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ATSDR > Public Health Assessments & Consultations

PUBLIC HEALTH ASSESSMENT

VOLUNTEER ARMY AMMUNITION PLANT
CHATTANOOGA, HAMILTON COUNTY, TENNESSEE

FACILITY NO. TN6210020933

September 7, 2004

Appendix C : Acid Cloud

Background
During the production of trinitrotoluene (TNT) and the acids required for TNT production, air emissions were likely. Anecdotal evidence provided by people who worked and resided around the Volunteer Army Ammunition Plant (VAAP) while TNT manufacturing processes were operational indicate that air emissions were at times visible, physically irritating, and damaging to clothing, plants and cars. Anecdotal information also suggests that the ambient concentrations may have been highest during the World War II production years. Apparently some air pollution control equipment was first added during the Korean War production years (Public Comment 2004a). This appendix attempts to identify the likely compounds that were released and the range of potential health effects that would be expected for people exposed to the emissions.

Summary Air Emissions from TNT Production
Gaseous by-products expected from the TNT and acid production processes include:

Nitrogen oxide (NO)
Nitrogen dioxide (NO₂)
Sulfur oxides (SO₂)
Nitric acid mist

Relative Emissions
The US Environmental Protection Agency (EPA) AP-42 (EPA 1983, 1998a, and 1998b) provides relative emission rates for the various compounds likely emitted during the TNT and acid production processes. The Agency for Toxic Substances and Disease Registry (ATSDR) used this information to identify the relative emissions of these compounds during the production of 2,000 pounds (lbs) or 1 ton of TNT. In most cases, AP-42 lists a range of emission factors measured at a variety of facilities and the average value. To be conservative, ATSDR used the highest value presented. Based on this process ATSDR calculated the emissions from TNT production shown Table C-1.

Table C-1: Emissions from the Production of 2,000 lbs of TNT
Nitrogen Dioxide (lbs)	Nitric Acid (lbs)	Sulfur Dioxide (lbs)	Sulfuric Acid (lbs)
507	277	181	231
lbs = pounds

Stoichiometrically, three molecules of nitric acid are needed to produce one molecule of TNT; based on the ratio of their molecular weights, approximately 0.83 lb of nitric acid is needed to react with toluene to produce 1 lb of TNT. Therefore 2,000 lbs of TNT would require 1,660 lbs of nitric acid; the total amount of nitric acid produced would need to be at least equal to the amount combined with the toluene and the amount lost to atmospheric emissions during the process (277 lbs). Therefore ATSDR assumed that approximately 2,000 lbs (1660 + 277 = 1937 ~ 2000) of nitric acid would be needed to produce 2,000 lbs of TNT.

AP-42 (EPA 1998a) estimates that 11.7 and 57 lbs of nitrogen dioxide and nitrogen oxides, respectively, would be emitted during the production of 2,000 lbs nitric acid from a process without air pollution control equipment. Nitrogen oxides are typically composed of nitrogen oxide and nitrogen dioxide with trace amount of other nitrogen-oxygen species-AP-42 does not provide the specific composition in TNT production. As such, ATSDR assumed that half of the 57 lbs of nitrogen oxides were nitrogen dioxide and the other half was nitrogen oxide. Using this assumption, ATSDR estimated that approximately 40 lbs of nitrogen dioxide (11.7 + [57/2] = 40.2 ~ 40) and 29 lbs of nitrogen oxide (57/2 = 28.5 ~ 29) would be released during the nitric acid production process.

The available information does not describe the amount of sulfuric acid necessary to produce TNT, only the amount emitted during TNT production (EPA 1983). Sulfuric acid is not directly consumed in the TNT production process. Therefore, ATSDR assumed that sulfuric acid was produced to replace that lost to the air and liquid waste stream and that air emissions (231 lbs) represented 1/3 of the total losses. ATSDR estimated a total of 700 lbs of sulfuric acid production (3 * 231 = 693 ~ 700) for the production of 2,000 lbs of TNT.

AP-42 (EPA 1998b) illustrates that the emissions from sulfuric acid production depend on a variety of unknown factors in the production process. ATSDR conservatively estimated that the sulfur dioxide emissions would be approximately 20 lbs (assuming 55 lbs SO2/2,000 lbs H2SO4 then [55 * 700]/2,000 = 19.25 ~ 20) and the sulfuric acid emissions would be approximately 2 lbs (assuming 6 lbs SO2/2,000 lbs then [6 * 700]/2,000 = 2.1 ~2) for the production of 2,000 lbs of TNT. The following table shows the total emissions estimated for the production of 2,000 lbs of TNT

Table C-2: Estimated Emissions for the Production of 2,000 lbs TNT
Process	Nitrogen Oxide (lbs)	Nitrogen Dioxide (lbs)	Nitric Acid (lbs)	Sulfur Dioxide (lbs)	Sulfuric Acid (lbs)
TNT Production	NA	507	277	181	231
Nitric Acid Production	29	40	NA	NA	NA
Sulfuric Acid Production	NA	NA	NA	20	2
Total	29	547	277	201	233

This analysis estimates only a rough approximation of the compounds released to the air to support the production of 2,000 lbs of TNT. The concentration of these compounds in an acid cloud that may have been released from VAAP is not estimated. However, the estimates provide a relative scale; showing which compounds likely dominated acid cloud composition. The greatest emissions were from the TNT manufacturing process and were much higher than the emissions from the acid production processes. In addition, nitrogen dioxide emissions were the dominant emission. The combination of nitrogen oxide, nitrogen dioxide, and nitric acid are much greater than the combination of sulfur dioxide and sulfuric acid. It is possible that much of the sulfuric acid used at VAAP was not produced at VAAP (Chattanooga Times April 18, 1969). As a result the actual sulfur dioxide and sulfuric acid emissions may be less than estimated.

Exposure to Gaseous By-Products
Large quantities of TNT and sulfuric and nitric acids were produced at VAAP. Sulfuric acid was produced to support TNT production. Nitric acid was produced to support the production of both TNT and agricultural fertilizer. By-products from these manufacturing processes could have migrated off site as a result of emissions from process exhaust stacks, leaks from tanks, and dispersion from work place environments. VAAP-33-New Acid Area is approximately 1,300 feet (ft) from VAAP's northern boundary. VAAP-2-CF Industries, Incorporated (CFI) Lease Area and VAAP-2-TNT Manufacturing Valley are approximately 1,000 to 2,000 ft from VAAP's western boundary. Residential homes are located across from VAAP at both locations.

Off-base concentrations of emissions would vary substantially based primarily on how much of a compound was released at VAAP, the height of the release, the location of the release, and meteorological conditions at the time of the release-predominantly wind speed. In addition many of these compounds are also found in the emissions of other industrial, commercial and residential activities. The actual concentration and potential health effects experienced by local residents would be a result of the combination of exposures from all of the potential sources.

No measured data exists to describe the concentration of sulfuric or nitric acid compounds in the air either onsite, offsite, or in the neighboring residential areas. As a result, quantifying the level of exposure that may have occurred is impossible. As described in the exposure evaluation section of this Public Health Assessment (PHA), the potential for health effects from an exposure to a chemical is related to a variety of factors including: the concentration of the chemical, duration of the exposure, and frequency of the exposure. Lacking measured data about the concentration of the compounds in the air, and the frequency and duration of the events when these compounds were in the air, evaluating if the exposures scenarios described by community members could lead to health effects is impossible.

However, people who resided near VAAP during the time that TNT was produced provided with ATSDR some useful information. Residents indicated that periodically, "clouds" would migrate from VAAP. The clouds tended to travel north through the Waconda Valley or south through Hickory Valley. They were described as having a yellow-orange-brown color and would burn the eyes and respiratory system of exposed individuals. Residents also described that the clouds turned laundry drying on a clothesline yellow, killed trees, and ruined the paint on cars. ATSDR combined information about the air releases provided by the residents with basic information about the likely composition of the emissions and the properties of those compounds in air to create a chart showing the most likely to least likely health effects to residents exposed to clouds migrating from VAAP (Figure C-1).

Nitrogen oxide (NO)
Nitrogen oxide in air is colorless and has a sharp sweet odor (ATSDR 2002). It is rapidly converted to nitrogen dioxide; the conversion rate depends primarily on the concentrations of nitrogen oxide and oxygen (NIOSH 1997; Meditext 2002). People who live near combustion sources such as coal burning power plants or near areas with heavy motor vehicle use, use wood or kerosene fuel for heating or cooking, or smoke tobacco or breathe in second-hand smoke are exposed to more nitrogen oxide than those who are not in these categories (ATSDR 2002). In addition, nitrogen oxide may be used as a medical treatment for some conditions of pulmonary hypertension (Meditext 2002).

Human toxicity data is limited, but nitrogen oxide appears to be 1/5 as toxic as nitrogen dioxide (Meditext 2002). It can irritate skin, eyes and mucous membranes. More serious effects appear to be due to inhalation. Acute exposures (exposures to a high concentration over a short period of time, generally minutes to hours) can result in a variety of symptoms. Common symptoms include: cough, hyperpnea (rapid breathing), and dyspnea (difficult, labored or uncomfortable breathing). These symptoms are usually accompanied by signs of pulmonary edema (fluid accumulation in the lungs) that can be recognized by a physician. Symptoms may occur up to 24 hours after the exposure. The initial symptoms may also include fatigue, restlessness, anxiety, mental confusion, lethargy, loss of consciousness, nausea and abdominal pain (Meditext 2002).

Chronic exposure (exposure to a low concentration over a long period of time, generally weeks to months) may also impair pulmonary (lung) function-possibly in the absence of acute symptoms (cough, hyperpnea, or dyspnea). Chronic exposures, as experienced occupationally by welders, that are too low to produce acute effects can result in pulmonary damage (Meditext 2002). Though not mentioned in the Meditext review, welders are also exposed to a variety of metals and other compounds in the fumes, which could confound study results.

The typical concentration of nitrogen oxide used to treat pulmonary hypertension is in the range of 10 to 20 parts per million (ppm); concentrations as high as 80 ppm have been well tolerated. Higher concentrations in the range of 60 to 150 ppm reportedly may cause immediate coughing and burning in the chest. Exposures to high concentrations (specific concentrations unavailable) are expected to cause serious burns on skin or eyes (ATSDR 2002). Concentrations above 100 ppm are characterized as immediately dangerous to life or health (NIOSH 1997). Concentrations in the range of 200 to 700 ppm reportedly may cause death (Meditext 2002).

