Skip directly to: content | left navigation | search

PUBLIC HEALTH ASSESSMENT ADDENDUM

LETTERKENNY ARMY DEPOT
USA LETTERKENNY SOUTHEAST AREA
CHAMBERSBURG, FRANKLIN COUNTY, PENNSYLVANIA

AND
USA LETTERKENNY - PROPERTY DISPOSAL OFFICE AREA
CHAMBERSBURG, FRANKLIN COUNTY, PENNSYLVANIA



PUBLIC HEALTH IMPLICATIONS

A. Introduction

The following three sections discusses potential health effects that may result from exposures to environmental contaminants, available health outcome data, public health concerns. The Toxicologic Evaluation section will assess the toxicologic and carcinogenic effects of exposure to contaminants that are above comparison values relative to the complete and potential exposure pathways. The Health Outcome Data Evaluation section evaluates available community health information to determine whether adverse health effects have occurred. The Community Health Concerns Evaluation section discusses public health concerns voiced by the community about possible exposure to contaminants relative to documented exposures and potential health effects.

B. Toxicologic Evaluation

In this section, ATSDR discusses health effects that could result from exposures to site-related contaminants. People can only be exposed to a site contaminants if they have contact with them. People can be exposed by breathing, eating, drinking, or touching air, soil, or water that contains contaminants.

In order to understand health effects that may be caused by a specific chemical, it is helpful to review factors related to how the human body processes the chemical after exposure. Those factors include the exposure concentration (how much), the duration of exposure (how long), the route of exposure (breathing, eating, drinking, or skin contact), and the multiplicity of exposure (combination of contaminants). Once exposure occurs, individual characteristics such as age, sex, nutritional status, health status, lifestyle, and genetics influence how the chemical is absorbed, distributed, metabolized (processed), and excreted (eliminated). Together, those factors determine potential health effects that exposed people may have.

To determine the possible health effects of specific chemicals, ATSDR researches scientific literature. The resulting information is compiled and published in a series of chemical-specific ATSDR documents called Toxicological Profiles. Toxicological Profiles are references that describe adverse health effects that could be associated with exposure to a specific chemical in the environment. In addition, they include health guidelines such as ATSDR's minimal risk levels (MRLs) and EPA's reference doses (RfDs), reference concentrations (RfCs), and cancer slope factors (CSFs). When RfDs, RfCs, and MRLs are not available, a no observed adverse effect level (NOAEL) or lowest observed adverse effect level (LOAEL) may be used to estimate levels below which no adverse health effects (noncancerous) are expected.

ATSDR compares a variety of health guidelines to contaminant concentrations detected in different environmental media (soil, air, water, and food) that populations may be exposed to daily. That will determine whether exposure to given levels of contaminants is likely to cause an increased risk of developing cancer and/or noncancerous adverse health effects. ATSDR's MRL is an estimate of daily human exposure to a chemical not likely to cause an appreciable risk of harmful effects (noncancerous) over a specified duration of exposure. MRLs are based on human and animal studies and are reported for acute (less than or equal to 14 days), intermediate (15-364 days), and chronic (greater than or equal to 365 days) exposures. If a person's daily exposure is below the MRL, adverse health effects are not expected. An RfD is EPA's estimate of the daily oral (ingestion) exposure not likely to cause appreciable risk of harmful noncancerous effects during a persons's lifetime (70 years). Likewise, an RfC is EPA's estimate of the daily inhalation exposure not likely to cause appreciable risk of harmful noncancerous effects during a person's lifetime (70 years). Both the RfD and RfC take into account sensitive subpopulations.

A NOAEL or LOAEL may be used when guidelines for noncancerous health effects, such as RfDs, RfCs, and MRLs, are not available. NOAELs and LOAELs are used to estimate a dose at which people are not expected to develop adverse noncancerous health effects.

Health guidelines such as MRLs and RfDs however, do not consider the risk of developing cancer. To evaluate exposure to carcinogenic chemicals, EPA has established cancer slope factors (CSFs) for inhalation and ingestion that define the relationship between exposure doses and the likelihood of an increased risk of cancer, compared with controls that have not been exposed to the chemical. Usually derived from animal or occupational studies, cancer slope factors are used to calculate the exposure dose likely to result in one excess cancer case per one million persons exposed over a lifetime (70 years).

