Health and Welfare Act 1972 (SA)
        and came into operation on 1 September 1976 - reg 59(2). The regulation
        requires the occupier of industrial premises where any asbestos procedure
        is carried on to comply with the regulations and envisaged that an
        "asbestos process" would be carried on within a building. Regulation 39
        makes reference to "exhaust ventilation equipment"; to "floor, walls,
        ceilings" and "interior parts of the roof". In September 1976 the
        regulation was amended to exclude processes in which asbestos dust is not
        given off in excess of the standards of exposure.

538          The Regulations reflect the standards of the era when it comes to the
        extent of asbestos. Except for Crocidolite, the use of asbestos was not
        banned (reg 39(15)), but the focus was on dust control through ventilation
        and cleaning. Smoking was not prohibited but the Chief Inspector had
        power to require the occupier to prohibit or regulate the employment in
        any asbestos process of smokers and to declare no smoking areas;


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        respiratory equipment was not required in all cases; there was no
        requirement that all workplaces where there might be asbestos exposure
        should be monitored for asbestos exposure levels; and there was no
        requirement for employees to be given information regarding the hazards
        of asbestos. Further amendments to the Regulations which came into
        effect on 29 June 1978 provided a prescribed maximum concentration of
        asbestos as a time-weighted average of 2 fb/ml. A further amendment on
        29 June 1978 inserted reg 39(2) which required the use of respiratory
        equipment when the level of asbestos exceeding 10 fb/ml was exceeded.
        (See Exhibits 163(1), (2) and (3)).
539          Against the second defendant, the plaintiff pleads (par 15 of the
        statement of claim):
              "That at all material times the second defendant knew or ought
              to have known that the inhalation of asbestos fibres and dust
              was extremely injurious to human health and caused, amongst
              other diseases, asbestosis, lung cancer, pleural disease and
              mesothelioma; that the asbestos cement pipes which the second
              defendant manufactured and supplied would, in the course of
              use, be likely to be handled, cut, filed and worked on by various
              methods which would release asbestos fibres and dust; that
              persons handling, cutting, filing and working with the asbestos
              cement pipes or working in the vicinity of others performing
              those activities would be exposed to asbestos fibre and dust and
              may, as a result, suffer injury unless measures were taken to
              prevent or minimise the release of asbestos fibre and dust; that
              if the second defendant did not provide any warning either at
              the time of supply of these asbestos cement pipes or on the
              pipes themselves it was unlikely that any or any sufficient
              measures would be taken to prevent inhalation of the asbestos
              fibre and dust; and that persons exposed to the risk of inhalation
              of asbestos from the use of its products may also be cigarette
              smokers and consequently exposed to significant additional risk
              of injury".

540          The plaintiff then asserts that at all material times the second
        defendant was under a duty to the deceased to warn him and other like
        workmen directly, whether by warning affixed to the asbestos cement
        pipes or otherwise, and also to warn those who purchased or received the
        asbestos cement pipes, including the first defendant, that because of the
        danger in using the materials it was essential that measures be taken when
        the pipes were handled, cut, filed and worked upon to prevent or minimise


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        the release of asbestos fibre and dust into the atmosphere (par 16). The
        plaintiff then alleges that the second defendant was in breach of these
        duties by failing to give any, or any sufficient, such warnings (par 17).

541          By its defence, the second defendant does not admit any of those
        allegations of fact and says further (defence, par 2) that at no material
        time did it know, nor should a reasonable person in the second defendant's
        position have known, that such alleged exposure to asbestos constituted a
        foreseeable risk of injury to the deceased. The second defendant further
        pleads that if the deceased suffered an injury related to the inhalation of
        asbestos, it was from sources and products for which the second defendant
        was not responsible and could not control [by implication from sources at
        the workplace at Australind]; that the amount of asbestos inhaled from
        any products for which the second defendant might be responsible was
        insufficient to cause Mr Cotton's injury; and that the second defendant
        could not foresee or control the fact that the deceased would continue to
        be placed in circumstances in which he might inhale asbestos.

542         There are, however, a number of facts formally admitted by the
        second defendant set out in Exhibit 8. These are that:

              (a)     The second defendant manufactured asbestos cement
                      water pipes in the period February 1976 to October 1978.

              (b)     Between February 1976 and October 1978 the second
                      defendant did not:

                      •         give the deceased any warning about any risk of
                                asbestos-related disease from handling, cutting or
                                rasping its asbestos cement water pipes;
                      •         instruct the deceased to minimise or avoid
                                inhalation of asbestos whilst handling, cutting or
                                rasping its asbestos cement water pipes;
                      •         warn the deceased to wear a mask or respirator
                                whilst handling, cutting or rasping its cement
                                water pipes.

              (c)     The second defendant never measured, or caused to be
                      measured, the amount of asbestos to which the deceased
                      (or any other employee of the first defendant in the period
                      February 1976 to October 1978) was exposed as a result
                      of handling, cutting or rasping asbestos water pipes.


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              (d)     In the period between February 1976 and October 1978
                      the second defendant did not warn the first defendant or
                      the deceased that the risk of lung cancer caused by
                      asbestos inhalation multiplied the risk of lung cancer
                      from smoking.

              (e)     When the second defendant sold or supplied asbestos
                      cement water pipes to the first defendant after February
                      1976 it did not know how long employees of t e firsth
                      defendant, such as the deceased, would work handling,
                      cutting or rasping its asbestos cement water pipes.
543          By par 20 of the statement of claim the plaintiff alleges that during
        the period of Mr Cotton's employment with the third defendant the third
        defendant knew or ought to have known :
              (a)     of the dangers of exposure to inhalation of asbestos
                      fibres, particles and dust;
              (b)     that Mr Cotton and other of its employees were likely to
                      be exposed to asbestos fibre and dust as a result of
                      working in areas of the third defendant's premises where
                      asbestos was used as lagging on plant and equipment;
              (c)     that in the absence of any sufficient warning, proper
                      supervision or implementation of the deceased's system
                      of work, no measures would be taken to prevent or
                      minimise the release of exposure of fibre and dust into the
                      atmosphere from lagging on the plant and equipment and
                      from other asbestos materials;
              (d)     some of the third defendant's employees, including
                      Mr Cotton, may have previously been employed in places
                      where they experienced exposure to asbestos so that
                      exposure to asbestos in the employ of a third defendant is
                      likely to be incremental to their risk of injury;
              (e)     some of the third defendant's employees, including the
                      deceased, would be cigarette smokers and, consequently,
                      be exposed to significant additional risk of injury.

544          Consequently, the plaintiff alleges that the third defendant was under
        a duty to take reasonable care to avoid unnecessary risk and injury to the
        deceased, to provide a safe place of work, to provide proper supervision,


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        to ensure that lagging on plant and equipment, including the band drier,
        did not contain asbestos or, if it did, that the lagging was contained and
        not allowed to fall into disrepair so that it would not expose employees to
        the risk of inhalation of asbestos dust.
545          The plaintiff also alleges that the third defendant was under an
        obligation to comply with the occupational health and safety regulations
        being Div 1 Pt 8 of the Occupational Health, Safety and Welfare
        Regulations 1988 (WA) and in particular regs 322, 803, 808, 815, 816,
        823 and Sch 3.

546          Then follows (par 22) an extensive series of allegations of breach of
        these alleged duties, by failing to take reasonable care to avoid
        unnecessary risk of injury, by failing to give any or any sufficient warning
        to the deceased or other employees of the risk of exposure to asbestos
        fibre and dust, by failure to provide proper supervision, by failure to
        provide a safe system of work, by failing to ensure that equipment
        requiring lagging was lagged with asbestos-free lagging, by failing to
        quantify the level of asbestos exposure and by failure to comply with the
        occupational health and safety legislation and regulations nominated.

547           The plaintiff also alleges that there were implied terms in the
        contract of employment between Mr Cotton and the third defendant that
        the latter would take all reasonable precautions for the safety of the
        deceased (statement of claim, par 8). In particular, the plaintiff alleges
        that there were implied terms in this contract of employment obliging the
        third defendant:

              (a)     not to expose the deceased to any risk, damage or injury
                      of which the third defendant knew or ought to have
                      known;

              (b)     to provide and maintain adequate and suitable plant and
                      equipment;

              (c)     to ensure that the deceased's workplace was safe;
              (d)     to provide and maintain a safe and proper system of work
                      and effective supervision of the same;
              (e)     to comply with occupational health and safety legislation
                      and regulations, being Div 1 Pt 8 of the Occupational
                      Health, Safety and Welfare Regulations 1988 and, in
                      particular, regs 322, 803, 808, 815, 816, 823 and Sch 3


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        and, consequently, that the third defendant was in breach of those
        contractual obligations.
548          The Occupational Health, Safety and Welfare Regulations 1988, and
        the Occupational Health, Safety and Welfare Act 1984, together with
        applicable amendments covering the period to 1990, comprise Exhibits
        166(1) and 166(2). It is sufficient if I summarise the gist of the particular
        regulations relied upon by the plaintiff as follows:

              •       Regulation 322: obliges any employer to ensure that no
                      worker is exposed to an atmospheric contaminant listed in
                      the schedule at a concentration which exceeds the level
                      set out in the schedule. This prevention is required to be
                      implemented, as far as practicable, by a suitable
                      ventilation or exhaust system or by other suitable means
                      but, if it is not practicable to avoid the atmospheric
                      contaminant by any other means then suitable respiratory
                      protective equipment must be provided.

              •       Schedule 3 lists various atmospheric contaminants and
                      the maximum time-weighted average exposure standards
                      for them. The contaminants include four references to
                      varieties of asbestos and the maximum exposure standard
                      for each of those is as follows:
                      •         Amosite - 0.1 fb/ml

                      •         Asbestos (not otherwise listed) - 0.1 fb/ml
                      •         Chrysotile - 1.0 fb/ml

                      •         Crocidolite - 0.1 fb/ml
              •       Regulation 803 is to be found in a section of the
                      regulations dealing with specified hazardous substances
                      and, in this particular instance, with asbestos. It obliges
                      any employer in charge of a workplace to ensure that
                      every asbestos surface is kept in a good condition; any
                      repair or sealing necessary to prevent the breaking up of
                      asbestos or the release of airborne asbestos is done
                      promptly; and maintenance, replacement, removal or
                      repair of an asbestos cement surface is carried out in the
                      approved manner.



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              •       Regulation 804 contains an express prohibition against
                      any person using, handling or causing or permitting
                      another to use or handle Crocidolite or Amosite or a
                      product containing Crocidolite or Amosite.
              •       Regulation 815 imposes an obligation on an employer to
                      ensure that the workplace is maintained in a clean
                      condition and, in particular, to ensure that where there is a
                      workplace at which an asbestos process is involved
                      (defined by reg 801 to include the repair, maintenance
                      and replacement of asbestos services and the cleaning and
                      disposal of asbestos materials, among other things), that
                      all machinery, apparatus, equipment and like furniture
                      and fittings; the external surfaces of any exhaust system
                      and cleaning equipment, and the floor, wall, ceilings or
                      inside part of the roof and other interior surfaces are kept
                      as far as practicable free of asbestos and other waste
                      material.      It specifically provides that in such
                      circumstances the employer shall ensure that cleaning is
                      carried out on completion of an asbestos process at least
                      daily and by means of an approved vacuuming equipment
                      or some other suitable method so that, as far as
                      practicable, asbestos is not discharged into the
                      atmosphere of the workplace.
              •       Regulation 816 obliges an employer to ensure that a
                      safety warning sign with the words "Danger - Asbestos"
                      is prominently displayed at each entry to every asbestos
                      processing area.

              •       Regulation 823 creates an offence for any person to carry
                      out or to cause or permit any other person to carry out
                      asbestos removal work unless the person carrying out the
                      work is licensed as required, has the approval in writing
                      of the Commissioner to commence the work, and
                      performs the work in accordance with the licence.

549           By par 5 of its defence the third defendant admits that it was a term
        of its contract of employment with Mr Cotton that it owed to him a duty
        that it would take all reasonable precautions for the safety of the deceased
        while he was engaged upon his work, as alleged by the plaintiff.
        However, the third defendant denies the plaintiff's allegations that prior to
        and during the course of its employment of Mr Cotton it knew, or ought to


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        have known, of the dangers alleged by the plaintiff in par 20 of the
        statement of claim except that it admits that it:
              •       knew that exposure to high levels of asbestos fibres,
                      particles and dust would be injurious to human health;
              •       that asbestos had been installed as lagging on plant and
                      equipment, including the band drier room, at a time prior
                      to the medical finding that high levels of asbestos fibres,
                      particles and dust could be injurious to human health;
              •       when it became aware of the dangers associated with
                      asbestos it implemented an active asbestos removal
                      programme using a licensed asbestos removal contractor;

              •       during this asbestos removal programme it kept the
                      plaintiff and other employees informed of the progress
                      and the importance of using respiratory protection in
                      effected areas;
              •       that it monitored the level of asbestos fibres, particles and
                      dust in the atmosphere of the workplace by air testing
                      over a prolonged period of time and that at no time during
                      the employment of the deceased did the tests reveal levels
                      of asbestos fibres, particles and dust in the air in the areas
                      in which the plaintiff worked which exceeded 0.01 fb/ml.
550          Further, by par 9 of its defence, the third defendant denies that it
        knew or ought to have known that Mr Cotton might have been exposed to
        asbestos in some previous employment and, consequently, that further
        exposure to asbestos might involve him in an incrementally higher risk of
        harm, and further denies that it knew or ought to have known that
        Mr Cotton or other employees would be cigarette smokers and thereby
        exposed to significant additional risk of injury.
551           By par 10, the third defendant further denies that it was under any
        duty to ensure that the lagging on plant and equipment, including the band
        drier, did not contain asbestos but, otherwise accepted, that it was under a
        duty to Mr Cotton to take reasonable care to avoid unnecessary risk of
        injury, to provide a safe place of work, to provide proper supervision, to
        ensure that if lagging was not contained or fell into disrepair it would not
        expose employees to the risk of inhalation of asbestos dust and to perform
        the other obligations alleged by the plaintiff in par 21 of the statement of
        claim.


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552          By Exhibit 4, a letter from its solicitors of 10 August 2005, the third
        defendant made certain admissions concerning Mr Cotton's employment.
        These are:

              (a)     that the third defendant was aware by 1990 that inhalation
                      of asbestos gave rise to a risk of asbestos-related disease;

              (b)     that the third defendant was aware that the plaintiff
                      smoked during his employment in the period 1990 until
                      1994; and
              (c)     that in the period between 1990 and 1994 the third
                      defendant did not warn Mr Cotton that the risk of lung
                      cancer caused by asbestos inhalation multiplied the risk
                      of lung cancer from smoking.
553           I am satisfied, from the testimony of all the witnesses who had
        worked for the South Australian Engineering and Water Supply
        Department during the period that Mr Cotton was employed by the first
        defendant from 1975 to 1978, that no precautions or steps were taken by
        the first defendant to avoid, prevent or diminish risks of contracting
        asbestos-related diseases as a result of working on asbestos cement pipes
        which were being laid by operations in which the deceased was employed.
        There were no respiratory devices provided, used or recommended. There
        was no restriction about the nature, frequency or degree of the working
        operations to be followed by the men in lifting, placing, cutting, filing or
        using the asbestos cement pipes. Although the device was, apparently,
        only seldom used in Mr Cotton's experience, there was no restriction upon
                                         o
        the use of a powered cutting t ol on the asbestos cement pipes which
        generated dust and fibres in the immediate vicinity. No sealant, or
        dampening liquid (such as water) was used for any of the cutting, rasping
        or fitting processes which the men followed when working with or laying
        the pipe. Nor were any steps taken to remove, control or otherwise render
        safe asbestos fragments which had come from the pipes that had been cut,
        rasped or otherwise worked upon and which lay on the ground in the
        vicinity of the operations and where the men were working and in a
        condition where they could be, and probably were, disturbed by
        continuing operations, by wind and by refilling the trenches. Nor was any
        warning given to Mr Cotton or to any other of the men about the hazards
        of working with asbestos and certainly not of the potential for increased
        hazard levels if a worker smoked.




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554           Accordingly, in my view, the issues of negligence, breach of
        contract, and breach of statutory duty insofar as they are made against the
        first defendant, come down essentially to whether or not the work in
        which Mr Cotton was employed involved any foreseeable risk of harm
        through the contraction of an asbestos-related disease and, further,
        whether having regard to the extent of knowledge available at that date,
        the general accepted standards of reasonable care prevailing at that time,
        and the potential significance of the risk to health from that form of
        employment, there was a failure by the employer to take reasonable care
        for its worker through the provision of a safe system of work or whether,
        because of hazards which could not adequately be controlled, there was an
        obligation to warn specifically of the hazard and/or to provide protective
        equipment and work practices.
555           The plaintiff's case against the second defendant is based solely in
        tort, namely, that there was a failure to take reasonable care for the
        deceased who should have been known to be a person who would work
        with the asbestos cement pipes supplied by the second defendant, in
        circumstances where it was known or should have known that such work
        would involve the hazards of contracting an asbestos-related disease, and
        where no warnings of these hazards, or the need for precautions to prevent
        or reduce them was given either to the worker, or to the purchaser of the
        asbestos cement pipes who, it was reasonably foreseeable, would employ
        others, including the plaintiff, to perform such hazardous activities unless
        warned of the need to take special precautions to eliminate or reduce the
        hazards involved.
556          There is no doubt from the evidence that the men who carried out
        activities similar to those performed by Mr Cotton in Adelaide during the
        second half of the 1970's, and indeed from the first defendant's own
        witness Mr Campbell, that the second defendant provided no warnings of
        any kind about the potential hazards of using or working with the asbestos
        cement pipes which it supplied, or of the need to take precautions to avoid
        or reduce risks involved by workers installing, cutting, rasping or
        handling those asbestos cement pipes. Nor did the second defendant
        measure or recommend the measurement of exposure levels to asbestos
        dust or fibres for men carrying out such operations employed by the first
        defendant.
557          Again, therefore, the area crucial for the determination of liability or
        otherwise by the second defendant is, in my view, the extent of the
        knowledge possessed by the second defendant, or knowledge of which the
        second defendant as a manufacturer and supplier of asbestos cement


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        products should reasonably have been aware, concerning the nature,
        extent and level of health hazards arising from the use of asbestos in an
        occupational setting.      This question involves, as an important
        consideration, the extent of the contemporary knowledge available about
        the risk, or level of risk, of working with asbestos products, and the
        contemporary standards of what were considered to be reasonable care
        when working with such materials. That, in turn, involves the
        examination of the nature or extent of hazard then reasonably known or
        believed to be associated with that degree of exposure to asbestos which
        could be expected to be associated with this form of activity.
558           Turning to the factors which are germane to the plaintiff's case
        against the third defendant, based as it is on breach of contract, negligence
        and breach of statutory duty, it is plainly the case that Mr Cotton, and
        other workers, were expected, indeed required, to work at the Australind
        factory, and to work at times within the confines of the BDR without any
        protective equipment or respiratory masks or the like. It is also the case
        that it must have been obvious to the third defendant that there were very
        large areas of asbestos cement sheeting on the cladding, internal walls and
        the roof areas of the various buildings on the Australind site where
        Mr Cotton and his colleagues were working. Similarly, it was known to
        the third defendant that there was asbestos lagging on the steam pipes in
        the BDR and that it had been mixed and made up on the premises and
        applied to the pipes during an earlier stage (see the evidence of
        Mr Savage). There is evidence to show that the third defendant was
        aware of the existence of asbestos in lagging in the BDR well before the
        Matprolab's assessment of March 1990. Exhibit 95(1) is a copy of the
        minutes of a Safety Meeting of the third defendant held on 9 September
        1987 which, at p 2, refers to samples of lagging having been collected
        from the top of the band drier and revealing asbestos in two of the
        samples. Exhibit 96 is a memorandum of the third defendant dealing with
        asbestos at the Australind site and dated 23 August 1988. This refers to a
        strike by all the contract personnel on this site employed by three-named
        contractors on 10 August 1988 over dissatisfaction with the owner's
        requirements to handle asbestos material. This led to the company
        contracting Amdel Ltd to undertake airborne asbestos fibre testing which
        was conducted on 12 and 16 August 1988 and these tests confirmed the
        presence of asbestos in various places. The report concluded by
        observing that contract personnel had raised concerns about their working
        environment being in close proximity to asbestos-related materials and
        that this concern was understandable based on the current publicity of
        asbestos in the media at that date. The presence of asbestos on the third


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        defendant's work site continued to be a subject of complaint by employees
        and was raised from time to time at company safety meetings - 29 July
        1988 (Exhibit 97).

559          The agitation from the third defendant's workforce from as early as
        1988 because of employees' concern about potential asbestos hazards was
        acted upon to engage Matprolabs to undertake detailed surveys and to
        provide recommendations for an asbestos removal programme. By March
        1990 (Exhibit 45) it was appreciated by the third defendant that steps
        needed to be taken to remove, reduce or control the hazards of asbestos
        exposure arising from these conditions of the workplace and the asbestos
        removal programme was embarked upon.

560          Whether this was an adequate response, both in extent and
        promptness, to the perceived hazard requires attention but it is clear that
        most of the asbestos lagging in the BDR was not removed until about
        April 1992; that the asbestos insulation in the hatches to the BDR doors
        and their seals was not removed until 1994; and that more asbestos was
        found on the top of the band drier machine accidentally causing exposure
        to workmen, including the deceased, in April 1995. The removal of the
        asbestos roofing took place over an extended period and it is clear that the
        asbestos cement roofing sheeting in the area of the packing sheds and the
        adjacent BDR where Mr Cotton continued to work was only replaced over
        the period of about 1994 to 1997.

