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					                                      Risk Assessment of INAAP




Risk Assessment of the Indiana Army Ammunitions Plant’s
         Effects on the Fetus of a Pregnant Adult

                   Mercury and Lead


                     April 29, 2005




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                                                           Risk Assessment of INAAP



                            TABLE OF CONTENTS

Chapter 1: Statement of Problem
1.1 Overview
1.2 Site History
1.3 Site Contaminants
1.4 Scope of Risk Assessment

Chapter 2: Hazard Identification
2.1 Introduction
2.2 General Site-specific Data Collection Considerations
2.3 General Site-specific Data Evaluation Considerations
2.4 Environmental Area

Chapter 3: Conceptual Site Model
3.1 Conceptual Site Table
3.2 Top-Down Site Map
3.3 Side-View Site Map


Chapter 4: Toxicity Assessment
4.1 Toxicity Information for Non-Cancer Lead Effects
       A. Description of Studies Used
       B. Endpoints Chosen and Why
       D. Reference doses
       E. Confidence
       F. Uncertainties


Chapter 5: Exposure Assessment
 5.1 Characterization of Exposure Setting5.2 Identification of Exposure Pathways
5.3 Quantification of Exposure
5.4 Identification of Uncertainties
5.5 Summary of Exposure Assessment


Chapter 6:     Risk Characterization
6.1 Current Land-use Conditions
6.2 Future Land-use Conditions
6.3 Uncertainties
6.4 Comparison of Risk Characterization Results to Human Studies
6.5 Summary discussion and Tabulation of the Risk Characterization



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Chapter 7: Risk Management
7.1 Site Goals
7.2 Corrective Measures for Site
7.3 Corrective Measures for Target Organism

References
Appendix A: Site Map
Appendix B:
Appendix C: Exposure Calculations for Non-cancer and Cancer Risk for Lead and
             Mercury
Appendix D: Exposure Calculations
Appendix E: Non-cancer Risk Table
Appendix F: Cancer Risk Table




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                                         Chapter 1
                                    Statement of Problem

1.1 Overview
        The Indiana Army Ammunition plant in Clark County, Indiana is contaminated with
VOC’s, SVOC’s, metals and pesticides making it a risk for the surrounding area and anyone
who enters the site. Soil, sediment, groundwater, and surface water samples indicate the
presence of many contaminates such as lead and mercury. These heavy metals can and most
likely are causing adverse health effects in both humans and biota in the area.

        INAAP’s has karst geology which includes enlarged fractures, sinkholes, swallets,
joints and caves in the limestone that influence the flow of groundwater in to the Ohio River
(see appendix A for site map). The area of focus for the pregnant adult female is the Jenny
Lind Pond Outfall Area which is located on the downstream side of the former Jenny Lind
Pond dam (DOC INAAP – Phase 1 RI Report Site 25 Jenny Lind Pond, 2001 pg 1-1).

       The objective of this risk assessment is to: 1. Assess the toxicity of lead, mercury and
methyl mercury in the area, 2. determine the pathways of exposure, 3. calculate the amount
of each chemical the fetus is exposed to though the blood levels of his/her mother, and 4.
develop a risk characterization of the site, including cancer and non-cancer risks for the fetus

1.2 Site History
        Indiana Army Ammunition Plant (INAAP), is located in Clark County (south central
Indiana) (See map in Appendix A), six miles north of Jeffersonville, Indiana and 10 miles
from Louisville, Kentucky and covers approximately 9,790 acres. The area is a Government-
Owned, Contractor-Operated (GOCO) military industrial installation that operated from 1941
to 1998 (www.globalsecurity.org/military/ library/report/enviro/INAAP_IAP.pdf) and is
currently inactive.

1.3 Site Contaminants
        INAAP was built during WWII to manufacture and assemble propellants and
explosives. Many contaminants were stored on site, specifically lead and mercury. The plant
is located on the north corner of the site with an elevation of 680 feet above sea level, the
highest point on the property. Due to the high elevation of the plant relative to the rest of the
area, during rainfall, stored contaminants leech into the soil and flow to areas down through
Jenny Lind Run and into the Ohio River. Due to the karst geology of the area, the
contaminants can freely flow into and out of the site, making it difficult to predict the
possible exposure range.
        Lead exposure to a fetus can lead to adverse health affects such as neurological
disorders and developmental problems. Mercury exposure can lead to brain and kidney
damage. Moreover, mercury, severely effects the neurological functioning/development of
the fetus and can cause infants to be born retarded, deaf, blind, and unable to speak.




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1.4 Scope of Risk Assessment
        This assessment of INAAP will determine the risks of lead and mercury exposure on
the fetus of a pregnant adult. Exposure from inhalation, ingestion and dermal pathways of the
contaminants will be quantified using air, soil, food, and water sample data from the Indiana
Department of Environmental Management (IDEM). The Risk Assessment Guide to
Superfund (RAGS) is the major guideline we will be following in order to achieve the most
accurate and consistent assessment of the heavy metals on the site and how they are affecting
our target organism. A management plan to effectively reduce the exposure to lead and
mercury will also be discussed.




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                                        Chapter 2
                                   Hazard Identification

2.1 Introduction
          Fetal development is the most susceptible to toxicological influences due to the
intense development taking place. The fetus grows at a rate incomparable to any other time
in its life span (Woollett, Laura Ann 2001). During pregnancy, the framework of an
individual is being created. The brain, central nervous system, organs, and limbs are being
developed; disruptions have significant and sometimes long lasting and permanent effects.
Often, these effects do not manifest themselves until adulthood. (Center for Environmental
Health and Susceptibility). Lead, mercury, and methylmercury can all disrupt this normal
embryonic and fetal development causing birth defects (Mekdeci, Betty ND).

2.2 General Site-specific Data Collection Considerations
Historical information relative to data collection:
         The Indiana Army Ammunition Plant (INAAP) was established in 1940 to produce
bagged propelling charges for large caliber ammunition and was one of over sixty (60) such
facilities eventually constructed in the United States. For over 50 years, INAAP was utilized
by the Army during World War II, the Korean War and the Vietnam War to produce
munitions to support the war efforts. Employment levels rose and dropped in accordance
with the operation (during national emergencies) and in operation of the plant. While the
plant was active it used and stored many contaminates such as nitrocellulose, nitroglycerin
and heavy metals (www.globalsecurity.org/military/ library/report/enviro/INAAP_IAP.pdf).
In December 1992 the facility was placed in ‘inactive’ status by the army but not closed.

Preliminary identification of human exposure:
       Past studies done on INAAP show that the area is contaminated with heavy metals,
however human exposure has yet be identified.

Modeling parameter requirements:
       Modeling parameter requirements included the risk investigation/feasibility study
(RI/FS) from the Risk Assessment Guidance for Superfund (RAGS), vol.1. The main
pathways studied are inhalation, dermal exposure, and ingestion and the media of
contaminant entry are air, soil, food, and water. We are aware that there are other potential
pathways and other media exists, but these are the most direct with respect to fetal exposure.

Background Sampling:
       Mike Tosick from the U. S. Fish and Wildlife Services provided us with on-site
sampling data preformed by IDEM. The fish mercury levels and air concentrations of
surrounding areas was done by IDEM. The sampling data was compiled and analyzed and
entered into our exposure calculations.

QA/QC methods:
      IDEM was responsible for Quality Assurance/Quality Control because they
conducted sampling. Lead does not require special precautions or requirements for testing.
Mercury, however, must be stored in a glass test tube and kept at a similar temperature to the


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location from which it was extrapolated. Extreme caution must be taken to ensure that none
of the contaminant comes into contact with human skin. Uncertainty exists because we can
not be sure that IDEM followed the proper sampling procedures.

2.3 General Site-specific Data Evaluation Considerations
Steps used:
        IDEM’s investigation methods included core-sampling, sampling of groundwater,
sampling of surface water and sediment content. There are over 60 areas of particular interest
within the property. Offsite sampling was also conducted on the Ohio River.

QA/QC methods during evaluation:
         There have been thousands of samples taken on the INAAP site. Each sample carries
the risk of becoming contaminated if not handled properly. In order to ensure accurate
results, many chemicals must be kept, tested and transported in specific ways; such as light
sensitive containers or cold temperatures. IDEM however, feels strongly about their results
and we can use these samples as a reliable source.

General data uncertainty:
       Exact procedures of the sampling process is unknown. Our air and fish concentrations
were not site specific leading to high uncertainty. The possibility for human error in
sampling, testing, or inputting data results leaves a large uncertainty. Overall, outside
contractors could have been hired in order to verify the results of IDEM sampling.

2.4 Environmental Area
Data from site investigations:
Data was taken from the U.S. Department of Fish and Wildlife.

Evaluation of qualified and coded data:
RAGS and the Dept of Fisheries and Wildlife.

Tentatively identified compounds:
Lead - Lead is a naturally occurring bluish-gray metal found in small amounts in the earth's
crust (ATSDR). Lead can be found in all parts of our environment. Much of it comes from
human activities including burning fossil fuels, mining, and manufacturing.

Mercury - Metallic mercury is a shiny, silver-white, odorless liquid. If heated, it is a
colorless, odorless gas (ATSDR). Mercury combines with other elements, such as chlorine,
sulfur, or oxygen, to form inorganic mercury compounds or "salts," which are usually white
powders or crystals (ATSDR).

Methylmercury-Mercury combed with carbon creates organic mercury or methylmercury.
This process is usually achieved by microscopic organisms in the water and soil (ATSDR).
Methylmercury is absorbed six times more easily than inorganic mercury and can migrate
through cells which normally form barriers to toxins (Environment Canada, 2004).




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                                       Chapter 3
                                  Conceptual Site Model

   3.1 Conceptual Site Table
TABLE 1            Source Locations         Geological              Target      Pathways of
                                            features                Organism    exposure
Lead (Pb)          Jenny Lind Outfall Run   karst geology           Pregnant    Inhalation –
                   & Jenny Lind Pond.       includes enlarged       Adult       Ground Water
                   (SW7/SD7,                fractures, sinkholes,   Female      and Air.
                   SW21/SD21,               swallets, joints and    Fetus       Dermal-
                   SW20,SD20 see map)       caves in the                        Groundwater and
                                            limestone that                      Soil
                                            influence the flow                  Ingestion-
                                            of groundwater in                   Groundwater
                                            to the Ohio River

Mercury (Hg)       Jenny Lind Outfall Run   karst geology           Pregnant    Inhalation- Air
                   & Jenny Lind Pond.       includes enlarged       Adult       Dermal- Soil
                   (SW20/SD20,              fractures, sinkholes,   Female      Ingestion - Food
                   25SW/SD32 see map)       swallets, joints and    Fetus
                                            caves in the
                                            limestone that
                                            influence the flow
                                            of groundwater in
                                            to the Ohio River




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3.2 Top-Down Site Map




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                         Risk Assessment of INAAP




3.3 Side-View Site Map




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                                                                 Risk Assessment of INAAP


                                         Chapter 4
                                     Toxicity Assessment

4.1 Toxicity Information for Non-Cancer Lead Effects

Fetal development is the most susceptible to toxicological influences due to the intense
development taking place. The fetus grows at a rate incomparable to any other time in its life
span (Woollett, Laura Ann 2001). During pregnancy, the framework of an individual is being
created. The brain, central nervous system, organs, and limbs are being developed;
disruptions have significant and sometimes long lasting and permanent effects. Often, these
effects do not manifest themselves until adulthood. (Center for Environmental Health and
Susceptibility). Lead, mercury, and methylmecury can all disrupt this normal embryonic and
fetal development causing birth defects (Mekdeci, Betty ND).


LEAD
--Non-cancer

Lead is a multi-targeted toxicant, causing effects in the gastrointestinal tract, hematopoietic
system, cardiovascular system, central and peripheral nervous systems, kidneys, immune
system, and reproductive system (Davidson, Kowetha A., 1994) It is exchanged in the blood,
soft tissue (liver, kidney, lung, brain, spleen, muscles, and heat) and mineralizing tissues
(bone and teeth ) (ATSDR 2000).

Once in the maternal bloodstream, lead readily crosses the placenta from mother to fetus,
causing venous blood lead levels in mother and infant to be nearly identical (Landrigan,
Philip J., et al. 2000). In adults, about 95% of the total body burden of lead is stored in the
skeleton (Shirng-Wern Tsaih, 2001). During pregnancy, especially during the third trimester
(6-8 months) of pregnancy when the fetal skeleton is developing, the lead from the maternal
skeleton is reabsorbed in to the blood stream, to meet the calcium requirements of the
developing fetus (See Chart #1 for critical times in fetal development) (Gulson, Brian L, et
al. 2004).

The incomplete development of the blood-brain barrier in the fetus makes the brain
susceptible for lead to enter into the developing nervous system, causing prolonged or even
permanent neurological damage (ASTDR 2000). Fetal blood lead levels of 10-20 ug/dl
causes a loss of intelligence, shortening of attention span and disruptive behavior, effects that
appears to be irreversible, untreatable and lifelong (Landrigan, Philip J, 2000). In addition to
neurobehavioural effects, there have been reports of effects on haeme synthesis and on a
number of enzymes and biochemical parameters, as well as of reduced gestational age (Shilu
Tong, 2000) Lead has been shown to decrease learning and memory, verbal ability, impair
speech and hearing functions. It has also been linked to hyperactivity and Attention Deficite
and Hyperactivity Disorder (ADHD). Low levels of prenatal exposure (maternal blood lead
levels of 14 ug/dL) increase the risk of reduced birth weight and premature birth (ASTDR
1999). Lead exposure has also been related to immunosuppression, increasing the
susceptibility or severity of infection (Hadden 1986).(Mekdeci, Betty….ND). There is also a
significant association between blood cord levels and the occurance of minor abnormalities

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in infants. The most common of which are hemangiomas, lymphangiomas, minor skin
anomalies (tags and papillae, and undescended testicles (Agency for Toxic Substances and
Disease Registry, 1999). A level of 80-100 ug/dL in children can result in irreversible, severe
mental brain damage or death (Davidson, Kowetha A., 1994). Frank anemia, which is a
result of reduced hemoglobin production and shortened life span of erythrocytes, is seen in
adults at blood lead concentrations of 80 ug/dL and in children at concentrations of 70 ug/dL
(Davidson, Kowetha A., 1994).

