Occupational Lung Diseases

Occupational Lung Diseases Guillermo do Pico MD FCCP Professor of Medicine 4/21/2008 INHALATION EXPOSURE Airways Bronchioles Alveoli Interstitium Blood Systemic effects Site & intensity of the injury  Physico-chemical properties  Particle size…<5u go deeper  Concentration…  Solubility  Density… Duration of exposure Signs of alertness  Rate / depth of breathing  Host response variability / susceptibility  Host defense mechanisms   Reactivity… lighter (as) go deeper higher (NH4) more damage Mechanisms Toxic Inflammatory Irritant : Allergic : Sensitizers : Infectious : Carcinogenic farm dust, chemicals flour (bakers) toluene di-isocyanates brucellosis uranium, Symptoms Cough Expectoration Hemoptysis Dyspnea at rest and/or on exertion Wheezing Chest tightness / pain Upper airways symptoms Fever, chills, other Threshold limit values ACGIH or OSHA TLV-TWA: time-weighted average concentration for 8 hours.Most workers will have adverse effects TLV-STEL: max concentration for up to 15 min that can cause chronic or irreversible changes in tissues or narcosis AIRWAYS EXPOSURE ALVEOLI UPPER ITIS  BRONCHITIS  ASTHMA-LIKE  ASTHMA BRONCHIOLITIS  BOOP PULM EDEMA PNEUMONITIS FIBROSIS   SYSTEMIC NEUROTOXINS FEVERS  BRONCHOGENIC   AIRWAYS Asbestos + Smoking Uranium + Smoking carcinogenic PLEURA •MESOTHELIOMA •Asbestos SYSTEMIC   LIVER Ca Polyvinyl chloride AIRWAYS  NEUROTOXINS  Malathion CO  FEVERS  EXPOSURE ALVEOLI Grain Moldy hay Endotoxin Tephlon fumes Metal fumes SYSTEMIC Occupational diseases Acute Chronic Progressive Regressive Intermitent Reversible Irreversible Asthma Bronchitis Silicosis HP Asthma Asthma Silicosis Airways exposure Acute massive chemical bronchitis Complete recovery Chronic low Acute low Chronic Bronchitis Asthma-like disease Allergic asthma POPULATION STUDIES CHRONIC BRONCHITIS 80 70 60 50 40 30 20 10 0 GS GNS CS CNS FS FNS GRAIN workers SM NS CONTROL S NS FARMER S NS SMOKERS NONSMOKER Definition Occupational asthma A. Asthma B. Onset after entering workplace C. Association of symptoms to workplace D1. Agent known to cause OA or D2. Work-related changes in lung function No latency……………..irritant exposure Latency…………………….allergic nonallergic sensitization Etiology Mechanism Inducers Immunologic IgE mediated High molecular wght Grain, crab, castor beans Woods, gum acacia Animal dander, urine Epoxy resins Chloramine T Platinum salts di-isocyanates Red Cedar Cobalt Ammonia, chlorine Low molecular haptens ? Cell mediated Low molecular Nonimmunologic Irritant-toxic Occupational Asthma in Finland Mean annual incidence 17/100000 workers Bakers, food industry Painters, Lacquerers Veterinarians Chemical workers Farmers Animal husbandry Welders Plastics industry 60 % related to: Animal epithelia hair secretions Flours Grains Fodder Kajalainen et al Am J Industr Med 2000 MILK TANK INSULATION Grain elevator Superior-Duluth CARGO SHIP Next slide Truck unloading grain No mask NIOSH tech w/mask       History Exam Lung Functions Skin tests Therapeutic trial   Obstructive pattern  On spirometry Bronchodilatadors Provocation tests FEV1 O IMMEDIATE REACTION LATE REACTION DUAL REACTION PROGRESSIVE-PROLONGED HOME-------------WORK-----HOME—WORK--HOMEWORK Rx therapy Same as other asthma Most important=avoidance of exposure Prognosis Can not be predicted by severity, exposure, type,... Progress Exposure ceases Persistent Recurrent Resolves HIGH IRRITANT UNCONDITIONED Stimulus RESPONSE Autonomic Activation “PANIC” CONDITIONED Stimulus RESPONSE GAS VAPOR LOW ODORANT Event-triggered reaction OCCUPATIONAL ALVEOLAR INJURY ORGANIC DUSTS: INORGANIC DUSTS:  Pneumoconiosis  Pulmonary  Allergic pneumonitis CHEMICALS: edema or Diffuse Alveolar Damage Hypersensitivity Pneumonitis Lung disease resulting from sensitization and recurrent exposures to organic dusts Symptoms hours after exposure Fever,chills, dyspnea, cough Xray = bilateral pneumonitis Abnormal lung functions Acute, subacute or chronic Organic Dust Toxic Syndrome Flu-like syndrome During exposure or delayed High level single exposure to dust No Xray or lung function changes Recovery without sequelae Incidence of Allergic Alveolitis or“Farmers Lung Disease” and Organic Dust Toxic Syndrome or Inhalation Fever EAA = 2-3/10000 farmers/year ODTS = 1/1000 farmers/year 6702 swedish farmers Malmberg et al 1988 