ATSDR's estimation of human exposure to contaminated media uses media-specific rates for adults and children. The rates are calculated by multiplying contaminant concentration by the ingestion rate for an adult or a child, and then dividing that number by the appropriate standard body weight (70 kg for adults, 16 kg for a child). The water ingestion rates used for adults and children are 2.0 L/day and 1.0 L/day, respectively. ATSDR uses an inhalation rate of 23 cubic meters per day (m3)/day for adults and 15 m3/day for children. Some exposures occur on an intermittent or irregular basis; in those cases, an exposure factor (EF) is calculated that averages the dose over the exposure period.

The maximum contaminant concentration detected in a particular medium is used to estimate exposure doses. Using the maximum concentration to evaluate exposure results in an evaluation protective of public health, because without historical exposure data, contaminants may have been greater or lower than the previously detected concentrations.

Off-site residents, adjacent to the SE Area, may have been exposed to multiple chemicals by ingestion of, skin contact with, and inhalation of VOC-contaminated well water. Most of the wells belonged to residents, but a few of them belonged to businesses. Data are very limited, however, on the health effects of multiple chemical exposures by oral, dermal, and inhalation routes. Effects of specific contaminants detected in multiple media may be additive, synergistic, or antagonistic. Although some studies indicate that simultaneous exposure to contaminants that are known or probable human carcinogens might increase the risk of developing cancer and/or noncancerous health effects, the levels at which those effects may occur are unknown (100-105). Current research involving complex chemical mixtures will eventually add new information that will be used in future evaluations.

Past Completed Pathway - Groundwater From Private Wells

Private well water contamination in neighborhoods east (adjacent to the SE Area) of Letterkenny Army Depot represent a past-completed exposure pathway for residents who used the water for drinking and other household purposes (such as cooking, bathing, mopping, and showering). Contaminants detected in those private wells (Table 6) were the following VOCs: 1,1-Dichloroethene, Trans-1,2-Dichloroethene, Chloroform, 1,1,1-Trichloroethane, Trichloroethylene, 1,1,2,2-Tetrachloroethane, 1,2-Dichloroethane, and Chlorobenzene.

Off-site private wells, east of the SE Area were abandoned as a potable water supply when contamination above MCLs was detected in 1982. Primary exposure points for the SE Area surface water/groundwater pathway were off-site private wells and springs. The main contamination source has been identified as the former industrial lagoon. Water from contaminated wells were replaced with bottled drinking-water. Those residences, and a few businesses, were later connected to the Guilford Water Authority System. Conversion to a centralized water-supply system began in October 1982 and was completed in 1987. Exposure to contaminated groundwater between 1982 and 1987 was through showering, bathing, mopping, washing cars, etc. It's unlikely that ingestion would account for exposure in those persons, since wells with VOCs exceeding MCLs were replaced with bottled water (109). Inhalation of and dermal contact with VOCs would have accounted for most of the exposure during 1982 to 1987. However, prior to 1982 (bottled water began), exposure via ingestion, inhalation, and dermal contact most likely occurred. Thirty-three years elapsed from the time disposal activities began at the lagoon area in 1954, until 1982, when VOCs greater than MCLs were detected in off-site private wells. However, it is very unlikely that exposure could have occurred for that length of time. The actual duration of exposure during the 33-year interval is unknown, and it would be difficult to reasonably predict the length of time that exposure could have occurred. Periodic monitoring of off-site wells/springs has indicated that contaminant concentrations have decreased since VOCs above MCLs were first discovered in 1982 (41, 42, 106).

Several studies have provided estimates of lifetime inhalation and dermal exposures to VOCs in tap water used for showering and other household purposes, such as laundry and dishwashing (52, 53, 114, 115, 116, 117). A recent report indicates that the lifetime inhalation dose from VOCs in tap water is probably roughly equal to the ingestion dose, but may be as high as about six times the ingestion dose. Similarly, the lifetime dermal dose from VOCs in tap water is probably roughly equal to 0.3 times the ingestion dose, but may be as high as about 1.8 times the ingestion dose (122).

The following paragraphs evaluate potential health effects from contaminant exposure via inhalation of and dermal contact with specific, individual chemicals (VOCS) (Figure 4). For purposes of this assessment, the inhalation dose is considered to be approximately equal to the estimated ingestion dose, and the dermal dose is estimated to be about equal to the estimated ingestion dose. Evaluation of potential risk for cancerous adverse health effects is based on the maximum concentration detected in private wells and EPA Cancer Slope Factors (CSFs), if available for the individual VOCs.