For our risk characterization we derived our No Observed Effect Level (NOEL) from a blood
lead level of 15ug/dL. This is in-between the 10-20ug/dL cited earlier and is based on a study
on infants between the ages of 6-24 months. Their blood was tested for lead levels,
erythrocyte protorphyrin, and hematocrit. The NOEL for the study was 15 ug/d, the point at
which there were no observed changes in the erythrocyte protorphyrin, meaning that the lead
had not inhibited the heme causing anemia, one of the first stages of lead poisoning
(Rabinowitz MB et al. 1986—Found on Google Scholar). This study, however is a
subchronic study, which was not aimed at our neurological endpoint and not based on known
fetal exposure. These were our uncertainties for all of our non-caner lead calculations,
making the uncertainty factor = 1,000 (10*10*10), (10 points from each uncertainty). It was
a credible study, however if I had more experience with risk assessments I might be able to
find more target organism specific study, so I gave myself a modifying factor of 10 for all of
my lead calculations.

The chemical form of lead, or lead compounds, entering the body is a factor in determining
the target organ. Organic lead compounds (rare cense the ban on lead gasoline additives) are
metabolized in the liver, inorganic lead, most common for of lead is absorbed into the body
and binds on to red-blood cells to be redistributed to the soft tissues and then end up
ultimately bioaccumulating in the bone (Agency for Toxic Substances and Disease Registry,
1999).Lead that is not retained in the body is excreted by kidney (urine) or feces (ATSDR
2000). Pregnant women can absorb 70% of the lead they ingest whereas as typical adults
absorb up to 20% (ATSDR 2000). At the Indiana Army Ammunitions Plant, we are dealing
with inorganic mercury from the production of lead shot.

One to ten-day exposure to lead can have serious and long term effects depending upon how
much is ingested and absorbed into the blood stream. As stated above, levels of 80-100ug/dL
can lead to severe brain damage and death. These levels, however are not common and it is
the gradual long term exposure which can do the most damage. If your child has ingested
lead it is recommended that you remove him from the area in which he ingested the lead.
Because most of the damage done by lead is caused by its behavior as a calcium mimic, if
the child intakes a large amount of calcium, you can minimize the amount he will intake into
the blood stream. Many tests have shown that eating can greatly decrease the amount of lead
absorbed (Rabinowitz, et al 1980).

--Cancer

Although there is no substantial data proving lead to be cancerous to humans, the National
Toxicology Program’s Report on Carcinogens Review Committee stated that lead and lead
compounds are considered “reasonably anticipated to be human carcinogens” (http://ntp-


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server.niehs.nih.gov/NewHomeRoc/roc11Bkgrnd2003.html EPA July 2003). There have
been extensive epidemiological studies on lead exposures in work places. These studies have
shown a relationship between lead exposure and lung and stomach cancer, however, the EPA
has lead classified as B2, probable human carcinogen, due to the lack the quantitative
exposure data needed to be accurate (Agency for Toxic Substances and Disease Registry,
1999).

Lead is a known animal carcinogen. The most common tumors developed are renal tumors. I
derived my lead slope factor from the Azar, et al. (1973) rat study referenced in the EPA
IRIS web site (http://www.epa.gov/IRIS/subst/0277.htm). The study was done in two stages,
each two years long. Because rats typically live for 2.5-3 years, this is considered a chronic
study. The rats were administered 10, 50, 100 and 500 ppm of lead acetate into their diet.
There were 100 control rats. The second study, under the same conditions, used 20 rats given
diets of 0, 1000, and 2000 ppm of lead acetate. No renal tumors were reported on 0, 10, or
100ppm. 5/50 rats developed tumors at 500 ppm (or 1/10), 10/20 developed tumors at 1,000
(5/10) and 16/20 developed tumors at 2,000 ppm (8/10).I combined these two studies to
generate the slope factor of 0.0086 mg/kg-d.

                           Lead Slope factor

                  20

                  15
  % with Tumors




                  10
                                        y = 0.0086x - 0.5516
                   5                         R2 = 0.9669
                   0
                       0   500   1000   1500    2000     2500
                  -5
                                    Dose

Figure 1. Slope Factor of for the carcinoginicy of Lead.
(Based on a rat kidney cancer study by Azar, et al. (1973))

Mercury
--Non-Cancer

Mercury is a naturally occurring metal and has several forms when combined with other
elements (ATSDR). Mercury is a toxin that has major effects on the nervous system.
Mercury may also interrupt neurological development of the fetus and cause spontaneous
abortions. It has been documented that the exposure of a mother to levels as low as
0.05mg/m^3 daily up until the 32 week of pregnancy can cause severe brain damage and
death to the born infant (Yoshida, 2002). Effects on brain functioning may result in
irritability, shyness, tremors, changes in vision or hearing, and memory problems. Exposure
to high levels of metallic, inorganic, or organic mercury can permanently damage the brain,
kidneys, and developing fetus (ATSDR). Short-term exposure to high levels of metallic
mercury vapors may cause effects including lung damage, nausea, vomiting, diarrhea,
increases in blood pressure or heart rate, skin rashes, and eye irritation.



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Fetuses can be exposed to mercury via exposure of their mothers either before or during
pregnancy (ATSDR). Maternal consumption of large amounts of fish or marina mammals
contaminated with mercury, dental amalgam fillings, and occupational exposure are the most
common source of mercury exposure for most individuals. Many consumer products also
contain mercury such as
fluorescent lamps and light switches.

Concentrations of mercury have been measured in cord blood studies that show prenatal
exposure. A study in ATSDR conducted by Pitkin (1976) used 100 maternal cord blood pairs
to measure concentrations of total mercury in cord blood samples from rural Iowa
inhabitants. The study results showed that the mean cord blood total mercury concentration
was 1.24 ppb, while the mean of the paired maternal blood samples was 1.01 ppb (ATSDR).
Another recent study conducted by Wheatley and Paradis showed that 523 cord blood
samples out of 2,405 (22%) were found to have total mercury elvels greater than 20 ppb,
with the highest cord blood sample containing 224 ppb (ATSDR).

Numerous studies have shown neurological effects on the fetus due to mercury exposure. A
study conducted in the Faroe Islands suggested that children born to mothers with high body
levels of mercury scored lower on brain function tests than mothers with low body levels of
mercury (http://enhs.umn.edu/5200/mercury/healtheffects.html).

--Cancer
There is inadequate human cancer data available for all forms of mercury (ATSDR). There is
no evidence of a link between metallic mercury exposure and cancer mortality. The EPA has
listed mercury as class D characterization – not classifiable as to human carcinogenicity.

Methylmercury

--Non-Cancer
Mercury combined with carbon creates organic mercury compounds the most common one
is, methylmercury. Methylmercury is produced mainly by microscopic organisms in the
water and soil. More mercury in the environment can increase the amounts of methylmercury
that these small organisms make (ATSDR). Methylmercury is absorbed six times more easily
than inorganic mercury and can migrate through cells which normally form barriers to toxins
(Environment Canada 2004). Organic mercury (methylmercury) affects developing fetuses.
Significant health risks, including neuropath logical and neurobehavioral effects are
associated with prenatal exposure to methylmercury (Zelikoff et al. 1995) (ATSDR).
Methylmercury is especially dangerous to developing fetuses because it can cross the
placenta and the blood-brain barrier. The mercury is then concentrated in the brain of the
fetus because the metal is absorbed quickly and is not excreted efficiently
(http://enhs.umn.edu/5200/mercury/healtheffects.html).

Methylmercury can be eaten or swallowed by a pregnant woman and is considered a
teratogen in the fetal brain (http://enhs.umn.edu/5200/mercury/healtheffects.html).
Methylmercury is a form of mercury that is associated with a risk in developmental effects. It
can pass from a mother’s body into breast milk and into the nursing infant. Effects of
methylmercury may not be apparent if the exposure was small during pregnancy. Small

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decreases in IQ or effects of the brain that can only be detected by sensitive
neuropsychological testing(ATSDR). Effects of mercury, where exposure to it was high
during pregnancy can be more serious. Exposure to a developing fetus may show effects
when they are beginning to walk or talk. More severe effects include brain damage with
mental retardation, lack of coordination, and inability to move (ATSDR). Eventual blindness,
involuntary muscle contractions, seizures, muscle weakness, and inability to speak can occur
if there were very toxic levels of mercury during pregnancy
(http://enhs.umn.edu/5200/mercury/healtheffects.html).

Studies of methylmercury effects on developing fetuses have been recorded. For example in
Minamata Bay, Japan during the 1950’s, large amounts of organic mercury were dumped
into the bay (http://enhs.umn.edu/5200/mercury/healtheffects.html). The fish in the bay were
contaminated by the mercury and then consumed by pregnant women. This resulted in many
children, born from the women who consumed the fish, who had severe nerve damage. In
Iraq a study of children born to mothers who consumed grain contaminated with organic
mercury, the effects showed the children walking at a later age than non-exposed children
(http://enhs.umn.edu/5200/mercury/healtheffects.html).

In the Minamata Bay disaster and the Iraq epidemic, mothers who were asymptomatic or
showed mild toxic effects gave birth to severely affected infants
(http://www.altcorp.com/DentalInformation/environmentalhg.htm). The study results showed
that at first after birth the infants appeared normal and showed no harmful effects from
exposure. However as they infants began aging psychomotor retardation, blindness, deafness,
and seizures developed throughout time.

-- Cancer
Mercury has not been shown to cause cancer in humans. There are inadequate human cancer
data available for all forms of mercury. Mercuric chloride has caused increases in several
types of tumors in rats and mice, and methylmercury has caused kidney tumors in male mice
(ATSDR). Human studies have no linked exposure to elemental mercury to cancer. The U.S.
Environmental Protection Agency believes methylmercury is a possible cancer causing agent
but elemental mercury is not classifiable as a cancer causing substance (EPA).

A. Description of Studies Used
I was unable to find a NOEL for lead with a fetal neurological endpoint, so I derived my own
NOEL based on a study (Rabinowitz MB et al. 1986) preformed on 232 infants between the
ages of 6 -24 months. The measurements of blood lead, erythrocyte protorphyrin and
hematocrit were made semi-annually. At the 15-17 ug/dL level, there was No Observed
Effects, however levels above 15 ug/dL resulted in erythrocyte protoporohyrin levels four
times the normal amount. I chose 15 ug/dL to account for the increased sensitivity for the
fetus.

My cancer slope factor was from the Azar, et al. (1973) rat study referenced in the EPA IRIS
web site (http://www.epa.gov/IRIS/subst/0277.htm). The study was done in two stages, each
two years long. Because rats typically live for 2.5-3 years, this is considered a chronic study.
The rats were administered 10, 50, 100 and 500 ppm of lead acetate into their diet. There
were 100 control rats. The second study, under the same conditions, used 20 rats given diets

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of 0, 1000, and 2000 ppm of lead acetate. No renal tumors were reported on 0, 10, or
100ppm. 5/50 rats developed tumors at 500 ppm (or 1/10), 10/20 developed tumors at 1,000
(5/10) and 16/20 developed tumors at 2,000 ppm (8/10).I combined these two studies to
generate the slope factor of 0.0086 mg/kg-d.

My mercury ingestion NOEL is from the US EPA AIR Mercury Study Report to Congress,
Volume 1: Executive Summary. This NOEL was based on studies from the high-dose fetal
exposures from pregnant women in Iraq who were exposed to methylmercury from the
ingestion of tainted flour used in baking bread. The U.S. EPA derived the NOEL from hair
mercury tests, which lead to the NOEL being based on 11ppm mercury in hair and the LOEL
of 52.5 ppm mercury in hair which correspond to ingestion levels of 1 ug/kg-day and 5.3
ug/kg-day, respectively. “These dose conversions were made by applying the methods for
converting hair mercury concentrations to ingestion levels in humans used in the derivation
of the Reference Dose (RfD) in Volume IV of this report.” (EPA 1997)

My mercury inhalation NOEL was from human occupational inhalation studies from the
EPA IRIS web site. The critical effects looked at in the study were: Hand tremor, increased
memory disturbance; slight subjective and objective evidence of autonomic dysfunction.
This correlated to a neurological endpoint. I used the Lowest Observed Effect Level (LOEL)
from the adjusted level (LOEL [ADJ]) for the extra-respiratory effect of the vapor (gas). The
conversion factors and assumptions used were: the LOEL was based on a 8 hour
occupational exposure. MVho = 10 cu.m/day, MVh = 20 cu.m/day. The LOEL [ADJ]= not
adjusted LOEL (0.025mg/cu.m) * (MVho (10 cu.m/day)/MVh(20 cu.m/day)) * (5 days/7
days) = 0.0089. Because I used data from inhalation studies, I do not need to include the
bioavailability (which would have been 80%)

B. Endpoints Chosen and Why
The endpoints that we chose to monitor for lead effects for non-cancer on the fetus are
neurological and nervous system developmental problems and disorders, and possible kidney
cancer in future, because they are most sensitive to lead exposure in humans. Endpoints
chosen for cancer on the fetus is kidney cancer because it is the most common and
hazardous. The endpoints chosen to monitor for mercury effects for non-cancer on the fetus
are the liver, brain, kidney, and umbilical cord accumulation. These endpoints were chosen
because they are the most common and sensitive to mercury exposure on the fetus. There
were no endpoints chosen for the cancerous effects of mercury because according to the EPA
mercury is not classifiable as a cancer causing substance due to the inadequate human cancer
data available for mercury. Effects were researched according to the neurological endpoint.
My lead NOEL was manually derived from a study preformed by Rabinowitz MB et al
(1986). I chose this study because it dealt with infants between the ages of 6-24 months.
Their blood was tested for lead, erythrocyte protorphyrin and hematocrit. Erythrocyte
protorphrin is converted to heme by ferrocheletase. Lead inhibits ferrocheletase, so less
protorphrin is converted to heme, resulting in a build up of protorphrin. So, if we have
elevated levels of protorphrin, we can deduce that we have impaired heme due to lead
inhibition. Iron deficiency and then anemia results from impaired heme synthesis (Family
Practice Notebook, ND). Due to the hyper sensitive nature of fetal development, I used the
lower bound limit at 15ug/dL for my NOEL. The NOEL was chosen from the best available



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data, with respect to exposure duration, animal type, and effects. NOELs are adjusted for
uncertainty and modifying factors before reaching an RfD.