561          Similarly, the air monitoring conducted at Australind was, for
        reasons already canvassed, largely associated with the asbestos removal
        activities and located at points within the extended factory areas which
        could not be regarded as being representative of the conditions under
        which Mr Cotton himself worked. In particular, none of the air
        monitoring could be regarded as sampling the conditions which applied in
        the BDR, or for that matter in the packing area, when sweeping up and
        cleaning operations were under way or during the times when Mr Cotton
        was clearly exposed to short-term peak loads of airborne dust
        concentrations.
562          With specific regard to the allegations made by the plaintiff of
        breach of statutory duty arising from the Occupational Health Safety and
        Welfare Regulations 1988, there are no air sampling results which record
        higher atmospheric contamination for Amosite, Chrysotile, Crocidolite or
        other asbestos greater than the exposure standards referred to reg 322 and
        Sch 3 but the evidence relating to the air sampling reveals that it was
        conducted at strategic points over time and that, therefore, the


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        probabilities are that it did not sample peak exposure levels at places or at
        times when dust was being agitated, such as during sweep up operations
        in the BDR or similar operations in the packing areas. In this respect the
        definition of "exposure standard" in reg 103 of the Regulations means the
        maximum exposure standard contained in Sch 3 in the breathing zone of
        the person concerned, determined by reference to either time-weighted
        average in respect of periods of exposure or a peak exposure level at any
        time. The evidence of Mr Kottek, which I consider is reliable in this
        respect, suggests very strongly, and I find, that during those periods of
        peak exposure when sweeping up in the BDR or elsewhere the
        probabilities are very high that the airborne dust concentration of asbestos
        exceeded 1.0 fb/ml and, consequently, that there were recurrent breaches
        of reg 322.
563          With reference to reg 804, I am satisfied on the evidence of the
        workmen and the Matprolab reports that the asbestos surfaces of the
        cladding to the piping within the BDR and the asbestos seals and
        insulation to the hatches of the BDR were not kept in good condition, that
        there was insufficient repair or sealing carried out to prevent the breaking
        up of the asbestos or the release of airborne asbestos either promptly or at
        all and that, apart from the eventual removal and replacement of the
        asbestos lagging to the pipes in the BDR under the supervision of
        Matprolabs in 1991 - 1992, and again in 1994, the daily removal of
        asbestos from the BDR by the sweeping up operations which the plaintiff
        complains was not carried out in the approved manner.

564          Again, with reference to reg 808, it is evident that the asbestos
        lagging to the pipes in the BDR contained Amosite and Crocidolite. The
        former was found and reported on by Matprolabs in Exhibit 52 and in the
        air sampling results (Exhibits 44 and 45) - latter was described by
        Mr Savage. Because of this it is almost certainly the case that pieces of
        asbestos lagging which broke away from the lagging to the pipes in the
        BDR, fragments of which fell to the floor and were swept up by
        Mr Cotton, contained Amosite and Crocidolite and that consequently the
        work practices which required him to sweep up the floor dust and debris
        containing such contaminants involved a breach of reg 808.
565          Exhibit 52, the Matprolab's report of 19 April 1995 revealed that
        Crocidolite and Chrysotile had been detected in a sample taken from the
        band drier area. Amosite was found in a sample taken from the south wall
        of the micronizer building (near the BDR) in August 1995 (Exhibit 100).
        Amosite was found in 12 of the 17 samples taken from within the BDR
        reported upon by Matprolabs in March 1990 (Exhibits 44 and 45).


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566          It also follows that because of the deposits of broken fragments of
        asbestos lagging from the pipes on the floor of the BDR, the shedding of
        asbestos insulation from the hatches and from the seals to the doors of the
        band drier, and the accumulation of these materials not only on the floor
        but upon other surfaces of the BDR without daily cleaning by means of an
        approved vacuum equipment or other suitable method, there were
        continuing breaches of reg 815.

567          I also find that there were not safety warning signs with the words
        "Danger - Asbestos" prominently displayed at each entry to the BDR as
        required by reg 816. These findings also involve the conclusion that the
        third defendant was in breach of reg 823 by requiring or permitting its
        employees, including Mr Cotton, to carry out the sweeping up of the
        BDR, involving as it did "asbestos removal work", otherwise than in
        accordance with reg 823.

568          I am satisfied that the Occupational Health and Safety Act, and the
        Regulations identified constitute legislation for "the safety of members of
        the public or a class of them" giving rise to "a correlative private right,
        although the sanction for breach of the regulation is penal, because it
        protects an interest recognised by the general principles of the common
        law", per Dixon J in O'Connor v S P Bray Ltd (1937) 56 CLR 464 at
        477 - 478. Indeed, this very legislation was treated as giving rise to a
        correlative civil right of action for damages by a decision of the Full Court
        in Wylie v South Metropolitan College of TAFE [2003] WASCA 34 and,
        if only in passing, also by the decision in McLachlan v Purchas & Ors,
        unreported; FCt SCt of WA; Library No 980749; 21 December 1998, a
        decision of Kennedy, Pidgeon and Miller JJ. It has also long been
        accepted in this State that the Occupiers Liability Act 1985 which imposes
        statutory duties on occupiers with respect to persons who enter upon their
        land or premises, confers duties which give rise to a correlative right of
        action for damages by any person who suffers injury, loss or damage
        through breach of the statutory duty and that such a statute defines the
        content of the relevant duty for the purposes of determining whether the
        occupier is liable in damages for negligence - Westralian Caterers v
        Eastment Ltd (1992) 8 WAR 139, per Malcolm CJ at 146.

569          In the present case I consider that the plaintiff has a correlative right
        of personal action for damages for loss or damage occasioned by the third
        defendant for breach of the duties imposed upon it under the Occupational
        Health, Safety and Welfare Regulations and, in addition, that the content
        of those regulations also informs the content of the relevant duty by the
        defendant in an ordinary civil action for damages for negligence.


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570           However, breach of such a statutory duty or of failure to comply with
        the standard of care which the law requires is only one step towards the
        establishment of the liability which the plaintiff alleges. The plaintiff
        must also prove that the breach of the regulation relied upon, or the
        relevant standard of care, in fact caused or materially contributed to the
        damage or loss of which she complains. As already canvassed this is the
        major area of contest in the present litigation but there are other issues
        involved in the allegations of breach of contract, negligence and breach of
        statutory duty which still require attention.

571          At this point, however, it is appropriate to conclude that, although I
        am satisfied that there was a breach of reg 816, which required the third
        defendant to place conspicuous warning signs at all the entrances to the
        BDR in terms "Asbestos - Danger" and that this was not done, I do not
        consider that that breach of the regulation caused or contributed to
        Mr Cotton's fatal disease. The reason for this is that there was no
        suggestion that, had such a warning been situated as required, he would
        not still have been obliged to carry out the sweeping, cleaning and other
        duties inside the BDR and elsewhere which resulted in his exposure to an
        atmosphere with asbestos dust and fibres, nor that the third defendant
        would have adopted a different working regime or employed safer
        working practices with relation to asbestos exposure had such a warning
        been posted.

Knowledge of the hazards of asbestos
572          Although it appears in various guises, I consider that the major issues
        on these questions of liability, whether framed in contract, negligence or
        breach of statutory duty, are whether conducting and requiring
        compliance with an occupational activity during the years when
        Mr Cotton was employed in Adelaide and at Australind in the vicinity of
        asbestos, involved a failure to take reasonable care for the safety of the
        workmen so exposed and, in particular, whether the reasonable standards
        of those times recognised that reasonable care demanded that precautions,
        including warnings, prevention, and protective working methods, be
        employed when men were working with, or in the vicinity of asbestos
        materials which could be expected to generate the types and nature of
        exposure to airborne particles which occurred during these two episodes
        of employment. To address those questions it is necessary to return to the
        substantial evidence dealing with the knowledge and attitude towards the
        health risks posed by asbestos in the workplace before 1976, in the case of
        the first and second defendants, and before 1990 in the case of the third
        defendant.


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573           I therefore revert to the evidence dealing with the extent and nature
        of the knowledge available in the scientific literature, among specialists in
        the field and in industry about the dangers posed by asbestos in 1976, and
        again in 1990. Much of this topic has been covered by the expert
        evidence and scientific literature adduced on the issue of whether or not
        Mr Cotton's alleged asbestos exposure could have caused his lung cancer
        and on what is the basis for making such a causal attribution. However, it
        was also specifically addressed by other witnesses, namely, Mrs Batt and
        Mr Russell and, in addition, by other evidence not so far specifically
        examined of Mr Kottek, Professor Musk, Mr Rogers and Dr Leigh.
574          It is convenient to turn again first to the evidence of Dr James Leigh,
        the occupational physician whose evidence on the issue of causation is
        discussed at length elsewhere in these reasons. In his statement
        (Exhibit 63, at p 7 - 14) Dr Leigh lists the progress in the literature,
        government inquiries and legislature and other responses showing that the
        hazards to health were understood from the beginning of the 20th Century
        and were studied and written about in Australia in New South Wales in
        1933 and 1938, in Victoria in 1939 and became more widely known in
        this country in the 1950's. In 1956 asbestos lagging or spraying and
        asbestos works or factories in which asbestos was used, manipulated,
        crushed or pulverised were declared in Victoria to be dangerous trades.
        The association between asbestos and lung cancer (bronchial carcinoma)
        was recognised in the USA and the UK in 1935, published internationally
        and was the subject of an international conference held in Sydney in 1950.
        The association between asbestos exposure and mesothelioma became
        widely known in the 1960's. The famous "Selikoff" paper was published
        in 1964 and it was followed by a New York conference that year, the
        results of which were published and became well known.
575           Attempts were made to set standards of cumulative lifetime exposure
        on the basis of a weighted average to minimise the risk of developing
        clinical asbestosis (1968) but no attempt was made to set a standard to
        prevent lung cancer or mesothelioma. By 1966 - 1968 that work had been
        critically evaluated and the standard chosen was shown to have been too
        high by a factor of about 10.
576          The interaction of asbestos and tobacco smoking in causing lung
        cancer was first recognised in 1968 and confirmed by 1972. In 1985 the
        UK Health and Safety Commission published its report on the effects on
        health of exposure to asbestos and in 1988 the Australian National
        Occupational Health and Safety Commission published its asbestos code



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        of practice. The Australian Mesothelioma Programme was established in
        1979 and is still continuing.
577           The very extensive literature and the steps in the progress towards
        national and worldwide recognition of these hazards is evident from the
        literature produced by Dr Leigh, summarised earlier in these reasons. For
        present purposes it is sufficient to say that there is no doubt whatever that
        well before 1978 it was widely known, internationally and nationally, that
        exposure to asbestos, particularly in the workforce, was potentially very
        hazardous and could cause the incurable fatal diseases of mesothelioma
        and lung cancer, as well as severely disabling conditions arising from
        asbestosis and other types of lung disease.

578          The same conclusions can be drawn from the evidence of the third
        defendant's witness, Mr Alan Rogers, who tabulated the steps in the
        progressive understanding about the hazards of asbestos in his statement
        (Exhibit 245). While I have, elsewhere, largely discounted or rejected the
        evidence of Mr Rogers when it comes to determining the quantification of
        asbestos exposure necessary to attribute to it the cause of a particular lung
        cancer, I accept his description about the progress of the knowledge of the
        hazards of asbestos contained in Appendix 1 of his report (Exhibit 245,
        pp 19 - 22), except where it enters into the field of the quantity of
        exposure known or believed to be hazardous.
579           In this respect I consider that there is great force in the observation
        made by Professor Musk during the course of his oral testimony that,
        there is really no controversy in the medical scientific or industrial fields
        about the extent or progress of knowledge about the hazards of working
        with asbestos and that now, and for quite some years past, the
        controversies which remain are about the extent of exposure associated
        with the development of different pathologies and, indeed, in cases of
        lung cancer, and whether diagnosis by reference to established cumulative
        exposure of the patient over time is really appropriate. Professor Musk
        does not quarrel with the proposition that, the greater cumulative
        exposure, the greater the risk of developing lung cancer or other
        asbestos-related diseases, but that observation is not significantly different
        from saying that the more frequently a sailor goes to sea the greater is his
        risk of drowning.

580          There are certainly some asbestos diseases, asbestosis being the most
        obvious, where the development and intensity of the disease depends upon
        the total cumulative exposure.       By contrast, it is believed that
        mesothelioma may be caused only by a short or transient exposure to


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        asbestos although, again, of course, even for mesothelioma the greater the
        exposure the greater the risk, but the diagnosis of that disease, unlike lung
        cancer, is highly indicative of its cause.

581           Mr Rogers confirmed that the risk of asbestos-related diseases was
        well-known from the 1930's onwards and that an association with lung
        cancer began to be appreciated before 1955 and was confirmed and
        accepted following the Doll paper of 1955. At that time it was believed
        that increased lung cancer risk occurred for workers who had sufficiently
        high cumulative exposures to be recognised clinically, that is through
        asbestosis apparent on X-ray or from lung function evidence. Mr Rogers'
        discussion then turns to the controversial issue of the extent of exposure
        or cumulative exposure to asbestos sufficient to be accepted as having
        caused the lung cancer. As mentioned now on more than one occasion, it
        is this aspect of the evidence of Mr Rogers which I consider is prone to
        criticism and which I have not accepted, at least in relation to the
        application of his quantitative methods for an evaluation of Mr Cotton's
        lung cancer.
582          Mrs Anne Cameron Batt holds the degrees of Bachelor of Science,
        Master of Applied Science and holds a diploma in library studies. Her
        professional career is that of a biomedical librarian and she has fulfilled
        that role at the West Australian Institute of Technology (now Curtin
        University), the University of Tasmania and as medical librarian in the
        Faculties of Medicine and Dentistry at the University of Western
        Australia. She was asked by the solicitors for the plaintiff to assemble a
        selection of the information and literature available in Australia from
        1967 onwards about the effects of asbestos in industry. She gave
        evidence at this trial explaining how she had done this and produced two
        lever arch files (Exhibits 77) containing copies of the materials which she
        had selected and a summary of the sources which she had consulted to
        gather this information. These included certain specified medical indexes,
        engineering and chemistry indexes, industrial arts indexes, the
        engineering index and the index of chemical abstracts. In these materials
        Mrs Batt also lists the libraries and resources in Australia which held
        some or all of these materials and which could be expected to be
        appropriate reference sources for any person or body who wished to carry
        out an adequate study of this learning.
583           It is sufficient to say that these materials demonstrate that there was
        an abundance of scientific literature available from the early 1970's and
        earlier showing the hazardous effects of working with asbestos, leading to
        asbestosis, lung cancer, mesothelioma and related diseases. As I have


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        recorded elsewhere, however, the pattern to be discerned from the
        literature is of an ever increasing awareness of the dangers posed by
        asbestos exposure, accompanied by a steady realisation that significant
        risks of asbestos disease arose with lower exposures than believed
        necessary in the past. There is really no doubt whatever that the risks of
        working with asbestos were well and widely known by the early 1970's
        and that this knowledge included the appreciation that asbestos could
        cause or contribute to the development of a variety of serious diseases at
        least two of which, mesothelioma and lung cancer, were incurable and
        fatal.
584          This was also the overall effect of the evidence of Professor Musk
        who, in his oral testimony, said that the association between asbestos
        exposure and asbestosis - or interstitial fibrosis - was well-known from the
        1930's. Another detailed description of the literature available and the
        growing extent of the knowledge of serious health hazards associated with
        asbestos occurs in the evidence of Mr Michael Kottek (Exhibit 71, p 1 - 8)
        which summarises the literature and in the materials chosen by Mr Kottek
        (Exhibit 72) which contains copies of the literature upon which he relied
        and which, again, I have summarised earlier in these reasons.
585          The literature clearly establishes that before 1976 there were
        widespread concerns about the risk to workers of occupational exposure
        to asbestos, and that asbestos exposure had the potential to cause a series
        of different, but grave, illnesses including mesothelioma, asbestosis and
        lung cancer. To establish breach of the obligation to exercise reasonable
        care for the safety of an employee or a person exposed to one's product, it
        is not essential to establish that the particular type of illness or injury, or
        the particular level of exposure which might produce it, was known or
        foreseeable by the defendant so long as the risk was, or should have been,
        foreseeable. The need for foreseeability of harm will be satisfied if it was
        foreseeable that exposure to asbestos could cause an injury generally of
        the kind suffered - Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383
        per Windeyer J at 402; Chapman v Hearse (1961) 106 CLR 112 at
        120 - 121; Beavis v Apthorpe [1963] NSWR 1176 and Bendix Mintex Pty
        Ltd v Barnes (1997) 42 NSWLR 307 at 332 and 334 - 335.

Evidence of Mr Peter Russell
586          Exhibit 80 is the statement of evidence of Mr Peter McKay Russell,
        now retired, who worked for James Hardie & Coy Pty Ltd between 1948
        and 1970 and was, for large portions of that time, involved in the testing
        and quality control work performed on asbestos cement products


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        manufactured by the second defendant under the direction of the
        company's Chief Chemist and Senior Research Engineer. He became
        Factory Superintendent of the insulation factory and about that time
        became aware of the hazards of asbestos and serious health problems
        being experienced by workers who had been engaged in the company's
        manufacturing and other activities over the years. He described how
        James Hardie obtained asbestos materials, Crocidolite from South Africa
        and Western Australia, Chrysotile from Canada and brown asbestos
        (Amosite) from South Africa.

587          During the 1960's Mr Russell said that James Hardie had an
        employment policy which avoided employing, if it could, smokers, mouth
        breathers and young people or those with a previous dusty work history.
        He spoke of a "dust file" kept by the company at its Camellia factory
        containing the names of employees who showed signs of being affected
        by asbestos dust levels. In this file Mr Russell found a report
        incorporating the results of two major surveys conducted, respectively, in
        1952/53 and in 1956/57, referring to the tests and X-ray results of some of
        the company's employees. This file contained recommendations against
        employees working in dusty conditions for more than two years and a
        document which referred to blue asbestos (Crocidolite) and white asbestos
        (Chrysotile), as causing chronic fibrosis of the lungs and of asbestos
        causing or contributing to lung cancer.

588           This prompted Mr Russell to undertake his own research at the
        Mitchell Library in Sydney, as a result of which he discovered the
        literature showing the hazards of asbestos dating from 1890 onwards. He
        said that this made it clear to him that some workers were affected with
        asbestos disease after relatively minimal exposure to asbestos dust. He
        was given a copy of a paper "Complications of Asbestos", published in
        the British Medical Journal in 1960 by Dr McCullagh of James Hardie.
        He continued his research interest in the literature of asbestos-related
        disease and discovered the reports of the New York Conference. He
        ordered a copy of these conference papers and distributed them around the
        company and placed them in the company library. These indicated a
        worldwide problem of greater magnitude and significance than he had
        previously appreciated about the severe health problems arising from
        asbestos manufacture and use.
589         Mr Russell discussed his concerns with the branch manager of James
        Hardie's factory at Brooklyn in Victoria and lent him copies of the New
        York Conference papers. He received other memoranda from James
        Hardie's staff demonstrating that they were aware of this literature. At


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        intra-company meetings in 1963 Mr Russell urged that warnings should
        be given, especially of the dangers of dry sawing or processing of the
        asbestos products and recommended that a written warning be placed on
        the products so that it would come to the notice of end users. However,
        his recommendations were not acted upon and warnings were not given to
        purchasers of supplies or to end users. He continued to press various
        officers in the company about his concerns but, as they appeared to be
        unresponsive, he became disillusioned. He took long leave in 1964 in
        order to consider his position arising from these concerns but, before this
        departure, prepared a confidential memorandum documenting his
        understanding of the problems and risks for distribution to senior officers
        of the first defendant.
590           The text of this memorandum appears at par 140 (pp 25 - 33) of
        Mr Russell's statement (Exhibit 80) and in it specific mention is made of
        the risk of a variety of serious lung diseases including asbestosis, cancer
        and heart failure due to lung disease. This memorandum included the
        passage (Exhibit 80, p 30):
              "It is a fallacy to assume exposure must be to high dust levels
              over a lengthy period. There is evidence to support the view
              that (ref: 3) the first few years of exposure to asbestos fibre are
              as important determinants of final outcome as are most of the
              remaining years of exposure. Continued exposure will, of
              course, aggravate the process."
        Mr Russell arranged for copies of his memorandum to be distributed to
        the first defendant's Branch Manager at Camellia, to the Personnel
        Manager, the Chief Engineer at the Camellia plant and to the Factory
        Manager at Camellia. During his leave Mr Russell decided to quit his
        employment with James Hardie but he was contacted by telephone by the
        company's technical director who persuaded to return to the company as
        quality controller in the brake lining division. He accepted that invitation
        and continued to work in that role from 1964 until 1970. During this time
        he continued to read the medical literature about the relationship between
        asbestos exposure and mesothelioma and noticed a series of articles which
        confirmed the belief which he had by then developed about the seriously
        harmful effects of asbestos. This led him to resign his employment with
        James Hardie in 1970.
591          Mr Russell said that, as a result of his discussions and interactions
        with staff, the senior officers at James Hardie were well aware of the
        problems with the use of asbestos and the difficulties which these were


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        causing in the longer term for the employees' health but that (Exhibit 80,
        par 161,p 37):
              "The company adopted an official line that asbestos exposure
              was not dangerous unless the exposure was very intense and of
              long duration. This was not true. It was a demonstrable
              falsehood. The company knew that it was false at the time, as
              detailed in the company's own documents ... "

592          There are in evidence a series of documents, correspondence and
        reports sourced from various officers of the second defendant which
        confirm the substance of Mr Russell's evidence concerning the internal
        appreciation by James Hardie's staff of the risks associated with asbestos
        exposure from an early date. This material comprises Exhibit 114 (a letter
        of 30 June 1954), Exhibit 115 (a letter from the Department of Public
        Health in South Australia, dated 5 September 1956), a letter and an
        accompanying report from the Director of the Division of Industrial
        Hygiene of the Department of Public Health of New South Wales of
        27 November 1957 (Exhibits 116 and 117). This report, which is
        presumably one of the reports to which Mr Russell made reference,
        contains a summary of the literature on asbestos-related disease (pp 4 - 8)
        including a summary of the literature dealing with the carcinogenic action
        of asbestos, together with a long list of the names of various workers who
        were believed to be affected, to varying degrees, by their occupational
        asbestos exposure.
593          Two further internal documents of the second defendant are of
        significance (Exhibits 118 and 119). The first is a copy of the
        memorandum from a Mr N Gilbert, Factory Manager to the city office in
        May 1966, which highlights a series of points requiring attention.
        Included is a reference to the need to protect the company's future
        compensation liability because virtually any lung cancer or lung disease
        contracted by its employees might be classified as being caused by contact
        with asbestos. Exhibit 119, being an extract from the company's Factory
        Managers' Conference in June 1967, acknowledged that recent research
        had established a relationship between contact with asbestos and
        mesothelioma and lung cancer.
594          Further internal documents of the second defendant show an early
        appreciation of the association between asbestos exposure and lung
        cancer, the aggravation of the risk and the condition in workers who
        smoked. A report of these risks distributed to James Hardie's Branch
        Managers in June 1968 is Exhibit 120 and it includes (at the page marked


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        103) the acknowledgement of some evidence at that time that lung cancer
        attributive to asbestos exposure may occur in the absence of asbestosis
        and other evidence which demonstrated the great extent to which cigarette
        smoking increased the likelihood of lung cancer in the asbestos exposed.
        The same acknowledgement can be seen in other James Hardie documents
        (Minutes of a Factory Managers' Conference in 1969 - Exhibit 121) and
        by a paper entitled: "Biological Effects of Asbestos in June 1971"
        (Exhibit 122).
595          There can be no doubt that these risks were appreciated within James
        Hardie, at least at the latest from the early 1970's and probably from the
        late 1960's (see Exhibits 123, 124, 125, 126 and 127); and the
        accompanying study by Elwood and Cochrane published in the British
        Journal of Industrial Medicine 1994 and Exhibits 128, 129, 130 and 131.
596           There are other internal documents of James Hardie's which confirm
        the recognition of the association between asbestos exposure and a variety
        of lung diseases, including lung cancer, and the elevated risk for workers
        who smoke, all dating from the mid-1960's. These include a summary of
        the literature in the New York Academy of Sciences Annals conducted by
        Dr S F McCullagh (Exhibit 132), an inter-house memo of James Hardie of
        16 June 1966 which referred to lung cancer in an electrician, not
        employed by James Hardie, but who was a regular caller for routine
        weekly maintenance on cranes and machinery at James Hardies' plant and
        who was, on occasion, on site for periods of up to three or four weeks
        (Exhibit 133), and other internal memos dating from June 1966 to May
        1967 (Exhibits 134, 135 and 136).
597           Mr Russell was not cross-examined by counsel for the first or third
        defendants and was only briefly cross-examined by counsel for the second
        defendant but this cross-examination did not produce any qualification or
        withdrawal of the evidence which I have described, nor demonstrate any
        reason which might cause me to hesitate in accepting the evidence of
        Mr Russell. I regarded him as a credible and convincing witness and I am
        satisfied that he did endeavour, assiduously and over a period of years
        during the 1960's, to bring to the attention of more senior management at
        the first defendant, his well-founded concerns about the dangers
        associated with working with the asbestos products and the need for some
        form of warning to customers and end users.
Knowledge about risks of asbestos
598         Further on this issue, counsel for the plaintiff tendered a series of
        documentary exhibits in support of the plaintiff's contention that the

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        hazards of working with asbestos were well known and understood from
        the early 1970's onwards. It will be sufficient if I mention these only
        briefly:

        •     Two extracts of the Hansard Reports of debates in the House of
              Assembly in South Australia in November and December 1968
              discussing the hazards associated with asbestos dust including its
              potential to cause lung cancer. The Minister responsible for the
              Department of Public Health in South Australia stated that officers of
              that Department were then (December 1968) well aware of the
              hazards associated with exposure to asbestos dust. The debate also
              made reference to workers who had been exposed to asbestos dying
              of lung cancer.
        •     Exhibit 85: A publication of the Department of Labour and Industry
              of South Australia: "Working Asbestos Safely", issued in June 1979
              describing, at p 2, the dangers of grinding, sawing, drilling or
              abrading action on the finished asbestos product, including pipes,
              because of the fibres liberated which can lodge permanently in the
              soft lining of the lungs and also warning (at p 7) of the health hazards
              from asbestos if people do not abstain from smoking or at least
              refrain from the habit in the work area.