1,1-Dichloroethene (1,1-DCE)

Exposure Prior to 1982
People were exposed to 1,1-DCE when off-site residents ingested, inhaled and dermally contacted 1,1-DCE-contaminated water from contaminated wells east of the SE Area boundary (Figure 4). All three exposure routes are believed to be equally significant with regard to absorption of 1,1-DCE based on reports in the literature (51).

A maximum concentration of 8.6 µg/L of 1,1-DCE was detected in contaminated private well water. Children and adults exposed to 8.6 µg/L of 1,1-DCE would have estimated ingestion exposures of 0.54 µg/kg/day and 0.25 µg/kg/day, respectively. Since the evidence for carcinogenicity in animals is restricted to two studies, addressing inhalation and dermal contact, respectively, of 1,1-DCE in mice (83, 99), and since information from humans is inconclusive (51), 1,1-DCE has been classified as a possible human carcinogen (Group C) by the EPA for both oral and inhalation exposure routes. (Group C is used by EPA to categorize chemicals for which there is limited evidence of carcinogenicity in animals, but inadequate evidence or no data from epidemiologic studies in people.) Prior to 1982, ingestion and inhalation of 1,1-DCE at the maximum detected level may have resulted in an increased cancer risk; however, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

Adverse noncancerous effects are not expected to result from ingestion of 1,1-DCE because the levels detected in private wells east of the SE Area would result in estimated exposure doses below the minimal risk level (MRL) of 9 µg/kg/day. The MRL is the estimated level below which adverse noncancerous effects are not expected.

For 1,1-DCE, ATSDR has calculated a chronic inhalation MRL of 30 ppb, which is approximately equal to estimated doses of 2.34 and 0.82 µg/kg/day in children and adults, respectively. Assuming the estimated exposures from inhalation of volatilized 1,1-DCE from showers and cooking are approximately equal to estimated ingestion exposures, no adverse noncancerous health effects would be expected from inhalation of volatilized 1,1-DCE from past contaminated well water east of Letterkenny.

Although it is recognized that dermal contact with 1,1-DCE also is a significant route of exposure (51), guidelines such as MRLs, RfDs, and NOAELS have not been established for dermal contact to 1,1-DCE. However, assuming all three exposure routes (ingestion, inhalation, and dermal contact) are equally significant with regard to absorption of 1,1-DCE and assuming the estimated exposures from ingestion of 1,1-DCE in well water would be approximately equal to estimated dermal exposures, no adverse health effects are expected from past dermal contact of 1,1-DCE contaminated water used for showering or other household activities such as mopping, washing dishes, and washing cars.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. Assuming that the inhalation dose and dermal dose are approximately equal to the ingestion dose, the respective estimated doses for children and adults would be three times the ingestion dose. The total dose for children and adults would be 1.62 and 0.75 µg/kg/day, respectively. Those total doses are below doses at which adverse health effects would be expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

Ingestion of 1,1-DCE at the maximum level detected (8.6 µg/l) would result in estimated exposure doses of 0.54 µg/kg/day and 0.25 µg/kg/day for children and adults, respectively. From 1982 until 1987, ingestion and inhalation of 1,1-DCE at the maximum detected level may have resulted in an increased cancer risk; however, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. Assuming that the inhalation dose and dermal dose may be approximately equal to the estimated ingestion dose, the respective estimated doses for children and adults would be three times the ingestion dose. Those total doses are below a concentration expected to cause adverse health effects.

Also known as vinylidene chloride, 1,1-DCE is used to make various plastics, such as packaging materials (flexible films, e.g., plastic food wraps) and flame-retardant fabrics (51). A national survey conducted by NIOSH (54), estimated that the largest numbers of workers potentially exposed to DCE in the workplace were special trade contractors or workers in the fabricated metal products or wholesale trade industries. The occupational groups with the largest numbers of exposed workers were carpenters, warehousemen (not otherwise classified) and miscellaneous machine operators (51). Residents east of the SE Area who were employed by those industries may have been exposed to 1,1-DCE in the workplace as well as at home from using private well water.