D. Reference doses
My reference doses were determined by calculating taking the NOEL and dividing it by our
uncertainty factors and modifying factor for each exposure pathway:

RfD = NOEL/[(UF*UF*…)*MF]

RfD = Reference Dose
NOEL = No Observed Effect Level
UF = Uncertainty Factor
MF = Modifying Factors
The uncertainty factors were assessed through possible errors in our use of the NOEL. For
example, my mercury NOEL for inhalation was based upon a occupational health study.
Because this is not the target organism we are looking at and our fetus is much more
sensitive, I used an uncertainty factor. Each uncertainty factor is equal to 10.
The modifying factor, >0 to 10, with 10 being the least professional, “is included to reflect a
qualitative professional assessment of additional uncertainties in the critical study and in the
entire data base for the chemical not explicitly addressed by the preceding uncertainty
factors.” (RAGS 7-7) The defaut value is 1.

LEAD
The EPA has not developed a reference dose (RfD) for lead because it is referred to as a non
threshold toxicant (Davidson, Kowetha A., 1994).

NOEL used—for all lead exposure pathways:
Ingestion
 NOEL: 0.156492319 mg/kg

Uncertainty Factors:
1) Subchronic study = 10
2) Data not for our chosen endpoint = 10
3) Not fetal data—sensitive population = 10
Modifying Factor: 10. It was a credible study, however I am an amateur at making calculations
        to find my own NOEL.

RfD—Ingestion--0.000015649mg/kg

Dermal
NOEL: 0.156492319 mg/kg

(Because I do not have dermal data, I had to multiply the oral study with the bioavailability
factor)

Bioavailability Factor: 30%



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                                                                 Risk Assessment of INAAP


Uncertainty Factors:
1) Subchronic study = 10
2) Data not for our chosen endpoint = 10
3) Not fetal data—sensitive population = 10
4) Data based upon oral ingestion = 10
Modifying Factor:10 Data is from a credible source, however I am an amateur at determining
        my own NOEL.

RfD—dermal--0.000000782 mg/kg-d

Inhalation
 NOEL: 0.104328158 mg/kg-d

(Because I do not have inhalation data, I had to multiply the oral study by the bioavailability
factor)

Bioavailability Factor = 40%

Uncertainties Factor:
1) Subchronic study = 10
2) Data not for our chosen endpoint = 10
3) Not fetal data—sensitive population = 10
4) Data based upon oral ingestion = 10
Modifying Factor: 10. The data comes from a credible source, however I am an amateur.

RfD—inhalation--0.000001043 mg/kg-d


MERCURY

NOEL’s Used

Ingestion
 NOEL: 0.001mg/kg-day

My NOEL is based upon methylmercury studies preformed on women and their babies who
were exposed to methylmercury in utero from contaminated flour supply used to make bread.
(Subchronic study)

Uncertainty
1) Subchronic study = 10
2) Extrapolation from maternal hair testing = 10
3) Methylmercury (which is more toxic) instead of mercury = 10
4) Sensitive Population = 10
Modifying Factor = 9 The data is from a credible source, however I am an amature and
       there are still uncertainties within the data set.



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                                                                 Risk Assessment of INAAP


RfD—food ingestion--0.000000011

Inhalation
 LOEL: 0.000010677mg/kg-d

My inhalation LOEL is based upon occupational exposure resulting in neurological problems
such as memory disturbance and hand tremors.


Uncertainty:
1) Population variability = 10
2) Sensitive Population—not fetal study = 10
3) LOEL instead of NOEL = 10
4) Conversion errors = 10
Modifying Factor: 10. Credible data, but I am an amateur.

RfD—inhalation--0.00000000010677

(SEE APPENXIC C FOR INDIVIDUAL EQUATIONS)


Confidence
Confidence in the key studies is medium. This is due to the use of a sufficient number of
pregnant fetus subjects, the inclusion of appropriate control groups, the significance level of
the reported results and the fact that three of them are derived from human epidemiological
studies (one of them was based upon a LOEL and not a NOEL). The exposure levels in one
of the studies had to be extrapolated from animal data. The adverse effects reported in these
studies are in agreement with the well-documented effects of lead and mercury hazards. The
lack of studies regarding the direct effect of lead and mercury on the fetus is the reason why
we are hesitant to assign this risk assessment with a high confidence rating due to the
database and inadequate quantification of exposure levels. Based on these considerations we
are assigning a confidence rating of medium.

Uncertainties
Our amateur status is probably the biggest uncertainty for this assignment.

Mercuric Mercury is not very highly absorbed into the skin or into the blood. Methylmercury
is highly absorbed (~100%) through all exposure pathways.
Mercury vapor is the most quickly absorbed of all forms of mercury. Roughly 80% of
mercury vapor is directly absorbed into the blood (Berlin, M. & Nordberg, F. G. 1969).

There are numerous uncertainties surrounding the NOEL’s; three of them were not for a
neurological endpoint, two of them were not focused on fetal exposure, and methylmercury
was used instead of mercury for my ingestion NOEL, which is much more toxic and readily
available to the fetus than elemental mercury. For my fetal intake calculation for the food
ingestion of mercury, because metallic mercury is absorbed at 0.01%, whereas 100% of
methylymercury is absorbed and mercury salts are absorbed around 30-40% and the data

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                                                                 Risk Assessment of INAAP


from the site did not specify what type of mercury was present, I averaged the three to get a
mean absorption rate of 40%.

Due to the length of pregnancy, only subchroinc studies can be preformed, so the two closest
studies to our target organism, our lead non-cancer study and our mercury ingestion study,
were both subchronic studies. The two chronic studies used were for our cancer slope factor
(rats for 2 years) and our mercury inhalation (occupational studies 15+ years); the least
relevant to our target organism (extrapolation from animal studies to human is also an
uncertainty) The fetus is classified as a highly sensitive population, which in of itself is
calculated as an uncertainty. Lastly, there are uncertainties regarding to quality assurance and
quality control of the data collected and used for the risk calculations. We are not sure if the
samples taken from INAAP were properly handled and tested for lead and mercury. Lead
mercury can also be mixed in with other chemicals on site that may affect transport,
accumulation and effects on the fetus.

Alternative effects not from contamination
The largest source of mercury vapor in most people is from amalgam fillings at a rate of 5
ug/day. There are, however, a wide range of other possible exposure locations for lead. For
example, our 30 year old could have been exposed to mercury thermometers as a child that
broke or any other range of chemicals that could aggravate or subdue mercury effects. Lead
could be ingested from our target organism’s home, if it was built before 1976, due to the
possibility of lead-based paint. Lead is also used in solder for water pipes and there is a high
background level for lead in soils due to its use in fuel until 1975.

Genetics plays a part in the susceptibility one has to chemicals. However, the results of my
exposure calculations show that there is a significant effect from some of the exposure
pathways from each of these contaminants.

Uncertainties for our target organism:
         For my dermal skin surface contact I used the hand and leg value for an adult male
and the arm value of a 9>10 year old, to account for the smaller size of an adult female.
         The transference of blood metal levels from mother to fetus is also an uncertainty. A
large amount of the lead the fetus will be exposed to is the lead that has accumulated in the
maternal bone structure for her entire life time. During times of stress, such as pregnancy,
especially during the third trimester when the fetus is developing its skeleton, the mother’s
body attempts to compensate for the increased need for calcium by getting it from her bones.
Because lead mimics calcium, much of the lead in the bone is released directly into the blood
and on to the fetus. There is little way for us to account for how much lead is being released
because the amount varies based on how much calcium the mother is taking into her body. If
she is taking calcium supplements, very little lead will be re-released into the blood stream.
So, because the amount of lead we have generated as fetal exposure does not include these
levels, it is very likely that our fetus will be exposed to much higher levels.
         We assumed that all of the fish that she consumed was from the site. In all likelihood
this is not the case. We also assumed that she always drank well water, never bottled water.
We did not include the possibility that she may be exposed to these chemicals from other
routs, such as lead based paint in her home or a broken mercury thermometer she cleaned up.



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                                                               Risk Assessment of INAAP


And as I stated previously, the amount of calcium she takes into her body greatly influences
the amount of lead that she will actually absorb into her bloodstream.

4.4 Summary of Toxicity Information

More studies need to be done on Lead to find its possible carcinogenicity to humans. Based
upon our data, cancer for both lead and mercury seems incidental and neurological damage is
the crucial endpoint.




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                                                                Risk Assessment of INAAP


                                        Chapter 5
                                    Exposure Assessment

5.1 Characterization of Exposure Setting
Physical Setting Clark County, Indiana

Groundwater at INAAP can be found in the bedrock formations and in the sand and gravel
deposits. Groundwater occurs primarily along the bedding planes.

Climate:
Moderate weather, four seasons; humid and hot in the summer, cold in the winter, medium
precipitation, and seasonal floods.

Vegetation:
Forest and farmlands surround the plant.

Soil types:
Fifteen different soil types have been identified and 10 of these are dominant. Four different
soil types the Crider-Grayford, Cincinnati-Trappist, Wheeling-Markland-Huntington, and
Corydon-Fairmount Associations. Soils within the terrace have developed from fluvial and
glacial outwash deposits (DOC INAAP – Phase 1 RI Report Site 25 Jenny Lind Pond, 2002
pg 3-8).

Surface hydrology:
Jenny Lind Run is the main stream in INAAP. Its flow begins on the northeastern corner and
extends to the Ohio River. Jenny Lind Run receives surface water runoff from over 20 sites
in INAAP, some of which contain high levels of lead and mercury.

Ground-water hydrology—
Joints, fracture planes, and caverns create an underground maze of water flow difficult to
track.

Potentially Exposed Populations

Relative locations of populations with respect to site:
Animal populations are located in the forest and stream areas surrounding plant. The Ohio
River borders the eastern edge with Louisville, Kentucky just across the river.
Approximatley 10 miles to the west is Interstate 65, surrounded by residential areas. Three
major highways intersect near the INAAP site; I-65, I-64, and I-71 (HNTB Corporation, ND)

Current land use:
The site is currently inactive. People in the surrounding area use the Jenny Lind Pond to fish.
Animals use contaminated land for eating, living, and breeding.




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                                                                  Risk Assessment of INAAP


Potential alternate future land uses:
1,140 acres, including the Jenny Lind Outfall area will be converted in to a State park. 2,810
acres are classified as commercial forests, and the remaining will for industrial use. The goal
is to clean the park areas of INAAP to a level of 1300ppm for lead and 5ppm for mercury.
Clean up is expected to begin this summer (Mike Tosick, 2005).

Subpopulations of potential concern:
There is a residential areas surrounding the North, West and South borders of the site.
Therefore, the populations of concern are those individuals living in the surrounding areas
and those who visit the site for recreational purposes.

5.2 Identification of Exposure Pathways
Sources and receiving media:
INAAP is the source of the contaminants and the receiving media is the air, water, soil, and
animals/fish surrounding it.

Fate and transport in release media:
The plant is located at the highest elevation on the site (640 feet above sea level). The karst
topography, and this geographic location, makes the pollutants susceptible to wide spread
exposure in any given direction through water flow, animal transport and bioaccumulation,
and wind blowing the dust particles; although the water typically flows south into the Ohio
River.

Exposure points and exposure routes:
Our target organism is exposed to the contaminants through fishing and recreational activites
on, and around the Jenny Lind Outfall area. Points of exposure are inhalation, ingestion, and
dermal. Routes of exposure are air, water, and soil. The combination of these exposure points
and routes can create a range of paths in which mercury and lead could travel making it
difficult to conclude what the specific exposure endpoints are. Main points include the
surrounding farmland area and the Ohio River..

Integration of sources, releases, fate and transport mechanisms, exposure points, and
exposure routes into complete exposure pathways:
The old INAAP facility still has residues of lead and mercury in and around its generation
points. When it rains, the lead and mercury seeps through the soil, possibly taking
underground streams that have eroded through the karst stone, and flow into the Jenny Lind
Lane. The Jenny Lind Lane once emptied into the Jenny Lind Pond, but upon the dam
breaking in 1997, there is no longer a pond. When the pond area did exist, the mercury and
lead settled to the bottom of the pond and accumulated through time. Now that the pond is
gone, the ground that has layers of contaminated soil that have been accumulating is not
exposed. The main source Jenny Lind Run Outfall area, and contaminants from the
surrounding soil, can seep in to groundwater. The exposure points and routes stated above
are a result of completed exposure pathway, which are soil, water, animals, and air

Summary of exposure pathways that will be quantified in this assessment:
Food, air, soil and water contaminants are calculated in respect to ingestion, inhalation, and
dermal exposure for our adult reproductive female target organism.