Nitrogen dioxide (NO₂)
As a liquid, nitrogen dioxide has a yellowish-brown appearance (NIOSH 1997). In air, nitrogen dioxide has been described as a reddish-brown or a reddish-orange-brown gas with a strong harsh odor (NIOSH 1997; UDEQ 2001a; ATSDR 2002). Nitrogen dioxide readily reacts with water to form nitric acid (acid rain) and sunlight to form ozone (ATSDR 2002). People who live near combustion sources such as coal burning power plants or near areas with heavy motor vehicle use, use wood or kerosene fuel for heating or cooking, or smoke tobacco or breathe in second-hand smoke are exposed to more nitrogen dioxide than those who are not in these categories (ATSDR 2002). Much of the information available about the health effects of exposure to nitrogen dioxide acknowledge the fact that nitrogen dioxide is typically found with nitrogen oxide. The information below follows the common procedure of discussing the health effects of exposure to nitrogen oxides, a combination of primarily nitrogen dioxide and nitrogen oxide.

The health effects associated with exposure to nitrogen oxides is due to the formation of nitric acid when the nitrogen dioxide reacts with water on the skin, in the eyes, or along the respiratory tract. The pulmonary and respiratory systems were most commonly identified with effects from nitrogen dioxide exposure. Symptoms usually develop after a 1 to 24 hour delay from the actual exposure; the chemical conversion of nitrogen dioxide in to nitric acid in the body is relatively slow (Meditext 2000).

Both acute and chronic effects have been identified in the pulmonary system following an acute exposure to nitrogen oxides. Typically the symptoms are mild-a slight cough, fatigue, and nausea. More serious symptoms may develop within 1 or 2 hours following the exposure; however, limited data suggests that airway restrictions may occur up to 4 weeks after the exposure. The delayed symptoms include: dyspnea (difficult, labored or uncomfortable breathing), tachypnea (rapid breathing), tachycardia (rapid heart rate), fine crackles and wheezing (abnormal sounds made by air moving in and out of the lungs), cyanosis (skin color change as a result of a change in the tissue's oxygen level), and signs of pulmonary edema (fluid accumulation in the lungs). Depending on the exposure, symptoms may subside within 2 to 3 weeks following the exposure, resulting in complete recovery. However, some amount of pulmonary function impairment is possible (Meditext 2002).

Chronic exposure to low concentrations of nitrogen oxides may aggravate asthma and allergic conditions. Reduced pulmonary function including reduced vital capacity, reduced maximum breathing capacity, reduced lung compliance, and increased residual volume, has been documented; however, the concentration or time of exposure was not reported. Studies of the effect of nitrogen dioxide concentrations normally found in air pollution do not conclusively link that level of nitrogen dioxide to health effects. Erosion of dental enamel has also been reported as a result of chronic exposure (Meditext 2000).

Nitrogen dioxide's odor can be detected at concentrations as low as 0.11 ppm. Acute symptoms begin to appear at approximately 13 ppm; however, some studies indicate asthmatics may experience increased airway reactivity at lower concentrations (0.5 to 3 ppm). In laboratory studies, emphysematous lesions were produced in the lungs of mice exposed to 10 ppm nitrogen dioxide for 2 hours/day, 5 days/week, for up to 30 weeks. In other laboratory studies, corneal opacities (clouding on the cornea of the eye) occurred in rabbits exposed to 70 ppm nitrogen dioxide, but not 20 ppm for 4 hours. Concentrations in the range of 60 to 150 ppm may cause immediate coughing and burning in the chest. The data is limited, but death is estimated to occur at concentrations above 100 ppm (Meditext 2000).

Nitrogen dioxide in air has been reported to damage certain types of vegetation. The degree of damage depends on the concentration of nitrogen dioxide, the duration of the exposure and the plant species. Vegetative damage was reported to occur after a 4-hour exposure to concentrations of 2 ppm. Leaf spotting was reported after a 48-hour exposure to concentrations of 1 ppm. Reductions in growth and yield of tomatoes, oranges, and Kentucky bluegrass were reported at concentrations of 0.1 to 0.25 ppm. In addition, chronic nitrogen dioxide exposure has been reported to fade dyes on cotton and rayon (0.05 ppm) and cause yellowing of white fabric (0.2 ppm) (UDEQ 2001a).

The average indoor air concentration of nitrogen dioxide in US home with gas appliances ranges from 0 to 0.1 ppm. The average ambient concentration of nitrogen dioxide in industrialized cities around the world ranges from 0.04 to 0.8 ppm. The average emission rate for nitrogen oxide and nitrogen dioxide in industrialized cities ranges from 56,000 to 440,000 tons/yr (HDSB 2003). Based on the amount of TNT annually produced at VAAP, the amount of nitrogen oxide and nitrogen dioxide likely emitted by VAAP would be much less; especially from 1953 when emissions controls were installed and run until the end of TNT production. Based on this brief review of data and reported plant and fabric damage, the average concentration of nitrogen oxide and nitrogen dioxide in the area surrounding VAAP was likely less than 1 ppm.

Air concentrations can greatly vary from an average value at a single measuring location due to variation in wind speed, wind direction or emission rates. The average concentration over a 1-hour time period for 214 different air quality monitoring stations in the US ranged from 0.02 to 0.05 ppm for nitrogen dioxide, whereas the maximum 1-hour concentration for these locations was 0.5 ppm (HDSB 2003). This suggests that the maximum concentration may be as much as 10 times higher than the average concentration. Using this assumption, the maximum concentrations around VAAP were likely less than 10 ppm.

Nitric acid
Nitric acid is colorless to yellow or brownish-red with a characteristic choking odor (Hazardtext 1989). Coloration is influenced by the type and quantity of nitrogen oxide species mixed with the nitric acid. Nitric acid can stain woolen fabric bright yellow and corrodes almost all metals, except gold (Meditext 1988a).

Nitric acid is a strong irritant. Acute exposure can cause headache, fatigue, cough, dryness of the throat and nose, chest pain, and dyspnea; symptoms may be delayed for up to 72 hours. Skin exposed to nitric acid may cause dermatitis or stain the skin yellow to yellowish-brown. Pulmonary edema and chemical pneumonitis can occur after severe exposure (Meditext 1988a).

If the exposure occurs in conjunction with nitrogen oxide, there is some risk of methemoglobin formation (a form of reduced oxygen carrying ability of the blood) in the mother and fetus. The most serious health effects would be for the fetus; possibly including neurological defects or developmental delays and stillbirths. Exposure during the final trimester of pregnancy would be of most concern because that's when fetal oxygen demand is greatest (Meditext 1988a). Exposure concentrations for concern, however, were not provided in the literature reviewed.

Prolonged or chronic exposure to nitric acid may be associated with pulmonary fibrosis (an illness of the lung where air sacs are gradually replaced by scar tissue), chemical pneumonia (inflammation of the lungs causing breathing difficulty), and bronchitis (inflammation of the air passages to the lungs). Prolonged exposure can also cause yellow discoloration or erosion of teeth; however tooth erosion is thought not to be as frequent as from exposure to sulfuric or hydrochloric acids (Meditext 1988a).

Air concentrations between 0.097 and 0.19 ppm have been reported to elicit some pulmonary function responses in adolescent asthmatics, but not healthy adults (HSDB 1998). Laboratory studies indicate rats, mice, and guinea pigs chronically exposed to 4 ppm of nitric acid in air had no apparent health effects. Air concentrations of approximately 13 ppm have been linked to respiratory system irritation. Laboratory studies indicate that rats experienced no apparent health effects following a single exposure to concentrations of 25 ppm. Concentrations between 50 to

150 ppm are reported to cause bronchitis or pneumonia; concentrations of 100 ppm are considered to be immediately dangerous to life or health (Meditext 1988a).

Sulfur dioxide (SO₂)
Sulfur dioxide is a colorless gas with an irritating pungent odor (NIOSH 1997). It is emitted by a variety of industrial activities including operations burning coal or oil (ATSDR 1998a) and as a result is a common air pollutant. Typical outdoor concentrations range from 0 to 1 ppm (ATSDR 1998a).

Concentrations found in occupational environments vary with industry and work practice. Reported occupational air concentrations ranged from 1 to 10 ppm in industrial environments using sulfur dioxide (IARC 1997). Current Occupational Safety and Health Administration (OSHA) regulations require work place concentrations of sulfur dioxide to be less than 5 ppm. The National Institute of Occupational Safety and Health (NIOSH) recommends a time-weighted average concentration of 2 ppm for an 8-hour work day. At the time VAAP was operational, the actual concentrations were likely higher than the current regulations permit or recommend.

Short-term exposures to high levels of sulfur dioxide can be life-threatening; concentrations of 100 ppm are considered to be immediately dangerous to life and health (ATSDR 1998a). Concentrations in this range are not normally found in the environment; they tend to result from occupational or other types of accidents. Studies involving healthy non-asthmatics suggest that sulfur dioxide concentrations of 1 ppm are not expected to cause adverse health effects. Asthmatics may be more sensitive when exercising. Some studies suggest that concentrations as low as 0.25 ppm may lead to brochoconstriction, wheezing, and increased respiratory resistance (ATSDR, 1998a). Factors, such as exercise and breathing cold air, can exacerbate the respiratory effects of sulfur dioxide (ATSDR, 1998a).

Several researchers have attempted to identify if a relationship exists between occupational or environmental exposure to sulfur dioxide and cancer. While an increased cancer incidence has been measured for workers in many industries where sulfur dioxide exposure is possible; any measured increases in cancer incidence appears to be more closely related to the other chemicals used in these industries. One study using mice indicated that short, frequent exposures to extremely high concentrations of sulfur dioxide (approximately 500 ppm) might be related to a higher incidence of lung tumors. However additional studies are necessary to identify if the observations truly represent carcinogenicity of sulfur dioxide, and, more importantly, if carcinogenicity could occur at concentrations measured under actual environmental or occupational conditions (ATSDR 1998a).

Sulfur dioxide in air has been reported to damage vegetation. Concentrations of 0.2 ppm for a 3-hour exposure, 0.5 ppm for a 1-hour exposure, and 1 ppm for a 5-minute exposure were reported to visibly injury sensitive vegetation in humid regions. The odor threshold for sulfur dioxide is approximately 0.5 ppm. Concentrations of 0.5 ppm for a 10-minute exposure were reported to cause increase airway resistance in exercising asthmatics while concentrations of 1 ppm for 10 minutes were reported to increase airway resistance for asthmatics at rest. In healthy adults, concentrations of 8, 20, and 400 ppm were reported to cause throat irritation, eye irritation, coughing; lung edema; and bronchial inflammation, respectively (UDEQ 2001b).