Although information about populations that may be especially sensitive to 1,1-DCE is from animal studies, the following groups may have been particularly susceptible to the chemical's toxic effects during the time the contaminated wells were used: infants and young children, pregnant women, consumers of alcohol, people with liver, kidney, thyroid and cardiac disease, certain central nervous system dysfunctions, and people who are fasting (51). Increased susceptibility to 1,1-DCE toxicity is largely caused by the formation of toxic intermediates during its metabolism (51).

Trans-1,2-Dichloroethene (T-1,2-DCE)

Exposure Prior to 1982
Residents east of the SE Area were exposed to T-1,2-DCE when they ingested, inhaled, and dermally contacted T-1,2-DCE-contaminated water from their private wells. Although dermal exposure was possible, dermal absorption of T-1,2-DCE is likely to be minimal compared to inhalation, because it rapidly evaporates into the air (55). Studies of Letterkenny indicate that most of the cis/trans 1,2-dichloroethene (1,2-DCE) in Letterkenny groundwater results from the breakdown of trichloroethene (TCE) used in SE Area operations (106).

The literature showed no exposure studies of animals or people that investigate the possible carcinogenicity of T-1,2-DCE, although one study is currently investigating the potential for cancerous effects of 1,2-DCEs following acute oral exposure (55, 56, 57). Prior to 1982, exposure occurred via ingestion and inhalation of and dermal contact with T-1,2-DCE. At this time, T-1,2-DCE is not believed to be a probable human carcinogen. When results of studies investigating the possible carcinogenicity of T-1,2-DCE are available, ATSDR can address the potential for cancerous adverse health effects from T-1,2-DCE exposure. At this time, T-1,2-DCE is not believed to be a probable human carcinogen.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. Assuming that the inhalation dose and dermal dose may be approximately equal to the estimated ingestion dose, the respective estimated doses for children and adults would be three times the ingestion dose. Those total doses are below the chronic ingestion RfD of 20 µg/kg/day for T-1,2-DCE. The RfD is the estimated level below which adverse noncancerous effects are not expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

A maximum concentration of 66 µg/L was detected in residential wells east of the Letterkenny. The estimated daily exposures from ingestion of 66 µg/L of T-1,2-DCE would have been 4.13 µg/kg/day for children and 1.89 µg/kg/day for adults. Those estimated doses are below the T-1,2-DCE chronic RfD of 20 µg/kg/day. The RfD is the estimated level below which adverse noncancerous effects are not expected. For T-1,2-DCE, no health guidelines, such as MRLs or RfCs, have been established for long-term exposure by inhalation or dermal contact in humans.

However, noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. Assuming that the inhalation dose and dermal dose may be approximately equal to the estimated ingestion dose, the total dose would be two times the ingestion dose. The total doses below the chronic ingestion RfD of 20 µg/kg/day for T-1,2-DCE. The RfD is the estimated level below which adverse noncancerous effects are not expected.

1,2-Dichloroethene is used mainly as an intermediate chemical in the synthesis of chlorinated solvents and compounds. It also has been used to produce organic materials such as dyes, perfumes, lacquers, and thermoplastics (55, 58). Thus, residents east of the SE Area who were employed with those industries may have had additional exposures to T-1,2-DCE in addition to exposures from their private well water.

Chloroform

Exposure Prior to 1982
People have been exposed to chloroform by ingestion, inhalation of, and dermal contact with chloroform-contaminated water from contaminated wells east of the SE Area boundary. Based on reports in the literature, all three exposure routes are believed to be equally significant with regard to absorption of chloroform (59).

A maximum concentration of 2.8 µg/L of chloroform was detected in contaminated private well water. Children and adults exposed to 2.8 µg/L of chloroform would have estimated ingestion exposures of 0.18 and 0.08 µg/kg/day for children and adults, respectively. Little information exists about the development of cancer in people who have been chronically exposed to chloroform. However, using animal studies, EPA has classified chloroform as a probable human carcinogen (Group B2) when ingested and inhaled (59). The term "Group B2" is used by EPA to categorize chemicals for which there is sufficient evidence of carcinogenicity in animals, but inadequate evidence or no data from epidemiologic studies in people (60, 61). Prior to 1982, ingestion and inhalation of chloroform at the maximum detected level would not have resulted in an increased cancer risk. It is not known how long persons were actually exposed or what concentrations they were exposed to.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. Assuming the estimated exposures from inhalation of volatilized chloroform from showers and cooking are approximately equal to the estimated ingestion exposure dose and assuming the dermal exposure approximates the estimated ingestion dose, the total estimated dose would be three times the estimated ingestion dose. Those doses are below the chronic oral RfD of 10 µg/kg/day for chloroform. Therefore, no adverse noncancerous health effects would be expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