Hypersensitivity Pneumonitis Farmer’s Lung Bird Breeder’s Metal worker’s Hot tub Mushroom workers Rodent handlers Cheese washers Bagassosis Summertype Humidifier Lung Suberosis Coptic Lung Malt workers Bathtub refinisher Composter’s lung Sauna takers Hypersensitivity Pneumonitis Microbial “moldy” Bacteria Thermophiles • S. rectivirgula NonThermophiles • P. fluorescens • B. cereus, B subtilis Animal Birds, rats dander,feathers, droppings, urine Insects:weevil Chemicals Metal fluid Diisocyanates Pyrethrum Fungi : Aspergillus sp,Penicillium, Amebae Mycobacteria avium Contaminated fluids Salami worker’s lung Rivero et al Medicina 1999 Biopsy proven Penicillium spp Water reservoirs related HP Hot tub Humidifiers home, office, industry Saunas Showers Swimming pools Air conditioning systems Endotoxin or Specific antigen?……….. Metal working fluid Metal working fluids Cool and lubricate machine parts Removal of metal waste Water-oil emulsions w/ soluble synthetic oils and biocide to reduce microbial contamination Respiratory symptoms Asthma Hypersensitivity Pneumonitis Hypersensitivity Pneumonitis to Metal working fluids Biopsy proven > 20 cases (US-Canada) Causative agent: unknown – Hodgson et al Am J Industr Med 2001 39:616 – Fox et al Am J Industr Med 1999 35:58- Wi Solutions Technical improvements • avoid cooling mists, • enclosures, • improve ventilation Workers education Surveillance for sentinel cases Treatment Corticosteroids for subacute or severe acute PROGNOSIS- OUTCOME Resolve Recurrent disease= outcome determinant Fibrosis / COPD Fatal,progressive Treatment –Avoidance of exposure –Corticosteroids Flock worker’s Lung Flocking Industry Flock=powder of fibers .2-5 mm Nylon, rayon, polyester, textile waste….. Precision-cut Random-cut Adhesive coated fabrics • Dull rotary blade • <10 μm particles Fleeced fabrics Clothing, carpets upholstery, cars … FLEECE INORGANIC DUST-INDUCED LUNG DISEASE barium •LOW-FIBROGENIC Deposits: iron, tin, titanium, glass wool Granulomatous: Berillium Silica (silicon dioxide) upper Silicates: Asbestos, lower Talc, Kaolin upper Coal dust Aluminum •FIBROGENIC Silica exposure Minning Foundry work Sand blasting Ceramics HOST Silicosis Calcified lymph nodes Upper lobe nodules Silicosis Massive fibrosis Acute silicosis quarry worker Kim et la Silicoproteinosis 25 yo dental technician Majo Barcelona Simple Carbomonoxide-fires Methane, CO2-manure pits Chemical (interfere with cell respiration H cyanide-burning plastics H sulfide-manure pits Neurotoxins Pesticides, herbicides, fumigants Warfare gases Irritants gases •Acrolein-burning plastics •Ammonia-fertilizer, transport •Chlorine-transport accidents paper mills •M-isocyanates plastics, fertilizers •N oxides=Farm silo, missile silo Zamboni disease •Phosgene=paint stripping, fires •Sulfur diox-paper mill, refrigeration Industrial or transportation accidents or intentional in wars Mustard gas Mustard Gas - Iran-Iraq war 10 years after single exposure 197 iranian veterans asthma chronic bronchitis bronchiectasis airway scars or granulation pulmonary fibrosis Emad et al Chest 97 11% 59% 9% 10% 12% Complex exposures Complex exposures Site and extent of damage depend on : Duration Concentration Depth of inhalation Solubility Reactivity Warning properties MASSIVE TOXIC INHALATION ASPHYXIA PULMONARY EDEMA IRRITATION UPPER AIRWAYS LOWER AIRWAYS OBSTRUCTION LARYNGOSPASM VENTILATORY ANOXIA FAILURE MECHANICAL VENTILATION DEATH RECOVERY Pulmonary edema Hemorrhagic alveolitis Acetaldehide Acrolein Ammonia Cadmium oxide Cobalt fumes Chlorine H chloride H fluoride H sulfide Methyl bromide Methylisocyanate Nickel carbonyl Nitrogen dioxide Organophosphates Sulfur dioxide Toluene diisocyanate Trimellitic anhidride Zinc chloride Exposure to Nitrous dioxide Silo Fillers Disease Within 10 days Went to rescue P.edema burns † Titan ll missile Missile Silo McConnel Accident Both pulmonary edema 1 † 20th Century castle for sale 2.3 million Diffuse alveolar Damage Non cardiogenic pulmonary edema=ARDS can be delayed OCCUPATIONAL LUNG DISEASES ARE PREVENTABLE Defective-Zamboni disease NO2 “Zamboni disease” 96 Hockey Players Cough Hemoptysis Dyspnea-rest Dyspnea-exertion Epistaxis Headache Nausea Weakness Chest pain 97 % 38 % 50 % 70 % 11 % 42 % 20 % 38 % 70 % PIGS PIG FEED NH3 CO2 H2S CH4 Occupational Lung diseases are preventable