Sulfur trioxide
Sulfur trioxide reacts rapidly with water to form sulfuric acid. As a result, sulfur trioxide quickly reacts with moisture in the air or human body (ATSDR 1998b). For this reason, health effects of sulfur trioxide would be the same as those described for sulfuric acid.

Sulfuric acid
Sulfuric acid may exist as a mist, vapor or gas, but is most commonly found as a mist because it does not easily volatilize (CCOHS, 1998) and tends to readily absorb to water droplets in the air. As a liquid, sulfur acid is colorless to dark-brown (NIOSH 1997).

Most health effects reported from brief exposures to high concentrations of sulfuric acid are related to respiratory system irritation and the severity of the symptoms seems to dissipate after the exposure ends. Human volunteers exposed to sulfuric acid for 5 to 15 minutes noticed no odor or irritation at concentrations below 0.2 ppm. The sulfuric acid became noticeable to all of the volunteers at 0.6 ppm; some of the volunteers found exposures at 1 ppm to be objectionable. In another study, human volunteers were exposed for 30 minutes to 1 hour at concentrations of 8 ppm (dry mist) or 4 ppm (wet mist). All subjects experienced irritation of the upper airways and signs of bronchial obstruction; these symptoms persisted for several days with two of the subjects. One report of a worker overcome by sulfuric acid fumes in a closed space indicated that there was injury to the upper airways and fluid accumulation and bleeding in the lungs. Most lung function tests were normal for the worker 6 weeks after the exposure (CCOHS 1998).

Sulfuric acid is commonly used in many industries. The average occupational exposures are typically below those described in the human volunteer tests or workplace accidents. Average exposures above 0.1 ppm have been measured for industrial processes using sulfur acid to pickle, electroplate or otherwise treat metals. Lower exposures are usually found in processes used to manufacture lead-acid batteries and phosphate fertilizer (IARC 1992).

Occupational exposure to acid mists has been related to a variety or cancer and non-cancer health effects (IARC 1992), including: bronchitis, emphysema and frequent respiratory infections (Meditext 1988b). The type and severity of health effects depend on a variety of factors, including: size of the aerosol particle, sulfuric acid concentration, humidity at the work site and in the respiratory tract, and where the particle is deposited within the respiratory system (CCOHS 1998; ATSDR 1998b). Growth of sulfuric acid aerosols due to contact with the higher humidity in the respiratory tract could potentially allow the aerosols to penetrate deeper into the lung than inert particles of the same size (ATSDR 1998b). Health effects reported for workers in these environments include dental erosion, and cancer and non-cancer respiratory conditions (CCPHS 1998).

Sulfuric acid mist can cause lacrimation (tearing) and conjunctivitis (inflammation) of the eye. Chronic exposure to concentrations of 3.3 to 8.6 ppm has been reported to cause discoloration, etching, or erosion of tooth enamel. The central and lateral incisors (front four teeth on the upper and lower jaw) are most likely to be affected (Meditext 1988b).

The International Agency for Research on Cancer (IARC 1992) indicated that several studies have linked sulfuric acid exposure to an increased rate of laryngeal and lung cancer. The evaluation concluded that there is sufficient evidence that occupational exposure to strong inorganic acid mists containing sulfuric acid is carcinogenic. The incidence rate ratios for laryngeal cancer ranged from 2.2 to 13.4; higher cancer incidence rates were linked to higher sulfuric acid exposure. For lung cancer, ratios ranged from 1.36 to 2.0 (DHHS 2002). Results from many of these studies, however, may have been confounded by exposure to other occupational chemicals.

Other, non-cancer, health effects were identified for occupational exposure to acid mists. These include irritation of the mucous epithelia, dental erosion, and symptoms and changes in pulmonary function. Asthmatics appear to be at particular risk for pulmonary effects (IARC, 1992). Results of studies with animal and human (asthmatics and non-asthmatics) volunteers suggest that adverse non-cancer health effects are uncommon at sulfuric acid concentrations less than or equal to 0.02 ppm; however, concentrations of 0.25 ppm did potentiate bronchoconstriction (ATSDR 1998b; Meditext 1988b). Asthmatics may develop transient bronchospasm at concentrations as low as 0.0125 to 0.025 ppm. Concentrations of 0.09 ppm caused an increased respiration rate in healthy volunteers (Meditext 1988b).

Exposure Summary
Based on the relative amount of each compound emitted, ATSDR created a figure which estimates the relative health effects possible from each of the compounds likely present in the clouds (Figure C-1). The chart is based on information from residents describing damage to clothing and vegetation and a literature review of potential health effects.

The results of this analysis indicate that clothing and vegetation damage could have resulted from exposure to compounds released during the TNT production process. Short-term health effects could have been experienced by people in the immediate vicinity of the cloud. Sensitive individuals may have experienced the effects sooner and the health effects may have been more pronounced.

Evaluating if long-term health effects would be expected from the clouds is impossible because too little is known about the actual concentrations, the frequency and the duration of the exposure. The majority of the compounds emitted are also found in the emissions from other industries and vehicle traffic. Long-term health effects would likely be influenced by combination of releases from VAAP and these other sources.

Figure C-1: Potential Exposure Effects Identified in teh Literature Review to Compounds Released during TNT

References

Amerada Hess 2000. Material Safety Data Sheet Sulfur. March 2000. Available at http://www.hess.com/about/msds/sulfur_6192_clr.pdf. Accessed on August 27, 2003.

ATSDR. 1998a. Toxicological Profile for Sulfur Dioxide. Department of Health and Human Services. December 1998.

ATSDR. 1998b. Toxicological Profile for Sulfur Trioxide and Sulfuric Acid. Department of Health and Human Services. December 1998.

ATSDR. 2002. ToxFAQs for Nitrogen Oxides (Nitric Oxide, Nitrogen Dioxide, etc.). Department of Health and Human Services. April 2002. Available at: http://www.atsdr.cdc.gov/tfacts175.html. Accessed on September 3, 2002.

Canadian Centre for Occupational Health and Safety (CCOHS). 1998. Health Effects of Sulfuric Acid. January 15, 1998. Available at: http://www.ccohs.ca/oshanswers/chemicals/chem_profiles/sulfuric_acid/health_sa.html. Accessed on July 17, 2003.

Department of Health and Human Services (DHHS). 2002. Strong Inorganic Acid Mists Containing Sulfuric Acid in Report on Carcinogens, Tenth Edition. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. December, 2002. Available at: http://ehp.niehs.nih.gov/roc/tenth/profiles/s164sulf.pdf. Accessed on July 28, 2002.

EPA. 1983. AP-42, Fifth Edition, Volume 1 Chapter 6, Organic Chemical Process Industry, Section 6.3 Explosives. May 1983. Available at: http://www.epa.gov/ttn/chief/ap42/ch086. Accessed on August 27, 2003.

EPA. 1998a. AP-42, Fifth Edition, Volume 1 Chapter 8: Inorganic Chemical Industry, Section 8.8 Nitric Acid. February 1998. Available at: http://www.epa.gov/ttn/chief/ap42/ch08. Accessed on July 10, 2003.

EPA. 1998b. AP-42, Fifth Edition, Volume 1 Chapter 8: Inorganic Chemical Industry, Section 8.10 Sulfuric Acid. February 1998. Available at: http://www.epa.gov/ttn/chief/ap42/ch08. Accessed on July 10, 2003.

Hazardous Substances Data Bank (HSDB). 1998. Nitric Acid. National Library of Medicine, Department of Health and Human Services. Last revised December 1999. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on September 5, 2003.

Hazardous Substances Data Bank (HSDB). 2003. Nitrogen Dioxide. National Library of Medicine, Department of Health and Human Services. March 2003. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on September 4, 2003.

Hazardtext. 1989. Nitric Acid. Last revised December 1999. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on September 5, 2003.

International Agency for Research on Cancer (IARC). 1992. Summary of Data Reported and Evaluation in Occupational Exposures to Mists and Vapours from Sulfuric Acid and Other Strong Inorganic Acids. Volume 54. Page 41. Available at: http://193.51.164.11/htdocs/monographs/vol54/01-mists.htm. Accessed on July 28, 2003.

Meditext. 1988a. Nitric Acid. Meditext Medical Management. Last revised October 1998. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on September 5, 2003.

Meditext. 1988b. Sulfuric Acid. Meditext Medical Management. Last revised October 1995. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on July 16, 2003.

Meditext. 2000. Nitrogen Dioxide. Meditext Medical Management. Last revised February 2002. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on September 3, 2003.

Meditext. 2002. Nitric Oxide. Meditext Medical Management. Last revised August 2002. Available at: http://csi.micromedex.com/fraMain.asp?Mnu=0. Accessed on September 3, 2003.

Montana Sulphur and Chemical Company 1977. Molten Sulfur MSDS. July 1977. Available at: http://montananasulphur.com/molten_sulphur.htm. Accessed on July 10, 2003.

National Institute for Occupational Safety and Health (NIOSH). 1997. NIOSH Pocket Guide to Chemical Hazards. Department of Health and Human Services. June 1997.

Utah Department of Environmental Quality (UDEQ). 2001a. Nitrogen Dioxide (NO2). Utah Department of Environmental Quality, Division of Air Quality. December 4, 2001. Available at: http://www.eq.state.ut.us/EQAMC/No2.htm. Accessed on September 5, 2003.

Utah Department of Environmental Quality (UDEQ). 2001b. Sulfur Dioxide (NO2). Utah Department of Environmental Quality, Division of Air Quality. December 4, 2001. Available at: http://www.deq.state.ut.us/EQAMC/So2.htm. Accessed on September 5, 2003.

Appendix D : Estimates of Human Exposure Doses and Determination of Health Effects

The Agency for Toxic Substances and Disease Registry (ATSDR) reviewed past, current, and planned activities at the Volunteer Army Ammunition Plant (VAAP) to identify how people living and working at VAAP may be exposed to contaminants released to the environment. ATSDR identified four potential exposure situations:

Past exposure to airborne contaminants.
Past exposure to groundwater contaminants in off-site private wells.
Past, current, and future exposure to contaminants in on-site surface soil.
Past, current, and future exposure to contaminants in on-site surface water and sediment.