The potential for cancerous adverse health effects were evaluated for exposure via inhalation and dermal contact. Children and adults who would have ingested 2.8 µg/L of chloroform (the maximum level detected) would have had estimated ingestion doses of 0.18 and 0.08 µg/kg/day, respectively. From 1982 until 1987, ingestion and inhalation of chloroform at the maximum detected level would not have resulted in an increased cancer risk. It is not known how long persons were actually exposed or what concentrations they were exposed to.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. Assuming the inhalation and dermal doses are approximately equal to the estimated ingestion exposure dose, the total estimated dose would be two times the estimated ingestion dose. Those doses are below the chronic oral RfD of 10 µg/kg/day for chloroform. Therefore, no adverse noncancerous health effects would be expected.

Chloroform has been used as a solvent or an extraction solvent for fats, oils, greases, resins, lacquers, rubber, alkaloids, gums, waxes, penicillin, vitamins, flavors, floor polishes, and adhesives in artificial silk manufacture, as a dry cleaning spot remover, in fire extinguishers, as an intermediate in the manufacture of dyes and pesticides, and as a fumigant (59, 62, 63).

Chloroform was previously used as an anesthetic, but it has been replaced by safer and more versatile materials (62). Chloroform, also known as trichloromethane, enters the environment from chemical companies, paper mills, waste water from sewage treatment plants, and drinking water that contains chlorine. Chlorine is added to most drinking water and many waste waters to destroy bacteria. Those who work in industries that use chloroform can be exposed to higher than normal amounts of chloroform (59). Residents east of the SE Area who were employed by such industries may have had work-related exposures to chloroform in addition to exposures from using private well water.

1,1,1-Trichloroethane (1,1,1-TCA)

Exposure Prior to 1982
Residents east of the SE Area were exposed to 1,1,1-TCA when they ingested and inhaled contaminated water from private well water. Although dermal exposure is possible, dermal absorption of 1,1,1-TCA is likely to be minimal compared with inhalation (64), because most of it evaporates into the air (65).

The literature showed no exposure studies in animals (68) or people that have conclusively shown 1,1,1-TCA to be a carcinogen following ingestion of 1,1,1-TCA. One study (Quast et al 1988) demonstrated no evidence of carcinogenicity by the inhalation route (66). Therefore, at this time, 1,1,1-TCA is not believed to be a probable human carcinogen.

A maximum concentration of 92 µg/L of 1,1,1-TCA was detected in off-site water wells east of Letterkenny. The estimated daily exposures from ingesting 92 µg/L would be 5.75 g/kg/day for children and 2.63 µg/kg/day for adults. Health guidelines have not been established for noncancerous health effects in people who inhale or ingest, or have dermal contact with 1,1,1-TCA. Guidelines are needed to determine what levels of 1,1,1-TCA could be associated with those exposure routes.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. One long-term occupational study found that central nervous system effects ranged from 200,000 - 900,000 ppb of 1,1,1-TCA (67). The study focused on inhalation exposures with an average duration of 6.7 years per study group. The results from that study was used to approximate inhalation doses for children and adults to be 214 µg/kg/day for children and 75 µg/kg/day for adults. Assuming the inhalation and dermal doses are about equal to the estimated ingestion dose, adverse noncancerous effects via inhalation, ingestion, and dermal contact are not expected. The total doses are below levels at which adverse health effects are expected to occur.

Exposure During 1982 - 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

A maximum concentration of 92 µg/L was detected in off-site water wells east of Letterkenny. The estimated daily exposures from ingesting 92 µg/L of 1,1,1-TCA would have been 5.75 µg/kg/day for children and 2.63 µg/kg/day for adults. Health guidelines have not been established for noncancerous health effects in people who inhale or ingest, or have dermal contact with 1,1,1-TCA. Guidelines are needed to determine what levels of TCA could be associated with those exposure routes.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. One long-term occupational study found a NOAEL for central nervous system effects (LOAELs) that ranged from 200,000 - 900,000 ppb of 1,1,1-TCA (67). The study focused on inhalation exposures with an average duration of 6.7 years per study group. Using the results from that study and assuming the inhalation and dermal doses are approximately equal to the estimated ingestion dose, adverse noncancerous effects via inhalation and dermal contact are not expected. The total dose is below the level at which adverse health effects are expected to occur.