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                                                                  Risk Assessment of INAAP



5.3 Quantification of Exposure
Exposure Concentrations:
     Air (lead)- .00003 mg/m^3 (Environmental Defense “Scorecard—pollution
      information site”)
          o Air (mercury)- .01184 mg/m^3 (Indiana Department of Environmental
              Management “Mercury: Air emissions and proposed utility rules” 2004) ,
     Water- .014175 mg/L (INAAP Phase 1 IR Report)
     Soil (lead)- 1506.67 (INAAP)
     Food Ingestion: fish- .1586 mg/L (IDEM “Mercury and Indiana Fish: A Brief
      Overview” 2004)

Estimation of chemical intakes for individual pathways:
     Air inhalation (lead)- .000006767 mg/kg-d
           o (mercury)- .0035778 mg/kg-d
     Water ingestion- .014175 mg/L
     Soil dermal (lead)- .000321
     Soil water (lead) – 3.5979E-9
     Food ingestion (mercury)- .000001781 mg/kg-d (source: exposure calculation
       homework)

5.4 Identification of Uncertainties
Current land use:
The plant is currently inactive. However, people in the local area visit the site to fish and for
other activities. There are uncertainties to how many people go to the site, how often they
go, and what activities they participate in while there.

Future land use:
The amount of land zoned for industrial use and the industries that lease the site is unknown.
It is possible that industrial use could additionally contaminate the area.

Environment and sampling analysis:
Data samples may not have accurate measures of the actual lead and mercury concentrations
due to sampling errors, bias, etc.

Exposure pathways evaluated:
Water concentration was measured from Jenny Lind Run. Air concentrations were measured
from an off source site. Soil concentrations are taken from a range of soil samples
surrounding the Jenny Lind Pond. In the risk assessment, the highest concentrations were
used in order to be safe.

The fate and transport modeling:
Lead and mercury have the potential to travel anywhere in the area because of the karst
geology and the uphill location of the plant and the extension of the Jenny Lind Run.




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                                                              Risk Assessment of INAAP


Parameter values:
Sampling data was taken from random areas on the site and around the outfall area. The
locations that are sampled may not pertain to the entire site. Some places not sampled may
have a higher level of lead and mercury than areas that have been sampled, so sampling data
may be inaccurate.

5.5 Summary of Exposure Assessment

Site-specific and other similar lead and mercury data will be used, in accordance with
RAG’s, to generate non-cancer and cancer exposure for our adult female reproductive target
organism by pairing the exposure routes of concern and the exposure pathways of concern.




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                                                                Risk Assessment of INAAP


                                        Chapter 6
                                   Risk Characterization

6.1 Current Land-use Conditions

(SEE APPENDIX D & E FOR CHART)

Carcinogenic risk--LEAD:
Water ingestion: 0.000000657 or 6.6x10^-7
Total dermal absorption: 0.000000001 or 1x10^-8
Inhalation: 0.00000002 or 2x10-8
(source: risk characterization homework, 4/24/05)

LEAD
Chronic hazard quotient calculation
No chronic studies were used
(source: risk characterization homework, 4/24/05)

Subchronic hazard quotient calculation
Water ingestion: 0.150
Total dermal absorption: 411.2053231
Inhalation: 6.488
(source: risk characterization homework, 4/24/05)


MERCURY
Chronic hazard quotient calculation
Inhalation: 33509412.76
(source: risk characterization homework, 4/24/05)

Subchronic hazard quotient calculation
Food ingestion: 161.945
(source: risk characterization homework, 4/24/05)

Chronic hazard index (Lead and Mercury)--33509412.76
(source: risk characterization homework, 4/24/05)

Subchronic hazard index (Lead and Mercury)—579.789
(source: risk characterization homework, 4/24/05)

Justification for adding risk across pathways:
Our target organism is exposed through a variety of different pathways throughout her daily
activities. She will eat mercury contaminated fish and drink lead contaminated well water in
one sitting. To account for this we generated a hazard index which is the total of all hazard
quotients out target organism is exposed to.



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                                                               Risk Assessment of INAAP


Noncarcinogenic hazard index (multiple pathways)
HI (for both lead and mercury)= 33509992.55 (for both lead and mercury
HI (for lead) = 417.04
HI (for mercury) = 33509574.17
(Risk characterization homework, 4/25/05)

Carcinogenic risk (multiple pathways)
RISK = 0.000021227 or 2.12x10^-5)
(Risk characterization homework, 4/25/05)

6.2 Future Land-use Conditions

On the INAAP site, 143 acres are classified as improved grounds, 635 are semi-improved
grounds, 6,202 are unimproved grounds, and 2,810 are classified as commercial forest 1,140
of the 9,790 acres is going to be cleaned up and then leased to the State as part of the
Charlestown State Park. Jenny Lind Pond is in located in the proposed park area. The
reconstruction of a dam is expected to be built on the pond to prevent sediment from
migrating into the Ohio River. The remaining land will be used for industrial purposes
(Indiana AAP, 2001). For the park area, including Jenny Lind Run, Mike Tossic informed us
that the clean up levels will be to 1300ppm for lead and because our average mercury and
lead concentrations are already below the target of 5ppm for mercury, there will be no
remediation for mercury or lead in our site (Our future calculations are the same as our
current calculations)

For our hazard identification calculations, three of our numbers were from off of the site
because there was no available data. We used fish mercury levels in the average fish in
southern Indiana and air levels of lead and mercury from five surrounding monitor stations.
Without these numbers, our site specific data is equal to 0.000000782 mg/kg-d, our dermal
calculation. This number is well below the “safe under 1” limit.

Carcinogenic risk--LEAD:
Water ingestion: 0.000000657 or 6.6x10^-7
Total dermal absorption: 0.000000001 or 1x10^-8
Inhalation: 0.00000002 or 2x10-8
(source: risk characterization homework, 4/24/05)

Chronic hazard quotient calculation
LEAD
Water ingestion: 0.150
Total dermal absorption: 411.2053231
Inhalation: 6.488
(source: risk characterization homework, 4/24/05)

MRECURY
Food ingestion: 161.945
Inhalation: 33509412.76
(source: risk characterization homework, 4/24/05)

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                                                                  Risk Assessment of INAAP



Chronic hazard index
HI (for both lead and mercury)= 33509992.55 (for both lead and mercury
HI (for lead) = 417.04
HI (for mercury) = 33509574.17
(Risk characterization homework, 4/25/05)

Justification for adding risk across pathways:
Our target organism is exposed through a variety of different pathways throughout her daily
activities. She will eat mercury contaminated fish and drink lead contaminated well water in
one sitting. To account for this we generated a hazard index which is the total of all hazard
quotients out target organism is exposed to.

Noncarcinogenic hazard index (multiple pathways)
HI (for both lead and mercury)= 33509992.55 (for both lead and mercury
HI (for lead) = 417.04
HI (for mercury) = 33509574.17
(Risk characterization homework, 4/25/05)

Carcinogenic risk (multiple pathways)
RISK = 0.000021227 or 2.12x10^-5)
(Risk characterization homework, 4/25/05)


6.3 Uncertainties

Site specific uncertainties—Hazard Identification
We did not get to visit the site, so we do not have a good idea of what the area looks like,
where places are located in relation to buildings and the accessibility of the area to outsiders.
It is also difficult for us to create a conceptual model. The testing is done by IDEM, so there
is little speculation for bias about generating ideal values. We do not know, however the
conditions in which the sampling was taken, the possibility for contamination from other
chemicals leaching onto the site nor can we guarantee the sterile nature of the process of
testing. We do not know if there are fish in Jenny Lind Pond or Lane for our target organism
to eat. Our target organism lives in the surrounding area and drinks from a private well, but
we have no data as to the possible chemical concentrations in surrounding area well water.
The only data generated is on site well water, which is the data we have used. We do not
know the influences the karst topography has on the flow of the contaminants into the
surrounding area.

Parameter values for fate/transport and exposure calculations
Our exposure values are based upon a 30 year old 66.5 kg pregnant adult female. The
inhalation rate is 1.25m^3/hr using the EPA suggested adult upper bound value due to
increased sensitivity of fetus from inhaled mercury vapors. Our exposure time differed for
inhalation is 24 hours/day. The exposure frequency for water ingestion is 365 days/year,
assuming she drank water very day from the contaminated well. Our exposure frequency for
food ingestion is 24 meals/year with a 1/1 fraction of ingested fish from the mercury

                                                                                               24
                                                                 Risk Assessment of INAAP


contaminated source. The ingestion rate is 0.284 kg/meal, the EPA’s 95th percentile for fin
fish. Dermal skin absorption exposure frequency was 40 events/year for soil and 365
days/year for water exposure (assuming she takes at least one shower every day) with the
skin surface area available for contact as 4420 cm—calculated from a adult male hands and
legs and a child 9<10 arms (there was no data on adult female). I used the skid adherence
factor of 2.11 mg/cm^2 based on the average of commercial potting soil (1.47) and kaolin
clay (2.77). The absorption factor of mercuric mercury through the skin is 0.01 and for lead it
is 0.00013 cm/hr. I used the EPA’s 95th percentile lower-bound water intake estimate for a
pregnant female of 2.674 L/day.
         To get the values of fetal exposure I used a 15% blood absorption rate from water
ingestion of lead, a 15% absorption rate for the intake of mercury in fish, a 0.04% absorption
rate for dermal lead absorption, a 67% inhalation absorption rate of mercury.(averaging the
three different absorption rates from methylmercury (100%), elemental mercury (75-85%)
and inorganic mercury (7-15%)), and a lead inhalation rate of 50%.
         In an adult female, roughly 90% of the absorbed lead is stored in the bone. In times of
stress, like pregnancy, depending upon the calcium intake of the individual, large amounts of
lead are released back into the blood stream. In the 3rd trimester of pregnancy when the fetus
is building its bone structure, there is an extra demand for calcium in the mother. To account
for this the lead in the mother’s bone will be released and reabsorbed into the blood stream,
reaching the fetus. I am unable to account for this in my calculations because the amount
released is determined by the calcium intake throughout the mother’s life span. The more
calcium she intakes, the less lead will bind onto the blood, mimicking calcium.

MERCURY:

On site tests resulted in: 3.146 mg/kg in the soil (however, this number was not used in this
risk assessment)

(off-site number used are: 158.6 ug/L—Common Carp mean Hg in the surrounding area, and
0.01184 mg/m^3 concentration in the surrounding air.)

LEAD

On-site tests resulted in: 14.165 ug/L in the groundwater and 1506.67 mg/kg in the soil.

Off-site number used: 0.00003 mg/m^3 concentration in the surrounding air

Summary of toxicity assessment uncertainty
Identification of Potential Health Effects:

LEAD

Lead causes effects in the gastrointestinal tract, hematopoietic system, cardiovascular
system, central and peripheral nervous systems, kidneys, immune system, and reproductive
system (Davidson, Kowetha A., 1994). For our fetus, the critical endpoint is neurological
damage due to the underdeveloped blood-brain barrier at this life stage (ATSDR 2000). Lead
does not have an significant known carcinogenic effects (EPA).

                                                                                             25
                                                                 Risk Assessment of INAAP



MERCURY

Mercury more severely effects the neurological functioning/development of the fetus and its
central nervous system causing infants to be born retarded, deaf, blind, and/or unable to speak.
It can also cause spontaneous abortion, mercury is unique in that concentrations accumulate in
the fetal cord blood meaning the fetus has higher levels than in the mother (EPA).

Derivation of Toxicity Value
LEAD

The RfD for lead was based upon a NOEL derived from a study preformed on infants
measuring the lead, erythrocyte protorphyrin and hematocrit levels in their blood. The NOEL
was derived from the indication that at 15-17 ug/dL there was no increases in erythrocyte
protorphyrin in the infants blood (I used 15 ug/dL for increased safety), however after that
level, erythrocyte protorphyrin levels multiplied four times quickly. (erythrocyte
protorphyrin in blood indicates lead presence and possible neurological damage) (Rabinowitz
MB et al. 1986).

The weight of evidence is classified as B2, a possible human carcinogen. It is a known
animal carcinogen.


MERCURY

My RfD for mercury ingestion was based upon a NOEL derived from a study on pregnant
females in Iraq who accidentally ingested high levels of methylmercury from contaminated
flour in home made bread. The tests were based upon hair sampling to formulate
corresponding ingestion levels. I used the NOEL of 1 ug/kg-day (EPA). The infants born to
the contaminated mothers had high incidences of neurological damage (Bakir, F. et al.1973)

My RfD for mercury inhalation was based upon a LOEL derived from an occupational health
study cited in EPA. The endpoint was neurological; looking at hand tremor, increased
memory disturbance and autonomic dysfunction. I used the adjusted LOEL value of 0.0089
mg/cu.m for increased sensitivity of the fetus.

The weight of evidence is classified as D, not classifiable as to human carcinogenicity.

Potential for synergistic or antagonistic interactions
LEAD

There is a synergistic interaction between lead and benzo[a]pyrene which impairs fertility of
mice that have been exposed in the womb causing longer gestation periods and a reduction of
the number of offspring (liters and litter size).(Kristensen, P, et al. 1995). However, I do not
know if benzo[a]pyyrene is at the site, or where our target organism might come into contact
with it.



                                                                                              26
                                                                 Risk Assessment of INAAP


Deficiencies of the antagonistic nutrient calcium and iron permit lead to be absorbed in
greater concentrations resulting in a more severe toxic effect, making meal interactions with
lead significant. Individuals who have been fasting have a higher intake of lead than those
who have not (Mushak, Paul and Annemarie F. Crocetti, 1996).

MERCURY

Mercury toxicity can be reduced by binding mercury ions with dimercaprol.
Acidification of a body of water can increase mercury residues in fish even when no new
input of mercury occurs due to the increased ventilation rat and membrane permeability of
fish at lower pH levels. Mercury readily binds to sulfur and organic compounds which cause
them to accumulate in eutrophic (nutrient and carbon rich) areas (Irwin, Roy J., 1997).