ATSDR also reviewed the environmental data for each of these pathways to identify the chemicals to which people may have been or may be exposed. ATSDR determined that insufficient data were available to evaluate exposures to airborne contaminants and groundwater contaminants in off-site private wells. These pathways pose an indeterminate public health hazard for past exposures. On-site soil, surface water, and sediment data were compared to ATSDR's health based comparison values (CVs). CVs are contaminant concentrations below which no adverse health effects would be expected. CVs are not thresholds for adverse effects; rather contaminants found above CVs are evaluated further. This appendix details the further evaluations of contaminants found above CVs in on-site soil, surface water, and sediment.

Deriving Exposures Doses

After identifying contaminants in site media above CVs and identifying potential pathways of exposure, ATSDR further evaluates exposures to detected contaminants considering information about exposures combined with scientific information from the toxicologic and epidemiologic literature. ATSDR estimates exposure doses, which are estimates of how much contaminant a person is exposed to on a daily basis. Variables considered when estimating exposure doses include the contaminant concentration in the environmental media, the exposure amount (how much of the substance the person was actually exposed to), the exposure frequency (how often), and the exposure duration (how long).

Evaluating Potential Health Hazards

The estimated exposure doses can be used to evaluate potential noncancer and cancer effects associated with contaminants detected in site media. When evaluating noncancer effects, ATSDR compares the estimated exposure dose to standard toxicity values, including ATSDR's minimal risk levels (MRLs) and the U.S. Environmental Protection Agency's (EPA) reference doses (RfDs), to evaluate whether adverse effects may occur. The chronic MRLs and RfDs are estimates of daily human exposure to a substance that is likely to be without appreciable risk of adverse noncancer effects over a specified duration. The chronic MRLs and RfDs are conservative values, based on the levels of exposure reported in the literature that represent no-observed-adverse-effects levels (NOAEL) or lowest-observed-adverse-effects-levels (LOAEL) for the most sensitive outcome for a given route of exposure (e.g., dermal contact, ingestion). Uncertainty (safety) factors are applied to NOAELs or LOAELs to account for variation in the human population and uncertainty involved in extrapolating human health effects from animal studies. ATSDR also reviews the toxicologic literature and epidemiology studies to further evaluate the evidence presented that might increase or decrease the likelihood of adverse health effects under site-specific exposure conditions.

ATSDR also evaluates the likelihood that site-related contaminants will cause cancer in people who would not otherwise develop it. As an initial screen, ATSDR calculates a theoretical increase of cancer cases in a population over a lifetime of exposure using EPA's cancer slope factors (CSFs), which represent the relative potency of carcinogens. This is accomplished by multiplying the calculated exposure dose by a chemical-specific CSF. CSFs are developed using data from studies of animals or humans exposed to known doses of a particular chemical. Because CSFs are derived using mathematical models which apply a number of uncertainties and conservative assumptions, risk estimates generated by using CSFs tend to be overestimated. Although no risk of cancer is considered acceptable, it is impossible to achieve a zero cancer risk. Consequently, ATSDR often uses a range of 10-4 to 10-6 estimated lifetime cancer risk (1 new case in 10,000 to 1,000,000 exposed persons), based on conservative assumptions about exposure, to determine the likelihood of excess cancer resulting from this exposure.

ATSDR also compared an estimated lifetime exposure dose to available cancer effects levels (CELs), including the effect levels seen in the study used to derive the CSF. An estimated lifetime exposure dose is generally defined as a dose that produces significant increases in the incidence of cancer or tumors. The CEL is the lowest dose of a chemical in a study, or group of studies, that was found to produce increased incidences of cancer (or tumors). In addition, genotoxicity studies are also reviewed to further understand the extent to which a chemical might be associated with cancer outcomes. This process enables ATSDR to weigh the available evidence in light of uncertainties and offer perspective on the plausibility of harmful health outcomes under site-specific conditions.

Estimated Exposure Doses for Incidental Ingestion of On-Site Soil

Explosives, volatile organic compounds (VOCs), polyaromatic hydrocarbons (PAHs), pesticides, polychlorinated biphenyls (PCBs), and inorganics elements were detected in on-site soil in industrial and/or future recreational areas of VAAP. The primary exposure pathway of concern is incidental ingestion of soil by on-site workers (adults) in industrial areas and recreational users (adults and children) in future recreational areas. As such, ATSDR derived exposure doses for soils in recreational areas, VAAP-2 (a mixed industrial and recreational area based on reuse plans), and industrial areas (excluding VAAP-32). At VAAP-32, substantially elevated contaminant concentrations, as compared to remaining portions of VAAP, were reported in soil samples, however the sample depth could not be clearly. As such, ATSDR concluded that insufficient data were available to further refine dose estimates and draw accurate conclusions regarding past surface soil exposures at VAAP-32.

Site-specific information about exposure was not available; therefore, ATSDR used standard default assumptions when deriving doses. These assumptions are considered protective of the general population and may overestimate actual exposures. ATSDR assumed that people would ingest only soil containing the maximum detected concentrations of contaminants. ATSDR also assumed that an adult using VAAP for recreation might incidentally ingest 100 milligrams (mg)/day of soil a day (EPA 1997), which is the default rate used when evaluating soil exposures. ATSDR also applied the default value for a child using VAAP for recreation (200 mg/day). For on-site workers in industrial areas, ATSDR assumed that half of the default soil ingestion rate would occur on-site (50 mg/day). These are likely conservative assumptions because people are not likely to contact this amount of soil from the same location on a daily basis. These protective assumptions enable ATSDR to evaluate the likelihood, if any, that detected levels of contaminants could cause harm to on-site workers or recreational users.

Tables D-1 through D-4 summarize the estimated exposure doses to contaminants in the soil future recreational areas, VAAP-2 (mixed industrial and recreational area), and industrial areas at VAAP. Estimated exposure doses were calculated using the following equation and assumptions:

where:

Conc.:	Maximum contaminant concentration in soil (mg/kilogram [kg] or parts per million [ppm])
IR:	Ingestion rate: 50 mg/day for an on-site worker; 100 mg/day for an adult; 200 mg/kg for a child (EPA 1997)
CF:	Conversion factor of 10-6 kg/mg
EF:	Exposure frequency (exposure events per year of exposure): 5 days/week for 50 weeks/year (250 days) for an on-site worker; 5 days/week for 39 weeks/year (195 days) for adult and child recreational users
ED:	Exposure duration or the duration over which exposure occurs: 30 years for an adult; 5 years for a child
BW:	Body weight: 71.8 kg (154 pounds) for an adult; 15.4 kg (34 pounds) for a child (EPA 1997)
AT:	Averaging time or the period over which cumulative exposures are averaged: 10,950 days (365 days/year for 30 years) for an adult and non-cancer effects; 1,825 (365 days/year for 5 years) for a child; 25,550 days (70 years x 365 days/year) for an adult and cancer effects

PAHs, Aroclor-1254 (a PCB), and metals were detected above CVs in soil at areas of VAAP designated for recreational reuse. At VAAP-2, which is proposed for mixed recreational and industrial reuse, PAHs, pesticides, PCBs, and metals were found above CVs. Industrial reuse areas of VAAP, excluding VAAP-32, contained PAHs, pesticides, PCBs, and metals at concentrations above CVs.

ATSDR estimated exposure doses for each of these scenarios: contact with soil by adults and children in recreational reuse areas (Table D-1), contact with VAAP-2 soil during recreation (adults and children, Table D-2) and industrial (workers only, Table D-3) use, and contact with soil by workers only in industrial reuse areas, excluding VAAP-32 (Table D-4).

Noncancer Effects

For contaminants found above CVs, ATSDR estimated doses for noncancer effects, as appropriate. For PAHs and some PCBs, potential cancer effects are a greater concern than noncancer effects. As such, research has focused on understanding doses and exposures related to cancer outcomes. No health guidelines for noncancer outcomes are available. PAHs and carcinogenic PCBs are considered in ATSDR's evaluation of cancer effects.

Estimated doses for noncancer effects resulting from exposure to contaminants in soil, for the most part, were below health guidelines. Estimated doses below health guidelines indicate that no adverse health effects are expected to occur. Doses found above health guidelines, however, require further evaluation before a conclusion regarding potential health effects can be made. For soil at VAAP, estimated doses were above health guidelines for Aroclor-1254 (adults, children and workers), heptachlor epoxide (children), arsenic (adults, children, and workers), chromium (adults, children, and workers), iron (children), and thallium (adults, children, and workers).

Aroclor-1254: The chronic oral MRL for Aroclor-1254 is 0.00002 milligrams of contaminant/kilogram body weight/day (mg/kg/day). Estimated doses above the MRL calculated using the exposure assumptions described above were 0.00002 mg/kg/day for child in a recreational reuse area; 0.0002, 0.002, and 0.0001 mg/kg/day for adults, children, and workers at VAAP-2; and 0.0004 mg/kg/day for workers in industrial reuse areas. The chronic oral MRL was derived from a LOAEL of 0.005 mg/kg/day seen in adult monkeys exposed to Aroclor-1254 for 23 and 55 months. Immunological effects (i.e., reduced antibody levels at 0.005 mg/kg/day and decreased numbers of T-cells at 0.08 mg/kg/day) were identified as adverse effects from Aroclor-1254 exposure. None of the derived doses at VAAP exceeded the LOAELs (ATSDR 2000c). In addition, areas with the maximum detected Aroclor-1254 concentration are slated for further investigation and remediation, as needed, to protect public health. Because doses were estimated assuming people were continuously exposed to the highest detected levels, a review of the toxicity literature found that these doses were below LOAELs, and further study and remediation is scheduled at VAAP, ATSDR concluded that incidental ingestion of Aroclor-1254 in soil is not expected to result in adverse health effects for adults, children, or workers.

Heptachlor epoxide: Only the estimated dose for children exposed to the maximum heptachlor epoxide concentration in soil during recreational use of VAAP-2 (0.00002 mg/kg/day) exceeded the RfD of 0.00001 mg/kg/day, and only slightly. EPA derived the RfD based on a 60-week study in dogs given heptachlor epoxide in their diets. The study established a LOAEL of 0.0125 mg/kg/day for an observed increased liver-to-body weight ratio. An uncertainty factor of 1,000 was applied to reach the RfD (EPA 2003). The doses estimated for VAAP are at least 600 times lower than the LOAEL. In 1993, ATSDR released the Toxicological Profile for Heptachlor/Heptachlor Epoxide. ATSDR did not derive MRLs, but complied available toxicological information about health effects resulting from oral exposure to heptachlor and heptachlor epoxide. The lowest NOAEL reported was 0.5 mg/kg/day in a 4-week study in rats. This NOAEL is 25,000 times higher than the estimated dose at VAAP (ATSDR 1993). ATSDR concluded that children exposed to heptachlor epoxide in soil at VAAP-2 are unlikely to experience adverse health effects because doses were estimated using conservative assumptions, were below the LOAEL and NOAEL, and further study and remediation is scheduled at VAAP-2.