        •     Exhibits 81(1) to (3): These are publications of the Department of
              Public Health In South Australia entitled "Good Health" in July
              1957, April 1960, July 1960.
        •     Exhibit 81(1) contains passages (at pp 28 - 29) to the effect that
              inhalation of asbestos dusts produce inflammatory conditions in
              lungs and produce characteristic peribronchiolar fibrosis. No
              asbestosis was found in the survey of asbestos workers in Adelaide at
              that time but none of them had been engaged in the work for more
              than two years.

        •     Exhibit 87(2) adverts to the historical knowledge of the disease
              known as asbestosis (p 6) and (at p 3) observes that in the
              implementation of a safety programme, the safety officer's principal
              duties are to aim at the elimination of all known hazards, to develop
              safe working conditions and methods and to see that protective
              equipment is utilised.

        •     In Exhibit 87(3) there is reference to the need for clean air and an
              observation that an ordinary person in leisurely activity breathes in
              and out about 1000 cubic feet of air each day. At p 3 it discusses

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              inanimate dusts and identifies common types of harmful particles as
              including asbestos dust. At p 4 the publication, speaking of asbestos
              dust, says that the damage it causes to the lung is very similar to that
              produced by silica but that some authorities consider that the effects
              of asbestos may develop more quickly. In the same report the
              authors observe that the prevention of dust diseases of the lungs is
              best approached as an engineering problem in dust suppression.

        •     Exhibits 88 and 89 are publications by the EWSD of South Australia
              in May 1958 and October 1959 relating to the procedures to be
              followed for the laying of asbestos cement pipes which are described
              as being manufactured by James Hardie & Coy Ltd. Although there
              is much detail about the procedures to be followed there are no
              recommendations or warnings about the potential danger of asbestos,
              nor of dust arising from cutting or rasping operations nor any
              recommendations to use a wet process or other dust suppression
              measures.

        •     Exhibit 91 is a booklet "Safety Policy Rules and Instructions" for the
              EWSD published in 1964 as a guide to supervisors, but there is no
              mention made of any disease risk involved in working with asbestos
              cement pipes or the need for any special measures or precautions
              when working with asbestos products.
        •     Exhibit 93 is a publication "Hardie's Textbook of Pipeline Design
              1981" which describes the composition, manufacture, properties,
              uses and methods of handling of asbestos cement pipe but it does not
              detail the types of asbestos used in the composition of these pipes.
              At p 5-62 there is a short section dealing with dust precautions
              warning that in cutting AC pipes care should be taken to avoid the
              production of dust. This observes that if it is necessary to cut the
              pipe other than with a Wheeler cutter that should be done with a
              portable electric cutter with a water cooled diamond blade. Although
              not recommended if an abrasive type disc is to be used or it is
              necessary otherwise to work in conditions where dust is produced,
              respiratory protective equipment such as the 3M8710 mask must be
              worn. If using a powered field lathe the service to the machine
              should be kept wet to reduce the generation of the airborne dust.

        I interpolate here that these recommendations contained in Exhibit 93
        were published after Mr Cotton had completed his employment with the
                                                        rom the other evidence,
        first defendant in Adelaide but I am satisfied, f
        that the knowledge of these risks and the need for such precautions was


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        available well before 1978, and there is no explanation offered for the
        second defendant's failure to inform its customers, or other end-users, of
        the need for such precautions much earlier, including during the period
        when Mr Cotton was employed in Adelaide. No wet system was used to
        suppress dust during cutting or rasping operations in which Mr Cotton
        was involved, nor was any respiratory protective equipment offered,
        available or worn.
599           Counsel for the plaintiff also tendered a large quantity of documents
        discovered by the second defendant, from both its own internal sources
        and from published materials and from third parties, relating to the
        knowledge of health hazards associated with asbestos including lung
        cancer and the aggravating effect of smoking. These materials were
        received as evidence only against the second defendant and, therefore, I
        have excluded them from consideration in relation to the claims against
        the first and third defendants.          These materials are collectively
        Exhibit 156 (four large folders) and they cover the period from
        16 February 1968 to mid-1976. There are repeated references in these
        materials to the known risks of contracting lung cancer, and other serious
        illnesses from asbestos exposure and of the potentiating effect of cigarette
        smoking. There is also much attention given to endeavours to establish a
        safe or tolerable level of asbestos dust concentration in a workplace but
        the materials on this topic stress the difficulties of doing so and the
        uncertainty that any level of exposure may be safe.
600          In this category of materials there are copious extracts from the
        proceedings of the first Australian pneumoniconiosis conference held in
        Sydney in February 1968 (Exhibit 156, vol 1, document D431 at 35 - 39).
        There, under the heading "Standards of Permissible Dustiness", a
        discussion of the attempts in various parts of the world to set exposure
        standards is described before the conclusion is reached (at 38), that, in
        general, prescribed dust standards in Australia are deficient to that date,
        and this topic was further addressed in papers by Dr J C McNulty, then a
        physician of the Occupational Health Division of the Public Health
        Department of Western Australia (Exhibit 156, vol 2, at 454 - 473) and by
        the physicist, Mr G Major, under the heading "Asbestos Dust Exposure"
        (Exhibit 156, vol 2, at 474 - 494), and in the discussion on these and other
        papers at 507 and following.
601          In vol 3 of Exhibit 156 (document D555) there is an internal
        memorandum from James Hardie to its Camellia plant dated 21 April
        1966, addressing the need to control dust in the Camellia area. It includes
        the observation that: "It is not possible nor is it, I feel desirable, to try and


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        define a safe concentration. All dust is harmful so that we must regard the
        best we can do as still inadequate". Another of these documents
        (Exhibit 156, vol 3, document D604, a letter of 17 October 1979) is a
        report from the company's principal occupational physician,
        Dr McCullagh, about the then recent meeting of specialists at Lyon.
        Dr McCullagh is recorded as expressing disappointment at the apparent
        consensus stated at the Lyon meeting that there is no safe limit of
        exposure to any carcinogen. He went on to observe that "We must try to
        show while this concept may, in principle be true to the academic
        oncologist it is, in practice, nonsense to practising epidemiologists".
        Nevertheless, Dr McCullagh's summary of this meeting of the
        International Agency for Research on Cancer, the French National
        Institute for Health and Medical Research and the UK Pneumoniconiosis
        Unit of the Medical Research Council reported (at 132) that as to lung
        cancer the risk among asbestos workers was not wholly confined to
        smokers, and that the data of Hammond et al suggested a multiplicative
        relationship between exposure and smoking, while McDonald's own data
        suggested something between the multiplicative and the added models.
        With respect to the concept of "no safe limit" for any carcinogen, there
        was considerable discussion of this matter and the general feeling at the
        meeting seemed to be that there was in fact no safe limit.
602          The documents include a memorandum of 6 April 1966 (Exhibit 156,
        vol 3, document 347) which recognised an accumulating mass of evidence
        in regard to asbestosis and lung cancer caused by a relatively short
        exposure to asbestos, leading to the possible need to prescribe a zero
        asbestos dust concentration within working factories.
603          There is also a pattern emerging in these documents of the second
        defendant during the 1970's of resistance and opposition to moves to
        amend public health regulations to reduce the maximum permitted
        occupational air concentrations of asbestos dust or to require warnings on
        asbestos products for the purchaser or end user. This can be seen in
        Exhibit 156 (vol 4, document D2307, a memorandum of 14 October 1976,
        a memorandum of 1 October 1974, document D2310), notwithstanding
        that other documents in the possession of the second defendant express
        concern about the use of asbestos products and the need for tighter
        controls (Exhibit 156, vol 4, document 75, a report of a visit to Canberra
        of 22 August 1977, and a report to the Industrial Commission of South
        Australia).
604         In October 1979 the 88th Session of the National Health and Medical
        Research Council published a statement concerning health hazards


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        associated with the use of asbestos in the construction industry. This was
        further amended in November 1981 and the amended document is
        Exhibit 104. The statement begins with a warning about the risks of
        careless use, or excessive exposure of workers, to asbestos fibres coming
        from asbestos materials extensively used in the construction industry. It
        warns that inhalation of excessive asbestos fibre may lead to asbestosis.
        Significantly, in present circumstances, it specifically notes that cigarette
        smokers occupationally exposed to asbestos exhibit markedly increased
        incidences of cancer of the lung compared to that of the general
        population and that there was then some evidence that non-smokers
        exposed to asbestos dust for long periods may have a higher incidence of
        lung cancer than for the general non-smoking population.
605           The NH & MRC statement recognised the problems occurring by the
        diverse work situations encountered in the construction industry and the
        difficulties faced in attempts to quantify the extent of asbestos dust, but
        the Conference expressed concern regarding the adequacy of the then
        current hygiene standards for asbestos dust in the workplace. It
        recommended, that in the light of the present knowledge:

              "(a) exposure to all forms of asbestos dust should be reduced
                   to the minimum that is reasonably practicable; and

              (b)     in any case, occupational exposure to asbestos dust when
                      averaged over a normal eight hour working day should
                      never exceed:
                      (i)       for Crocidolite 0.1 fibres per millilitre;

                      (ii)      for Amosite       and    Chrysotile    1.0 fibre   per
                                millilitre."
        and, in pars 2.2 and 2.4, the statement drew attention to the existence of
        asbestos in laggings for pipes, boilers, refinery equipment etc. and the
        potential hazards to health associated with the removal of sprayed
        asbestos and pipe insulation. With regard to asbestos cement products,
        the statement observed (at par 4.1) that care should be exercised to avoid
        making dust even when hand tools are used and that residues left after
        cutting with fibro cutters, score and snap tools and hand saws should not
        be walked upon unnecessarily but, rather, a high standard of housekeeping
        should prevail and waste collected with an approved vacuum cleaner or
        the surface wet with water before sweeping. Rasping, planing and filing
        should be avoided whenever possible.


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606          Another publication by the NH MRC of June 1981 set out a Code of
        Practice for working with asbestos cement building materials. This is
        Exhibit 105 which, at p 9, when speaking of the need for regular clean-ups
        in an approved manner to avoid the build-up of deposited dust containing
        asbestos, stated:

              "Dust and swarf should not be swept dry, but should be
              regularly collected with an approved vacuum cleaner."

607          In an information leaflet published by the Workers' Health Centre in
        1981 (Exhibit 107), there are warnings that asbestos exposure can cause
        asbestosis, lung cancer, mesothelioma and gastro-intestinal cancers and
        that there is no safe level for asbestos exposure. It contains an
        observation that 2 fb/ml was then the legally prescribed "safe" level in
        New South Wales for asbestos exposure and that this was probably true
        when it came to asbestosis but that for asbestos-caused cancer it was not
        possible to establish any safe level of exposure. At p 4 of the brochure
        there was an explanation of how smoking, in combination with exposure
        to asbestos, increases the risk of developing lung cancer by a factor of
        about 11.

Newspaper and media publications
608           A further source of evidence of information generally available to the
        public about the risk of asbestos exposure in the workplace is the
        collection of many articles relating to the perceived threat of asbestos
        published in various Australian newspapers. There is a large quantity of
        these publications. They comprise Exhibit 150(1), (2) and (3), being three
        lever arch files of newspaper or media articles of such work which cover
        the period from 1967 to 1992, and include extracts from Western
        Australian newspapers - "The West Australian", "Weekend News",
        "Sunday Times", "Daily News", other Australian newspapers - "The
        Age", "The Herald", "The Canberra Times", "The Geelong Advertiser",
        "The Australian Financial Review", "The Sydney Morning Herald",
        scientific magazines such as "The New Scientist" and other local or
        regional newspapers. A second set of collections of media articles about
        the risk of asbestos is to be found in Exhibit 162, documents 7 - 25.

609          All these clearly demonstrate that from 1978 onwards it was widely
        known publicly that: asbestos was a hazard in the workplace; that its
        dangers had not been fully understood in the past; but that with the
        understanding then current there was a need for increased vigilance
        against the risks posed of working with asbestos; there was a need to
        modify many working environments to change working systems and to

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        remove or secure asbestos materials or products which, because a lack of
        full understanding of the danger which they presented in the past, were
        very prevalent in many workplaces. It clearly was the case that, from the
        mid-1970's onwards the public was on notice that asbestos in the
        workplace was a serious danger to health.

610           Not all of these documents can be used for all purposes in this
        litigation. The newspaper articles comprising Exhibit 162 include
        documents 21, 22 and 25 which were admitted into evidence only in the
        case against the third defendant. The remaining documents in Exhibit 162
        were admitted against all defendants. Similarly, with respect to
        Exhibit 156 (the four volumes of documents discovered by the second
        defendant coming from its internal records), they were mainly received in
        evidence only against the second defendant. None was admitted in
        support of the case against the third defendant, but those documents
        which, on their face, showed that they came from, or were dispatched to,
        an agency or instrumentality of the Government of South Australia or that
        such a State instrumentality or agency was aware of them, were also
        received against the first defendant - subject to the reservation of liberty to
        apply to object against such use of the documents: a right not exercised
        by the first defendant.

Findings of negligence, breach of contract and breach of statutory duty
             against each of the three defendants
611          Mr Major of the Occupational Health Section of the University of
        Sydney - the same physicist who had written at the Inaugural
        Pneumoniconiosis Conference - wrote on 4 February 1976, reporting on
        inspections of the Elizabeth and Larges Bay factories conducted by James
        Hardie & Coy Pty Ltd. In p 1 of that report Mr Major observed that any
        areas where dry wall asbestos or asbestos cement dust occurred in a
        factory should be considered as potentially harmful unless proved
        otherwise by dust sampling.
612          The prescription by various health standards of a maximum of
        2 fb/mls, and later 1 fb/ml, and still later, 0.2 fb/mls of asbestos in South
        Australia and 0.1 fb/mls (for amphiboles) in Western Australia as detected
        on the membrane filter sampling system during periods from 1972
        onwards, including the periods when Mr Cotton was working in Adelaide
        and then from 1990 onwards in Australind, has led to the first and second
        defendants submitting that the working conditions experienced by
        Mr Cotton complied with those standards and that, therefore, that this
        means there was no lack of reasonable care for the workers' safety by the


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        respective employers according to the standards of those times, even if
        more recent developments and contemporary standards may suggest that
        exposure at those levels could be harmful.

613          This is a powerful submission by the defendants but it needs to be
        examined with some care. In the first place, there is simply no record at
        all of the asbestos dust air concentration which was experienced by
        Mr Cotton and other workmen while working in laying pipes in and
        around Adelaide. The evidence as to the asbestos concentrations
        associated with this work all comes from retrospective estimations or
        from data assembled in the literature of conditions applying in broadly
        comparable activities. Insofar as it has been possible to make such
        estimations, it has been attempted by Mr Kottek, Professor de Klerk and
        Professor Berry, whose evidence I generally accept, or by Mrs Sowden,
        Mr Rogers and Professor Fox, whose opinions I have rejected. None of
        the evidence comes from any measurement, by the membrane filter
        method or any other objective sampling method, of the actual working
        conditions and levels of exposure experienced by Mr Cotton.
614          The evidence of concentrations which I have found probable, while
        admittedly estimating transient and relatively short-term peak exposures,
        are in excess of the maximum exposure limits recommended by the
        authorities. Accordingly, there is no basis for the first or second
        defendant to claim that the exposure levels associated with the work in
        Adelaide were at, or below, levels of exposure then thought acceptable
        because of the absence of sampling or objective testing.

615           Nevertheless, it is implicit in the submissions of the first and second
        defendants that, despite the absence of sampling, their general
        understanding of the risks associated with working with asbestos cement
        pipes in the open, supported by studies of comparable activities in the
        literature, was that such operations did not, or were most unlikely to,
        involve asbestos dust exposures beyond thresholds then believed to be
        acceptable and that, therefore, the absence of actual sampling or studying
        Mr Cotton's working environment, belies no lack of reasonable care or
        indifference to the health and safety of the workforce.

616          Similar considerations apply in relation to Mr Cotton's exposure to
        asbestos dust while working at the third defendant's premises as
        Australind but with the variation that, at crucial times during the asbestos
        removal operations, scientific air sampling by the membrane filter method
        was conducted, supervised by properly licensed qualified contractors, and
        analysed in an independent laboratory but none of the reports suggested


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        any concentrations above the 0.1 fb/ml limit then prescribed by the
        authorities in Western Australia for amphiboles.
617           However, there are shortcomings in the air sampling procedures
        carried out at Australind both as to extent, location of the testing pumps
        and the comparative infrequency of the tests except during periods of high
        activity during asbestos removal operations. This has led me to conclude,
        earlier in these reasons, that such sampling as did occur at Australind did
        not measure the peak exposure levels probably experienced by Mr Cotton
        when working in sweeping operations in the BDR, or in the packing area.

618          There is, in addition, a more fundamental problem associated with
        accepting the defendants' submissions that compliance with the exposure
        standards prescribed from time to time itself demonstrated that reasonable
        care for the health and safety of the worker, or for that matter the
        provision of a safe system of work, had occurred. This is the problem,
        revealed by the literature already discussed, and by the various scientific
        conferences, dating back to the Lyon conference in 1974 reported on by
        Dr McCullagh; the first Pneumoniconiosis Conference held in Sydney in
        1968; the New York Conference of 1964, the Helsinki Protocols and the
        AWARD Criteria that there is no safe level of exposure to airborne
        asbestos and that the entire emphasis of industrial hygiene and safety
        should be devoted to reducing the occasions and extent of exposure to
        asbestos to a minimum rather than attempting to prescribe maximum
        permissible exposure levels.
619           The literature, the scientific conferences and the various reports of
        official or semi-official public bodies all show that the science of
        measuring exposure was inexact, and that the history of attempts had
        revealed over the years that the danger of airborne asbestos particles had
        generally been underestimated, leading to progressive reductions in the
        maximum exposure levels as the danger became more widely accepted by
        governments responsible for exposure standards. Because of this and to a
        very real degree, the prescription of maximum exposure standards by the
        regulatory authorities trailed quite some distance behind informed medical
        and scientific opinion of the day.

Differential risks
620           Of equal, or perhaps greater importance for the present case, the risk
        of serious illness was not the same for all forms of asbestos disease. For
        example, it has long been realised that mesothelioma can be caused by
        relatively low or short exposures to asbestos dust, whereas it was
        believed, and still believed, that much higher levels of exposure and for

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        longer periods, are necessary before clinical asbestosis would develop.
        The controversy over whether or not similar high and long-lasting levels
        of exposure, sufficient to result in asbestosis, are needed for the
        development of lung cancer has been very apparent in this case, but the
        preponderant prevailing view, which I have accepted, is that it is not. The
        literature also demonstrates that, in comparison with the number of cases
        of asbestosis, the presentations of asbestos-related cases of mesothelioma
        and lung cancer are each, mercifully, vastly fewer.
621          There is, therefore, no justification to conclude that practices at work
        places with asbestos exposure standards less than the prescribed maxima
        by the applicable industrial safety regulations for the periods when
        Mr Cotton was employed in Adelaide and again at Australind, were
        sufficient to constitute reasonable care for the prevention of mesothelioma
        or lung cancer, as distinct from asbestosis. This is not to decry in any way
        the importance of those industrial hygiene regulations, or the care or
        knowledge of those persons entrusted with the responsibility of devising
        them and enforcing them. It is, rather, a recognition that any form of
        exposure to asbestos which could reasonably be avoided is dangerous and
        that there are no safe thresholds which have been accepted. The
        historical, and continuing emphasis of the maximum emission standards
        published by the various industrial authorities has obviously been to force
        down, by the threat of penal sanction, the degrees of exposure which were
        widely known at the times to be dangerous as far as possible as part of
        public health measures to reduce the risk of asbestos exposure. It is
        simply not correct to place an interpretation on those efforts that,
        compliance with those standards had solved or eliminated the known
        public health risk associated with asbestos, as distinct from reducing it.