Uncertainty in evaluating a less-than-lifetime exposure
Our target organism has had a lifetime exposure


6.4 Comparison of Risk Characterization Results to Human Studies

Our risk characterization for cancer is much smaller than the studies conducted on animals
and know accounts of human accidental exposure studies. Our mercury inhalation study was
based upon a study in which exposed workers has mean blood levels of 10 ug/L
(0.0104mg/kg) and 11.6 ug/L (0.012mg/kg). Our fetus is exposed to 0.003578 mg/kg-d (a
chronic study) from the maternal blood. Our mercury ingestion study was based upon the
hair testing which lead to the ingestion NOEL being 0.001mg/kg-d. Our ingestion exposure
levels were 0.00000178 mg/kg-d. Our lead levels were based on a study of 232 infants blood
levels between the ages of 6-24 months. The NOEL limit they found was 15 ug/dL, or
0.1565 mg/kg. Our exposure results were much lower, at 0.0000855 mg/kg-d for water
ingestion. Our dermal exposure was 0.0003216mg/kg-d and our inhalation was 0.000006767
mg/kg-d. These are all significantly lower than the study levels. However, because of the
uncertainty factors, our reference doses were smaller than the NOEL’s from the studies. We
did therefore get a positive number on some of the exposure pathways that we might not
have otherwise.

Site-specific health studies (plot of epidemiological studies)
I was unable to locate any site specific health studies.

Incorporation of studies into the overall risk characterization.
I have incorporated many studies based on both animal and human data from peer-reviewed
documentation of studies from scientific journals and governmental departments and web
sites, such as IRIS, ATSDR, EPA, and INAAP. These resources are vital to the assessment of
risk for our target organism and for the possible developmental, neurological, etc. problem(s)
that may result in our fetus at our calculated level of exposure.




                                                                                            27
                                                                 Risk Assessment of INAAP



6.5 Summary discussion and Tabulation of the Risk Characterization

Key site-related contaminates and key exposure pathways
Lead and Mercury are our key contaminants for the site and our exposure pathways are
dermal absorption, inhalation and ingestion through the water, soil, air, and food.

Types of health risks of concern
LEAD

Lead causes effects in the gastrointestinal tract, hematopoietic system, cardiovascular
system, central and peripheral nervous systems, kidneys, immune system, and reproductive
system (Davidson, Kowetha A., 1994). For our fetus, the critical endpoint is neurological
damage due to the underdeveloped blood-brain barrier at this life stage (ATSDR 2000).

MERCURY

Mercury more severely effects the neurological functioning/development of the fetus and its
central nervous system causing infants to be born retarded, deaf, blind, and/or unable to speak.
It can also cause spontaneous abortion, mercury is unique in that concentrations accumulate in
the fetal cord blood meaning the fetus has higher levels than in the mother (EPA).

Level of confidence in the quantitative information used to estimate risk
The data used for my risk estimation all came from credible peer-reviewed or governmental
agency sources. My only reservation is that some of the data does not directly relate to my
specific target organism at the INAAP site. I had to extrapolate some data to use in my
calculations and there is a great chance for error in that process. I have a high level of
confidence in the credibility of the source data, but a low level of confidence in my usage of
said data.

Confidence in the key exposure estimates for the key exposure pathways
Our exposure estimates were created for and adult pregnant female using the information
provided to us by RAGS and through our own decisions on how she lives. I have confidence
that there are individuals who fit our profile and I have made her sufficiently above average,
leaving room for more sensitive individuals. The only errors may be in the calculation.

Magnitude of the carcinogenic and non-carcinogenic risk estimates.
The Superfund site remediation goals for cancer risk range from 10^-4 to 10^-6 and our
cancer risk is 3.4x10-7, well within the “goal” range. Therefore, the carcinogenic risk at our
site is not high.

Our non-carcinogenic hazard index was 33509992.55 and the “safe” level is under 1, so it is
safe to say, that there is a significant hazard for non-carcinogenic effects at our site.

Major factors contributing to uncertainty
Three of my chemical concentrations were from sources other than the INAAP site. My data
for fish contamination was based on a southern Indiana Common Carp mean Hg

                                                                                              28
                                                               Risk Assessment of INAAP


concentration from between 1997-2002, not from the INAAP site. My air concentrations for
lead and mercury were based upon the ambient air concentration data from 5 monitoring
stations surrounding the location; one in Martin County, one in Lawrence County, and the
two closest were from Clark County.

Many of the studies I used to extrapolate my NOELs and LOEL were not from fetal
neurological endpoints.

My lead NOELs were from the same source and based upon oral exposure, I had to adjust
them for inhalation and dermal absorption by multiplying the equivalent bioavailability
factor.

My slope factor was based upon oral absorption, not dermal or inhalation, so I had to adjust
my data as I saw appropriate. Also, my non-cancer hazards were based upon the fetus being
my target organism, however as there is little/no data, that I found, on fetal cancer
development from these two metals, I used my adult pregnant female as the target organism.

Exposed population characteristics
My initially exposed pregnant adult was: 30 years old, weighs 66.5 kg, has lived near the
INAAP her entire life, and goes to the site for fishing and recreational purposes. Her diet
includes 24 meals of contaminated fish per year and drinks 2.675 Liters of well water per
day. Our fetus is in his third trimester at 8 months. The blood transfer rate from mother to
fetus is 240 mL/min or 345600mL/day. The mother has a blood volume of 97.5 mL/kg,
weighing 66.5kg she has 6483.75 mL of blood in her body. This means, the fetus will cycle
the blood in mom’s body 53.3 times per day. Because both mercury and lead freely transfer
from the mother to the fetus, I will assume that 100% of the metal levels in the blood are
transferable to the fetus.

Comparison with site-specific health studies
No studies are currently available.




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                                                                Risk Assessment of INAAP


                                        Chapter 7
                                     Risk Management


7.1 Site Goals
        This management plan proposes corrective measures aimed to protect ecological
receptors while at the same time protecting human health. This plan also aims to be
consistent with reasonable future land use in the future for example, inclusion of a state park
and industrial use. According to Michael J. Tosick the safe target level for mercury is 5 parts
per million and 1300 parts per million for lead for the Jenny Lind Outfall area.

7.2 Corrective Measures for Site
        The proposed removal and disposal activities would include 1st areas that are above
5ppm for mercury and 1300ppm for lead will be removed of contaminated soils and
sediments. The contaminated soils and sediments will be removed to an estimated average
depth of about 4 feet in the western area and about 8 feet deep in each of the other two areas
(DOC INAAP – Phase 1 RI Report Site 25 Jenny Lind Pond, 2002 pg 3-13). After removal
of contaminated soils and sediment we suggest to leave a layer of soil or sediments at least
24 inches thick that does not contain any lead above 1300 ppm and mercury at 5ppm. 2nd
characterize and dispose of contaminated media in a permitted solid waste landfill or a
hazardous waste landfill. Some material may be characterized as hazardous and will need to
be handled accordingly. “The subtitle D solid waste will be transported to the local RCRA
Subtitle D Landfill about 20 miles away from the site for disposal” (DOC INAAP – Phase 1
RI Report Site 25 Jenny Lind Pond, 2002 pg 3-13). “The subtitle C hazardous waste will be
transported to the nearest Subtitle C landfill. After the removal of hazardous material is
complete the remaining sediments and soils will be graded to establish finish site grades with
even slopes and positive drainage” (DOC INAAP – Phase 1 RI Report Site 25 Jenny Lind
Pond, 2002 pg 3-13). 3rd restore the site by removing the damn and lower the stream water
level by pumping in order to prevent water from flowing over the spillway by stabilizing the
Jenny Lind Run channel. Vegetation in combination with geotextiles and rock will be used to
stabilize the channel and to protect against erosion ((DOC INAAP – Phase 1 RI Report Site
25 Jenny Lind Pond, 2002 pg 3-13). 4th a complete removal Action, as necessary, to address
the hotspot downstream of the dam (DOC INAAP – Phase 1 RI Report Site 25 Jenny Lind
Pond, 2002 pg 3-13).

7.3 Corrective Measures for Target Organism
        Specific to our adult pregnant female we suggest that the local community council
implement social programs for mothers in living the area. These social programs
will advise mothers of the hazards of lead and mercury, how they can be exposed to these
metals and how to avoid future exposure. Next we recommend that monthly community
meetings are help for local expecting mothers and advice them of the harmful effects of lead
and mercury on the fetus. These meetings will show expecting mother’s how to avoid
exposure to lead and offer blood testing to detect for lead exposure. Moreover, the expecting
mother’s will be encouraged to eat organic foods, not drink well water, and be warned of
products such as paints and pigments that are used as make-up or hair coloring that contain
lead. In terms of mercury pregnant mothers will be encouraged to carefully handle and


                                                                                             30
                                                               Risk Assessment of INAAP


dispose of products that contain mercury, such as thermometers or fluorescent light bulbs.
Do not vacuum up spilled mercury, because it will vaporize and increase exposure. Most
importantly pregnant women will be told keep away from rooms where liquid mercury has
been used and refrain from eating fish from the Jenny Lind Outfall Run.
        The proposed removal and disposal activities combined with the community outreach
programs will significantly reduce the affects of lead and mercury to the fetus of a pregnant
women living in the area. The removal and disposal activities will make sure that safe target
levels for lead and mercury are met. Furthermore, the implementation of the community
outreach programs will further ensure that pregnant mothers are knowledgeable regarding the
hazardous metals and are taking proper steps to eliminate exposure.




                                                                                          31
                                                                     Risk Assessment of INAAP


                                                References


ASTDR, Management Guidelines for Mercury. Last Accessed April 22 2005.
     http://www.atsdr.cdc.gov/MHMI/mmg46.html


Azar, A., H.J. Trochimowicz and M.E. Maxfield. 1973. Review of lead studies in animals
       carried out at Haskell Laboratory - Two year feeding study and response to hemorrhage
       study. In: Barth D., A. Berlin, R. Engel, P. Recht and J. Smeets, Ed. Environmental health
       aspects of lead: Proceedings International Symposium; October 1972; Amsterdam, The
       Netherlands. Commission of the European Communities, Luxemberg. p. 199-208.

Bakir, F., S. F. Damluji, L. Amin-Zaki, M. Murtadah, A. Khalidi, N. Y. Al-Rawi, S.
        Tikriti, and H. I. Dhahir. 1973. Methylmercury Poisoning in Iraq. Science.
        Volume 181 p. 230-239.

Berlin, M. & Nordberg, F. G. 1969. The uptake of mercury in the brains of mammals
        exposed to mercury vapor and to mercuric salts. Arch. Environ. Health, 18, 719-
        729.

DOC. Indiana Army Ammunition Plant—Phase I RI Report. Site 17 & 60
Burning Ground (Site 17). Table 16.2-7, May 1997

DOC. Indiana Army Ammunition Plant—Phase I RI Report. Jenny Lind Pond--,
May 1997

Environmental Defense “Scorecard—The Pollution Information Site

EPA “Estimated Per Capita Water Ingestion and Body Weight in the United
States—An Update” October 2004, pg 6-4

EPA “Estimate Per Capita Water Ingestion and Body Weight in the United
States—An Update” October 2004, pg 7-2

EPA http://www.epa.nsw.gov.au/leadsafe/leadinf3.htm, 2003

EPA IRIS website for lead http://www.epa.gov/IRIS/subst/0277.htm


Indiana Department of Environmental Management “Mercury: Air Emmisions and Proposed
Utility Rules” 2004

Karanth, K.U., Nichols, J. Seidensticker, E. Dinerstien, D. L., D. Smith, C. McDougal, A. J. T.
Johnsingh, R. S. Chundawat, and V. Thapar. 2003. Schience deficiency in conservation
practice; the monitoring of tiger populations in India. Animal Conservation 6:141-146.

Danielsson, B.R.G., Fredriksson, A., Dahlgren, L., Reling, O., Gerdlund, A., Olsson, L.,
        Dencker, L. & Archer, T. 1993. Behavioral effects of prenatal metallic mercury
        inhalation exposure.



                                                                                                    32
                                                                      Risk Assessment of INAAP

Davidson, Kowetha A., Ph.D, D.A.B.T.; TOXICITY SUMMARY FOR LEAD
       (Inorganic). OAK RIDGERESERVATION ENVIRONMENTAL
       RESTORATION PROGRAM. Chemical Hazard Evaluation Group
       Biomedical and Environmental Information Analysis Section, Health Sciences Research
       Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee. December 1994

Indiana AAP, 2001. Installation Action Plan for Indiana Army Ammunitions Plant

Irwin, Roy J., 1997. Environmental Contaminants Encyclopedia—Mercury Entry.
        National Parks Service.

Kristensen, P., E Eilertsen, E Einarsdottir, A Haugen, V Skaug and S Ovrebo. 1995.
        Fertility in mice after prenatal exposure to benzo[a]pyrene and inorganic lead.
        Environmental Health Perspectives 103(6): 588-590.

Mushak, Paul, Annemarie F. Crocetti. 1996. Biologic interactions of lead with nutrients—Lead and
      Nutrition, Part 1. Nutrition Today.

Rabinowitz MB, Leviton A, Needleman HL. Occurrence of elevated protoporphyrin
       levels in relation to lead burden in infants. Environ Res. 1986 Apr;39(2):253-7.

Risk Assessment Guidance for Superfund (RAGS) EPA website:
       http://www.epa.gov/oswer/riskassessment/ragsa/index.htm Last accessed April 24, 2005

Schoof, Rosalind A. (updated by); Guide for Incorportating Bioavailability Adjustments
        into Human Health and Ecological Risk Assessments at U.S. Department of Defense
         Facilities Part 1: Overview of Metals Bioavailability. Tri-Service Ecological Risk
        Assessment Workgroup. June 2003.

Sydney Southwest Area Health Service, 2005

The RiskAssessment Information System. “Toxicity & Chemical-Specific Factor Data
       Base Search Results” March 2005

Tchirikov M, Rybakowski C, Huneke B, Schoder V, Schroder HJ. Umbilical vein blood volume
        flow rate and umbilical artery pulsatility as 'venous-arterial index' in the prediction of
        neonatal compromise. Ultrasound Obstet Gynecol. 2002 Dec;20(6):580-5.