Arsenic: Estimated doses above the arsenic MRL (0.0003 mg/kg/day) were 0.0008 mg/kg/day for child in a recreational reuse area and 0.001, 0.01, and 0.0008 mg/kg/day for adults, children, and workers at VAAP-2. ATSDR derived the chronic MRL based on a 1977 epidemiological study of Blackfoot disease and dermal lesions seen in Taiwanese farmers exposed to arsenic (170 to 800 parts per billion [ppb]) in their drinking water. The NOAEL in this study was 0.0008 mg/kg/day and the LOAEL was 0.014 mg/kg/day. Other studies of arsenic exposure in humans have reported dermal effects at chronic dose levels of 0.01 to 0.1 mg/kg/day. (ATSDR 2000a). Conservatively derived doses for VAAP did not exceed the LOAEL of 0.014 mg/kg/day. A number of uncertainties exist in directly comparing health effects from exposure to arsenic in water versus arsenic in soil. Arsenic has varying toxicity depending on the form it takes-organic or inorganic. Arsenic in water is typically found in its inorganic and more toxic form, whereas arsenic is found in both organic and inorganic forms in soil. ATSDR assumed that all arsenic detected in soil at VAAP was the more toxic, inorganic form. Unlike arsenic in soil, arsenic in water is very well absorbed across the human gastrointestinal tract. Most arsenic in water will enter the bloodstream, whereas a substantial portion of the arsenic in soil will pass directly through the body without entering the bloodstream. Uncertainties of the 1977 study should also be considered: lack of individual exposure information, no accounting for arsenic exposure from other sources, and the poor nutritional status of the study population. These weakness and uncertainties may limit the study's usefulness in evaluating health effects for adults, children, and workers exposed to arsenic in soil. In a 1998 study, researchers reanalyzed the data from the 1977 study and considered dietary arsenic intake. They concluded that, the 1977 study would have identified a NOAEL of 0.016 mg/kg/day if a 50 micrograms (ug)/day intake of arsenic from food was considered (ATSDR 2000a). All doses estimated for VAAP were below this revised NOAEL.

Furthermore, various studies indicate that at low level exposures, arsenic compounds are detoxified (or metabolized)-that is, changed into less harmful forms-and then excreted in the urine. At higher levels of exposures, our bodies' capacity to detoxify arsenic may be exceeded. Certain studies suggest that the dose at which this happens is somewhere between 0.25 and 0.5 mg/kg/day, which is higher than the doses estimated for VAAP (ATSDR 2000a). Based on the toxicity information, the conservative assumptions used to estimate doses, and planned remediation, ATDR concluded that incidental ingestion of soil at VAAP is not expected to result in adverse health effects for adults, children, or workers.

Chromium: EPA established an RfD of 0.003 mg/kg/day for chromium VI-the most toxic form of chromium. At VAAP, estimated doses exceeding the RfD were 0.009, 0.08, and 0.006 for adults, children, and workers at VAAP-2. EPA derived the RfD for chromium VI based on a 1-year drinking water study in rats where a NOAEL of 2.5 mg/kg/day was identified. An uncertainty factor of 900 was applied to this NOAEL to derive the RfD (EPA 2003). The NOAEL is at least 35 times higher than our estimated doses for exposure to children using VAAP-2 for recreational use.

Similar to arsenic, chromium is found in a number of different forms in the environment. Because no information about the form of chromium detected was available, ATSDR assumed that all the chromium found at VAAP was present in its more toxic form-chromium VI. However, chromium in soil is predominantly found as chromium III-a less toxic form (ATSDR 2000b). Based on the conservative exposure assumptions, assumptions about the form of chromium, toxicity information, and planned investigations and remediation at VAAP-2, ATSDR concluded that no adverse health effects were expected from incidental ingestion of soil at VAAP.

Iron: Iron is an important mineral found naturally in the environment. Without sufficient iron, the body cannot produce enough hemoglobin or myoglobin to sustain life. Iron deficiency anemia is a condition occurring when the body does not receive enough iron (ANR 2001). Doses for children exposed to iron in recreational areas of VAAP (0.5 mg/kg/day) and at VAAP-2 (1 mg/kg/day) exceeded the EPA provisional RfD of 0.3 mg/kg/day. The oral health guideline for iron is based on dietary intake data collected as part of EPA's Second National Health and Nutrition Examination Survey in which no adverse health effects were associated with average iron intakes of 0.15 to 0.27 mg/kg/day. These levels were determined to be sufficient for protection against iron deficiency, but also low enough to not cause harmful health effects (EPA 2001).

Although conservatively derived doses for children at VAAP exceed the NOAEL, iron is not generally considered to cause harmful health effects except when swallowed in extremely large doses, such as in the case of accidental drug ingestion. Acute iron poisoning has been reported in children less than 6 years of age who have accidentally overdosed on iron-containing supplements for adults. According to the FDA, doses greater than 200 mg per event could poison or kill a child (FDA 1997). To reach this exposure level, a child would need to consume over 2,500 mg of soil containing the maximum iron concentration found in recreational areas or 950 mg of soil containing the maximum iron concentration found in VAAP-2. Studies have found that most children consume only 200 mg or less of soil over the course of a day. It is unlikely that a child would consume at least 5 times this amount from a single location during recreational use of VAAP. Further, the body uses a homeostatic mechanism to keep iron burdens at a constant level despite variations in the diet (Eisenstein and Blemings 1998). As such, no adverse health effects are expected in children exposed to iron in soil at VAAP.

Thallium: Conservatively estimated doses for exposure to thallium exceed its health guideline (0.00007 mg/kg/day) as follows: children (0.0007 mg/kg/day) and adults (0.00008 mg/kg/day) in recreational areas; adults, children, and workers (0.002, 0.02, and 0.002 mg/kg/day) at VAAP-2. Much of what we know about thallium is from human poisoning cases reports and a relatively sparse animal data set that describe effects associated with various thallium compounds (e.g., thallic oxide, thallium sulfate, or thallium chloride). Only limited amounts of data are available regarding dose-response relationships. EPA Region III reports an RfD of 0.00007 mg/kg/day. A review of the literature identified the lowest reported LOAEL (changes to the testis) to be 0.7 mg/kg/day, based on a 30 to 60 day study in which rats were exposed to thallium sulfate via gavage (i.e., administered directly into their gut). A NOAEL of 0.2 mg/kg/day was reported in a study of rats exposed to thallium sulfate via gavage for 90 days (ATSDR 1992). The highest dose estimated for exposures at VAAP were at least 10 times lowest than the NOAEL reported in the literature and at least 35 times lower than the lowest reported LOAEL. ATSDR concluded that no adverse health effects were likely to result from thallium exposures at VAAP based on a review of the toxicological literature and the assumptions used to overestimate actual risks.

Aroclor-1254 and Aroclor-1260: Estimated doses were 0.00009/0.0002 mg/kg/day for adults at VAAP-2 exposed to Aroclor-1254/Arochlor-1260, 0.0001 mg/kg/day for workers exposed to Aroclor-1260 at VAAP-2, and 0.0002/0.0002 mg/kg/day for workers exposed to Aroclor-1254/Arochlor-1260 in industrial reuse areas. These doses assume that daily exposures occur to the highest detected concentrations of these Aroclors. To derive estimated theoretical excess cancer risks, which were no greater than 5 x 10-4, these doses were multiplied by the CSF for PCBs, which is 2 (mg/kg/day)-1. EPA derived the CSF for PCBs based on two different rats studies. In these studies, study rats were exposed to Aroclor-1254 and Aroclor-1260 at doses ranging from 0.35 to 1.59 mg/kg/day (human equivalent doses) for durations from 52 to 104 weeks. Increases in liver cancers were seen, however the lowest exposure dose was 1,700 times higher than the conservatively estimated cancer doses for exposures at VAAP-2. The lowest CEL reported in the ATSDR toxicological profile for PCBs was 1 mg/kg/day for rats exposed to Aroclor-1254 or Aroclor-1260 in their feed for 2 years. Liver and thyroid tumors were observed. Estimated cancer doses for VAAP are at least 5,000 times lower than this CEL (EPA 2003). In addition, the maximum Aroclor concentrations used to estimate doses were detected at VAAP-1 and VAAP-2, both of which are schedule to undergo additional investigation and remediation to protect public health. As such, ATSDR concluded that contact with Aroclors in soil at VAAP is unlikely to result in an increased risk of cancer based on conservative assumptions applied when estimating doses, a review of the toxicological literature, and ongoing remediation.

Arsenic: Using conservative assumptions, estimated doses were 0.0005 mg/kg/day for adults exposed to arsenic at VAAP-2 and 0.0004 mg/kg/day for workers exposed at VAAP-2. The highest estimated excess theoretical cancer risk (8 x 10-4) was calculated by multiplying the doses with the CSF for arsenic-1.5 (mg/kg/day)-1. Similar to the MRL for arsenic, EPA derived the slope factor based on a 1968 and 1977 epidemiological study Taiwanese farmers exposed to arsenic in drinking water. Other studies of people exposed to inorganic arsenic in drinking water have identified a link between ingestion of inorganic arsenic and cancer (mainly skin cancer); exposure doses for these studies were not provided (EPA 2003, ATSDR 2000a).

As previously discussed, a number of uncertainties exist in directly comparing health effects from exposure to arsenic in water versus arsenic in soil. ATSDR conservatively assumed that all arsenic detected in soil at VAAP was the more toxic, inorganic form. More likely, both forms of arsenic are present in soil. Uncertainties of the epidemiology studies limit their usefulness in comparing drinking water and soil exposures. The lowest CEL reported in the toxicological profile for arsenic is 0.0011 mg/kg/day (EPA 2003; ATSDR 2000a). Conservative doses estimated for VAAP soils were below this level. This study investigated internal cancers in Chileans exposed to arsenic in drinking water at concentrations ranging from 40 to 800 ppb. Researches concluded that the study supports the reported link between arsenic in drinking water and internal cancers (Ferreccio et al 1998).