622          The unequivocal state of the medical and scientific opinion
        throughout was that there was no safe threshold and that exposure levels
        less than those prescribed by the regulations could still lead to serious
        consequences, for example, mesothelioma. While analogies are never
        entirely apt, the situation can be compared to that of road speed limits.
        These are prescribed by the responsible authorities having regard to the
        general knowledge of public behaviour and the perceived requirements of
        the locality, but compliance with the prescribed speed limit will not
        always be conclusive of the discharge of the obligation of reasonable care
        by a motorist. There may be local circumstances, such as weather
        conditions, the proximity of children, or a congested inner city locality,
        which make driving at the speed limit positively dangerous. So it is with
        asbestos exposure. I do not consider that demonstrating, even if it could
        have been demonstrated in this case, that Mr Cotton's average level of

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        asbestos exposure calculated over an eight hour day was less than the
        prescribed maximum exposure levels by the applicable regulation in force
        at the time, demonstrated the exercise of reasonable care if, in addition,
        the fact of the matter is that he was exposed to regular but transient short
        periods of high level exposure in an uncontrolled operation involving
        sweeping up of dust containing asbestos particles including Amosite and
        Crocidolite and when it was known that he was an habitual smoker.

623          Compliance with the maximum exposure standards recommended by
        bodies such as the NH & MRC or even prescribed by applicable industrial
        safety regulations does not, necessarily, discharge a relevant duty of care -
        Thompson v Johnson & Johnson Pty Ltd [1991] 2 VR 449 per Murphy,
        O'Bryan and McDonald JJ at 494.
624          The literature referred to in [528] of these reasons specifically
        mentions that it is not only the average long-term exposure which needs to
        be controlled but that even short-term exposures of 10 minutes or so of
        10 fb/mls or above should be avoided. Consequently, I am unable to
        accept the submissions advanced by the defendants in this case that, if it
        could be concluded that Mr Cotton's exposure was less than the maximum
        exposure levels stipulated by applicable regulations at the relevant times,
        that would exclude any finding of lack of reasonable care.

625          There is some force in the submissions of counsel for the first
        defendant that reg 39 of the Industrial Safety Code Regulations (SA) as
        amended (Exhibits 161(1) to (3)) does not expressly apply to the working
        conditions in which Mr Cotton was engaged while with the MWSD
                                                                         h
        because he was, at most times, working in the open rather t an in any
        closed site. That does not entirely dispose of the plaintiff's resort to
        reg 39 for the support of her case. The existence of reg 39 in a section of
        the Regulations dealing especially with asbestos shows particular
        recognition by the State of South Australia that the use of asbestos in
        industry was potentially very dangerous and called for special
        precautions, for the protection of workers. True it is that the particular
        precautions which the regulation prescribed contemplated protective
        practices, exhaust systems, ventilation and the like within factory
        premises but the very point of these precautions was the then widespread
        recognition that asbestos was hazardous and that any industrial use of it
        called for special care, regular supervision, and appropriate precautions.
626          While it may be the case that an employer could not be prosecuted
        for conducting, or tolerating, hazardous working practices involving the
        use of the asbestos in the open under the Regulations, because the


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        Regulations were limited to internal working conditions, that does not
        mean that uncontrolled use of asbestos outside the precise limits of the
        Regulations, was regarded as tolerable or reasonable. Regulation 39 is,
        therefore, indicative of the public recognition in South Australia from
        1972 onwards that working with asbestos is hazardous and that reasonable
        care on the part of an employer in the design of a safe system of work,
        involved an obligation to take suitable and appropriate precautions
        whenever using asbestos or asbestos products.
627          The evidence in this case is clear that no specific precautions were
        taken or exercised by the first defendant in relation to the conduct of
        asbestos cement pipe laying operations by the EWSD in and around
        Adelaide during the years that Mr Cotton was employed and exposed to
        dust from those products between 1976 and 1978. There were no
        respirators, there were no warnings given by the employer or supervisors,
        or for that matter by the second defendant, and no attention was given to
        whether the men were smokers or non-smokers. This meant that the
        asbestos cement pipes were delivered to the site, direct from the factory or
        a storage depot and were, as the evidence disclosed, often coated with thin
        films of dust which had presumably been deposited at the place of
        manufacture or while in store. This was not cleaned by any specific
        process and when the men worked in cutting the pipes, and rasping the
        ends, that was undertaken by a dry process which generated dust and
        fragments of the product.
628           No attempt was made to eliminate this hazard or to gather up the
        fragments which were left lying nearby, subject to agitation by wind,
        weather, the passage of feet and the ultimate earthmoving process that
        filled in the trenches. This was also the case in cutting holes in the pipes
        for the attachment of outlets or making other connections. There were
        also some occasions, rather few, when a powered cutting tool, again using
        a dry process, was employed and generated dust. No monitoring or
        testing was conducted in the workplace and, therefore, Mr Cotton and his
        other employees were subject to regular but intermittent exposure to
        asbestos cement dust containing Chrysotile, Amosite and some
        Crocidolite. These levels of short-term peak exposures cannot be known
        precisely but only estimated.

629          I have little doubt that this was hazardous to all the workmen
        because, clearly enough, even short limited exposures are sufficient to
        cause mesothelioma. While it is not the case Mr Cotton contracted this
        disease, the possibility that it might result from these working conditions
        is itself enough to reveal their shortcomings. However, the view


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        prevailing from before 1975 was that there was no safe level of exposure
        or threshold to asbestos, especially with regard to the potential
        development of lung cancer and, consequently, the obligation upon the
        employer was to take all reasonable steps to eliminate exposure to
        asbestos as far as was practicable and, to the degree that it was
        impracticable, to implement protective measures by the use of wet
        processes, respirators, protective clothing and the like to minimise this.
        Neither approach was adopted at the time by the first defendant for
        Mr Cotton and his fellow employees and this leads to my conclusion that
        there was a failure by the first defendant to exercise reasonable care to
        provide a safe system of work.

630           Reliance was placed on the submission that the average
        time-weighted level of exposure which could be expected to arise from
        the use of asbestos cement pipes in pipe laying operations in the open was
        below the accepted tolerable limits of asbestos exposure for the times and,
        consequently, that the absence of protective work practices, warnings or
        special instructions for the employees, by the first defendant was not
        negligent. This proposition has already been partly dealt with by the
        observation that it was realised at the time that there were no safe
        thresholds and that there was a positive obligation on any employer
        requiring workers to work with asbestos products to take the steps to
        minimise any potential exposure to asbestos dust and that this was not
        done. Secondly, however, this argument takes no account of transient
        peak exposures at high levels which, even if brief, are for the reasons
        already given potentially very dangerous. Thirdly, any assumption by the
        first defendant that a maximum prescribed level of asbestos was tolerable
        in the workplace (and the first defendant did not present any evidence that
        this was its view or assumption at the relevant time) is, on the evidence,
        entirely unjustified. The literature and research which was available at the
        time, and to which the framers of the Regulations must have had, or
        should have had, access was overwhelmingly to the effect that efforts
        should be taken to avoid or reduce to the maximum possible any asbestos
        exposure. There was no support in science or in the literature for the view
        that a particular level was safe or reasonable but, rather, the research and
        the widespread medical and scientific discussion was to the one effect that
        whenever and wherever asbestos products were in use precautions needed
        to be taken to eliminate or to minimise the risk from dust exposure. This
        was simply not addressed by the first defendant.
631          With respect to the second defendant, it was well aware of the risks
        of asbestos exposure and of the vast quantity of literature, scientific
        investigations and worldwide reports about the hazards involved. It

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        actively assembled these records and its senior staff, medical advisors and
        several of its factory managers were fully aware of this. Not only is this
        apparent from the evidence of Mr Russell but the collection of materials
        in the second defendant's own documents (Exhibits 156, vols 1 - 3,
        Exhibits 114 to 113 and Exhibits 133 to 136) all demonstrate this. In my
        view, the second defendant had a clear duty to its customers and to the
        end users of their products to bring to attention the risks associated with
        handling, working with, and particularly cutting asbestos cement pipes
        and other products and to recommend special work procedures which
        would minimise this. None of this was done in the case of the supply of
        the AC pipes to the first defendant during the years that Mr Cotton was
        employed and, in my view, this constituted a breach of the duty of care
        due by the second defendant to Mr Cotton.
632          Turning to the case against the third defendant, it is necessary to
        consider both the allegations of negligence and the allegations that there
        were breaches of the provisions of the Occupational Health, Safety and
        Welfare Regulations 1988, discussed at [548] above. I am satisfied that
        there were failures to comply with the Regulations, in particular reg 322,
        reg 803, reg 804 and reg 815 as discussed in [561] - [570] above and that
        these have resulted in the third defendant being in breach of its statutory
        duty towards Mr Cotton.
633           In relation to the claims against the third defendant, it is necessary to
        take account of the steps which the third defendant took to identify the
        existence of potential asbestos hazards at the workplace at Australind, to
        remove the risk posed by those items of asbestos and to carry out air
        monitoring in the workplace in order to ensure that its workers were not
        exposed to hazards. Clearly, the third defendant did embark upon a major
        asbestos eradication programme, which was very extensive and very
        expensive and that, from time to time, air monitoring was conducted in
        the workplace. The problem is that the asbestos removal programme was
        only conducted in stages over a period of years commencing in 1990 and
        lasting until 1997, notwithstanding the fact that there had been industrial
        action by subcontractors on the site protesting about the asbestos
        environment as early as 1988.
634           The asbestos removal programmes conducted began with the
        asbestos lagging on the pipes in the BDR during 1991/1992 but did not
        involve the removal of all asbestos from the BDR, leaving the insulation
        and seals on the band drier hatch doors, other lagging on the top of the
        BDR and, of course, the asbestos cement roofing which was old and in a
        friable and deteriorating condition. The removal programmes to eliminate


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        those further asbestos components in the BDR again took place in stages
        (during shut downs or maintenance periods) over the years from 1990 to
        April 1995 and the roof removal was not completed until late 1997.
        Removal of the asbestos cladding on the walls, internal walls and roofing
        in the packing areas and in which Mr Cotton was also employed was not
        completed until about 1998 [206].
635           During these periods there was an ever present risk of exposure to
        asbestos dust and, in Mr Cotton's case, particularly during sweeping up
        operations. In the time that he was working periodically in the BDR from
        the second half of 1991 until late 1992 he was sweeping up the dust from
        the floor which contained the fragments and shedding from the exposed
        lagging containing Chrysotile, Amosite and Crocidolite on the steam
        pipes and was, as I have found, exposed to short-term, but regular, high
        peak exposures of asbestos containing Chrysotile, Amosite and
        Crocidolite. No efforts were taken to avoid this, to conduct dust
        suppression by wetting or other methods or to provide protective
        equipment to the men working on those tasks. Again, the danger of
        development of any asbestos disease, including mesothelioma, was clearly
        patent and the failure to take steps to minimise this was, in my view, in
        breach of duty by the third defendant towards Mr Cotton. The question in
        this case is whether it caused to a material degree his fatal disease.
636          I have discussed elsewhere in these reasons the air monitoring
        programmes carried out at Australind and have concluded that they were
        mainly conducted during the asbestos removal operations. They were
        certainly not conducted in relation to the kind of intensive sweeping up
        operations in which Mr Cotton was employed and, for that reason, I
        cannot regard them as indicative of the conditions under which he and his
        colleagues were working of which the third defendant should have been
        aware.

Approach to causation
637           For the plaintiff to succeed, not only must she establish negligence or
        breach of duty on the part of one or more of the defendants in this action
        but she must also satisfy the court, on the balance of the probabilities, that
        that negligence or other breach of duty by that particular defendant caused
        or contributed to the fatal lung cancer which, in turn, caused the death of
        Mr Steven Cotton. Proof of causation has been the real battleground in
        this case and not without reason.

638         The diagnosis of lung cancer in Mr Cotton's case was not in itself
        conclusive or indicative of the cause of the cancer. There was no

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        histological, radiological or other forensic evidence upon which to basis a
        specific attribution of the cause of the disease. This is not unusual
        because, as Professor Musk described, the location, size and type of a lung
        cancer such as this was not indicative of the cause, in the sense that it did
        not positively confirm or suggest the likelihood of a particular cause nor,
        negatively, exclude or diminish the prospect of some other possible cause.
        The finding, in that sense, was inscrutable. According to Professor Musk
        and the other medical experts, the attribution of the particular cause or
        causes for Mr Cotton's cancer required a clinical decision based largely on
        the history provided by the patient and the known effects of particular
        carcinogens operating alone or in combination with others.

639           In the light of Mr Cotton's history, the major potential causes of his
        lung cancer were the effects of his chronic smoking and his history of
        exposure to asbestos fibres. In addition, however, as is always the case,
        there is the possibility that the lung cancer may have developed from
        some other unknown, and unidentifiable cause because it has been long
        recognised that such a cancer may develop in the absence of exposure to
        asbestos or to smoking and be due to one or more other unrelated causes.
        To say that such a cancer may develop from other unrelated causes
        requires no qualification but it remains the case that people who have
        never smoked, or who have never worked or spent any time in an
        environment of asbestos contamination, can still be exposed to the effects
        of smoking and asbestos because in most places and at most time there is
        a low background level of smoke or asbestos in the atmosphere or
        environment. This cannot be avoided and presents an inescapable risk
        that those who do not smoke or work with or in the vicinity of asbestos
        may, nevertheless, develop cancers due to asbestos or smoking or to other
        causes. This is known as the background level of risk. It is in those
        environments in which the background level of asbestos is increased, due
        to the use of asbestos or asbestos products, which might be avoided by the
        exercise of reasonable care, where the elevated risk of contracting an
        asbestos-related disease becomes significant.
640          Accordingly, in Mr Cotton's case, his lung cancer may have been
        caused by his smoking, or by his exposure to asbestos, or by the possible
        influence of some unknown and unidentified carcinogen which has
        escaped notice, or by the background risks of asbestos or smoking, or the
        combination of one or more of these factors. The undisputed medical
        evidence is that chronic smokers who are exposed to asbestos are at a
        greater risk of developing a variety of asbestos-related diseases including
        lung cancer and that the toxic effects of smoking and of asbestos combine
        with each other in a synergistic way to increase the risk of developing that

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        disease. The medical evidence is to the effect that the combined effects of
        tobacco smoking and asbestos exposure in some unknown way enhance
        the risks of developing lung cancer and that the cumulative or synergistic
        effect is not additive but multiplicative, or nearly multiplicative.
641          In the present case therefore, the plaintiff will succeed if the evidence
        establishes that it is more probable than not that Mr Cotton's lung cancer
        was caused by asbestos arising from one or both of his periods of
        occupational exposure to that mineral or if it supports the conclusion, on
        the probabilities, that his cancer was caused to a material extent by the
        combined effects of his periods of asbestos exposure with the effects of
        his chronic smoking.

642          By contrast, however, the plaintiff will fail if the probabilities are
        that the cancer was caused by Mr Cotton's smoking alone, or by some
        other unknown carcinogen, or because of the ever present background
        risks for the entire population of exposure to smoking or asbestos other
        than in his working environments with the first and third defendants. Put
        another way, the plaintiff will fail unless the evidence allows a conclusion
        to be drawn, on the balance of probabilities, that one or both of these two
        periods of occupational exposure to asbestos alone or in combination with
        other potential carcinogens, particularly cigarette smoking, made a not
        insignificant contribution to the development of Mr Cotton's lung cancer.
        More particularly, as the case was conducted, the plaintiff's case will
        succeed or fail according to whether or not the evidence establishes that
        one or both of the occupational periods of exposure to asbestos, acting in
        combination with the long smoking history, caused this lung cancer
        because all the consultants accepted that Mr Cotton's smoking was a
        significant, probably the most significant, contributing cause of his
        disease.
643          The legal principles applying in such a situation involve some
        complexities. Causation is a question of fact to be determined by the
        application of commonsense to the facts of each case: March v E & M H
        Stramare Pty Ltd (1991) 171 CLR 506 at 515 per Mason CJ; Bennett v
        Minister for Community Welfare (1992) 176 CLR 408 and Bendix
        Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 per Beazley JA at 335.
        The onus remains on the plaintiff to prove causation on the balance of
        probabilities; Bonnington Castings Ltd v Wardlaw [1956] AC 613;
        McGhee v National Coal Board [1973] 1 WLR 1; Wilsher v Essex Area
        Health Authority [1988] AC 1074 and March v E & M H Stramare Pty
        Ltd (supra) and this onus is not discharged by establishing that a
        particular matter cannot be excluded as a cause of the injury because, as


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        said by Hope AJA in Sydney County Council v Furner (1991) 7
        NSWCCR 210 at 214:
              "In other words, to establish that medical evidence supports a
              conclusion that the cause could not be excluded as a cause of
              injury does not establish, without more, that particular cause in
              fact resulted in or caused the injury."
        But, if the plaintiff can establish a prima facie case, an evidentiary onus
        shifts to the defendant which, if not discharged, may enable the plaintiff to
        succeed on the basis of an inference drawn from even slight evidence
        adduced on his or her behalf - Bendix Mintex Pty Ltd v Barnes (supra) at
        339. It will be sufficient for the plaintiff to establish that his injuries were
        "caused or materially contributed to" by the defendant's wrongful conduct,
        and this remains the principle when the plaintiff sues more than one
        defendant but in that case a plaintiff must demonstrate that each defendant
        from whom he seeks a verdict caused or materially contributed to his
        injury: Bendix Mintex Pty Ltd v Barnes (supra) at 311.
644           Where, as in the present case, there is no forensic evidence which
        directly indicates, or tends to indicate, that the lung cancer was caused by
        asbestos it is possible, indeed necessary, for the plaintiff to seek to
        establish the alleged causal connection by circumstantial evidence as has
        been the approach in this case. The circumstantial evidence may include,
        as it has in this case, details of the nature and duration of known
        exposures of the deceased to asbestos, the absence of other potential
        carcinogens as possible causes of the disease as far as they can be
        eliminated, the presence of another potential carcinogen (chronic tobacco
        smoking) and its effects, as far as they are known, in interacting with the
        asbestos carcinogen and other circumstances about the frequency, periods
        of latency and likely onset of the disease when caused by one or more of
        such carcinogens.

645          Other pieces of circumstantial evidence, which in this case are relied
        upon by the defendants, are the opinions of expert epidemiologists about
        the relative risks of contracting such a lung cancer as measured from
        studies of the general population, or from studies of industry groups,
        including those contracting this and other asbestos-related diseases. The
        epidemiological evidence will be another source of circumstantial
        evidence which may, or may not establish, or refute, a probability that
        Mr Cotton's lung cancer was due in whole or in part to one or both of his
        periods of occupational exposure to asbestos. A detailed examination of
        the potential significance of such epidemiological evidence in an asbestos
        carcinoma case can be found in the judgment of Spigelman CJ in Seltsam

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        Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262 in
        which, by a majority, Spigelman CJ and Davies AJA with Stein JA
        dissenting, held that the plaintiff/respondent had failed to establish that
        exposure to asbestos had caused the renal cell carcinoma from which he
        later died. As said by Spigelman CJ at [59] and [60]:

              "[59] Epidemiology is the study of the distribution and
              determinants of disease in human populations. It is based on
              the assumption that a disease is not distributed randomly in a
              group of individuals. Accordingly, sub groups may be
              identified which are at increased risk of contracting particular
              diseases.

              [60] Epidemiological evidence identifies associations between
              specific forms of exposure and the risk of disease in groups of
              individuals. Epidemiologists do make judgments about whether
              a statistical association represents a cause-effect relationship.
              However, those judgments focus on what is sometimes called in
              the epidemiological literature 'general causation': Whether or
              not the particular factor is capable of causing the disease.
              Epidemiologists are not concerned with 'specific causation':
              Did the particular factor cause the disease in an individual
              case?"
        And then, the learned Chief Justice went on to say at [78] - [80]:
              "[78] Epidemiology is, as I have noted above, concerned with
              the study of disease in human populations. It is not, of itself,
              directed to the circumstances of an individual case. For the
              purpose of determining whether exposure to a particular
              substance is the legal cause of a particular disease,
              epidemiology only provides evidence of possibility.
              [79] Evidence of possibility, including expert evidence of
              possibility expressed in opinion form and evidence of
              possibility from epidemiological research or other statistical
              indicators is admissible and must be weighed in the balance
              with other factors, when determining whether or not, on the
              balance of probabilities, an inference of causation in a specific
              case could or should be drawn. Where, however, the whole of
              the evidence does not rise above the level of possibility, either
              alone or cumulatively, such an inference is not open to be
              drawn.



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              [80] The common law test of balance of probabilities is not
              satisfied by evidence which fails to do more than establish a
              possibility. See especially the unanimous joint judgment of the
              High Court in St George Club Ltd v Hines (1961) 35 ALJR 106
              at 107; [1962] ALR 39 at 41, where the court referred to
              Bonnington Castings v Wardlaw [1956] AC 613 as authority for
              the following proposition:-

                 'In an action at law a plaintiff does not prove his case
                 merely by showing that it was possible that his injury was
                 caused by the defendant's default.' "
646           Central to the approach of the epidemiological studies of the
        statistical risk of developing a disease as a result of a particular cause or
        precipitant is the notion of relative risk. As Spigelman CJ said in Seltsam
        Pty Ltd v McGuiness (supra) at [67]:

              "[67] Most epidemiological studies identify the strength of an
              association by a measure called relative risk (RR). RR is
              defined as the ratio of the incidence of disease in exposed
              individuals compared to the incidence in unexposed individuals.
              If the relative risk equals 1.0, the risk in exposed individuals is
              the same as the risk in unexposed individuals. If the relative
              risk is greater than 1.0 the risk in exposed individuals is greater
              than the risk in unexposed individuals."