U.S. EPA. “Dermal Exposure Assessment Principles and Applications” 1992

World Health Organization, 1995

Yoshida, Minoru 2002. Placental to Fetal Transfer of Mercury and Fetotoxicity. Tohoku
       J. Exp. Med., 2002, 196, 79-88

Yoshida, Minoru, Yamamura, Y. & Satoh H. 1986. Distribution of mercury in guinea pig
       offspting after in utero exposure to mercury vapor during late gestation. Arch. Toxicol., 58,
       225-228.




                                                                                                     33
             Risk Assessment of INAAP


Appendix A

Site Map




                                        34
             Risk Assessment of INAAP


Appendix B




                                        35
                                                                  Risk Assessment of INAAP


Appendix C

Non-cancer Hazard for Lead and Mercury
For each exposure pathway, I will divide my non-cancer hazard characterization into three
sections. In part A, I will calculate the Reference Dose (RfD) for each exposure pathway.
The equation for calculating the RfD is:
RfD = NOEL/ [(UF) * MF]
Where:
NOEL = No Observed Effect Level
UF = Uncertainty Factor (A factor of 10 for each)
MF = Modifying factor (“a number ranging from >0 - 10 based upon the qualitative
professional assessment of additional uncertainties in the critical study and in the entire data
base for the chemical not explicitly addressed by the preceding uncertainty factors. The
default value is 1” (RAGS pg.7-7)
 Background on how I found Fetal exposure levels from adult female intake:

 To determine how much blood was transferred to the fetus from the mother in one day, I
 found the transfer rate of blood from mother to fetus;
 240/min (Tchirikov, M. 2002). The average blood Volume of an adult woman is 65
 mL/kg and pregnant females increase their blood volume by 40-50% (Sydney
 Southwest Area Health Service, 2005), so using 50% to allow for all populatins, I
 calculated the average blood volume for a pregnant adult female to be:
 65*1.50=97.5 mL/kg.

 Our Pregnant Female weighs 66.5 kg (See exposure calculations) so, the blood volume of
 our pregnant female is:
  97.5mL/kg*66.5kg = 6483.75 mL.

 With our mother to fetus exchange rate of 240mL/min or 345600mL/day, our fetus cycles
 the blood in mom’s body 53.3 times/day. Because both Mercury and Lead freely transfer
 from mother to fetus, it is safe to say that 100% of metal levels in the blood are
 transferable to the fetus.

  To calculate the blood exposure level of the fetus, I first calculated the amount of exposed
  metal absorbed into maternal blood stream by multiplying the absorption rate of the metal
  through the specific pathway by the intake amount calculated in my exposure
  calculations.
  For example, if the maternal absorption rate is 15% of the metal and the maternal intake
   part B, I will show the calculated exposure intake of my target organism by .15 pathway.
Inwas 0.000786553 mg/kg/day, we would multiply 0.000786553 mg/kg/dayfor eachto get
  0.000011798mg/kg-d. Because 100% of the metals transfer into the fetus,
  0.000011798mg/kg-d is exposure value for the fetus.
In part C, I will calculate the Hazard Quotient (HQ) for each pathway.

After I have determined the HQ for all of my exposure pathways, I will add them together to
create the Hazard Index (HI), the overall non-cancer risk for my target organism. A HI less
than one is considered ‘safe’ or, negligible risk.

                                                                                               36
                                                                Risk Assessment of INAAP



I did not calculate the dermal absorption rate of mercury because most studies have stated
that it is negligible.(“ Dermal reactions associated with dermal contact with liquid elemental
mercury or the vapor are rare” (ASTDR, Management Guidelines for Mercury.
http://www.atsdr.cdc.gov/MHMI/mmg46.html).



1). Non-Cancer Effects From Water Ingestion of Lead.

Part A—Finding Reference Dose (RfD)

Pregnant female ingests lead from the ground water in her well.
I was unable to find a NOEL with a fetal neurological endpoint, so I derived my own NOEL
based on a study (Rabinowitz MB et al. 1986) preformed on 232 infants between the ages of
6 -24 months. The measurements of blood lead, erythrocyte protorphyrin and hematocrit
were made semi annually. At 15-17 ug/dL, there was No Observed Effects, however levels
above 15 ug/dL resulted in erythrocyte protoporohyrin levels four times the normal amount. .
I chose 15 ug/dL to account for the increased sensitivity for the fetus.

NOEL = 15 ug/dL (deciliter) = (1000ug=1mg, so 15ug=0.015mg)

 0.015mg    1dL      1L             1oz              0.015mg
--------- x ---- x --------- x --------------- = -------------- = 0.156492319 mg/kg
  dL        0.1L   33.81oz      0.02835 kg        0.0958514kg

NOEL = 0.156492319 mg/kg

--Uncertainty Factors:
1) Population variability = 10
2) Data not for our chosen endpoint = 10
3) Not fetal data—sensitive population = 10

--Modifying Factor: 10 The data is from a credible source, however due to my amateur
judgment, I have chosen 10.

                            0.156492319 mg/kg
RfD = NOEL / ((UF)* MF) = ------------------------ = 0.000015649mg/kg
                            (10*10*10) * 10


Part B—Finding exposure intake for fetus from adult pregnant female water ingestion
(RAGS, p. 6-35).

Intake (mg/kg-d) =        CF * IR * EF * ED
                          --------------------------
                                 BW * AT

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                                                                    Risk Assessment of INAAP



CF = Chemical concentration in ground water (mg/L) = 14.165 ug/L (1000 ug= 1mg, so
      14.175 ug= 0.014175 mg/L
      (DOC. Indiana Army Ammunition Plant—Phase I RI Report. Site 17 & 60
      Burning Ground (Site 17). Table 16.2-7, May 1997)

IR = Ingestion Rate (Liters/day) = 2.674 L/d (Based on 95% for increased safety)
       (EPA “Estimated Per Capita Water Ingestion and Body Weight in the United
       States—An Update” October 2004, pg 6-4)

EF = Exposure Frequency (d/yr) = 365 day/yr

ED = Exposure Duration (years) = 30 years

BW = Body Weight (kg) = 66.5 kg (Estimated mean weight)
      (EPA “Estimate Per Capita Water Ingestion and Body Weight in the United
      States—An Update” October 2004, pg 7-2)

AT = Average time (ED (30) * 365 day/yr) = 10950 days

INTAKE (mg/kg-d) =

0.014175 mg/L * 2.674 L/d * 365 day/yr * 30 yrs
---------------------------------------------------------------------- = 0.000569984 mg/kg-d
                   66.5 kg * 10950 days

(conversion units cancel out to get mg/kg-d)

Intake from mother: 0.000569984 mg/kg/day
Absorption rate: 15% (high end for ingestion)(EPA)
http://www.epa.nsw.gov.au/leadsafe/leadinf3.htm, 2003)

E = Fetal intake from blood = 0.000569984 mg/kg/day * .15 = 0.000085498mg/kg/d

Part C—Calculating the hazard quotient (HQ) for oral water intake


            0.000085498mg/kd-d
HQ = E/RfD= ------------------------- = 0.150
            0.000569984mg/kg-d




2) Non-Cancer Effects From Food Ingestion—Mercury

Part A—Finding the RfD:

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                                                              Risk Assessment of INAAP



My pregnant female is ingesting mercury through contaminated fish from the site.
My ingestion NOEL is from the US EPA AIR Mercury Study Report to Congress, Volume
1: Executive Summary. This NOEL was based on studies from the high-dose fetal exposures
from pregnant women in Iraq who were exposed to methylmercury from the ingestion of
tainted flour used in baking bread. The U.S. EPA derived the NOEL from hair mercury tests,
which lead to the NOEL being based on 11ppm mercury in hair and the LOEL of 52.5 ppm
mercury in hair which correspond to ingestion levels of 1 ug/kg-day and 5.3 ug/kg-day,
respectively. “These dose conversions were made by applying the methods for converting
hair mercury concentrations to ingestion levels in humans used in the derivation of the RfD
in Volume IV of this report.” (EPA 1997)

NOEL for ingestion = 1 ug/kg-day (1000ug=1mg) = 0.001mg/kg-day

--Uncertainty Factors:
1) Subchronic study to Chronic = 10
2) Extrapolation from maternal hair testing = 10
3) Methylmercury (which is more toxic) instead of mercury = 10
4) Sensitive Population = 10

--Modifying Factor: = 9. Data is aimed at fetal development, and is good and credible;
however, I am an amateur.

                           0.001mg/kg-d
RfD = NOAEL / ((UF)* MF) = ----------------- = 1.00E-08 or 0.000000011mg/kg-d
                          (10*10*10*10)*9


Part B—Finding exposure intake for fetus from adult pregnant female food ingestion.


Intake (mg/kg-d) = CF * IR * FI * EF * ED
                   --------------------------
                          BW * AT

CF = Chemical concentration in fish (mg/kg) = 158.6 ug/L (Common Carp mean HG
      concentration 1997-2002 )
      (1000 ug= 1mg, so 158.6 ug= 0.1586 mg/L)
      (James R. Stahl, IDEM “Mercury in Indiana Fish: A breif overview” 2004.)

IR = Ingestion Rate (kg/meal) = 0.284 kg/meal
       (RAGS. 95th % for fin fish)


FI = Fraction Ingested from Contaminated Source (unitless) 1/1 = 1
       (Assumption: All fish consumed comes from this site)

EF = Exposure Frequency (meals/yr) = 24 meals/yr

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                                                                    Risk Assessment of INAAP



ED = Exposure Duration (years) = 30 years

BW = Body Weight (kg) = 66.5 kg (Estimated mean weight)
      (EPA “Estimate Per Capita Water Ingestion and Body Weight in the United
      States—An Update” October 2004, pg 7-2)

AT = Average time (ED (30) * 365 day/yr) = 10950 days


INTAKE (mg/kg-d) =

0.1586 mg/L * 0.284 kg/meal * 1 * 24 meals/yr * 30 day/yr
---------------------------------------------------------------------- = 0.000044536 mg/kg-d
                   66.5 kg * 10950 days

(conversion units cancel out to get mg/kg-d)

Intake = .000044536 mg/kg-d
Take into account maternal absorption rate = 15%
-Uncertainty…metallic mercury is absorbed at 0.01%, whereas 100% of methylymercury is
absorbed and mercury salts are absorbed around 30-40%. Because the data from the site did
not specify what type of mercury was present, I averaged the three to get a mean absorption
rate of 40%.

E = fetal exposure through blood = 0.000044536 mg/kg-d*.40 = 0.0000017814mg/kg-d

Part C—Calculating the HQ for mercury food ingestion


            0.0000017814 mg/kg-d
HQ = E/RfD= ------------------------- = 161.945
            0.000000011 mg/kg-d




3)Non-Cancer Effects From Dermal Absorption—Lead

Part A—Finding the RfD:

My pregnant female absorbs lead dermaly in the shower and through interaction with the
sediment and dirt while visiting the site (to get this number, I added my exposure intake from
both soil dermal exposure and water dermal exposure).
Pregnant female ingests lead from the ground water in her well.
I was unable to find a NOEL with a fetal neurological endpoint, so I derived my own NOEL
based on a study (Rabinowitz MB et al. 1986) preformed on 232 infants between the ages of

                                                                                               40
                                                               Risk Assessment of INAAP


6 -24 months. The measurements of blood lead, erythrocyte protorphyrin and hematocrit
were made semi annually. At 15-17 ug/dL, there was No Observed Effects, however levels
above 15 ug/dL resulted in erythrocyte protoporohyrin levels four times the normal amount. .
I chose 15 ug/dL to account for the increased sensitivity for the fetus.
Because this is data from an oral test, I will multiply the NOEL by the Bioavailability factor
for lead (which was based on in vitro and speciation tests ((Schoof, Rosalind A. 2003).

NOEL for lead/dermal = 25 ug/dL * Bioavailability = 30% (0.30) = 7.5 ug/dL
(1000ug = 1mg, so 7.5 ug = 0.0075mg) =


0.0075mg     1dL     1L              1oz             0.0075mg
--------- x ---- x --------- x --------------- = -------------- = 0.078246118 mg/kg-d
  dL        0.1L   33.81oz      0.02835 kg        0.0958514kg

--Uncertainty Factors:
1) Population variability = 10
2) Data not for our chosen endpoint = 10
3) Not fetal data—sensitive population = 10
4) Data based upon oral ingestion = 10

--Modifying Factor: 10. Data is from a credible source, however I am an amateur.

                       0.078246118 mg/kg-d
RfD = NOEL/[(UF)*MF]= ------------------------- = 0.000000782 mg/kg-d
                       (10*10*10*10) * 10

Part B—Finding exposure intake for fetus from adult female skin absorption

Intake = CS * CF * SA * AF * ABS * EF * ED
            -----------------------------------------------
                              BW * AT

CS = Chemical Concentration in soil (mg/kg) = 1506.67 mg/kg
             (DOC. Indiana Army Ammunition Plant—Phase I RI Report. Jenny Lind
Pond--,
             May 1997)

CF = Conversion Factor (10 E-6 kg/mg) = 0.000001 kg/mg

SA = Skin Surface Area Available for Contact (cm^2/event) = 0.442 (m^2) (0.442 m^2 *
      10^4 cm^2 = 4420 cm^2/event.
      (RAGS, pg. 6-41)
      (Uncertainty—There is no data for adult female, so I used the hand and leg values for
      an adult male and the arm value of a 9<10 year old, to account for the smaller size of
      the average female to the average male.)



                                                                                           41
                                                              Risk Assessment of INAAP


AF = Soil to Skin Adherence Factor (mg/cm^2) = (1.45 mg/cm^2 (commercial potting soil)
+
      2.77 mg/cm^2 (kaolin clay)/2 = 2.11 mg/cm^2
      (RAGS pg. 6-42)
      (Uncertainty—Actual consistency of soil is unkown, because we were unable to visit
      the site, so I averaged commercial potting soil with kaolin clay.)