Various studies indicate that at low level exposures, arsenic compounds are changed into less harmful forms and then excreted in the urine. Certain studies suggest that the dose at which this happens is somewhere between 0.25 and 0.5 mg/kg/day, which is much higher than the dose levels estimated for VAAP (ATSDR 2000a). Based on ATSDR's conservative assumptions and the toxicity data, no increase in cancer is expected from exposure to arsenic in soil at VAAP.

Estimated Exposure Doses for Incidental Ingestion of On-Site Surface Water

Explosives, VOCs, delta-BHC, heptachlor, and inorganics were detected above drinking water CVs in surface water samples collected throughout VAAP. The primary exposure pathway of concern is through incidental ingestion of surface water during recreational use of the streams, such as wading or hiking.

In deriving the exposure doses, ATSDR assumed that people would repeatedly contact the maximum detected contaminant concentrations found anywhere at VAAP. Adults were assumed to ingest 10 milliliters (mL) and children 50 mL during wading (EPA 1989). ATSDR also assumed that people would be directly exposed to the surface water 5 days a week for 39 weeks a year (March through November). These are conservative assumptions because people are not likely to contact only the maximum detected contaminant concentrations on a nearly daily basis. These assumptions enable ATSDR to evaluate the likelihood, if any, that detected levels of contaminants could cause harm to recreational users.

Table D-5 summarizes the estimated exposure doses to contaminants in surface water. Estimated exposure doses were calculated using the following equation and assumptions:

where:

Conc.:	Maximum concentration in surface water (ppm or mg/liter)
IR:	Ingestion rate: 10 mL per day for an adult; 50 mL per day for a child (EPA 1989)
CF:	Conversion factor of 10-6 mL/L
EF:	Exposure frequency (exposure events per year of exposure): 5 days/week, 39 weeks/year (195 days)
ED:	Exposure duration or the duration over which exposure occurs: 30 years for an adult; 5 years for a child
BW:	Body weight: 71.8 kg (154 pounds) for an adult; 15.4 kg (34 pounds) for a child (EPA 1997)
AT:	Averaging time or the period over which cumulative exposures are averaged: 10,950 days (365 days/year for 30 years) for an adult and non-cancer effects; 1,825 (365 days/year for 5 years) for a child; 25,550 days (70 years x 365 days/year) for an adult and cancer effects

Noncancer Effects

For contaminants found above CVs, ATSDR estimated doses for noncancer effects, as appropriate. Estimated doses for noncancer effects resulting from exposure to contaminants in surface water, for the most part, were below health guidelines. Estimated doses below health guidelines indicate that no adverse health effects are expected to occur. Doses found above health guidelines, however, require further evaluation before a conclusion regarding potential health effects can be made. For exposure to on-site surface water, only the estimated dose for children exposed to 2,4-dinitrotoluene was above its health guideline.

2,4-Dinitrotoluene: The estimated dose for children exposed to 2,4-dinitrotoluene in on-site surface water at VAAP was 0.004 mg/kg/day, which slightly exceeds the MRL of 0.002 mg/kg/day. ATSDR derived this MRL based on a NOAEL of 0.2 mg/kg/day identified in a 24-month study in dogs. The LOAEL for this study was 1.5 mg/kg/day. Blood and liver affects were observed at the LOAEL (ATSDR 1998). The dose for children exposed to 2,4-dinitrotoluene is 50 times lower than the NOAEL and 375 times lower than the LOAEL. As such, ATSDR concluded that the estimated exposure doses, designed to overestimate actual exposures, are unlikely to result in adverse health effects.

Cancer Effects

For contaminants found above CVs and considered carcinogens, ATSDR estimated doses for cancer effects. Estimated doses for cancer effects resulting from exposure to contaminants in surface water exposures were below the theoretical excess cancer risk of 10-6. The highest estimated theoretical excess cancer risk was for exposure to 2,4,6-trinitrotoluene (7 x 10-7). Because doses were estimated using conservative exposure assumptions designed to overestimate actual risk and the theoretical excess cancer risks were below 10-6, ATSDR concluded that no adverse cancer risks are likely to be associated with exposure to contaminants in on-site surface water during recreational use.

Estimated Exposure Doses for Incidental Ingestion of On-Site Sediment

PAHs, Aroclor-1260 (a PCB), and inorganics were detected above surface soil CVs in sediment samples collected throughout VAAP. The primary exposure pathway of concern is through incidental ingestion of sediment during recreational use of the streams, such as wading or hiking.

In deriving the exposure doses, ATSDR assumed that people would repeatedly contact the maximum detected contaminant concentrations found anywhere at VAAP. Adults were assumed to ingest 100 mg and children 200 mg of sediment during recreational use of VAAP (EPA 1997). ATSDR also assumed that people would be directly exposed to the sediment 5 days a week for 39 weeks a year (March through November). These are likely conservative assumptions because people are not likely to contact only the maximum detected contaminant concentrations on a nearly daily basis. These assumptions enable ATSDR to evaluate the likelihood, if any, that detected levels of contaminants could cause harm to recreational users.

Table D-6 summarizes the estimated exposure doses to contaminants in the sediment. Estimated exposure doses were calculated using the following equation and assumptions:

where:

Conc.:	Maximum contaminant concentration in sediment (mg/kg or ppm)
IR:	Ingestion rate: 100 mg/day for an adult and 200 mg/day for a child (EPA 1997)
CF:	Conversion factor of 10-6 kg/mg
EF:	Exposure frequency (exposure events per year of exposure): 5 days/week, 39 weeks/year (195 days)
ED:	Exposure duration or the duration over which exposure occurs: 30 yrs for an adult; 5 yrs for a child
BW:	Body weight: 71.8 kg (154 pounds) for an adult; 15.4 kg (34 pounds) for a child (EPA 1997)
AT:	Averaging time or the period over which cumulative exposures are averaged: 10,950 days (365 days/year for 30 years) for an adult and non-cancer effects; 1,825 (365 days/year for 5 years) for a child; 25,550 days (70 years x 365 days/year) for an adult and cancer effects

Noncancer Effects

For contaminants found above CVs, ATSDR estimated doses for noncancer effects, as appropriate. For PAHs and Aroclor-1260, potential cancer effects are a greater concern than noncancer effects. As such, research has focused on understanding doses and exposures related to cancer outcomes. No health guidelines for noncancer outcomes are available. PAHs and PCBs are considered in ATSDR's evaluation of cancer effects.

Estimated doses for noncancer effects resulting from exposure to contaminants in on-site sediment, for the most part, were below health guidelines. Estimated doses below health guidelines indicate that no adverse health effects are expected to occur. Doses found above health guidelines, however, require further evaluation before a conclusion regarding potential health effects can be made. For sediment at VAAP, estimated doses were above health guidelines for arsenic (children), chromium (adults and children), iron (children), and thallium (adults and children).

Arsenic: Based on assumptions, estimated doses above the arsenic MRL (0.0003 mg/kg/day) were 0.0007 mg/kg/day for children exposed to the maximum arsenic concentration found in on-site sediment. As previously discussed, ATSDR derived the chronic MRL based on a 1977 epidemiological study of Taiwanese farmers exposed to arsenic in their drinking water. The NOAEL in this study was 0.0008 mg/kg/day and the LOAEL was 0.014 mg/kg/day. Other studies of arsenic exposure in humans have reported dermal effects at chronic dose levels of 0.01 to 0.1 mg/kg/day. (ATSDR 2000a). A number of study uncertainties, which may bias study result to inflate arsenic toxicity have been identified, as previously mentioned. Nonetheless, the NOAEL in this study is higher than the estimated dose for children exposed to arsenic in sediment. Unlike arsenic in soil, arsenic in water is very well absorbed across the human gastrointestinal tract. Most arsenic in water will enter the bloodstream, whereas a substantial portion of the arsenic in soil will pass directly through the body without entering the bloodstream. In addition to applying conservative exposure parameters (e.g., intake rate, exposure frequency, and exposure duration), assuming that all arsenic in sediment is found in its more toxic, inorganic form further overestimates actual exposure. As such, ATSDR concluded that exposure to arsenic in on-site sediment during recreational use is not expected to result in adverse health effects.

Chromium: EPA established an RfD of 0.003 mg/kg/day for chromium VI-the most toxic form of chromium. At VAAP, estimated doses exceeding the RfD were 0.009 and 0.08 mg/kg/day for adults and children exposed to the maximum detected chromium concentration found in on-site sediment. EPA derived the RfD for chromium VI based on a 1-year drinking water study in rats in which a NOAEL of 2.5 mg/kg/day was identified. An uncertainty factor of 900 was applied to this NOAEL to derive the RfD. The NOAEL more than 30 times higher than the conservatively derived doses for exposure to children. In addition, ATSDR assumed that all chromium found in sediment was present as chromium VI, whereas chromium III-the less toxic form-is typically predominant in soil and sediment (ATSDR 2000b). Based on exposure assumptions and toxicity data, ATSDR concluded that exposure to chromium in sediment is not expected to result in adverse health effects.

Iron: As previously noted, iron is naturally occurring mineral that is required by people to maintain normal body functions (ANR 2001). Doses for children exposed to the maximum detected iron concentration in on-site sediment (2 mg/kg/day) exceeded the EPA provisional RfD of 0.3 mg/kg/day. The oral health guideline for iron is based on dietary intake data collected as part of EPA's Second National Health and Nutrition Examination Survey in which no adverse health effects were associated with average iron intakes of 0.15 to 0.27 mg/kg/day (EPA 2001). Iron, however, is not generally considered to cause harmful health effects except when swallowed in extremely large doses. Acute iron poisoning has been reported in children less than 6 years of age who have accidentally overdosed on iron-containing supplements for adults. According to the FDA, doses greater than 200 mg per event could poison or kill a child (FDA 1997). To reach this exposure level, a child would need to consume over 900 mg of soil containing the maximum iron concentration found in sediment. Studies have found that most children consume only 200 mg or less of soil over the course of a day. Sediment intake would likely be less than that for soil. It is unlikely that a child would consume sediment at over four times this amount from a single location containing the maximum detected iron concentration during recreational use of VAAP. Further, the body uses a homeostatic mechanism to keep iron burdens at a constant level despite variations in the diet (Eisenstein and Blemings 1998). As such, no adverse health effects are expected in children exposed to iron in sediment at VAAP.