647           In the present case the defendants submit that unless the plaintiff
        could establish that Mr Cotton's RR of developing lung cancer was 2.0 or
        more the plaintiff should fail because an RR of 2.0 signifies that the
        exposed group is twice as likely as the unexposed group to contract the
        disease, meaning that in a group comprising individuals who had been
        exposed to the risk and who had contracted the disease there could be
        expected to be 50 per cent caused by the general background risk of the
        disease and 50 per cent caused by the exposure to the known carcinogen,
        that is twice as many affected patients as would be expected to occur in
        the general unexposed population. This would mean that in such a group
        of affected patients 50 per cent could be expected to have had their
        cancers caused or contributed to by their known exposure to the
        carcinogen and the other 50 per cent to have had their cancers caused by
        the background risk. As the RR increases beyond 2.0 the proportion in
        that sample group whose cancers could be expected to be caused by the
        specific exposure to the known carcinogen would increase and,
        consequently, so it is argued, the probability that any individual suffering


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        from cancer in that group had his or her cancer caused by the known
        exposure, rather than by the general background risks would increase.
        But that would not be the case unless and until the RR exceeded 2.0.

648           Immediately it is obvious that this analysis is effective at a
        macro-statistical level when dealing with large populations or groups but
        that it is entirely inconclusive when dealing with an individual member of
        that group when attempting to deduce whether or not his or her illness was
        actually caused by exposure to the known carcinogen. The point can be
        established in a slightly different way. If a person is a member of a group
        which has the known risk of 70 per cent of developing a certain disease
        due to the effects of a suspected carcinogen and he does develop that
        disease, this does not exclude the possibility that he may be one of the
        30 per cent in that group whose disease was not caused by that particular
        exposure. Similarly, if a person is a member of a group where the risk of
        developing a disease due to occupational exposure is only 10 per cent, and
        he does develop that disease, that does not mean that his disease was not
        caused by that exposure only that it is less likely, by odds of nine to one
        that it did.

649           These limitations upon the significance and application of
        epidemiological evidence when determining a controversy concerning
        causation in a particular case are ever present and insidious and must
        constantly be acknowledged. The question for decision must always be
        whether the increased risk of contracting the disease due to the known
        exposure to the potential carcinogen did cause or materially contribute to
        the injury actually suffered.
650           There is a line of authority dealing with causation in Australia, traced
        by McLure JA in her Honour's judgments in Shire of Brookton v Water
        Corporation [2003] WASCA 240 at [65] - [70] and again in City of
        Stirling v Tremeer [2006] WASCA 73; (2006) 32 WAR 155 at 171 - 174
        at [72] - [80] which includes consideration of McGhee v National Coal
        Board (supra); Bonnington Castings Ltd v Wardlaw (supra) and which
        refers to the judgment of Gaudron J in Bennett v Minister for Community
        Welfare (1992) 176 CLR 408 at 420 - 421, to Chappel v Hart [1998]
        HCA 55; (1998) 195 CLR 232 in the dissenting judgment of McHugh J at
        the particular passage which, however, was later approved in Naxakis v
        Western General Hospital [1999] HCA 22; (1999) 197 CLR 269 and
        which appears to have been endorsed by Gummow J in Rosenberg v
        Percival (2001) 205 CLR 434 that, in the language of Gaudron J in
        Bennett (supra):



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              " ... generally speaking, if an injury occurs within an area of
              foreseeable risk, then, in the absence of evidence that the breach
              had no effect, or that the injury would have occurred even if the
              duty had been performed, it will be taken that the breach of the
              common law duty caused or materially contributed to the
              injury."
        The proposition was formulated by McHugh J in Chappel v Hart (supra)
        at 244 - 245, [27]:
                "If a wrongful act or omission results in an increased risk of
                injury to the plaintiff and that risk eventuates, the
                defendant's conduct has materially contributed to the injury
                that the plaintiff suffers whether or not other factors also
                contribute to that injury occurring. If, however, the
                defendant's conduct does not increase the risk of injury to
                the plaintiff, the defendant cannot be said to have materially
                contributed to the injuries suffered by the plaintiff."
        In Seltsam Pty Ltd v McGuinness (supra) Spigelman CJ pointed out at
        [107] that the justification for this approach depended upon the
        conclusion, of whether, by way of finding or inference, that it was the
        actual risk of suffering harm from the recognised potential cause which
        was postulated to have occurred because if that risk had not eventuated
        and some other risk had instead materialised, the conclusion of effect
        from exposure to a potential cause could not be drawn.
651           However, it is very difficult if not impossible always to maintain a
        distinction between exposure to an increased risk of harm from a known
        potential cause, on the one hand, and the question of whether or not the
        elevated risk of harm from known exposure to that potential cause did in a
        particular case eventuate, because the asserted distinction is not between
        unrelated and distinct concepts. McLure J recognised the interrelationship
        of these concepts in Shire of Brookton v Water Corporation (supra) at
        [69] where, although addressing suggested distinctions between breach of
        duty and causation, her Honour cited Gaudron J in Bennett (supra), at
        422, for the proposition that:

              " ... there is usually no reason to separate or distinguish the
              question of breach of a common law duty from that of causation
              because the duty relates to precautions a reasonable person in
              the position of the person sued would have taken to prevent a
              foreseeable risk of the harm of the kind suffered. A precaution
              would not be classified as reasonable unless its performance


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              would, in the ordinary course of events, avert the risk that called
              it into existence."
652          Similarly, it can be said that as the risk of contracting a particular
        disease from exposure to one of several potential causes for that disease
        increases because of the increasing effect of that exposure, so it becomes
        more likely that if the person so exposed contracts that disease, it is this
        known exposure rather than other potential causes which has actually
        caused it. As this approach to causation is circumstantial, the increasing
        level of exposure to the risk is itself a potent circumstance which may lead
        to the inference of causation being drawn but it is still necessary to
        consider all material circumstances.

653          After conducting a comprehensive review of the authorities,
        including American decisions in Seltsam Pty Ltd v McGuinness (supra)
        which addressed the significant epidemiological evidence and the
        significance of increases in relative risk, Spigelman CJ said, at
        [135] - [137]:

              "[135] Some of the American cases indicate that the RR of 2.0
              should not be applied as a rigid mathematical formula. Others
              appear to apply it in that way.
              [136] The predominant position in Australian case law is that a
              balance of probabilities test requires a court to reach a level of
              actual persuasion. This process does not involve a mechanical
              application of probabilities ... [citations omitted].
              [137] In Australian law, the test of actual persuasion does not
              require epidemiological studies to reach the level of the relative
              risk of 2.0, even where that is the only evidence available to a
              court. Nevertheless, the closer the ratio approaches 2.0, the
              greater the significance that can be attached to the studies for
              the purposes of drawing an inference of causation in an
              individual case. The 'strands in the cable' must be capable of
              bearing the weight of the ultimate inference."

654          Nevertheless, what appears to be an insistence that supplementary
        evidence of causation is essential before a conclusion could be drawn that
        a material increase in the risk of injury from a potential cause had in fact
        occurred, arises from the decision of the New South Wales Dust Diseases
        Tribunal in Judd v Amaca Pty Ltd (No 2) (2003) 25 NSWCCR 488 on
        which counsel for the second defendant in this case placed reliance. That
        was a lung cancer case of a man who had smoked heavily for more than

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        40 years, where the plaintiff alleged that the cancer was materially
        contributed to by occupational exposure to asbestos. Curtis J held that in
        a case where exposure to a toxic substance is alleged but no direct injury
        mechanism is proved, it is necessary to decide the issue of causation on
        the basis of statistical probabilities and that where a claimant has lung
        cancer but no asbestosis and there is no other particular causal
        circumstance, the cancer can be attributed to asbestos if the degree of
        exposure more than doubled the risk of lung cancer. His Honour went on
                     f
        to find that i a plaintiff has to rely upon epidemiological evidence alone
        he or she must usually show an RR higher than 2.0. In that case the
        combined effect of smoking and asbestos exposure elevated the RR but,
        not in his Honour's view beyond 2.0 and that although such a case cannot
        be decided only by strict analysis of probabilities, the claimant had not
        demonstrated proof of causation and therefore failed.
655          In Judd v Amaca Pty Ltd (No 2) (supra) Curtis J rejected the two
        essential contentions of the claimant which were (at 491):

              "1.     His cancer is more likely to have been induced by
                      asbestos, or asbestos in combination with smoking than
                      either the background risk to which the whole population
                      was exposed, or to smoking alone, or

              2.      all lung cancers which develop after exposure to both
                      cigarette smoke and asbestos fibre are caused by the
                      agency of both toxins operating in combination and his
                      asbestos exposure has contributed to that pathological
                      process which resulted in his cancer."
        The reason for the rejection of these contentions were very similar, to a
        significant extent, to the reasons for acceptance by his Honour of the
        relevance of the Helsinki Protocol which included the proposition that "in
        the absence of any causal circumstances peculiar to the plaintiff,
        carcinoma of the lung may be attributed to asbestos exposure in the
        absence of asbestosis when the exposure was sufficient to more than
        double the risk of contracting lung cancer in an individual".
656           However, in the present case, in the opinions of Professor Musk,
        Professor Leigh, Dr Kendall and Professor de Klerk and Professor Berry
        the Helsinki Protocol is not universally accepted as being a definitive
        guide of attribution, for clinical purposes, of asbestos as a cause for lung
        cancer and is, instead, principally concerned with protocols for the
        attribution of levels of exposure to support conclusions of occupationally
        induced asbestosis and, further, did not deal adequately with the issue of

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        attribution of asbestos as a cause of lung cancer where the persons
        exposed were also chronic smokers.
657           There are issues in the present case which do not appear to have been
        raised in Judd v Amaca Pty Ltd (No 2) (supra) and, although any decision
        of the NSW Dust Diseases Tribunal commands great respect, because of
        the special proficiency and expertise of that Tribunal in cases of
        industrially induced lung disease, that decision is not binding on me and I
        must consider the evidence and submissions in this case without
        constraint arising from the findings in Judd v Amaca Pty Ltd (No 2)
        (supra). Nevertheless, I have given careful consideration to the reasons
        for decision in that case but these do not appear to me to cover the
        situation which has been reached in this case, namely whether or not, on
        the probabilities it has been established that asbestos exposure made a not
        immaterial contribution to the fatal tumour, together with tobacco, where
        other potential carcinogens or background risks have effectively been
        excluded.

658          The second defendant also places reliance on another decision of the
        Dust Diseases Tribunal of New South Wales - McDonald (Executrix of
        the estate of late T G H McDonald) v State Rail Authority (NSW) [1998]
        NSWDDT 4; (1998) 16 NSWCCR 695. This was also a claim arising
        from a death due to lung cancer following occupational exposure to
        asbestos and in which the deceased showed no signs of asbestosis.
        Nevertheless, the claimant sought to prove causation by evidence
        suggesting that the cumulative fibre burden which the deceased had
        ingested due to his asbestos exposure raised a probability that this had
        made a material contribution to the development of the disease.
659          The expert evidence differed on the cumulative burden ingested by
        the deceased ranging from 29.3 fibre/ml years to 5.0 fibre/ml years.
        O'Meally J had reservations about the accuracy of the estimations of
        cumulative exposure and was unable to make a finding about cumulative
        exposure. Earlier, having examined the scientific literature, his Honour
        accepted that proof of a probability of a certain cumulative fibre burden
        could lead to an inference that the asbestos exposure had made a material
        contribution to the development of the particular cancer but he adopted
        the approach that an RR of 2.0 would first need to be established and that
        on the basis of the Helsinki Protocol and other writings a 25 fibre/ml year
        cumulative exposure or more would need to be demonstrated. In other
        words, his Honour accepted evidence that a cumulative fibre burden
        sufficient to account for a diagnosis of asbestosis was necessary before an
        inference could be drawn that asbestos exposure associated with a


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        non-specific lung cancer had made a causal contribution. The evidence
        before his Honour also suggested that the presence of asbestosis, or a
        cumulative exposure sufficient to cause asbestosis, was essential to such
        an attribution. To my mind that is essentially a finding of fact made on
        the evidence presented in the particular case, rather than the establishment
        of any principle or rule of law.
660           The evidence adduced in this present case has been far more
        extensive and by far the greater preponderance of the expert scientific
        opinion, including the AWARD Criteria has rejected the hypothesis that
        the presence of asbestosis is an essential concomitant before an attribution
        of causal effect can be made between asbestos exposure and a
        non-specific lung cancer. Furthermore, I have also found that the opinion
        evidence presented before me, and the weight of the very extensive
        scientific literature in evidence, accepts that lung cancers can develop due
        to asbestos from cumulative exposure doses less than regarded as
        sufficient to cause asbestosis - in other words, that asbestosis is a disease
        occuring after higher cumulative exposures to asbestos than lung cancer.
        It follows that the decision in McDonald's case (supra) can be
        distinguished on the facts and that it does not support the submissions
        made by the defendants in the present actions.

661           At this point it is also necessary to mention, if only to put to one side,
        the existence of a doctrine which may or may not be applicable in
        different circumstances but which would, if applicable, assist a plaintiff
        alleging disability or death from an occupationally induced asbestos
        exposure, in overcoming some of the evidential problems on causation
        issues which stem from current limitations in medical and scientific
        understanding of the cause and development of such diseases. The
        problem which this expedient addresses is that which occurs when the
        claimant's asbestos disease is known to have been caused by wrongful
        exposure to asbestos hazards by one or more of several defendants but it is
        not possible to prove, because of the lack of scientific knowledge, which
        one or more of those episodes of exposure caused the onset of the asbestos
        disease and, therefore, not possible to prove which one or more of the
        defendants, to the exclusion of another or others is liable on conventional
        grounds. It arises in those cases where it can be said with confidence that
        the particular disease contracted is an "indivisible disease".
662          This problem was addressed by the House of Lords in Fairchild v
        Glenhaven Funeral Services Ltd [2002] UKHL 22; [2003] 1 AC 32. In
        that case the claimant widow was able to prove to the requisite standard
        that her late husband had died of mesothelioma as a result of asbestos


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        exposure in the workplace due to negligence of his employer. There were
        three periods of employment with three different employers each
        involving negligent exposure to asbestos and while the evidence showed
        that the mesothelioma occurred as a result of one of those exposures it
        was not possible, on the state of scientific knowledge, to say which.
        Accordingly, one of the three defendants must have caused the fatal
        mesothelioma but it was not possible to show that one, rather than either
        of the other employers was responsible. To avoid injustice the House of
        Lords modified the rules of causation by providing an exception for this
        type of case to the effect that proof of material contribution to the
        elevation of the known risk, in cases where the victim contracted the
        actual disease which the exposure threatened, would be treated as
        causative of the contraction of the disease so that damages could be
        recovered against each of the employers who had wrongfully exposed the
        deceased to the elevated risk.
663          In Fairchild's case (supra) it was clear that the deceased's
        mesothelioma had been caused by exposure to asbestos, and not by some
        other carcinogen, and that the only significant exposures occurred during
        the three separate periods of employment with the three defendants. It
        followed that one of these periods of exposure must have caused the
        disease, although which one it was could not be ascertained. In
        recognising that the exception so created would inevitably need revision
        and adjustment in the future, their Lordships in Fairchild (supra)
        recognised the probable emergence of variations on the facts which would
        pose questions for future decision about whether or not the exceptional
        rule should be applied in those different cases. One such variation
        postulated was where the deceased had been exposed in the course of his
        employment by one of the defendants to other sources of asbestos where
        that exposure was not negligent. Lord Bingham would have excluded
        such a case from the application of the principle - see [34] and Lord
        Hoffmann ventured a similar opinion at [61] and [73], but Lord Rodger of
        Earlsferry allowed for a non-tortious exposure by a defendant w washo
        also responsible for a tortious exposure but reserved his position on any
        other non-tortious exposure: see [169] - [170].
664          In the later case of Barker v Corus (UK) Ltd [2006] UKHL 20;
        [2006] 3 All ER 785 at 793 when speaking of the variety of approaches
        taken in Fairchild (supra), Lord Hoffmann said at [11]:

              "The assistance which can be derived from these various
              formulations is limited. No one expressly adverted to the case
              in which the claimant was himself responsible for a significant


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              exposure. Lord Bingham's formulation requires that all possible
              sources of asbestos should have involved breaches of duty to
              the claimant; Lord Rodger allowed for a non-tortious exposure
              by a defendant who was also responsible for a tortious exposure
              but reserved his position on any other non-tortious exposure.
              The most that can be said of the others is that they did not
              formulate the issue in terms which excluded the possibility of
              liability when there had been non-tortious exposures."
        Barker v Corus (UK) Ltd (supra) was both an application and a
        modification of the exception developed in Fairchild. The result in
        Fairchild was that, upon the application of the exceptional rule as to
        causation, all defendants who had materially elevated the risk of
        contracting the fatal disease by negligent exposure to asbestos were found
        liable in solidum and, for that reason, there was no basis available for
        apportionment of their liability as between the defendants. This
        conclusion of liability in solidum was discarded in Barker v Corus (UK)
        Ltd where the House of Lords decided that, in such cases, it would be the
        responsibility of the court to apportion the liability for damages between
        the defendants on a basis, thought appropriate by the trial Judge, for
        reflecting the apparent contribution of each such defendant to the
        development of the disease - whether by reason of the duration of the
        exposure in the course of the employment, its intensity or otherwise.
665          The origin and development of the principle applied in Fairchild was
        discussed by all their Lordships in Barker v Corus (UK) Ltd (supra) and
        in one of those explanations Lord Walker said at [104]:
              "In Fairchild v Glenhaven Funeral Services Ltd the House
              explicitly established or affirmed a new principle (already
              emerging in McGhee v National Coal Board [1973] 1 WLR 1)
              and began to mark out the field in which that principle applies.
              A defendant who is under a duty to protect a worker from the
              risk associated with a single noxious agent, and who breaches
              that duty by exposing the worker to that very risk, may be held
              liable even though the worker cannot (on the traditional 'but for'
              test) prove that his ensuing disease was caused by that exposure.
              Exposing the claimant (or the deceased worker whose personal
              representative is the claimant) to the risk of injury is in this
              situation equated with causing his injury. This result is
              achieved not by a manipulation of the burden of proof, or some
              other comparable fiction, but as an explicit variation of the
              ordinary requirement as to causation, adopted in order to avoid


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              injustice: see the speech of Lord Bingham of Cornhill [2003] 1
              AC 32; Lord Nicholls of Birkenhead at [42] - [45]; Lord
              Hoffman at [47] - [61], [62] and [65] and Lord Rodger of
              Earlsferry at [155] and [168] - [170] (only Lord Hutton based
              his conclusion on an inference of causation (at [107] - [112])).
              All those speeches must be read in full, to do justice to their
              closely-reasoned surveys of principle, authority and policy; but
              the above references contain the salient statements of the new
              principle."
666          In Barker v Corus (UK) Ltd (supra) Lord Scott identified four
        further issues or questions which arose from the development the
        Fairchild principle - see [58]. The fourth of these questions, which did
        not directly arise, and which was only addressed by Lord Scott, was:
              "does the Fairchild principle apply only where exposure to a
              single injurious agent has caused the risk of the disease that the
              victim has eventually contracted or can it also apply where the
              victim has been exposed to more than one injurious agent each
              of which has subjected the victim to a risk of the outcome and it
              cannot be ascertained which agent has been responsible?"
        In addressing that question at [64] Lord Scott observed:
              "Everything I have said in regard to the previous three questions
              has been on the footing that only a single injurious agent was
              involved (and as at present advised I would regard different
              types of asbestos as constituting a single agent). If, however,
              the case were not one of an eventual outcome produced by a
              single agent but of an outcome that might have been produced
              by one of a number of different agents and where the guilty
              agent could not be identified e.g. cases like Wilsher v Essex
              Area Health Authority [1988] AC 1074 or Hotson v East
              Berkshire Area Health Authority [1987] AC 750, I would not
              regard the Fairchild principle as applicable. Fairchild v
              Glenhaven Funeral Services did not establish an overarching
              principle. It established a narrow exception to the causation
              requirements applicable to single agent cases. I would not
              extend the exception to cover multi-agent cases as well. One
              reason why I would not do so is that the identification of the
              proportion of risk of the eventual outcome attributable to each
              particular agent would, to my mind, be well nigh impossible
              and highly artificial. At least in the asbestos cases it is known
              that asbestos was responsible for the eventual outcome and that

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              the negligent defendants are to be held liable for subjecting the
              victim to a risk that has materialised."
667          The auspices for the possible application of the Fairchild principle to
        cases in which the victim has been exposed to two or more carcinogens,
        only one of which exposures is due to negligence or breach of duty, are,
        therefore, by no means positive. If, as the question posed by Lord Scott
        assumes, only one of the carcinogens could have caused the development
        of the disease, then there would appear to be no basis in justice to hold
        that the party who exposed the victim to the other non-causative
        carcinogen liable if that other exposure was not negligent or in breach of
        duty. However, if the exposure to the other carcinogen (the non-causative
        one which is incapable of being reliably identified) were the result of
        negligence or breach of duty, it is not altogether obvious why the
        Fairchild principle should not be applied because, on that hypothesis, two
        or more defendants negligently exposed the victim to a toxic carcinogen
        known to be capable of producing the disease which was contracted but
        where it is not possible to identify which was the sole cause. There really
        does not seem to be any difference between that scenario and the situation
        to which the Fairchild principle was originally developed and applied.

668          It is important to note, of course, that Lord Scott's question and this
        discussion proceeds on the basis that in the so-called multiple
        carcinogenic agent situations examined, it can only be one carcinogen
        acting solely which causes the disease - an indivisible disease: an obvious
        example being asbestos in a case of mesothelioma. The question and the
        analysis, however, does not address the situation of multi-carcinogenic
        agents which act in combination and, cumulatively, have a more toxic
        effect than any one in isolation which is the situation in the present case.