ABS = Chemical-Specific Permeability Constant (absorption of lead through skin)= 0.01
      (The RiskAssessment Information System. “Toxicity & Chemical-Specific Factor
Data
      Base Search Results” March 2005)
      (Uncertainty—the number is based upon organic lead.)

EF = Exposure Frequency = 40 events/year
      (Uncertainty—I do not know the average amount of times an individual will interact
      with the soil. I do know she will need to interact with the soil and sediment when she
      is fishing (at least 24 times/year) and during general usage of the park area.)

ED = Exposure Duration = 30 years

BW = Body Weight = 66.5 kg

AT = Averaging Time (ED * 365 days/yr) = 30 * 365 days/year = 10950 days

Intake (mg/kg-d) =

1506.67 mg/kg*0.000001 kg/mg*4420 cm^2/event*2.11 mg/cm^2*0.01*40 events/yr*30
yrs.
                                66.5 kg * 10950 days

(conversion units cancel out to get mg/kg-d)

Intake (mg/kg-d) = 168.681
                  -------------- = 0.000231563 mg/kg-d
                    728175

Intake: soil intake (0.000231563mg/kg-d) + water intake (0.00009mg/kg-d)=
0.000321563mg/kg-d
Maternal absorption rate = 0.04% (The Risk Assessment Information System. “Toxicity &
Chemical-Specific Facotrs Data Base Search Results” March 2005) was already calculated in
the ABS section of the exposure calculations, so I do not need to calculate again.


E = Fetal exposure through blood= 0.000321563 mg/kg-d

Part C—Calculating the HQ


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                                                               Risk Assessment of INAAP


            0.000321563 mg/kg-d
HQ = E/RfD= ------------------------- = 411.2053231
            0.000000782 mg/kg-d



4)Non-Cancer Effects From Air Inhalation—Mercury

Part A—Finding the RfD

Pregnant woman inhales mercury vapor from ambient air amounts at the site. My data is
based on human occupational inhalation studies from the EPA IRIS web site. The critical
effects looked at in the study were: Hand tremor, increased memory disturbance; slight
subjective and objective evidence of autonomic dysfunction. This correlated to a
neurological endpoint. I used the LOEL from the adjusted level (LOEL [ADJ]) for the extra-
respiratory effect of the vapor (gas). The conversion factors and assumptions used were: the
LOEL was based on a 8 hour occupational exposure. MVho = 10 cu.m/day, MVh = 20
cu.m/day. The LOEL [ADJ]= not adjusted LOEL (0.025mg/cu.m) * (MVho (10
cu.m/day)/MVh(20 cu.m/day)) * (5 days/7 days) = 0.0089. Because I used data from
inhalation studies, I do not need to include the bioavailability (which would have been 80%)

LOEL for inhalation = 0.0089 mg/cu.m

0.0089 mg        0.004546 cu.m        1 gallon       1 lb
------------- x ------------------- x ---------- x ----------------- = 0.000010677mg/kg-d
1 cu.m              1 gallon           8.354 lb 0.45359237 kg

--Uncertainty Factors:
1) Population Variability = 10
2) Sensitive Population—not fetal study = 10
3) LOEL instead of NOEL = 10
4) Conversion errors = 10

--Modifying Factor: 10. Credible data, but I am an amateur.

                        0.000010677mg/kg-d
RfD = LOEL/[(UF)*MF] = -------------------------- = 1.0677E-10 (0.00000000010677)
                        (10*10*10*10) * 10

Part B—Finding exposure intake for fetus from pregnant adult female inhalation of
mercury.

INTAKE (mg/kg-d) = CA * IR * ET * EF * ED
                           BW * AT
CA = Chemical concentration in Air (mg/m^3) = 0.01184 mg/m^3
      (Indiana Department of Environmental Management “Mercury: Air Emmisions and
Proposed

                                                                                            43
                                                                Risk Assessment of INAAP


        Utility Rules” 2004)
        (Uncertiainty—Not site specific, I averaged the amount from the five monitoring
stations in
        Southern Indiana)

IR = Inhalation Rate (m^3/day (30m^3/day/24 hours/day) = 1.25m^3/hr
       (RAGS)

ET = Exposure Time (hours/day) = 24hr/day

EF = Exposure Frequency (day/yr) = 365 day/yr

ED = Exposure Duration (yrs) = 30 years

BW = Body Weight (kg) = 66.5 kg

AT = Avaraging Time (ED * 365days/yr) = 30yr * 365 day/yr = 10950 days

INTAKE (mg/kg-d) = 0.01184 mg/m^3 * 1.25 m^3/hr * 24 hr/day * 365 day/yr * 30 yr
                                       66.5 kg * 10950 days

(conversion units cancel out to get mg/kg-d)

INTAKE = 3889.44 mg = 0.00534 mg/kg-d
         728175 kg/day

Adult female intake: 0.00534 mg/kg-d
Absorption rate into blood = 67% (methylmercury 100% absorbed, Elemental mercury 75-85
% aborbed and Inorganic mercury 7-15 % aborbed. I averaged the three, using the highest
numbers to account for sensitivity of fetus, to get 67%.)

E = Fetal exposure through blood = 0.00534mg/kg-d*0.67 = 0.0035778mg/kg-d
Part C—Calculating the HQ

                 0.0035778 mg/kg-d
HQ = E/RfD = ---------------------------------- = 33509412.76
              0.00000000010677 mg/kg-d



5)Non-Cancer =Effects From Air Inhalation—Lead

Part A—Finding the RfD

Pregnant woman inhales lead from ambient air amounts at the site. Pregnant female ingests
lead from the ground water in her well.


                                                                                           44
                                                              Risk Assessment of INAAP


I was unable to find a NOEL with a fetal neurological endpoint, so I derived my own NOEL
based on a study (Rabinowitz MB et al. 1986) preformed on 232 infants between the ages of
6 -24 months. The measurements of blood lead, erythrocyte protorphyrin and hematocrit
were made semi annually. At 15-17 ug/dL, there was No Observed Effects, however levels
above 15 ug/dL resulted in erythrocyte protoporohyrin levels four times the normal amount. .
I chose 15 ug/dL to account for the increased sensitivity for the fetus.
The study was based on oral exposure, so I multiplied the NOEL by the bioavailability
(40%). The Bioavailability was based on in uetro rat tests ((Schoof, Rosalind A. 2003)

NOEL = 25 ug/dL * bioavailability=40% (0.40) = 10 ug/dL

(1000ug = 1mg, so 10 ug = 0.01mg)


0.01mg       1dL     1L             1oz                0.01mg
---------   x ---- x --------- x --------------- = -------------- = 0.104328158 mg/kg-d
  dL          0.1L   33.81oz      0.02835 kg        0.0958514kg

--Uncertainty Factors:
1) Population variability = 10
2) Data not for our chosen endpoint = 10
3) Not fetal data—sensitive population = 10
4) Data based upon oral ingestion = 10

--Modifying Factor: 10. Credible data, but I am an amateur.

                         0.104328158 mg/kg-d
RfD = NOEL/[(UF) * MF] = ---------------------------- = 0.000001043 mg/kg-d
                         (10*10*10*10) * 10

Part B—Finding exposure intake for fetus from pregnant adult female inhalation.

Intake (mg/kg-d) = CA *       IR * ET * EF * ED
                              BW * AT

CA = Chemical concentration in Air (mg/m^3) = 0.03 ug/m^3 (1000ug = 1 mg) = 0.00003
mg/m^3
        (Environmtnal Defense. “Scorecard—The Pollution Information Site)
        (Uncertiainty—Not site specific, I averaged the amount from theambient air
concentrations
        of lead from Martin County and Lawrence County, and the two closest monitoring
stations to
        Clark Count).
IR = Inhalation Rate (m^3/day (30m^3/day/24 hours/day) = 1.25m^3/hr
        (RAGS)

ET = Exposure Time (hours/day) = 24hr/day

                                                                                          45
                                                                   Risk Assessment of INAAP



EF = Exposure Frequency (day/yr) = 365 day/yr

ED = Exposure Duration (yrs) = 30 years

BW = Body Weight (kg) = 66.5 kg

AT = Avaraging Time (ED * 365days/yr) = 30yr * 365 day/yr = 10950 days

INTAKE (mg/kg-d) = 0.00003 mg/m^3 * 1.25 m^3/hr * 24 hr/day * 365 day/yr * 30 yr
                                       66.5 kg * 10950 days

(conversion units cancel out to get mg/kg-d)

INTAKE = 3889.44 mg = 0.000013534 mg/kg-d
         728175 kg/day


Adult Female Intake = 0.000013534 mg/kg-d
Absorption rate into blood from inhailation = 50% (World Health Organization, 1995)

E = Fetal exposure through blood = 0.000013534mg/kg-d * 0.5 = 0.000006767 mg/kg-d

Part C—Calculating HQ

              0.000006767 mg/kg-d
HQ = E/RfD = ----------------------------- = 6.488
              0.000001043 mg/kg-d

HAZARD INDEX (HI)

The hazard index tells us the overall hazard to our target organism. If it is less than 1, then it
is considered ‘safe’.

To get the HI, we must add together all of the HQ’s from each exposure pathway.

HI = 0.15 + 161.945 + 411.2053231 + 33509412.76 + 6.488 = 33509992.55

This is larger than 1, so our fetus is not ‘safe’.

Cancer Risk for Lead and Mercury
To determine my cancer risk for lead and mercury, I used the following low risk equation
form RAGS:

Cancer risk = Chrinic Daily Indake (CDI) * Slope Factor (SF)


                                                                                                46
                                                                   Risk Assessment of INAAP


If the risk is greater than 0.01, I will recalculate the data using the high risk equation from
RAGS:

Cancer risk = 1 – the exponential * (-CDI * SF)

To determine Chronic Daily Intake, we use the same data as in our non-cancer exposure
calculations, with the exception of the Averaging Time. For cancer, the Averaging Time
(AT) is 70 years (for it to manifest) multiplied by 365 days/year.

I used the same slope factor for each exposure pathway.

I calculated my slope factor for oral intake from a two studies documented on the EPA’s
IRIS Lead web page (http://www.epa.gov/IRIS/subst/0277.htm). The first study, done by
Azar et al. (1973), was on the carcinogenic potential of lead acetates administered in 10, 50,
100, 500 ppm dietary concentrations to 50 rats for 2 years. The second study, by the same
group, in the same way, had 20 rats and they were given 0, 1000 and 2000 ppm.
Carcinogenicity was based upon the appearance of renal tumors.
No renal tumors were reported on 0, 10, or 100ppm. 5/50 rats developed tumors at 500 ppm,
10/20 developed tumors at 1,000 and 16/20 developed tumors at 2,000 ppm.
I combined these studies to generate the slope factor. There is uncertainty in my calculations.

Slope factor = 0.0086 mg/kg-d
                           Lead Slope factor

                  20

                  15
  % with Tumors




                  10
                                        y = 0.0086x - 0.5516
                   5                         R2 = 0.9669
                   0
                       0   500   1000   1500    2000     2500
                  -5
                                    Dose

Figure 2 Dose were administered in ppm.



Each exposure pathway will be devided up into three sections. In part A, I will determine the
CDI using the equation above. In part B, I will calculate the slope factor. In part C, I will I
will calculate the risk for cancer for the exposure pathway. If the risk is greater than 0.01, I
will then recalculate using the high risk equation.

I was unable to determine the slope factor for mercury. Based on the EPA website, mercury
is “Classification –D; not classifiable as to human carcinogenicity”
(http://www.epa.gov/IRIS/subst/0370.htm). There have been no studies done that have
shown a correlation between mercury exposure and increased cancer mortality. There are six
separate studies on the EPA website indicating that despite drastic increases in mercury
levels in the blood of those tested, the cancer incidence was comparable to the average


                                                                                                  47
                                                                    Risk Assessment of INAAP


population. Because it is better to have no data rather than wrong data as to not lead people
into a false security in the data (Karanth, K.U. et al. 2003), I have not included mercury
calculations in my Cancer risk characterization.

-Uncertainty: None of my slope factors are based off of fetal development cancer studies.


1). Cancer Risk From Water Ingestion of Lead.
Part A—Finding the CDI: (RAGS, p. 6-35, with cancer AT)

CDI = Intake (mg/kg-d) = CF * IR * EF * ED
                        --------------------------
                               BW * AT

CF = Chemical concentration in ground water (mg/L) = 14.165 ug/L (1000 ug= 1mg, so
      14.175 ug= 0.014175 mg/L
      (DOC. Indiana Army Ammunition Plant—Phase I RI Report. Site 17 & 60
      Burning Ground (Site 17). Tabel 16.2-7, May 1997)

IR = Ingestion Rate (Liters/day) = 2.674 L/d (Based on 95% for increased safety)
       (EPA “Estimated Per Capita Water Ingestion and Body Weight in the United
       States—An Update” Octover 2004, pg 6-4)

EF = Exposure Frequency (d/yr) = 365 day/yr

ED = Exposure Duration (years) = 30 years

BW = Body Weight (kg) = 66.5 kg (Estimated mean weight)
      (EPA “Estimate Per Capita Water Ingestion and Body Weight in the United
      States—An Update” October 2004, pg 7-2)

AT = Average time (70 years for cancer * 365 days/year) = 25550 days


INTAKE (mg/kg-d) =

0.014175 mg/L * 2.674 L/day * 1 * 365 day/yr * 30 day/yr
---------------------------------------------------------------------- = 0.000244279 mg/kg-d
                   66.5 kg * 25550 days

(conversion units cancel out to get mg/kg-d)

Part B—Finding the Slope Factor

Slope factor = 0.0086 mg/kg-d


                                                                                                48
                                                               Risk Assessment of INAAP


Part C—Calculating Risk for water lead ingestion

Risk = CDI * SF = 0.000244279 mg/kg-d * 0.0086 mg/kg-d = 0.000021




2) Cancer Risk for Dermal Lead Exposure
Part A—Finding the CDI: (RAGS, pg. 6-41)

CDI Intake = CS * CF * SA * AF * ABS * EF * ED
            -----------------------------------------------
                              BW * AT

CS = Chemical Concentration in soil (mg/kg) = 1159.9 mg/kg
      (DOC. Indiana Army Ammunition Plant—Phase I RI Report. Site 17 & 18 Burning
      Ground (Site 17). Table 16.6, May 1997)

CF = Conversion Factor (10 E-6 kg/mg) = 0.000001 kg/mg

SA = Skin Surface Area Available for Contact (cm^2/event) = 0.442 (m^2) (0.442 m^2 *
      10^4 cm^2 = 4420 cm^2/event.
      (RAGS, pg. 6-41)
      (Uncertainty—There is no data for adult female, so I used the hand and leg values for
      an adult male and the arm value of a 9<10 year old, to account for the smaller size of
      the average female to the average male.)