Thallium: Estimated doses for exposure to thallium in sediment exceed the health guideline (0.00007 mg/kg/day) for adults (0.0002 mg/kg/day) and children (0.002 mg/kg/day). Only limited data are available regarding dose-response relationships between thallium exposure and adverse health effects. Human poisoning cases reports and a relatively sparse animal data set describing effects associated with various thallium compounds (e.g., thallic oxide, thallium sulfate, or thallium chloride) are the primary sources of data. EPA Region III reports an RfD of 0.00007 mg/kg/day. A review of the literature identified the lowest reported LOAEL (changes to the testis) to be 0.7 mg/kg/day, based on a 30 to 60 day study in which rats were exposed to thallium sulfate via gavage (i.e., administered directly into their guts). A NOAEL of 0.2 mg/kg/day was reported in a study of rats exposed to thallium sulfate via gavage for 90 days (ATSDR 1992). The highest dose estimated for exposures at VAAP were at least 100 times lower than the NOAEL reported in the literature and at least 350 times lower than the lowest reported LOAEL. ATSDR concluded that no adverse health effects were likely to result from thallium exposures at VAAP based on a review of the toxicological literature and the conservative assumptions used to overestimate actual risks.

Cancer Effects

For contaminants found above CVs and considered carcinogens, ATSDR estimated doses for cancer effects. Estimated doses for cancer effects resulting from exposure to contaminants in sediment were below the theoretical excess cancer risk of 10-4. The highest estimated theoretical excess cancer risk was for exposure to arsenic (5 x 10-5). Because doses were estimated using exposure assumptions designed to overestimate actual risk and the theoretical excess cancer risks were below 10-4, ATSDR concluded that no adverse cancer risks are likely to be associated with exposure to contaminants in on-site sediment during recreational use.

References

Agency for Toxic Substance and Disease Registry (ATSDR). 1992. Toxicological Profile for Thallium. Atlanta: US Department of Health and Human Services. July 1992.

ATSDR. 1993. Toxicological Profile for Heptachlor/Heptachlor Epoxide. Atlanta: US Department of Health and Human Services. April 1993.

ATSDR. 1998. Toxicological Profile for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene (Update). Atlanta: US Department of Health and Human Services. December 1998.

ATSDR. 2000a. Toxicological Profile for Arsenic (Update). Atlanta: US Department of Health and Human Services. September 2000.

ATSDR. 2000b. Toxicological Profile for Chromium. Atlanta: US Department of Health and Human Services. September 2000.

ATSDR. 2000c. Toxicological Profile for Polychlorinated Biphenyls (Update). Atlanta: US Department of Health and Human Services. November 2000.

Austin Nutritional Research (ANR). 2001. Reference guide for minerals. Available from: http://www.realtime.net/anr/minerals.html. Last accessed December 1, 2003.

US Environmental Protection Agency (EPA). 1997. Exposure Factors Handbook. 1997 August. http://www.epa.gov/ncea/exposfac.htm.

EPA. 2001. Risk assessment issue paper for: derivation of the provisional RfD for iron (CASRN 7439-89-6) and compounds. National Center for Environmental Assessment. Superfund Technical Support Center.

EPA. 2003. Integrated Risk Information System. Available at: http://www.USEPA.gov/iris/. Last accessed December 1, 2003.

Ferreccio C, Gonzalez Psych C, Milosavjlevic Stat V, Marshall Gredis G, Sancha AM. 1998. Lung cancer and arsenic exposure in drinking water: a case-control study in northern Chile. Cad Saude Publica. 1998;14 Suppl 3:193-8.

US Food and Drug Administration (FDA). 1997. Preventing iron poisoning in children. FDA Backgrounder. January 15, 1997. Available from URL: http://www.cfsan.fda.gov/~dms/bgiron.html. Last accessed December 1, 2003.

Table D-1. Estimated Exposure Doses-Incidental Ingestion of On-Site Soil in Future Recreational Areas
Contaminant	Maximum Concentration (mg/kg)	Estimated Non-Cancer Exposure Dose (mg/kg/day)		Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Contaminant	Maximum Concentration (mg/kg)	Adult	Child	Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Benzo(a)anthracene	6	N/A	N/A	N/A	N/A	0.000002	0.73	1 x 10^-6
Benzo(a)pyrene	6	N/A	N/A	N/A	N/A	0.000002	7.3	1 x 10^-5
Benzo(b)fluoranthene	6.8	N/A	N/A	N/A	N/A	0.000002	0.73	2 x 10^-6
Dibenz(a,h)anthracene	0.78	N/A	N/A	N/A	N/A	0.0000003	7.3	2 x 10^-6
Aroclor-1254	3.3	0.000002	0.00002	0.00002	Chronic oral MRL	0.000001	2	2 x 10^-6
Arsenic	116	0.00009	0.0008	0.0003	Chronic oral MRL	0.00004	1.5	6 x 10^-5
Iron	78,200	0.06	0.5	0.3	NCEA	N/A	N/A	N/A
Manganese	4,200	0.003	0.003	0.02	RfD (non-food value)	N/A	N/A	N/A
Thallium	106	0.00008	0.0007	0.00007	Other	N/A	N/A	N/A
Notes: mg/kg/day milligrams contaminant per kilogram body weight per day; MRL ATSDR minimal risk level NCEA EPA National Center for Environmental Assessment Provisional Value Other Other toxicity value as reported in EPA Region III Risk-Based Concentration Table (April 2003) ppb parts per billion; RfD EPA reference dose. Bold indicates a dose above the non-cancer health guideline or a theoretical excess cancer risk greater than 10^-4.

Table D-2. Estimated Exposure Doses-Incidental Ingestion of On-Site Soil at VAAP-2 under Recreational Use
Contaminant	Maximum Concentration (mg/kg)	Estimated Non-Cancer Exposure Dose (mg/kg/day)		Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Contaminant	Maximum Concentration (mg/kg)	Adult	Child	Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
3,3-Dichlorobenzidine	27	N/A	N/A	N/A	N/A	0.000009	0.45	4 x 10^-6
Benzo(a)anthracene	40	N/A	N/A	N/A	N/A	0.00001	0.73	9 x 10^-6
Benzo(a)pyrene	40	N/A	N/A	N/A	N/A	0.00001	7.3	9 x 10^-5
Benzo(b)fluoranthene	60	N/A	N/A	N/A	N/A	0.00002	0.73	1 x 10^-5
Benzo(k)fluroanthene	21	N/A	N/A	N/A	N/A	0.000007	0.073	5 x 10^-7
Dibenz(a,h)anthracene	4.2	N/A	N/A	N/A	N/A	0.000001	7.3	1 x 10^-5
Indeno(1,2,3-c,d) pyrene	19	N/A	N/A	N/A	N/A	0000006	0.73	4 x 10^-6
4,4'-DDT	27	0.00002	0.0002	0.005	RfD	0.000009	0.34	3 x 10^-6
Dieldrin	0.0505	0.00000004	0.0000004	0.00005	RfD	0.00000002	16	3 x 10^-7
Heptachlor epoxide	2.6	0.000002	0.00002	0.00001	RfD	0.0000008	9.1	8 x 10^-6
Aroclor-1016	0.41	0.0000003	0.000003	0.00007	RfD	0.0000001	2	3 x 10^-7
Aroclor-1221	0.81	N/A	N/A	N/A	N/A	0.0000003	2	5 x 10^-7
Aroclor-1232	0.41	N/A	N/A	N/A	N/A	0.0000001	2	3 x 10^-7
Aroclor-1242	1.88	N/A	N/A	N/A	N/A	0.0000006	2	1 x 10^-6
Aroclor-1248	0.41	N/A	N/A	N/A	N/A	0.0000001	2	3 x 10^-7
Aroclor-1254	280	0.0002	0.002	0.00002	Chronic oral MRL	0.00009	2	2 x 10^-4
Aroclor-1260	592	N/A	N/A	N/A	N/A	0.0002	2	4 x 10^-4
Aluminum	120,000	0.09	0.8	2	Intermediate oral MRL	N/A	N/A	N/A
Antimony	55	0.00004	0.0004	0.004	RfD	N/A	N/A	N/A
Arsenic	1,700	0.001	0.01	0.0003	Chronic oral MRL	0.0005	1.5	8 x 10^-4
Barium	4,200	0.003	0.03	0.07	RfD	N/A	N/A	N/A
Chromium	12,000	0.009	0.08	0.003	Chronic oral RfD (hexavalent)	N/A	N/A	N/A
Iron	210,000	0.2	1	0.3	NCEA	N/A	N/A	N/A
Manganese	37,000	0.03	0.3	0.5	RfD (non-food value)	N/A	N/A	N/A
Thallium	3260	0.002	0.02	0.00007	Other	N/A	N/A	N/A
Zinc	26,000	0.02	0.2	0.3	Chronic oral MRL	N/A	N/A	N/A
Notes: mg/kg/day milligrams contaminant per kilogram body weight per day; MRL ATSDR minimal risk level; ppb parts per billion; RfD EPA reference dose. Bold indicates a dose above the non-cancer health guideline or a theoretical excess cancer risk greater than 10^-4.