669           The evidence establishes that the risk of contracting lung cancer
        through exposure to asbestos is much greater for a worker who is a
        chronic smoker and that the effect of smoking and the effect of asbestos
        somehow enhance the risk of contracting the disease and are associated
        with its earlier onset. The evidence in this case suggests strongly that the
        cause of Mr Cotton's lung cancer was either the cumulative effect of his
        history of long smoking alone, or the combined effect of his long smoking
        with the potentiating or multiplicative effect of exposure to asbestos even
        if only by a relatively low aggregate dose over time.
670          Had he not been a smoker it is more than likely that Mr Cotton
        would not have contracted lung cancer when he did. Had he not been
        subjected to the occupational exposure to asbestos during these two


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        periods of employment, it is more than probable that he would not have
        developed lung cancer when he did although, as a smoker he was certainly
        prone to the development of that disease later. The question, therefore,
        must be whether, notwithstanding the relatively low aggregate exposure to
        asbestos experienced by Mr Cotton, the evidence supports a conclusion,
        on the balance of probabilities, that in combination with his tobacco
        smoking the asbestos made a material contribution to the development of
        his lung cancer.
671           This conclusion leads to a necessity to view the epidemiological
        evidence and, in particular the submissions that the RR of Mr Cotton
        developing lung cancer should be 2.0 or more before the plaintiff can
                                        u
        succeed and/or that this in t rn requires a conclusion that the deceased
        was exposed to at least 25 fibre/ml years of asbestos with particular
        discrimination. Do those protocols hold good for cases of lung cancer for
        persons who are exposed to both asbestos and who are chronic smokers or
        do they fail to distinguish between the cumulative and multiplicative
        effect of those two carcinogens acting in combination? In that case what
        suffices for a plaintiff to discharge the enduring obligation of proving that
        the particular carcinogen, asbestos, probably made a material contribution
        to the onset and development of the disease?
672           This is not to suggest that the Fairchild principle, even if extended to
        multi-agent carcinogens, would apply in Australia to a case such as this.
        Fairchild v Glenhaven Funeral Services (supra) has been referred to, in
        this State with apparent approval by McLure J in the Shire of Brookton v
        Water Corporation (supra) at [65] and by the Court of Appeal in City of
        Stirling v Tremeer (supra) at [75] - [76]; (2006) 32 WAR 155 at
        172 - 173. McGhee v The National Coal Board (supra) of which it is
        said to be a development, has long been followed in this country. As
        recognised in Bennett v Minister for Community Welfare (supra) at 420
        and 422; March v E M & H Stramare Pty Ltd (supra) at 514 and 515 and
        Chappel v Hart (supra) 238 at [8] and Henville v Walker [2001] HCA 52;
        (2001) 206 CLR 459 at 480 when, relying on McGhee's case (supra),
        among other authorities, Gaudron J said at [59] - [60]:

              "[59] There is nothing novel in the idea that, on occasions, loss
              or injury is the result of two or more events, neither of which is
              sufficient, of itself, to bring about that result. The events in
              question may be sequential or concurrent. March v Stramare
              (E & M H) Pty Ltd was a case involving an injury which
              resulted from the conjunction of two separate acts or events, the
              injury in question having resulted from the plaintiff, who was


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              driving at excessive speed running into a negligently parked
              vehicle.
              [60] For the purpose of the law of negligence, where two or
              more events combine to bring about the result in question, the
              issue of causation is resolved on the basis that an act is legally
              causative if it materially contributes to that result. The same is
              true for the tort of deceit."

        See also McHugh J at [107] and [108].
673          In Australia the tendency, rather than expanding the legal concept of
        causation as was done in Fairchild (supra), is to allow a finding of
        causation to be made in situations of elevated risk where there is no
        evidence to displace or reject that inference - a course which maintains the
        significance of the obligation of the plaintiff to discharge the onus of
        proof of causation - see, for example, Purkess v Crittenden (1965) 114
        CLR 164 at 167 - 168.
674          Fairchild v Glenhaven Funeral Service Ltd (supra) was discussed
        but distinguished in Rufo v Hosking [2004] NSWCA 391; (2004) 61
        NSWLR 678 at [434] - [446] by M W Campbell AJA but the tenor of his
        Honour's reasons for judgment suggested that his Honour regarded the
        decision as contrary to established principles in Australia. The same
        reserve about the application of that "principle" is evident in Orica Ltd v
        CGU Insurance Ltd (2003) 59 NSWLR 14 per Santow JA at [92], [93]
        and [204] and in Australian Capital Territory v Kitt [2004] NSWCA 444;
        (2004) 43 MVR 249 (CA NSW per Santow JA) at [34], and it was said
        not to represent the law in Australia by Barker J in Misiani (as Executor
        of the Will of Misiani (Dec)) v Welshpool Engineering Pty Ltd (In Liq)
        [2003] WASC 263 at [158] where his Honour considered that the
        approach in Australia was determined by a passage already cited from the
        judgment of Gaudron J in Bennett v Minister for Community Welfare
        (supra) and repeated by her Honour in Naxakis v Western General
        Hospital (supra) at 278 - 279.

675          On this basis, therefore, the crucial test on the issue of causation in
        the present case is whether or not the plaintiff has demonstrated, on the
        probabilities, that an inference of causation should be drawn that the
        asbestos exposure, in combination with the history of chronic smoking,
        materially contributed to Mr Cotton's lung cancer.




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More aspects of causation
676          There can never be any departure from the fundamental obligation of
        the plaintiff to prove, on the balance of probabilities, that the alleged
        negligence, breaches of statutory duty or breach of contract did cause the
        injury or loss of which she complains while acknowledging always that
        proof of causation does not require that the breach of duty should be the
        sole cause of the loss of damage so long as it makes a material
        contribution to that end. Problems with the legal concept of causation are
        by no means infrequent but the doctrine which the law has applied
        remains uniform. Explanations of this doctrine, however, need to be
        understood having regard to the particular controversy which is being
        addressed by the case in which those explanations are found. Questions
        of causation in cases where the alleged breach of duty arises from an
        omission, or a failure to warn, have special complexities of their own, for
        example, Bennett v Minister of Community Welfare (1992) 176 CLR 408
        and Rosenberg v Percival (2001) 205 CLR 434.

677           Another category of cases which gives rise to distinct problems of
        causation is that involving multiple causes. These cases contain their own
        sub-categories, including multiple concurrent causes, multiple sequential
        causes, multiple but independent and unrelated causes, and multiple
        causes some of which involve a breach of duty by the defendant and
        others which do not. Again, the distinction between indivisible and
        divisible diseases or conditions becomes significant because such cases
        usually involve the need to identify and prove the effect of one single
        causative event or agent in a situation where there are a number of rival
        possibilities. Accordingly, it becomes essential to address the problem of
        causation in the case in hand with a realisation of its distinct features so as
        to place it in this spectrum.
678           Mr Steven Cotton's death was undoubtedly caused by the progress of
        his lung cancer. On the facts of this case the only possible causes of that
        lung cancer which have been suggested are: his tobacco smoking; his
        occupational exposure to asbestos; or some one or more unidentified
        background risks; or a combination of one or more of these factors. As
        the evidence progressed it became clear that, in reality, the only
        carcinogens which are at all likely to have caused or contributed to the
        initiation or progress of Mr Cotton's fatal tumour are his smoking and his
        asbestos exposure or a combination of them.

679          For reasons explained earlier, I have concluded that his particular
        disease must be regarded as a divisible disease, that is one which was


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        either caused or aggravated, or both, by accumulation, that is, from
        repeated exposure over time, to one or both of those carcinogens. The
        causal agent or agents acted alone or in combination progressively and
        with cumulative effect to produce and advance the tumour. This means
        that having established so much, the plaintiff still has the onus of proving,
        on the probabilities, that the asbestos exposure caused by the conduct of
        each of the defendants made a material contribution, even if in
        combination with the effect of chronic smoking, to the development
        and/or progress of the fatal tumour.

680           This, therefore, identifies the issues of causation in the present case
        as involving an allegation of a material contribution to the loss and
        damage that was produced by one agent to which the deceased was
        exposed as a result of breaches of duty by the defendants, acting in
        combination and cumulatively, with another, probably more powerful,
        toxic agent for which none of the defendants was directly responsible.
        The qualification "directly responsible" is made to accommodate that part
        of her case which involves the plaintiff alleging that the defendants were
        negligent or in breach of duty for failing to warn or prevent Mr Cotton
        from smoking while he was working with or in the vicinity of asbestos,
        when that defendant knew or should have known of the greater risks of
        developing asbestos-related disease by exposed persons who were
        smokers. However, it is not necessary to pursue or explore the
        significance of that qualification because analysis of the principal issue,
        just described, will suffice to produce a resolution of this case.

681           Accordingly, it is to those authorities which discuss causation in a
        setting of multiple cumulative causes not all of which involve a breach of
        duty by a defendant, and where questions of identifying the meaning of
        "material contribution", that I now turn for exposition of the applicable
        principles. A very helpful review of these authorities may be found in the
        judgment of Campbell AJA, with whom Hodgson and Santow JJA both
        agreed in these respects in Rufo v Hosking (2004) 61 NSWLR 678. That
        was a case in which the claimant complained of the loss of a chance of
        achieving a better outcome from a medical procedure due to alleged
        negligence. Campbell AJA, at 695 - 701, collected and considered a
        number of the authorities dealing with material contribution to the loss or
        damage by the alleged causal event or omission, including E M Baldwin
        & Son Pty Ltd v Plane [1999] NSWCA 130; (1999) 17 NSWCCR 434.
        His Honour also cited the judgment of Mason P in TC (by his Tutor
        Sabatino) v State of New South Wales [2001] NSWCA 380, as follows:




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              "[119] There is a tension between the suggestion that any
                    increased risk is sufficient to constitute a 'material
                    contribution', and the clear line of authority that a mere
                    possibility is not sufficient to establish causation for legal
                    purposes. The latter is too well established to be
                    qualified by the former. The reconciliation between the
                    two kinds of references is to be found in the fact that, as
                    in Chappel v Hart (1998) 195 CLR 232 and in the cases
                    that suggest the former, the actual risk had materialised.
                    The 'possibility' or 'risk' that X might cause Y had in fact
                    eventuated, not in the sense that X had happened and Y
                    had also happened, but that it was undisputed that Y had
                    happened because of X."
682         His Honour also examined, in detail, the decisions of the House of
        Lords in McGhee v National Coal Board [1973] 1 WLR 1 and
        Bonnington Castings Ltd v Wardlaw [1956] AC 613. Fitzgerald AJA,
        had summarised Bonnington Castings Ltd v Wardlaw (supra) in
        E M Baldwin & Son Pty Ltd v Plane (supra) in these terms:

              "In Bonnington Castings v Wardlaw (supra), which was
              referred to in Tubemakers (1976) 50 ALJR 720, the plaintiff
              (pursuer) had inhaled silica dust concurrently from two different
              work activities, one of which involved negligence on the part of
              the employer and the other of which did not. The House of
              Lords held that the effect of the silica dust was cumulative and
              that the plaintiff had established, as was necessary, that the
              silica dust from the activity which involved negligence on the
              part of the defendant had probably materially contributed to his
              disease."
        In Bonnington Castings Ltd v Wardlaw (supra) Lord Reid said, at
        622 - 623:
              "It appears to me that the source of his disease was the dust
              from both sources, and the real question is whether the dust
              from the swing grinders materially contributed to the disease.
              What is a material contribution must be a question of degree. A
              contribution which comes within the exception de minimis non
              curat lex is not material, but I think that any contribution which
              does not fall within that exception must be material. I do not
              see how there can be something too large to come within the
              de minimis principle but yet too small to be material."


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683          There are some suggestions in the cases that, in certain special
        circumstances, an elevation of the risk of an adverse outcome occurring
        because of exposure to a potentially causative factor will, of itself, allow
        an inference of causation to be drawn - see Commonwealth v McLean
        (1996) 41 NSWLR 389 at 408 - 410 per Handley JA and Beazley JA, but
        the potential causative agents in McLean's case were complicated in their
        interaction and I do not consider that that decision supports any departure
        from the established rule that a material contribution, even if only indirect,
        to the cause of harm must be proved - see Bendix Mintex Pty Ltd v
        Barnes (1997) 42 NSWLR 307; ICI Australia Operations Pty Ltd v
        Walsh (1997) A Tort Rep 81-452 but much depends upon whether or not
        the alternative agent or agents which might potentially have caused the
        disease - especially in cases of indivisible disease, can be excluded on the
        facts, or as a matter of inference, from any causative role - Birkholz v
        R J Gilbertson Pty Ltd (1985) 38 SASR 121 per King CJ at 130 and Rufo
        v Hosking (supra) at 695 - 696.

684           Complicated though the application of these principles may
        sometimes be in certain cases, most particularly those involving the need
        for a plaintiff to identify one single cause, in a situation where there are a
        number of rival potential causes, whether involving breaches of duty or
        not, the difficulties are less acute in cases involving cumulative multiple
        causes. It has been said, and I accept correctly, in a note "The Causation
        Conundrum of Mesothelioma" (2003) 11 Tort Law Rev 9 that:
              "If the causal relationship was definitely cumulative, then the
              decisions in Bonnington Castings Ltd v Wardlaw [1956] AC
              613 and Nicholson v Atlas Steel Foundry and Engineering Co
              Ltd [1957] 1 WLR 613 provided an answer - the defendant was
              a cause or materially contributed to the injury whenever the
              exposure to the dust was not de minimis."

685          A court is not compelled to abandon the task of determining whether
        an alleged breach of duty has, in fact, caused loss or damage in situations
        where medical or other sciences are unable to identify the actual cause or
        the causal mechanism. There are many instances in which scientific
        understanding of natural phenomena is absent or incomplete but, even in
        those cases, the common experience of humanity may enable a decision,
        whether by inference or otherwise, of cause and effect to be made to the
        requisite degree of proof. The plaintiff has relied on a line of authority,
        adopting this approach, to support her present case. This authority
        includes the well-known observations of Dixon J in Betts v Whittingslow e
        (1945) 71 CLR 637 at 649; and his Honour's earlier remarks to similar


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        effect (although in dissent) in Adelaide Stevedoring Company v Forst
        (1940) 64 CLR 538 at 569 - 570; Tubemakers of Australia Ltd v
        Fernandez (1976) 50 ALJR 720; (1976) 10 ALR 303; Western Australia
        v Watson [1990] WAR 248 and CSR Ltd v Culkin, unreported; FCt SCt
        of WA; Library No 940570; 18 October 1994. Certainly, the plaintiff is
        entitled to call in aid these authorities and the court must be astute to
        ensure that all inferences which may properly be drawn, even in the
        absence of scientific proof or probability, are drawn but whether in fact
        proof of elevated exposure to risk can be treated as allowing an inference
        that, on the probabilities, that elevated risk caused or contributed to the
        misfortune is another matter. Seltsam v McGuiness (2000) 49 NSWLR
        262 and the cases referred to in [650] to [654] above are powerful
        reminders that elevation of risk and material contribution in fact are not
        necessarily the same thing but, as Commonwealth v McLean (supra) and
        other authorities such as Tubemakers (supra) reveal, the elevation of the
        risk may, in the particular circumstances, be of such a kind that the
        inference of causation can and should be drawn.
686           Whether that dichotomy is real or is simply part of a continuum may
        well involve an obligation "to consider the view that there is no real
        distinction between breach and duty and causation" - per Mason CJ,
        Deane and Toohey JJ in Bennett v Minister of Community Welfare
        (1992) 176 CLR 408 at 416 and per Gaudron J at 418 - 420 which, in turn,
        is explained by Gaudron J at 422 where her Honour said:
              "And so far as general sufficiency is involved in the question of
              causation, there is usually no reason to separate or distinguish
              the question of breach of a common law duty from that of
              causation [see McGhee v National Coal Board [1973] 1 WLR at
              page 8 per Lord Simon of Glaisdale, where it is said that in
              certain cases there is no real distinction between breach of duty
              and causation. See also Quigley v The Commonwealth (1981)
              55 ALJR at 581 per Stephen J.] That is because a duty is
              imposed by the common law by reason that it is a precaution
              which a reasonable person in the position of the person sued
              would have taken to prevent a foreseeable risk of harm of the
              kind suffered."

        So it will be seen that where the particular duty which is in question,
        reflects widespread human knowledge, that breach of that duty usually
        leads to harm (for example in the case of a breach of a duty to place
        effective guards around dangerous cutting machinery in a workplace) if
        harm follows the question of causation is often axiomatic. The problem,


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        however, arises in cases such as the present where breach of duty and
        exposure to the toxic agent will not always, or even necessarily, cause the
        feared damage. In this latter category of cases, of which I accept the
        present is one, there is still a need by the plaintiff to establish the
        probability that the breach of the duty, that is exposure to the toxic agent,
        did in fact contribute to the damage alleged.
687           Here, if one concentrates on the effect of Mr Cotton's occupational
        exposures to asbestos alone, and takes that in combination with the
        epidemiological evidence, the probabilities are quite high that the asbestos
        exposure alone did not cause his lung cancer. On the other hand, I am
        satisfied that the situation is very different if the question is posed,
        whether on the probabilities, Mr Cotton's two sequential periods of
        occupational exposure to asbestos, acting in combination with his habit of
        smoking, contributed to the development and/or progress of his fatal
        tumour. Then there is really no answer to the evidence of Professors
        Musk, Wan, Dr Kendall, Professor de Klerk, Dr Leigh and Professor
        Berry that a not insignificant contribution to the combined causative effect
        was due to this asbestos exposure. That is all that the plaintiff needs to
        establish and I am satisfied that she has demonstrated this.
688           This analysis has, of course, proceeded upon the basis that the effects
        of exposure to asbestos experienced by Mr Cotton both at Adelaide, and
        then, years later at Australind, contributed, in a cumulative way, to the
        development or progress of his fatal lung disease. Against that
        submission of combined or cumulative effect are the submissions for the
        first and second defendants that the asbestos exposure at Adelaide was, on
        a time-weighted basis only low and lasted, at the most, for about two and
        a half years from March 1976 until October 1978. Similarly, but to
        opposite effect, are the submissions advanced by the third defendant that
        the period of exposure to asbestos at Australind, that is from early 1991
        to, it would say, mid-1994 (although I have found that exposure to
        asbestos at Australind continued until late 1997), was too recent to allow
        it to be attributed as having a causal connection with Mr Cotton's lung
        cancer because of a short latency period of nine years from exposure to
        diagnosis.
689          With regard to these contentions by the defendants, however, I do
        not consider that either of the two periods of occupational exposure to
        asbestos can be analysed or evaluated without regard to the other. All the
        evidence is to the effect that the risk of developing lung cancer due to
        exposure to asbestos, whether alone or in combination with other
        carcinogens, increases with cumulative exposure. Both Professor Musk


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        and Professor de Klerk treat asbestos as a complete carcinogen, in the
        sense that it has both an initiating and an aggravating affect in the cause
        and progress of that disease. The exposure to asbestos in Adelaide was at
        a time which is certainly consistent with the common duration of latency
        resulting in the appearance of diagnosable cancer more than 20 years
        later. On the other hand, the initial exposure at Australind, nine years
        before diagnosis and 11 years before death, as recognised by Professor
        Berry, is also within the recognised period of latency. Where the
        probabilities are that the toxic effect of the carcinogens of tobacco and
        asbestos had synergistic effect, and that their effects were also cumulative
        upon previous exposures, I am satisfied that both periods of occupational
        exposure to asbestos made material contributions to the onset and/or
        development of Mr Cotton's disease.
690           At some places in the evidence of Professor Musk, Professor Kottek,
        Dr Leigh, and Professor Berry, some attempts were made to estimate the
        proportions by which each exposure may have contributed to the final
        fatal result, but these were rather superficial and approximate and were
        not pursued, either by further examination, or by further evidence. As
        there is no issue between the defendants seeking contribution or
        apportionment it is unnecessary and undesirable for me to embark on any
        such attempt.
691           That leaves a position where I am satisfied that breach of duty by
        each of the defendants has made material contribution towards the
        development or progress of Mr Cotton's fatal lung cancer. In the case of
        the first and second defendants this involves concurrent breaches of duty,
        each causing the consequences of the exposure to asbestos which
        Mr Cotton experienced in Adelaide. In the case of the third defendant,
        each breach of duty, contractual, tortious and in breach of the
        Occupational Health Safety Regulations also caused and aggravated the
        development of Mr Cotton's lung disease. The third defendant's breaches
        of duty were, therefore, cumulative upon the effects of the breaches of
        duty by the first and second defendants but combined with them to
        contribute to the fatal outcome.

692          When there are separate and independent acts of negligence or other
        breaches of duty on the part of two or more persons who have directly
        contributed to cause injury to another, the person injured may recover
        damages from any one of the wrongdoers or all of them - Grant v Sun
        Shipping Co Ltd [1948] AC 549 at 563.




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693           Therefore, subject to the differing measures of the quantum of
        damages arising under the law of South Australia, as it applies to the case
        against the first and second defendants, and the law of Western Australia,
        as it applies to the claim against the third defendant, I consider that each
        of the defendants is fully liable for the damages which are recoverable by
        the plaintiff, whether in the estate actions or in the dependants' actions, for
        the loss which has been caused by those harmful exposures.

Contributory negligence and voluntary assumption of risk - the effects of
             smoking
694           Each of the defendants has pleaded that Mr Cotton's long history of
        smoking covering, as it did, years when there was a well developed public
        awareness of the severe health risks of smoking has an important bearing
        on the plaintiffs claim. The first and the second defendants allege that
        Mr Cotton's smoking history reveals that he voluntarily assumed the risk
        associated with the development of lung cancer due to tobacco smoking,
        either alone or in combination with some other carcinogen such as
        asbestos exposure, with the consequence that his conduct in this regard
        constitutes a complete defence to any action based in negligence or breach
        of statutory duty. The justification for such a view, if established on the
        facts, will be examined later.

695           The defence of voluntary assumption of risk will not arise unless the
        defendant pleading it establishes, the onus being upon it, on the balance of
        probabilities that the plaintiff both knew of and voluntarily agreed to run
        the risk of the hazard which actually caused any ensuing damage -
        Insurance Commissioner v Joyce (1948) 77 CLR 39 at 45 - 46 and
        Roggenkamp v Bennett (1950) 80 CLR 292 at 298. Whatever may have
        been Mr Cotton's attitude towards the risks of smoking there is simply no
        evidence to establish that he was aware of the existence of significant risk
        to his health through working in the conditions in which he was employed
        either in Adelaide or at Australind, or the greater risks involved from such
        occupational exposures to asbestos because he was also a smoker.