AF = Soil to Skin Adherence Factor (mg/cm^2) = (1.45 mg/cm^2 (commercial potting soil)
+
      2.77 mg/cm^2 (kaolin clay)/2 = 2.11 mg/cm^2
      (RAGS pg. 6-42)
      (Uncertainty—Actual consistency of soil is unkown, because we were unable to visit
      the site, so I averaged commercial potting soil with kaolin clay.)

ABS = Chemical-Specific value (absorption of mercury through skin) = 0.01
      (The Risk Assessment Information System. “Toxicity & Chemical-Specific Factors
      Data Base Search Results” March 2005.)
      (Uncertainty—the number is based upon organic lead.)

EF = Exposure Frequency = 40 events/year
      (Uncertainty—I do not know the average amount of times an individual will interact
      with the soil. I do know she will need to interact with the soil and sediment when she
      is fishing (at least 24 times/year) and during general usage of the park area.)

ED = Exposure Duration = 30 years

BW = Body Weight = 66.5 kg

                                                                                           49
                                                               Risk Assessment of INAAP



AT = 70 years for cancer * 365 days/year = 25550 days

CDI (mg/kg-d) =

1159.09 mg/kg*0.000001 kg/mg*4420 cm^2/event*2.11 mg/cm^2*0.01*40 events/yr*30
yrs.
                                66.5 kg * 25550 days

(conversion units cancel out to get mg/kg-d)

CDI (mg/kg-d) = 129.71886
                -------------- = 0.000076347 mg/kg-d
                  1699075

Part B—Finding the Slope Factor

I used the same slope factor from my lead water ingestion but converted it to dermal
exposure by multiplying it by the bioavailability factor (30%)

Slope factor = 0.0086 mg/kg-d * Bioavailability 0.30 = 0.00258 mg/kg-d

Uncertainty Factor: This slope factor is based on oral absorption rather than dermal
absorption.

Part C—Calculating cancer risk for dermal lead absorption

RISK = CDI * SF = 0.000076347 mg/kg-d * 0.00258 mg/kg-d = 0.000000657




3) Cancer Risk for Dermal Water Exposure to Lead
Part A—Finding the CDI: (RAGS pg. 6-37)

CDI Intake = CW * SA * PC * ET * EF * ED * CF
            ---------------------------------------------
                            BW * AT

CW = Chemical Concentration in Ground Water (mg/L) = 14.175 ug/L (1000ug = 1mg, so
14.175
                                                      ug = 0.014175mg) =
                                              0.014175mg/L
       (DOC. Indiana Army Ammunition Plant – Phase I RI Report. Site 17 & 60 Burning
Ground
       (Site 17). Table 16.7-2, May 1997)

                                                                                          50
                                                                  Risk Assessment of INAAP


       (Uncertainty—do not know exactly how much will travel off site to the target
organisms
       private well)

SA = Skin Surface Area Available for Contact (cm^2) = 0.442 m^2 = (0.442m^2 *
10^4cm^2)
                                                                         4420 cm^2
      (RAGS pg 6-41)
      (Uncertainty—There is no data for adult female, so I used the hand and leg values for
      an adult male and the arm value of a 9<10 year old, to account for the smaller size of
      the average female to the average male.)

PC = Chemical-Specific Dermal Permeability Constant (cm/hr) = 0.00013 cm/hr
      (U.S. EPA. “Dermal Exposure Assessment Principles and Applications” 1992)

ET = Exposure Time (hrs/day) = 73.44 hrs/d
      (Assuming my target organism spends approximately 4 hours per visit (40 visits/year)
      4*40=160/365(days/yr) = 0.438356 hours/day for dermal water surface contact. For
      dermal contact while showering I will assume; one shower/day at 12 min/shower =
      365day*12 min = 4380min/60min/hr = 73 hours So, Total water dermal contact =
      73.44 hrs/day.)

EF = Exposure Frequency (day/yr) = 365day/yr

ED = Exposure Duration (yrs) = 30 yrs

CF = Volumetric Conversion Factor for Water ( 1 L/1000cm^3) = 1 L/1000cm^3

BW = Body Weight (kg)= 66.5 kg

AT = Averaging Time (70 years for cancer * 365days/yr) = 25550 days

CDI Intake =
0.014175mg/L * 4420 cm^2 * 0.00013 cm/hr * 73.44 hrs/d * 365day/yr *30 yrs *1
L/1000cm^3
                                 66.5kg * 25550 days

(Conversion factors cancel out to get mg/kg-d)

CDI = 6.5499 = 0.000003855 mg/kg-d
     1699075

Part B—Finding Slope Factor

I used the same slope factor for all cancer risk calculations adjusted for the bioavailability
(30%).



                                                                                                 51
                                                                         Risk Assessment of INAAP


SF = 0.0086 mg/kg-d * Bioavailability 0.30 = 0.00258 mg/kg-d

Part C—Finding cancer risk for water dermal absorption

RISK = CDI * SF = 0.000003855 mg/kg-d * 0.00258 mg/kg-d = 0.00000001




4)Cancer Risk for Inhalation of Lead
Part A—Finding the CDI: (RAGS pg. 6-44)

CDI Intake (mg/kg-d) = CA * IR * ET * EF * ED
                      --------------------------------
                                 BW * AT

CA = Chemical concentration in Air (mg/m^3) = 0.03ug/m^3 (1000ug = 1mg) =
                                                                          0.00003mg/m^3
        (Environmental Defense “Scorecard—The Pollution Information Site)
        (Uncertainty—Not site specific, I took the average from the ambient air
concentratiosns
        of lead from Martin County and Lawrence County, the two closest monitoring
stations
        to Clark County)

IR = Inhalation Rate (m^3/hr) = 30m^3/day (30m^3/day/24 hr/day) = 1.25 n^3/hr
       (RAGS)

ET = Exposure Time (hrs/day) = 24hr/day

EF = Exposure Frequency (d/yr) = 365day/yr

ED = Exposure Duration (yrs) = 30 yrs

BW = Body Weight (kg) = 66.5 kg

AT = Averaging Time = 70 years * 365days/yr for cancer = 25550 days

CDI (mg/kg-d) = 0.00003mg/m^3 * 1.25 m^3/hr * 24hr/day * 365day/yr * 30 yrs
                 ------------------------------------------------------------------------------
                                           66.5 kg * 25550 days
(Conversion units cancel out to reach mg/kg-d)

CDI (mg/kg-d) = 9.855mg
               ------------- = 0.0000058 mg/kg-d


                                                                                                    52
                                                                 Risk Assessment of INAAP


                   1699075

Part B—Finding the SF:
I used the same slope factor as the two previous calculations adjusted for inhalation by
multiplying it by the bioavailability factor (40%).

SF = 0.0086 mg/kg-d * Bioavailability 0.40 = 0.00344

Part C—Calculation of cancer risk for inhalation of lead

RISK = CDI * SF = 0.0000058 mg/kg-d * 0.00344 mg/kg-d = 0.00000002


Sum of Cancer Risk Across All Exposure Pathways

Total exposure for cancer risk = risk for food (water) ingestion + risk of inhalation + risk of
dermal exposure (soil + water) =
       0.000021 + (0.000000197 +0.00000001) + 0.00000002 = 0.000021227

Total cancer risk = 0.000021227




                                                                                              53
                                                                               Risk Assessment of INAAP


         Appendix D

         Non-Cancer Risk Characterization Table

                        Exposure pathway: ingestion of contaminated private water well

Chemical     NOEL*        NOEL            Tests        Modifyi   Uncertainty       RfD          Fetal      Hazard      Total
                                                                      e
             mg/kg-d      Source          Based          ng                     Uncertainty   Exposure*   Quotient*    Exp.
                                           On:         Factor                     Adj.*        mg/kg-dg    (HQ)h      Hazard
                                                       (1-10)a                   mg/kg-df                             Index
                                                                                                                       (HI)b
Mercury          n/a        n/a             n/a          n/a         n/a            n/a          n/a         n/a
 Lead          2.E-01      Rabino       erythrocyte      10         10^3          1.6E-05      9.E-05      2.E-01
                            witz      protoporohyrin
                           MB et         increases
                             al.
                           1986d

 HQ for                                                                                                    2.E-01
  water
ingestion

                                        Exposure pathway: food ingestion

Mercury       1.E-03      US EPAc      Hair mercury      9          10^4          1.E-08       2.E-06       161.9
                                           tests
  Lead        2.E-01     Rabinowit      erythrocyte      10         10^3          1.6E-05      9.E-05          0.2
                          z MB et     protoporohyrin
                         al. 1986 d      increases

 HQ for                                                                                                     162.1
  food
Ingestion

                              Exposure pathway: dermal contact in soil and water

Mercury         n/a          n/a            n/a          n/a         n/a            n/a          n/a         n/
 Lead         8.E-02     Rabinowit      erythrocyte      10         10^4          8.E-07       3.E-04       411.2
                          z MB et     protoporohyrin
                         al. 1986 d      increases

HQ for                                                                                                      411.2
Dermal

                                          Exposure pathway: inhalation

Mercury       1.E-05       EPA--       neurological      10         10^4          1.1E-10      4.E-03     33509412.
                            IRIS        problems                                                              8


 Lead         1.E-01     Rabinowit      erythrocyte      10         10^4          1.E-06       7.E-06          6.5
                          z MB et     protoporohyrin
                         al. 1986 d      increases



                                                                                                          54
                                                                                     Risk Assessment of INAAP

  HQ for                                                                                                               33509419.
inhalation                                                                                                                 3
TOTAL                                                                                                                              335099
  HI                                                                                                                                92.55



        NOEL = No Observed Effect Level
        RfD = Reference Dose
             *All values are expressed as no significant value—values for illustration only

             a Modifying Factor is on a 1-10 scale; 1 being the most reliable data and/or experience, 10 being the least.

             b Hazard Index (HI) = Total HQ for water ingestion + HQ for food ingestion + HQ for dermal + HQ for
                  inhalation.
             c US EPA AIR Mercury Study Report to Congress, Volume 1: Executive Summary
             d Rabinowitz MB, Leviton A, Needleman HL. Occurrence of elevated protoporphyrin levels in relation to
                           lead burden in infants. Environ Res. 1986 Apr;39(2):253-7.
             e. Each uncertainty = 10. Total uncertainty is all uncertainties multiplied together.
             f. RfD Adj. = NOEL / ((UF)* MF)
             g. Fetal exposure (E) = Adult Intake * Absorption rate into blood
             h. Hazard Quotient (HQ) = E/RfD




                                                                                                                       55
                                                                                  Risk Assessment of INAAP


            Appendix E

      Cancer Risk Table

      Exposure pathway: ingestion of contaminated private water well

Chemical       CDI         CDI             SF         Type      SF        SF Basis    Chemical-     Total          Total
               (mg/kg-     Adj. for        (mg/kg-    of        Source    (Vehicle)   Specific      Pathway        Exp.
               d)a         Absorption?     d)         Cancer                          Riskb         Risk           Risk
Mercury        n/a         n/a             n/a        n/a       n/a       n/a         n/a
Lead           2.E-04*     no              9.E-3*-    Renal-    Azar et   Water       2.E-05*       2.E-05*
                                                                al.
                                                                (1973)c

      Exposure pathway: dermal contact in soil and water

Mercury        n/a        n/a            n/a         n/a       n/a        n/a          n/a
Lead-soil      8E-05*     No             3.E-3*-     Renal-    Azar et    Water        2.E-07*
                                                               al.
                                                               (1973) c
Lead-water     4E-06*     No             3.E-3*-     Renal-    Azar et    Water        1.E-08*
                                                               al.
                                                               (1973) c
                                                                                                    2.E-07*

      Exposure pathway: inhalation

Mercury        n/a         n/a             n/a       n/a       n/a        n/a         n/a
Lead           6.E-06*     no              3.E-3*-   Renal-    Azar et    Water       2.E-08*
                                                               al.
                                                               (1973) c
                                                                                                    2.E-08*
TOTAL                                                                                                              2.E-05*
CANCER
RISK

            SF = Slope Factor
            CDI = ChronicDaily Intake

            * All values are expressed as no significant value—values for illustration only
            - slope factor based on two studies done by Azar et al. (1973), on the carcinogenic potential of
                 lead acetates. 10, 50, 100, 500 ppm dietary concentrations to 50 rats for 2 years in the first
                 study. 0, 1000 and 2000 ppm to 20 rats for 2 years for the second study.
                 Carcinogenicity was based upon the appearance of renal tumors.
            a CDI = Exposure Calculation with an Averaging Time of 70 years * 365 days (for cancer to manifest)
            b Risk = CDI * SF
            c Azar, A., H.J. Trochimowicz and M.E. Maxfield. 1973. Review of lead studies in animals carried out
                 at Haskell Laboratory - Two year feeding study and response to hemorrhage study. In: Barth D.,
                 A. Berlin, R. Engel, P. Recht and J. Smeets, Ed. Environmental health aspects of lead:
                 Proceedings International Symposium; October 1972; Amsterdam, The Netherlands. Commission
                 of the European Communities, Luxemberg. p. 199-
                 208.




                                                                                                                   56

				
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