Table D-3. Estimated Exposure Doses-Incidental Ingestion of On-Site Soil at VAAP-2 under Industrial Use
Contaminant	Maximum Concentration (mg/kg)	Estimated Non-Cancer Exposure Dose (mg/kg/day)		Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Contaminant	Maximum Concentration (mg/kg)	Adult	Child	Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
3,3-Dichlorobenzidine	27	0.00001	N/A	N/A	N/A	0.000006	0.45	3 x 10^-6
Benzo(a)anthracene	40	N/A	N/A	N/A	N/A	0.000008	0.73	6 x 10^-6
Benzo(a)pyrene	40	N/A	N/A	N/A	N/A	0.000008	7.3	6 x 10^-5
Benzo(b)fluoranthene	60	N/A	N/A	N/A	N/A	0.00001	0.73	9 x 10^-6
Benzo(k)fluroanthene	21	N/A	N/A	N/A	N/A	0.000004	0.073	3 x 10^-7
Dibenz(a,h)anthracene	4.2	N/A	N/A	N/A	N/A	0.0000009	7.3	6 x 10^-6
Indeno(1,2,3-c,d) pyrene	19	N/A	N/A	N/A	N/A	0.000004	0.73	3 x 10^-6
4,4'-DDT	27	0.00001	N/A	0.005	RfD	0.000006	0.34	2 x 10^-6
Dieldrin	0.0505	0.00000002	N/A	0.00005	RfD	0.00000001	16	2 x 10^-7
Heptachlor epoxide	2.6	0.000001	N/A	0.00001	RfD	0.0000005	9.1	5 x 10^-6
Aroclor-1016	0.41	0.0000002	N/A	0.00007	RfD	0.00000008	2	2 x 10^-7
Aroclor-1221	0.81	N/A	N/A	N/A	N/A	0.0000002	2	3 x 10^-7
Aroclor-1232	0.41	N/A	N/A	N/A	N/A	0.00000008	2	2 x 10^-7
Aroclor-1242	1.88	N/A	N/A	N/A	N/A	0.0000004	2	8 x 10^-7
Aroclor-1248	0.41	N/A	N/A	N/A	N/A	0.00000008	2	2 x 10^-7
Aroclor-1254	280	0.0001	N/A	0.00002	Chronic oral MRL	0.00006	2	1 x 10^-4
Aroclor-1260	592	N/A	N/A	N/A	N/A	0.0001	2	2 x 10^-4
Aluminum	120,000	0.06	N/A	2	Intermediate oral MRL	N/A	N/A	N/A
Antimony	55	0.00003	N/A	0.004	RfD	N/A	N/A	N/A
Arsenic	1,700	0.0008	N/A	0.0003	Chronic oral MRL	0.0004	1.5	5 x 10^-4
Barium	4,200	0.002	N/A	0.07	RfD	N/A	N/A	N/A
Chromium	12,000	0.006	N/A	0.003	Chronic oral RfD (hexavalent)	N/A	N/A	N/A
Iron	210,000	0.1	N/A	0.3	NCEA	N/A	N/A	N/A
Manganese	37,000	0.02	N/A	0.5	RfD (non-food value)	N/A	N/A	N/A
Thallium	3,260	0.002	N/A	0.00007	Other	N/A	N/A	N/A
Zinc	26,000	0.01	N/A	0.3	Chronic oral MRL	N/A	N/A	N/A
Notes: mg/kg/day milligrams contaminant per kilogram body weight per day; MRL ATSDR minimal risk level; ppb parts per billion; RfD EPA reference dose. Bold indicates a dose above the non-cancer health guideline or a theoretical excess cancer risk greater than 10^-4.

Table D-4. Estimated Exposure Doses-Incidental Ingestion of On-Site Soil in Industrial Use Areas1
Contaminant	Maximum Concentration (mg/kg)	Estimated Non-Cancer Exposure Dose (mg/kg/day)		Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Contaminant	Maximum Concentration (mg/kg)	Adult	Child	Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
2,4-Dinitrotoluene	1100	0.0005	N/A	0.002	RfD	N/A	N/A	N/A
2,4,6-Trinitrotoluene	2000	0.001	N/A	0.005	RfD	0.0004	0.03	1 x 10^-5
Bis(2-ethylhexyl) phthalate	80	0.0004	N/A	0.06	Chronic oral MRL	0.00002	0.014	2 x 10^-7
Benzo(a)anthracene	56	N/A	N/A	N/A	N/A	0.00001	0.73	8 x 10^-6
Benzo(a)pyrene	44	N/A	N/A	N/A	N/A	0.000009	7.3	7 x 10^-5
Benzo(b)fluoranthene	36	N/A	N/A	N/A	N/A	0.000007	0.73	5 x 10^-6
Dibenz(a,h)anthracene	6.7	N/A	N/A	N/A	N/A	0.000001	7.3	1 x 10^-5
Indeno(1,2,3-c,d) pyrene	3.9	N/A	N/A	N/A	N/A	0.0000008	0.73	6 x 10^-7
Pentachlorophenol	20	0.00001	N/A	0.001	Chronic oral MRL	0.000004	0.12	5 x 10^-7
Dieldrin	0.091	0.00000004	N/A	0.00005	RfD	0.00000002	16	3 x 10^-7
Heptachlor epoxide	0.28	0.0000001	N/A	0.00001	RfD	0.00000006	9.1	5 x 10^-7
Aroclor-1254	800	0.0004	N/A	0.00002	Chronic oral MRL	0.0002	2	3 x 10^-4
Aroclor-1260	1160	N/A	N/A	N/A	N/A	0.0002	2	5 x 10^-4
Arsenic	91.2	0.00004	N/A	0.0003	Chronic oral MRL	0.00002	1.5	3 x 10^-5
Iron	490,000	0.2	N/A	0.3	NCEA	N/A	N/A	N/A
Thallium	129	0.00006	N/A	0.00007	Other	N/A	N/A	N/A
Notes: mg/kg/day milligrams contaminant per kilogram body weight per day; MRL ATSDR minimal risk level; ppb parts per billion; RfD EPA reference dose. Bold indicates a dose above the non-cancer health guideline or a theoretical excess cancer risk greater than 10^-4. ¹Excluding VAAP-32

Table D-5. Estimated Exposure Doses-Incidental Ingestion of On-Site Surface Water during Recreational Use
Contaminant	Maximum Concentration (mg/L)	Estimated Non-Cancer Exposure Dose (mg/kg/day)		Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Contaminant	Maximum Concentration (mg/L)	Adult	Child	Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
1,3-Dinitrobenzene	0.003	0.0000002	0.000005	0.0005	Intermediate oral MRL	N/A	N/A	N/A
2,4-Dinitrotoluene	2.37	0.0002	0.004	0.002	RfD	N/A	N/A	N/A
2,6-Dinitrotoluene	0.23	0.00002	0.0004	0.004	Intermediate oral MRL	N/A	N/A	N/A
2,4,6-Trinitrotoluene	0.74	0.00006	0.001	0.005	Chronic Oral MRL	0.00002	0.03	7 x 10^-7
RDX	0.007	0.0000005	0.00001	0.003	RfD	0.0000002	0.11	2 x 10^-8
Bromodichloromethane	0.001	0.00000009	0.000002	0.02	Chronic oral MRL	0.00000004	0.062	2 x 10^-9
Toluene	0.3	0.00002	0.0005	0.02	Intermediate oral MRL	N/A	N/A	N/A
Bis(2-ethylhexyl) phthalate	0.011	0.0000008	0.00002	0.06	Chronic oral MRL	0.0000004	0.014	5 x 10^-9
delta-BHC	0.000006	0.0000000005	0.00000001	0.008	Chronic oral MRL	0.0000000002	6.3	1 x 10^-9
Heptachlor	0.00002	0.000000002	0.00000004	0.0005	RfD	0.0000000007	4.5	3 x 10^-9
Arsenic	0.01	0.0000007	0.00002	0.0003	Chronic oral MRL	0.0000003	1.5	5 x 10^-7
Cobalt	0.138	0.00001	0.0002	0.01	Intermediate oral MRL	N/A	N/A	N/A
Chromium	0.054	0.000004	0.00009	0.003	RfD	N/A	N/A	N/A
Manganese	16	0.001	0.03	0.5	RfD (non-food value)	N/A	N/A	N/A
Notes: mg/kg/day milligrams contaminant per kilogram body weight per day; MRL ATSDR minimal risk level; ppb parts per billion; RfD EPA reference dose. Bold indicates a dose above the non-cancer health guideline or a theoretical excess cancer risk greater than 10^-4.

Table D-6. Estimated Exposure Doses-Incidental Ingestion of On-site Sediment during Recreational Use
Contaminant	Maximum Concentration (mg/kg)	Estimated Non-Cancer Exposure Dose (mg/kg/day)		Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Contaminant	Maximum Concentration (mg/kg)	Adult	Child	Health Guideline (mg/kg/day)	Health Guideline Source	Estimated Cancer Exposure Dose (mg/kg/day)	Cancer Slope Factor (mg/kg/day)^-1	Theoretical Excess Cancer Risk
Bis(2-ethylhexyl) phthalate	80	0.00006	0.0006	0.06	Chronic oral MRL	0.00003	0.014	4 x 10^-7
Acenaphthylene	2.9	0.000002	0.00005	0.02	RfD	N/A	N/A	N/A
Benzo(a)anthracene	8.5	N/A	N/A	N/A	N/A	0.000003	0.73	5 x 10^-6
Benzo(a)pyrene	12	N/A	N/A	N/A	N/A	0.000004	7.3	3 x 10^-5
Benzo(b)fluoranthene	11	N/A	N/A	N/A	N/A	0.000004	0.73	3 x 10^-6
Benzo(k)fluroanthene	12	N/A	N/A	N/A	N/A	0.000004	0.073	3 x 10^-7
Dibenz(a,h)anthracene	1.5	N/A	N/A	N/A	N/A	0.0000005	7.3	3 x 10^-6
Phenanthrene	9.2	0.000007	0.00006	0.02	RfD	N/A	N/A	N/A
Aroclor-1260	5.1	N/A	N/A	N/A	N/A	0.000002	2	3 x 10^-6
Aluminum	102,000	0.08	0.7	2	Intermediate oral MRL	N/A	N/A	N/A
Antimony	57	0.00004	0.0004	0.004	RfD	N/A	N/A	N/A
Arsenic	100	0.00007	0.0007	0.0003	Chronic oral MRL	0.00003	1.5	5 x 10^-5
Chromium	12,000	0.009	0.08	0.003	RfD	N/A	N/A	N/A
Iron	220,000	0.2	2	0.3	NCEA	N/A	N/A	N/A
Manganese	7,000	0.005	0.05	0.05	RfD	N/A	N/A	N/A
Thallium	254	0.0002	0.002	0.00007	Other	N/A	N/A	N/A
Vanadium	293	0.0002	0.002	0.003	Intermediate oral MRL	N/A	N/A	N/A
Notes: mg/kg/day milligrams contaminant per kilogram body weight per day; MRL ATSDR minimal risk level; ppb parts per billion; RfD EPA reference dose. Bold indicates a dose above the non-cancer health guideline or a theoretical excess cancer risk greater than 10^-4.

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Department of Health and Human Services

PUBLIC HEALTH ASSESSMENT

VOLUNTEER ARMY AMMUNITION PLANT CHATTANOOGA, HAMILTON COUNTY, TENNESSEE FACILITY NO. TN6210020933

Appendix C : Acid Cloud

Appendix D : Estimates of Human Exposure Doses and Determination of Health Effects

VOLUNTEER ARMY AMMUNITION PLANT
CHATTANOOGA, HAMILTON COUNTY, TENNESSEE

FACILITY NO. TN6210020933