696          Secondly, all the defendants submit that Mr Cotton's long history of
        smoking covering periods when he knew or should have known of the
        health risks associated with smoking, including the risk of developing
        lung cancer either due to smoking alone or to smoking in combination
        with another carcinogen such as asbestos, constitutes contributory
        negligence which should result in an appropriate apportionment of any
        damages which are otherwise recoverable, either for breach of statutory



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        duty or negligence or, in the case of the first and third defendants, breach
        of the implied terms of the contract of employment.
697            Whether a defence of contributory negligence is available in these
        circumstances for claims based on breach by an employer of implied
        terms of the contract of service will also require separate examination
        later.
698          The plaintiff replies to these defences by taking issue with the basic
        assertions about the availability and effect of those defences but also by
        pleading that, along with many smokers, Mr Cotton began smoking at a
        young age and then became addicted to cigarette smoking to such an
        extent that he was unable to give it up and that, to persist in his smoking
        habit while subject to that addiction, could not constitute either any
        voluntary assumption of the risks involved in smoking, nor any failure to
        take reasonable care for his own safety so as to constitute contributory
        negligence. This has generated issues of fact about the nature and effect
        of smoking, the extent of any addiction resulting and the capacity of
        Mr Cotton to cease smoking in his own interests either because of
        becoming aware of the public health campaigns about the danger of
        smoking or because of specific medical advice and recommendation given
        to him by his doctors or similar recommendations made to him by
        members of his family. It is necessary to address the evidence on these
        issues.

699           These specific defences were raised, in various forms, and to
        different degrees, by the defendants. The first defendant pleaded (by
        par 9 of its defence) that by smoking and continuing to smoke when he
        knew or ought to have known that cigarette smoking was a health hazard
        and involved a risk of disease to the lungs including lung cancer, Mr Paul
        Cotton voluntarily assumed the risk of contracting the injuries alleged.
        Further, by par 10 of its defence, the first defendant alleged that if,
        contrary to its primary position, Mr Cotton's lung cancer was contributed
        to by the negligence of the first defendant, Mr Cotton's action in smoking
        and continuing to smoke when he knew or ought to have known that
        cigarette smoking was a health hazard and involved a risk of disease to the
        lungs including lung cancer, was a new intervening cause and the sole
        effective cause of him contracting the injuries alleged. Finally, by par 11
        of its defence, the first defendant pleaded that if Mr Cotton's lung cancer
        was caused as alleged, then the lung cancer was caused or materially
        contributed to by the negligence of the deceased, particulars of which
        were then set out. Those involved, in substance, his commencement and
        continuation of smoking cigarettes at a time when Mr Cotton knew or


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        ought to have known that cigarette smoking was a health hazard; and by
        failing to heed health warnings on cigarette packets, in advertisements in
        newspapers, magazines and on television, and in failing to give up
        smoking until his diagnosis in May 2000.
700           Similar defences are also raised by the second defendant which
        pleads, by pars 4, 5 and 6 of its defence, that by continuing to smoke
        cigarettes after a time when he knew or should have known of the risks
        associated with tobacco smoking, any cause or connection between the
        inhalation of asbestos emanating from sources for which the second
        defendant was responsible, and that of the disease, was severed by the
        conduct of the deceased. I take this to be a plea of lack of causation
        and/or a variation of the first defendant's plea of new intervening cause.
        The second defendant then pleads that the continuation of smoking by
        Mr Cotton after a time when he knew or ought to have known that
        smoking constituted a risk of injury was a voluntary acceptance of the risk
        of lung cancer. Finally, the second defendant also pleads contributory
        negligence essentially on the same grounds as those alleged by the first
        defendant but, additionally, on the ground that Mr Cotton failed to seek
        medical advice about the risks and dangers to health associated with
        smoking cigarettes and, further, failed to heed medical advice about those
        risks and dangers.
701           The third defendant, by par 13 of its defence, also raised a plea of
        contributory negligence on essentially the same grounds advanced by the
        first defendant. However, the third defendant does not raise a plea of
        voluntary assumption of risk nor, expressly, a plea of new intervening
        cause although its position clearly is that Mr Cotton's lung cancer was
        caused by his smoking and that any influence of exposure to asbestos at
        Australind (which it had of course denied) made no material contribution
        to the development or progress of that fatal disease.

702          These defences were each addressed at some length by the plaintiff
        in her three replies. Although there are some variations in those replies it
        is sufficient to identify the principal features which raise common issues
        in each of the three claims. The plaintiff has pleaded that there was no
        voluntary assumption of risk by Mr Cotton nor any contributory
        negligence by him because:

        •     to the extent, if any, to which smoking contributed to the
              development of the lung cancer, Mr Cotton's smoking habit did not
              constitute contributory negligence because it played no part in the
              contribution to his exposure to the carcinogen asbestos caused by the


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              alleged breaches of duty of the defendants. In other words, if the
              event which caused his damage was exposure to asbestos because of
              the negligence of the defendants, his smoking habit was independent
              of that and did not lead him (at least knowingly) to neglect
              reasonable care for his own safety, by continuing to work in the
              environments in which his employers had exposed him;
        •     that at no time during the period when he was smoking, did
              Mr Cotton fail to take adequate care for his own safety because of
              potential exposure to asbestos, having regard to his absence of
              knowledge of any association between asbestos exposure and
              smoking;
        •     in any event the continuation of smoking by Mr Cotton was due to
              his addiction to tobacco and, therefore, did not constitute any failure
              by him to take reasonable care for his own safety;
        •     at the time when he commenced smoking, and during the period
              leading to the establishment of his addiction to smoking, Mr Cotton
              did not know nor should he reasonably have known, that
              consumption of tobacco products posed any significant risk to his
              health;
        •     until the diagnosis of his lung cancer, Mr Cotton did not know nor
              should he reasonably have known, that a smoker who was exposed to
              asbestos dust was subject to a materially increased risk of contracting
              lung cancer;
        •     any lack of reasonable care for his own safety by Mr Cotton due to
              his use of tobacco products did not cause any additional injury or
              damage beyond the damage which was produced by the combination
              of smoking and tobacco exposure, where that combined effect was
              not known to him;
        •     because of the material greater risk of developing lung cancer for a
              person exposed to asbestos who also smoked, the employers (first
              and third defendant) had failed in their duty to warn the deceased of
              that enhanced risk. This seems to be, in substance, a plea that the
              continuation of smoking by a person working in an environment
              involving asbestos exposure, could not be regarded as a lack of care
              for his own safety, unless the otherwise unknown degree of danger
              arising from the combination of those two carcinogens was brought
              to that person's attention by the employer;
        •     for this last reason the alleged contributory negligence or assumption
              of risk by Mr Cotton in continuing to smoke, was not in fact any lack
              of care for his own safety nor any voluntary assumption of risk

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              because it was a product of the employers' failure to discharge the
              alleged duty of care to warn him of the enhanced effects of the
              combination of tobacco and asbestos and that this was not known,
              nor could it reasonably have been known, to the deceased until the
              time of his diagnosis.
703          A feature of the replies by the plaintiff to these allegations of
        contributory negligence and voluntary assumption of risk is their attempt
        to address, discretely, the consequences of smoking, on the one hand, and
        asbestos exposure on the other when it comes to the effect which each had
        in causing Mr Cotton's lung cancer and as conduct which might be
        regarded as risky behaviour or involving a lack of reasonable care for
        one's own health and safety. For the same reasons which, in my view,
        make it unrealistic to attempt to examine or measure the effects of each of
        the two carcinogens separately, that is independently of each other, as the
        sole cause of Mr Cotton's lung cancer, I am of the view that it is equally
        unreal to attempt to evaluate alleged contributory negligence or voluntary
        assumption of risk by treating Mr Cotton's smoking conduct from the
        point of view that only consequences due solely to the effects of smoking
        would be determinative.
704          As the evidence makes clear, the adverse consequences to one's
        health from chronic smoking are not confined to diseases solely or
        principally associated with tobacco. Smoking is known to render the
        smoker more prone to cardiovascular disease and hence heart attacks and
        strokes; it is associated with a large range of respiratory diseases,
        emphysema, bronchitis, chronic obstructive airways disease and others. It
        is known to be associated with a higher incidence of a whole variety of
        cancers, not merely lung cancers. In short, the overwhelming body of
        medical opinion, and the messages from the public health authorities and
        public health campaigns lasting for many years, is that smoking is
        generally bad for the smoker, not only because of the immediate effects of
        smoking but because it renders him or her susceptible to a whole range of
        other diseases which can arise in other ways. Another way of stating the
        position is to say that, by heavy smoking for any lengthy period, the
        smoker makes himself or herself far more vulnerable to a whole range of
        diseases or adverse health conditions which, while they could develop in a
        non-smoker, are less likely to develop without heavy smoking. It will be
        necessary to return to this aspect of the case later but for the present the
        major issues of fact arising from these defences and replies are the extent
        of the knowledge which the deceased had, or in the case of contributory
        negligence, should have had of the risks of smoking and the significance,
        if any, of the fact that smoking soon becomes an addiction.


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705           This last reply by the plaintiff to the defence of the third defendant
        led to leave being sought and granted to the third defendant to file a
        rejoinder. By this extra flourish in the pleadings arena, the third
        defendant denied that it owed any duty to the deceased to warn him before
        the commencement of his employment or in the course of his employment
        that a person exposed to asbestos who was also a smoker was at a
        materially increased risk of contracting lung cancer and that this was a
        risk greater than the risk to smokers who had no exposure to asbestos and
        substantially greater than the risk to the general population who had no
        exposure to asbestos and who were not smokers. By this same pleading
        repêchage, the third defendant pleaded that, if which it denied, it had
        owed the asserted duty to warn the deceased of any material increase of
        risk in developing lung cancer for a person exposed to asbestos who also
        smoked, then any such warning which it might have given to the deceased
        would not have resulted in him ceasing to smoke. Not surprisingly, there
        was no evidence led which could, or did, support the alleged fact involved
        in this second degree of anticipation.
706          The plaintiff sought to establish that, at least at the time when
        Mr Cotton took up smoking and when he was still smoking during his
        employment with the first defendant in Adelaide, and again with the third
        defendant at Australind, the adverse health risks of smoking were not
        extensively known or accepted by the community and that, significantly,
        various groups associated with the tobacco company were conducting
        public campaigns to challenge the assertions of the medical profession,
        and other health representatives, that smoking caused lung cancer. The
        plaintiff also sought to establish that, once established in the smoking
        habit, addiction set in so that a smoker who wished to give up the habit
        found it very difficult to do so and that most smokers who made the
        attempts were unsuccessful so, as it was argued, leading to the conclusion
        that a continuation of the smoking habit should not be regarded either as
        any voluntary assumption of risks involved or as a form of contributory
        negligence.
Significance of anti-smoking campaigns
707          The first second and third defendants have adduced a large quantity
        of evidence consisting of newspaper articles, advertisements, statements
        by public health authorities and other health representatives from about
        1972 onwards about the significant dangers to the public of tobacco
        smoking and of the need for smokers to quit their habit or at least to
        reduce it substantially. This evidence was led in support of the
        defendants' various contentions that Mr Cotton's long history of smoking


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        afforded the first and second defendants a defence of voluntary
        assumption of risk together with the defences of new intervening cause.
        Further, all the defendants relied on this evidence to support their pleas of
        contributory negligence and lack of causation. In this regard the second
        defendant relied upon decisions and dicta in Commonwealth of Australia
        v McLean (1996) 41 NSWLR 389 CA, Simmons v Commonwealth of
        Australia, unreported; SCt of Vic; 8 October 1991, per Coldrey J
        (BC 9100603); and Margolis v Imperial Tobacco Ltd & Ors - UK Court
        of Appeal [2000] EWCA Civ 114 - 6 April 2000, all being decisions
                          h
        which support t e availability of such defences in the abstract in cases
        such as the present.

708           In this respect the first defendant tendered a bundle of newspaper
        articles including letters and advertisements published in "The Advertiser"
        in Adelaide from 21 February 1972 until 30 June 1977 illustrating its
        submission that such dangers were widely publicised in the South
        Australian community during those years - Exhibits 170(1) - (103).
        Further evidence of this kind is contained in Exhibits 171(1) - (11), being
        newspaper articles published in South Australia from 18 January 1972 to
        23 September 1981 highlighting, in various ways, the dangers to health of
        continuation of tobacco smoking. In addition, the first defendant tendered
        Exhibits 172(1) - (26), being newspaper articles published in the Northern
        Territory from 15 January 1980 to 23 July 1981 covering the period when
        Mr Cotton was working in the Territory and before moving to Western
        Australia.

709           Similarly, there was evidence of the practices adopted by the
        authorities in South Australia, the Northern Territory and Western
        Australia concerning the control of the release of tobacco products and
        legislation relating to the imposition of warning labels on cigarettes and
        other tobacco products offered for sale which showed the prevalence of
        these warnings and the increasing starkness in the language on the labels
        of cigarette packets by which they were conveyed (Exhibits 173(1) - (5)).

710          The second defendant joined in this effort by tendering Exhibits 210,
        211 and 212, comprising photographs of warnings on cigarette packets at
        various dates and of other health warning messages.
711          The most dramatic example of evidence of this character is
        Exhibit 231 the "Yul Brynner advertisement", being a CD recording of a
        television advertisement broadcast at many times and places in Australia
        depicting that famous actor, by then subject to a diagnosis of incurable
        lung cancer due to smoking, warning a global audience of the dangers of


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        smoking and advising them, in the most emphatic terms, never to take up
        smoking or to quit the habit.
712          The unmistakable point of this evidence was to establish a very high
        degree of probability that Mr Cotton must, on many occasions, have seen
        and become aware of warnings involving the grave dangers of smoking.
        The submission of the defendants is that Mr Cotton must inevitably have
        seen many of these warnings and become aware of the dangers inherent in
        his continuation of smoking.
713           Among the third defendant's records is a note of a medical health
        check of Mr Cotton by a staff member conducted in 1994 - perhaps on
        2 September that year (Exhibit 79). This contains an observation that
        Mr Cotton appeared to become very sweaty during the examination and
        had elevated blood pressure, resulting in a recommendation that he should
        be seen by his GP for investigation of hypertension. The health staff
        member also noted that she had spoken to him about smoking and diet and
                                              o
        noted that he would be interested in j ining a "Quit" group if he had not
        been able to stop smoking alone. The defendants also point to advice,
        recorded in the clinical notes of Dr Mincham (Exhibit 149) of a
        consultation with Mr Cotton on 31 August 1992 when he had a throat and
        respiratory infection (U.R.T.I.) in which the doctor warned him to stop
        smoking yet, as the evidence discloses, Mr Cotton did not act, at least in
        any sustained way, upon that advice.

714           The defendants' positions are that Mr Cotton's conduct not only gives
        rise to a defence of contributory negligence justifying a reduction by
        apportionment of any damages which may be proved if an actionable
        wrong is established against that defendant but that "where a clear line can
        be drawn, the plaintiff's intervening negligence breaks the chain of
        causation between the original wrong and the later damage": see March v
        E & M H Stramare Pty Ltd (1991) 171 CLR 506 at 510 and McKew v
        Holland & Hannen & Cubitts (Scotland) Ltd [1969] 3 All ER 1621 - see
        generally, Commonwealth v McLean (supra) at 41 NSWLR 398.

715          The response of the plaintiff to these allegations rests on two broad
        propositions. The first is that an established smoking habit produces a
        physical, and sometimes a psychological, addiction and dependence by
        the smoker upon the harmful substance so that the smoker becomes
        unable to cease the noxious habit even though he or she may wish to.
        Equally, it is submitted that even determined attempts at giving up
        smoking by a person so addicted, maintained with considerable sincerity,
        often nevertheless fail in a very high proportion of cases so that


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        continuation of a smoking habit is not so much conduct by the smoker in
        disregard of reasonable care for his or her own safety but a physical
        consequence of the addiction or dependence which develops.

716          This proposition is manifest by the many examples in the literature
        and by anecdotal observation of physicians who have studied the effects
        of smoking who describe chronic smokers as people who are only too
        well aware of the potentially harmful consequences of their habit, and
        deplore its continuance, but find themselves unable to resist. At the same
        time it must also be acknowledged that the evidence reveals that there are
        significant numbers of smokers who continue to smoke under
        circumstances of self-denial about the magnitude and extent of the risks
        associated with their habit. Consequently, so the submissions for the
        plaintiff go, conduct of this kind cannot, or should not, be regarded as a
        voluntary assumption by the smoker of the risks of smoking because the
        will of the smoker, so long as it is subject to voluntary control, is to give
        up the habit but it is the addiction which prevents this. This is not to
        convert the smoker into some kind of automaton devoid of personal
        responsibility for his or her actions but, rather, so the argument goes, is a
        recognition that part of the harmful effects of smoking is the addiction
        which develops which, varying from individual to individual, may prevent
        or delay the ability of the smoker to take precautions which his or her
        mind recognises should be taken, to give up or to reduce the habit. That
        contention has given rise to controversy about the strength of the
        addiction in any particular case; the acknowledged fact that many people
        who have been smokers, have succeeded in giving up the habit; and the
        degree of personal autonomy which the law expects as an objective
        content in determining whether or not conduct constitutes contributory
        negligence.
717           The second form of the plaintiff's response to these allegations is that
        the prevailing climate of opinion from the mid 1970's onwards about the
        risks to health from continued tobacco smoking was not so unequivocal or
        settled as the defendants contend. This involves an issue raised by the
        plaintiff that, while the mainstream health authorities from the early
        1970's onwards took every opportunity to warn the public against the
        health dangers of smoking, there was a well orchestrated and widespread
        counter-campaign from the tobacco industry which sought to downplay
        these warnings; to suggest that medical opinion was significantly divided
        about the risks of smoking; and that the warnings represented an alarmist
        view from a section only of the medical health professions. At the same
        time, so the plaintiff contends, the organised tobacco lobbies, represented
        by the large cigarette manufacturing firms and the Tobacco Institute of

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        Australia, fought a rearguard action strenuously opposing and delaying
        the implementation of stronger warnings on cigarette packets and other
        restrictions upon the advertising, sale and distribution of tobacco products.

718          In such a climate, the plaintiff argues, an individual smoker such as
        Mr Cotton was being faced with powerful conflicting messages and may
        be excused for believing that there was propaganda being generated to
        influence his maintenance of a longstanding habit which had been
        practised for many generations and, in the past, with a large degree of
        cultural acceptance. In that situation the plaintiff's submission is that for a
        man such as Mr Cotton to continue to smoke was no more than the
        exercise of a personal choice to consume a lawful product which, despite
        the development of strong views in many quarters, was still largely
        condoned and practised by the community.
719           To establish the climate of opinion of the extent of public knowledge
        at these material times the plaintiff led evidence f     rom Professor Simon
        Chapman, a Professor of Public Health and Director of Teaching and
        Learning at the School of Public Health, University of Sydney. The
        extensive detail of Professor Chapman's evidence is set out in Exhibit 142.
        Before I turn to that, however, I must record that Professor Chapman
        holds the degrees of Bachelor of Arts from the University of New South
        Wales in 1972, and Doctor of Philosophy from the University of Sydney
        in 1984. He is the Associate Dean of Communications in the Faculty of
        Medicine at the University of Sydney, he advises State and
        Commonwealth Health Departments and is a consultant to the World
        Health Organisation on issues relating to the control of cancers due to
        smoking, and he has published many books and articles in the scientific
        literature on these and associated topics. He has special awards from the
        British Medical Association and the World Health Organisation and has
        been recognised as a leading researcher in his area by the NH & MRC.
        Initially there was some objection to his evidence when he was first
        called, but, in the light of that, the taking of his evidence was deferred and
        was ultimately received by video link from Sydney later in the trial.
        Professor Chapman impressed me as being extremely experienced in his
        special area, as being measured, thorough and of international repute in
        this important field of public health. His evidence addressed first the
        extent of information available in the public domain relating to
        contentions that risks of smoking to health and in particular of lung cancer
        were either not established or inclusive or were greatly exaggerated.




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720          The substance of Professor Chapman's evidence is contained in his
        report dated 7 September 2005 (Exhibit 142) which, after addressing the
        issues which I have just described, observes:

              " ... It is argued by some that the large volume of news
              reportage on smoking and health matters in the Australian news
              media published since particularly the early 1960's should be
              taken to mean that all Australian smokers should be assumed to
              be fully informed about the risks to their health arising from the
              smoking.

              There is no dispute with the fact that since the 1960's
              newspapers, radio and television news reports about smoking
              have overwhelmingly described smoking [as] a health hazard.
              It certainly would have been almost impossible for any ordinary
              citizen to avoid being exposed to such information. However
              against this must be balanced the deliberate efforts of the
              tobacco industry at the manufacturing and retailing levels to
              cast doubt on the veracity of that information and also by the
              vast expenditures by the tobacco industry on tobacco
              advertising which often featured images that implicitly
              repudiated health concerns by showing vital, energetic,
              discerning and apparently health[y] people smoking."
721           Professor Chapman's evidence and report contains very detailed
        appendices which describe the efforts by the Australian tobacco
        manufacturing industry to, at first, avoid, and then to delay and dilute,
        health warnings on Australian cigarette packs between 1969 and the most
        recent generation of warnings introduced in 1995. His evidence also
        describes efforts by the Australian manufacturing and retail tobacco
        industries to reassure their smoking customers that the "jury was still out"
        on smoking and health matters and that smokers should therefore take
        comfort that their smoking was not necessarily harmful to health. He also
        emphasised the history of the Australian tobacco industries' sponsorship
        of travelling scientists to Australia for the purposes of giving publicity to
        views to the effect that science was divided on whether smoking caused
        diseases like lung cancer and heart disease.
722          Professor Chapman expressed the opinion, which I accept he is
        qualified to give, that the effects of this campaign by the tobacco industry
        to respond to the anti-smoking campaigns of the health authorities was to
        encourage smokers to reject the statements and warnings as representing



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        wisdom and that they should necessarily adopt a view for themselves. In
        Professor Chapman's words:
              "The intended effects of this industry conduct were that
              smokers should feel that health warnings on packs did not
              represent the consensus of medical opinion, and that it was
              likely that the true causes of diseases said to be caused by
              smoking were in fact unknown and as likely as not to be caused
              by other factors such as pollution, petrol fumes or genetic
              factors."

        Professor Chapman summarised his evidence ultimately by stating four
        propositions which, I consider I should accept, namely:
              "1.     The great majority of Australian smokers would be aware
                      of claims made by medical authorities that smoking was
                      harmful to health and caused diseases like lung cancer.

              2.      That many smokers would also have been exposed to
                      tobacco industry generated arguments that the health
                      warnings did not reflect medical consensus because
                      scientists around the world were seriously divided in the
                      beliefs about whether smoking indeed was hazardous and
                      caused diseases.

              3.      Accordingly, it is likely that many smokers discounted
                      warnings on cigarettes, genuinely holding beliefs that the
                      causes of cancer were unknown and were likely as not to
                      involve cigarette smoking.