Animal studies show that nicotine enhances the harmful effects of 1,1,1-TCA (69), suggesting that simultaneous exposure to nicotine and 1,1,1-TCA could pose an increased health risk in people. Therefore, smokers exposed to 1,1,1-TCA could have an increased risk of health effects compared with nonsmokers. Low doses of ethanol also enhances the harmful effects of 1,1,1-TCA (70), suggesting that increased health risks may be associated with simultaneous exposure to those two chemicals. Phenobarbital, which is prescribed for certain cases of epilepsy, reportedly enhances the hepatotoxicity of 1,1,1-TCA in rats (71). Thus, an increased risk of hepatotoxicity may be associated with simultaneous exposure to that drug and 1,1,1-TCA. The literature suggests that people who have cardiac arrhythmias also may be more susceptible to the health effects of 1,1,1-TCA (65). Persons belonging to groups previously described and who also were exposed to 1,1,1-TCA in contaminated well water east of Letterkenny may have been more susceptible to the health effects from 1,1,1-TCA exposure.

1,1,1-TCA, is a synthetic chemical with many industrial and household uses. It is often used as a solvent to dissolve other substances, e.g., glue and paint. In industry, it is widely used to remove oil and/or grease from manufactured metal parts. It also may be in household products such as spot cleaners, glues, and aerosol sprays (65). Thus, residents east of the SE Area who were employed by those industries may have had other exposures to 1,1,1-TCA in addition to other exposures from private well water.

Trichloroethylene (TCE)

Exposure Prior to 1982
Residents east of the installation were exposed to TCE when they ingested contaminated private well water. Ingestion, inhalation, and dermal contact were the routes of exposure to contaminated water. Dermal contact appears to be a more significant route of exposure if large amounts are applied on the skin, which would be more likely to happen in an occupational setting (72, 73, 74). Therefore, dermal contact is not as significant (but is evaluated) as the inhalation route of exposure to residents who used contaminated well water for household purposes.

From water samples collected from private drinking water wells near the SE Area, a maximum concentration of 48 µg/L of TCE was detected. The estimated daily exposures of children and adults who would have ingested a concentration of 48 µg/L of TCE from well water are 3 µg/kg/day and 1.37 µg/kg/day, respectively. The carcinogenicity of TCE is currently being re-evaluated by EPA, however it is considered to be a probable carcinogen (Group B2) until it's reevaluation is completed. Prior to 1982, ingestion and inhalation of TCE at the maximum detected level may have resulted in an increased cancer risk; however, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. Assuming the estimated exposures from inhalation of and dermal contact with TCE are approximately equal to the estimated ingestion exposure dose, the total estimated dose would be three times the estimated ingestion dose. The total dose is below the chronic intermediate MRL of 100 µg/kg/day for ingestion of TCE. Therefore, no adverse noncancerous health effects would be expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

The potential for cancerous adverse health effects were evaluated for five years of exposure via inhalation and dermal contact. From 1982 until 1987, ingestion and inhalation of TCE at the maximum detected level may have resulted in an increased cancer risk; however, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

ATSDR has derived an intermediate MRL of 100 µg/kg/day for ingestion of TCE. The estimated ingestion doses described previously for children and adults (3 µg/kg/day and 1.37 µg/kg/day, respectively) do not exceed the MRL of 100 µg/kg/day.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal exposure) are evaluated. Assuming the inhalation dose and dermal dose may approximate the ingestion dose, the respective estimated doses for children and adults would be two times the estimated ingestion dose. Those total doses are below doses at which noncancerous adverse health effects would be expected.

Persons particularly susceptible to TCE exposures are chronic consumers of alcohol, people with heart disease, people taking disulfiram (a medication used to treat alcoholism), and people taking the anticoagulant warfarin (72). Those medications increase the toxicity of TCE in the liver by interfering with its normal metabolism. Thus, residents who used contaminated wells east of the SE Area and belonged to the above groups may have been more susceptible to health effects from TCE exposure.