              4.      The tobacco industry in Australia, having actively
                      pursued decades long campaigns of smoker reassurance
                      between 1950 and the late 1990's is highly likely to have
                      contributed to delays and half-hearted quitting attempts
                      by many Australian smokers, which in the absence of this
                      conduct might otherwise have translated into much more
                      smoking cessation in the Australian community."

723           I realise that these opinions and conclusions contain heavy criticisms
        of the organised tobacco industry in Australia and that this industry is not
        represented in these proceedings and has not been given any opportunity
        to respond or to defend itself. However, this case does not involve the
        trial of any issues against the tobacco industry or any individual tobacco
        manufacturer or retailer. It does, however, involve an assessment of the


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        consequences of Mr Cotton apparently failing to act on the warnings of
        the risks of smoking which must have been known to him and I can only
        do that by accepting, as I do, that Professor Chapman has given a fair and
        reliable account of the climate of public reaction to the anti-smoking
        campaigns which the defendants have convincingly described and of the
        reaction to them by the tobacco producing interests.
724           I conclude, therefore, that Mr Cotton must have been aware for a
        long time, in a general way, of the risks of smoking and that he had been
        counselled by his doctor, and implored by his children, to reduce or give
        up his smoking. He did not do so but in this regard he was no different to
        many smokers who, subject to similar influences, continued to smoke at a
        time when the community sought to discourage this activity by
        persuasion, but did not prohibit it. I consider that it is far more probable
        than not that he was addicted by physical or psychological effects to
        smoking and that this conclusion is most evident from the fact that even
        after his diagnosis of inoperable lung cancer in May 2000 and the obvious
        role which smoking had played in the development of the disease he tried
        to stop smoking altogether but, as the plaintiff related, still occasionally
        smoked up until his death.
725           Major steps in the public anti-smoking campaigns were identified by
        Professor Chapman. Significantly, in 1964, the Surgeon General in the
        United States of America announced his conclusion that smoking caused
        lung cancer. In 1973 written warnings were introduced to cigarette
        packets in Australia and from September 1976 onwards all television and
        radio advertisements for tobacco products (excluding cigars) were banned
        in this country. There was a second generation of warnings introduced in
        about 1985 or 1986 and these were the first to be placed on the front of
        cigarette packets.
726          However, Professor Chapman described how people can maintain
        contradictory beliefs simultaneously and, indeed, do so, especially when it
        comes to the use of tobacco.

727          In cross-examination, Professor Chapman explained that the tobacco
        companies first acknowledged in public that smoking caused lung cancer
        during 1999 but that documents subsequently obtained by various
        processes revealed that they had privately acknowledged this well before.
        He made reference to the notorious episode of the senior representatives
        of the tobacco industry in the United States appearing before a
        Congressional Committee in 1994 and 1995 and solemnly each declaring
        that nicotine was not addictive. This was given as an illustration of the


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        industry reaction to the public health warnings as late as the mid 1990's.
        Also, as an illustration of the change in the development of public opinion
        on this topic, Professor Chapman explained that tobacco advertising in
        Australia is now completely banned but that this did not occur until 1995.
728          The addictive effect of smoking was described by Professor
        MacDonald J Christie, a consultant pharmacologist called by the plaintiff.
        Professor Christie has an Honours Degree in Science and the degree of
        Doctor of Philosophy in Pharmacology and is a specialist
        neuro-pharmacologist. He has been a professor of pharmacology at the
        University of Sydney and a consultant at the Royal Northshore Hospital in
        New South Wales. He has published widely upon the effects of nicotine
        addiction and nicotine replacement therapy. He was engaged by the
        plaintiff's solicitors to provide an opinion on: the pharmacological and
        psychological bases for addiction; the chemical and pharmacological
        mechanisms of addiction; the effect of warnings on cigarette packaging
        and otherwise in the media upon a person addicted to smoking; the
        strength of addictions; and the likelihood of a smoker breaking his or her
        addiction. His report containing the substance of his evidence on these
        topics is Exhibit 78.
729          Professor Christie explained how nicotine has now been long
        accepted as producing addiction notwithstanding that, unlike narcotic
        drugs and alcohol, no obvious intoxication occurs from its use. He
        explained that intoxication resulting from the use of a drug was no longer
        regarded as a necessary feature of addiction and that many intoxicating
        drugs had very low addiction liability and some non-intoxicating drugs
        (eg nicotine) are highly addictive. He also described that the severity of
        any withdrawal syndrome from nicotine may be much less than the
        withdrawal syndrome experienced from ceasing narcotic use but,
        nevertheless, that significant withdrawal symptoms from ceasing nicotine
        use did occur. He also described a chemical and pharmacological effect
        upon the brain which led to compulsive use of drugs, including nicotine,
        which reinforced the empirical data that the substance is addictive.
730          With regard to the strength of nicotine addiction, Professor Christie
        mentioned that the first indicator of addiction addresses the proportion of
        the population who experiment with a drug but go on to use it in a
        dependent or addictive manner, pointing out that approximately one-third
        of the adult population uses tobacco in a dependent manner which is
        higher than observed for any other drug and which suggests that nicotine
        addiction is particularly strong. A second measure of the strength of an
        addiction is the success rate of those who attempt to break the addiction.


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        He described the success rate of individuals attempting to quit smoking as
        being very poor. In Professor Christie's opinion from study and
        observation, at six months after initiation of smoking cessation only
        approximately 5per cent of individuals remain abstinent. The use of
        therapeutic aids to give up smoking, such as nicotine gum or patches,
        improve the success rate by 1.5 to twofold. This means that, at best, only
        about 10 per cent of individuals attempting to quit smoking succeed for
        more than six months - another demonstration of the power of the
        addictive force of the drug.

731           In his oral evidence Professor Christie elaborated on these figures by
        pointing out that about 50 per cent of lung cancer victims still smoke after
        their diagnosis, as do about 60 per cent of heart attack victims who were
        smokers. He then went on to describe how warnings by labelling of
        cigarette packets and by other advertising had only a very small impact
        upon smokers largely, it seems, because of levels of denial which they
        maintained. Studies had revealed that the warnings placed on cigarette
        packets from 1973 onwards had a much less effect on smokers than on
        non-smokers, again because of their level of denial and the nature of the
        addiction. By contrast, social use of alcohol was much less addictive but
        nevertheless approximately 5 per cent of men and 3 per cent of women
        become dependent on alcohol with all the attendant social problems which
        this entails.

732          In cross-examination by counsel for the second defendant, Professor
        Christie went on to say that the term "dependence" was sometimes used in
        preference to "addiction" and that, in certain individuals, some potentially
        addictive substances do not produce addiction, notwithstanding large
        numbers of users. Alcohol is an example of this phenomenon and even
        with such a notoriously addictive substance as heroin, about 50 per cent of
        users can manage a restrictive controlled pattern of use. He agreed that
        there is a component of compulsive behaviour in the use of such
        substances analogous with the compulsive behaviour arising from
        uncontrolled gambling.
733          Turning to the ability to give up the addictive or dependent or
        compulsive behaviour, Professor Christie was generally guarded about
        accepting high success rates but acknowledged that about 2 per cent of
        smokers succeed in giving up the habit each year. He acknowledged that
        pregnant women have a high success rate of abstinence and that health
        specialists also had a high success rate, leading to his agreement with the
        proposition that highly motivated persons can give up the habit. Professor
        Christie was not, however, prepared to accept that as an unqualified


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        statement pointing out that, even for highly motivated persons who have
        had surgery, the success rates were low and that even during periods of
        abstinence the addiction can remain and last for periods of five years or
        longer. For such a person, on receipt of bad news, attempts are made to
        reduce or give up smoking but there are only limited degrees of success.
        In cross-examination by counsel for the third defendant, Professor
        Christie said that for a person with a nicotine addiction the response to
        anti-smoking warnings is only likely to be small.
734          I am satisfied having regard to the evidence of Professor Chapman
        and Professor Christie that one should not unhesitatingly adopt the
        position that the reasonable man, if he should happen to be a smoker of
        long-standing, could or would abandon the habit and remain abstinent
        once he had learned of the health hazards associated with the habit from
        warnings on cigarette packets or from public health campaigns from
        respected sources. If it were as easy as that our community would not still
        be confronted with the vast public health problems associated with
        smoking which remain even in the current age when the social climate
        and anti-smoking regulation, has moved far more closely to a position of
        prohibition and disapproval than existed during Mr Cotton's lifetime.
735           I accept that there is a complicated relationship deriving from the
        addictive nature of nicotine, self-denial by smokers, and by
        encouragement for some time by the tobacco industry itself, which
        inhibits the informed individual from acting entirely rationally or in his
        own best interests. Consequently, I reject the submission that Mr Cotton's
        continued smoking, in the face of the many health warnings which he
        must have experienced, constituted a voluntary assumption of the risk of
        illness or disease associated with cigarette smoking. Even more so, I am
        satisfied that it did not constitute any voluntary assumption of the risk of
        developing lung cancer or other serious lung disease from the combined
        effect of tobacco smoking and asbestos exposure because there is simply
        no evidence to suggest, or to infer, that Mr Cotton was ever aware of the
        greater hazards of lung disease associated with the combination of
        cigarette smoking and asbestos exposure.

736          Again, because of the multiplicative or synergistic effect of asbestos
        exposure and chronic smoking which, as discussed in so much detail
        elsewhere, gives rise to an enhanced risk of developing the disease, I
        conclude that, assuming the combined effect of the two carcinogens, there
        is no basis for concluding that the continuation of the smoking effectively
        displaced any causative effect of the asbestos exposure so as to break the
        chain in causation of lung disease of the asbestos exposure or so as to act


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        as a new intervening cause. Those aspects of the defences of the first,
        second and third defendants must also be rejected. In reaching this
        conclusion, I hasten to acknowledge that a very significant issue in this
        case is whether or not Mr Cotton's experience of exposure to asbestos,
        materially contributed to the development of his fatal disease. For reasons
        already given, I have concluded, on the balance of probabilities, that it did
        have this effect. This conclusion itself is sufficient to displace the various
        submissions by the defendants that the smoking constituted a new
        intervening cause or became the sole or dominant cause of the lung
        cancer.
Contributory negligence
737          The conduct relied upon by a defendant asserting that a claimant was
        contributorily negligent must be conduct which is assessed from the
        viewpoint of a reasonable person placed in the same circumstances as the
        claimant. That is, it is an objective standard of conduct rather than a
        subjective one: Astley v Austrust Ltd (1999) 197 CLR 1 at 16. The issue
        for consideration is whether or not the conduct alleged to constitute
        contributory negligence, contributed not to the accident or event which
        caused the loss, but to the loss itself, which the claimant suffered - see
        Wynbergen v Hoyts Corporation Pty Ltd [1997] HCA 52; (1997) 149
        ALR 25; Astley v Austrust Ltd (supra) at 11; and Henville v Walker
        (2001) 206 CLR 459 at 504. The authorities are consistent that, even in
        cases involving multiple potential causes of harm or multiple potential
        defendants, there must be proof that the actual breach of duty, as a matter
        of inference, caused or contributed to the ensuing harm - see also
        Santow JA in Orica Ltd v CGU Insurance Ltd (2003) 59 NSWLR 14 at
        32 - 35.

738           Hence it is said that contributory negligence is independent of the
        idiosyncrasies of the particular person whose conduct is in question - per
        McHugh J in Joslyn v Berryman [2003] HCA 34; (2003) 214 CLR 552 at
        [39] and per Gummow and Callinan JJ at [70] and Hayne J at [153]. By
        analogy, the second defendant submits that the court should not permit
        any personal condition, inclination or weakness of the claimant, to alter
        the standard of care of the duty due to him or to her by a defendant - Cole
        v South Tweed Heads Rugby League Football Club Ltd [2004] HCA 29;
        (2004) 217 CLR 469 per Gleeson CJ at [13] - [15] or in relation to the
        significance, from the claimant's viewpoint, of conduct alleged to
        constitute contributory negligence - Jones v Bradley [2003] NSWCA 81
        and the intermediate appeal in the New South Wales Court of Appeal in
        South Tweed Heads Rugby League Club Ltd v Cole [2002] NSWCA


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        205; (2002) 55 NSWLR 113 per Santow JA at [20] and per Ipp JA at
        [179]. While there may be limits to this inflexibility which arise at a point
        where the plaintiff can no longer be regarded as acting voluntarily, or
        where unconscientious behaviour by the defendant has induced the
        plaintiff to act in a particular way (as to which see Gleeson CJ in Cole v
        South Tweed (supra)) at [13]; and Callinan J at [121] and [131]), the
        submission is that any addiction or dependence which Mr Cotton may
        have developed upon his tobacco smoking will not avoid or diminish
        what, otherwise, might be contributory negligence.

739           I certainly do not accept that the obvious addic tion or dependence
        which Mr Cotton developed as a result of cigarette smoking went so far as
        to deprive him of voluntary control or constituted some form of
        unconscientious interference with his free will by anybody for whom any
        of the defendants might be responsible. I therefore accept that the issue of
        whether or not Mr Cotton's smoking may amount to contributory
        negligence must be answered on an objective basis without regard to any
        actual addiction or dependence upon nicotine, however real that may be in
        fact, as it appears to be in his case.

740           The second defendant has drawn attention to several cases dealing
        with whether or not smoking can constitute contributory negligence. Of
        those, two determined that smoking could not constitute contributory
        negligence, namely Haar v Uneedus Scaffolding Pty Ltd, unreported; SCt
        of VIC (O'Bryan J); 30 March 1990 and Refalo v Stevedoring Industry
        Finance Committee [2002] NSWDDT 20 but which, on this point the
        first second defendant submits was decided per incuriam. Two cases
        which upheld the potential availability of smoking as contributory
        negligence are Simmons v Commonwealth of Australia, unreported; SCt
        of Vic (Coldrey J); 8 October 1991, where the defence was allowed to go
        to the jury; Commonwealth of Australia v McLean (1996) 41 NSWLR
        389 where the court unanimously held that the defence was arguable and
        should have gone to the jury. McLean's case was regarded by O'Meally
        as deciding that smoking could constitute contributory negligence in
        Dalby v Wallaby Grip Ltd [2002] NSWDDT 15. The second defendant
        also points to authorities in England and Canada as supporting its
        submission that smoking may constitute contributory negligence for the
        purposes of equivalent apportionment legislation, citing Margolis v
        Imperial Tobacco Ltd (2000) EWCA Civ 114 and Dumais v Hamilton
        [1998] ABCA 218, a decision of the Court of Appeal of the Province of
        Alberta.




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741          Since this case was argued there has been the decision of Badger v
        Ministry of Defence [2005] EWHC 2941; [2006] 3 All ER 173 upholding
        a submission that smoking may constitute contributory negligence in a
        lung disease case and reducing the damages by apportionment on this
        account by 20 per cent.

742          The second defendant also puts its submissions in relation to
        contributory negligence not only on the basis that smoking by Mr Cotton
        enhanced the prospects of him contracting lung cancer, in combination
        with the carcinogen of asbestos, but also on the basis that it aggravated the
        effects and rate of progress of the disease and that, consequently, his
        damages should not include such degree of loss as is attributable to his
        unreasonable conduct in continuing to smoke - Robertson v Hobart
        Police and Citizens Youth Club (1984) A Torts Rep 80-629.

743           I consider that I should accept that Mr Cotton's long habit of
        smoking did increase the risks of him of developing lung cancer from
        exposure to asbestos and, once the carcinogenic process had begun,
        aggravated and probably accelerated the onset and impact of the disease.
        However, I reject the submission that it ever became the sole cause of the
        disease or its progress so as to amount to an intervening cause, or that it
        ever displaced the effect which asbestos exposure had, either as an
        initiator or promoter acting in combination, to the point where the causal
        effect of the asbestos exposure disappeared.

744          The question therefore becomes whether or not the effect which his
        smoking had upon the development of progress of his fatal lung cancer
        means that Mr Cotton was contributorily negligent by failing to meet the
        objective standards which a reasonable person is expected to exercise for
        his or her own safety. That chronic smoking is harmful to health is only
        too obvious, but this does not mean that a chronic smoker who was
        severely injured as the result of a motor vehicle accident due solely to a
        car driver's negligence, will have his damages apportioned for
        contributory negligence in failing to exercise reasonable care for his
        general health - although it may mean that if his smoking was so severe as
        to diminish his working life, or life expectancy, that his damages may be
        reduced because the victim's losses would be less than they might have
        been if he were healthy, had a longer working life and life expectancy. If
        the partial defence of contributory negligence is to apply, the defendant
        must satisfy the court that either the injury which the plaintiff has suffered
        has been caused in part by his contributory negligence or the losses
        flowing from that injury have been increased because of the claimant's
        own lack of reasonable care for himself. Is smoking, therefore, viewed


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        objectively, a failure to take reasonable care for one's own health and
        safety? It may have little or no effect on the risk of injury or loss caused
        by traumatic events but, when it comes to loss or harm caused by diseases,
        to which smokers are more susceptible, then it may be.
745          For example, take a case where a claimant who is susceptible to
        some form of harm or disease if he or she fails to adhere to a prescribed
        regime of preventative medication, fails to take the medication as
        recommended. The significance of this example is to reveal that
        reasonable care for one's own health or safety may demand that an
        individual takes particular precautions by following a recommended
        regime or by abstaining from particular conduct which may be especially
        harmful for that individual - by way of further example, the need for a
        diagnosed diabetic to avoid knowingly ingesting a high sugar load.
746           So it may well be said that, in the modern state of informed public
        and medical opinion about the risks of smoking, a person who continues
        to smoke heavily after receiving warnings of the risk, that by doing so, he
        or she may be more susceptible to congestive heart disease or to a variety
        of respiratory diseases, would, in my view, probably be regarded by
        ordinary reasonably-minded people in the community as failing to
        exercise reasonable care for his or her own safety. If that person did
        develop such a disease the ordinary reasonable onlooker in the community
        would, no doubt, be sympathetic but would also be inclined to say of the
        unfortunate patient that he or she must accept part of the blame (should
        blame be attributable for the illness) or otherwise bear part of the
        responsibility for the misfortune. The reality to which that assumed
        human response is the reaction, derives from the general community
        belief or norm that, if an individual has the opportunity to avoid harm or
        risk by some action or precaution of his own which will not unduly
        interfere with reasonable enjoyment of life, then personal responsible
        autonomy demands that the individual should act accordingly. The
        community expectation is that if he or she fails to do so, that person
        should not attribute all the consequences of that risk falling in to someone
        else whose act or omission, in breach of duty, results in that risk becoming
        an actual event of loss or harm.
747          Decisions of this kind involve the application of generally accepted
        norms of behaviour in society. In places or at times when decisions on
        such matters of fact were or are made by juries, a jury is pre-eminently
        suitable to give the representative judgment of the community. Because
        these decisions are so normative it is difficult to articulate a principle, or
        any measure of scale for their assessment, which is applicable in anything


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        but the individual case. Because they are decisions of fact and degree,
        they are not susceptible to precise criteria.
748           Adding to the difficulties is the changing climate of public opinion
        about the risks of smoking. When Mr Cotton was only 17 when he began
        smoking in 1973 it is unlikely that he would then have been regarded as
        failing to exercise reasonable care for his own health or welfare, because
        of the prevalence and widespread acceptance of smoking then current in
        the community. However, I consider that when the anti-smoking
        campaigns from the public health authorities had become advanced, and
        when cigarette advertising was banned progressively from 1976 to 1995,
        according to Professor Chapman, a distinct change in public opinion
        developed, and hence the norms of behaviour expected for the
        preservation of one's health altered over these years.
749           There is a record in the notes of Dr Mincham of Bunbury,
        Mr Cotton's GP, on 31 August 1992 (Exhibit 149), of a recommendation
        that he should give up smoking. Equally, there is evidence from the
        plaintiff that over the period of 1992 to 1994, Mr Cotton attempted to give
        up smoking. I consider that it must be said that by continuing to smoke
        from then on Mr Cotton did fail to take reasonable care for his own safety
        and his failure to do so must be regarded as contributing to the severity of
        his fatal lung disease. That is, of course, long after his last exposure to
        asbestos while in the employ of the first defendant in Adelaide, and also
        after, but not long after, his first exposure to asbestos at the third
        defendant's premises as Australind. On the evidence it seems probable
        that the process of carcinogenesis which I have found was begun by
        Mr Cotton's exposure to asbestos in Adelaide, was then in its latent phase,
        and the same may be said of the contribution to the carcinogenesis which I
        have concluded was played by his exposure to asbestos at Australind.
        Nevertheless, the process was, as I have found, cumulative and was
        synergistic with the constant exposure to tobacco.
750           There is no detailed evidence about what course would probably
        have followed had Mr Cotton successfully given up smoking in 1992 or,
        for that matter, at any time after his first exposure to asbestos in Adelaide.
        There is, however, general evidence to the effects that his risk of
        developing lung cancer due to tobacco would, over time, have declined. It
        is not possible, therefore, to make any attempt to analyse quantitatively
        what would have occurred had he then quit, but it is nevertheless clearly
        implicit that his risks of developing the disease would have been
        diminished or, alternatively, that the onset of the disease may have been
        delayed by quite some time. However, having regard to the estimations of


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        Professor Musk who put the relative risk of developing lung cancer from
        smoking in Mr Cotton's case at 20; Professor Wan who put it at 10;
        Dr Leigh who put it at 8; and Professor Berry initially put the RR at 15
        but then reduced it to 8, the scope for reducing the risk would appear to be
        considerable had Mr Cotton stopped smoking. But no close attention was
        given in this case to the extent to which the risk of lung cancer for a
        former smoker diminishes over time after smoking has stopped, let alone
        what the variations in risk are for a reformed smoker who has been, and
        continues to be, subject to asbestos exposure.
751          In Badger v Ministry of Defence (supra) there was quantitative
        evidence about the reduction in risks after giving up smoking at particular
        times, leading to the decision to make the ultimate reduction by
        apportionment for contributory negligence by continuing to smoke,
        20 per cent. Mr Badger died at the age of 63 years, 15 years after a 23
        year period of employment involving exposure to asbestos dust and fibres
        which had caused him to develop asbestosis and, ultimately, his fatal lung
        cancer. He had continued to smoke at the rate of about 20 cigarettes per
        day throughout his adult life, probably until the year of his death or the
        year before - a total of about 44-pack years. He had a number of other
        smoking-related conditions, including emphysema and ischaemic heart
        disease, with a reduction of seven years' life expectancy due to those
        conditions alone. He therefore had smoked for far longer and, as