According to the literature, TCE exposure usually occurs in occupational settings where the chemical is used as a solvent to remove grease from metal parts (72). Products that may contain TCE are some types of typewriter correction fluids, paints and paint removers, glue, spot removers, rug-cleaning fluids, and metal cleaners (72). Thus, residents east of the installation who were employed by those industries or used those household products may have been exposed to TCE in addition to contaminated water from private wells.

1,1,2,2-Tetrachloroethane (1,1,2,2-PCA)

Exposure Prior to 1982
People have been exposed to 1,1,2,2-PCA by ingestion, inhalation of, and dermal contact with 1,1,2,2-PCA-contaminated water from contaminated wells east of the SE Area boundary. Based on reports in the literature, all three exposure routes are believed to be equally significant with regard to absorption of PCA (75).

Water samples collected from private drinking-water wells east of Letterkenny contained a maximum concentration of 13 µg/L of 1,1,2,2-PCA. The estimated daily exposures of children and adults who would have ingested a concentration of 13 µg/L of 1,1,2,2-PCA are 0.81 µg/kg/day and 0.37 µg/kg/day, respectively. Since the evidence for carcinogenicity in animals is restricted to two studies in mice (76, 77), and since information from humans is inconclusive (78), 1,1,2,2-PCA has been classified as a possible human carcinogen (Group C) by the EPA for both oral and inhalation exposure routes (79). Prior to 1982, ingestion and inhalation of 1,1,2,2-PCA at the maximum detected level may have resulted in a slight increased cancer risk; however, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or concentrations they were exposed to.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. Assuming the estimated exposures from inhalation of and dermal contact with 1,1,2,2,-TCA are approximately equal to the estimated ingestion dose, the total estimated dose would be three times the estimated ingestion dose. The total doses are below a level at which adverse health effects are expected to occur.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

The potential for cancerous adverse health effects were evaluated for five years of exposure via inhalation and dermal contact. From 1982 until 1987, ingestion and inhalation of 1,1,2,2-PCA at the maximum detected level may have resulted in a slight increased cancer risk; however, it is not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

There are no health guidelines for noncancerous health effects caused by chronic exposure from ingestion and inhalation of or dermal contact with 1,1,2,2-PCA. However, workers in India's bangle (ornamental bracelet or anklet) industry who dipped their hands in 1,1,2,2-PCA, as well as inhaled it, had tremors, headaches, and dizziness in addition to gastric pains during 3 to 6 months of exposure (80). Specific exposure levels are not known, but air concentrations were detected to be between 9 and 98 ppm (or between 9,000 ppb and 98,000 ppb for the LOAEL). Using the results from that study and assuming the inhalation and ingestion doses to be approximately equal, adverse noncancerous effects are not expected.

Although it is recognized that dermal contact with 1,1,2,2-PCA is also a significant route of exposure, (75) guidelines such as MRLs, RfDs, and NOAELS have not been established for that type of exposure route. However, assuming all three exposure routes (ingestion, inhalation, and dermal contact) are equally significant with regard to absorption of 1,1,2,2-PCA (75) and assuming the estimated exposures from inhalation of 1,1,2,2-PCA in well water would be approximately equal to estimated dermal exposures, no adverse health effects are expected from dermal contact of 1,1,2,2-PCA-contaminated water.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. Assuming the inhalation dose is approximately equal to the estimated ingestion dose associated with the contaminated water and assuming the dermal exposure dose is about equal the ingestion exposure dose (0.81 µg/kg/day and 0.37 µg/kg/day for children and adults, respectively), the total estimated dose would be two times those estimated ingestion dose which would correspond to respectively 1.62 and 0.74 µg/kg/day for children and adults). Those doses are below levels expected to result in adverse health effects.

1,1,2,2-PCA has been used in large amounts to produce other chemicals and as an industrial solvent. It is also used to separate other substances, to clean and degrease metals, and in paints and pesticides. However, worker exposure to high concentrations of 1,1,2,2-PCA is not likely, because it is generally used to produce other chemicals. That process takes place in automatic systems, in which there is no human contact with the product (75). Therefore, residents east of the installation who were employed by industries that use 1,1,2,2-PCA are not expected to have had additional exposures to 1,1,2,2-PCA other than those from contaminated water from private wells.

1,2-Dichloroethane (1,2-DCA)

Exposure Prior to 1982
Residents east of the SE Area were exposed to 1,2-DCA by inhalation, ingestion, and dermal absorption of contaminated groundwater from residential wells. People are exposed to 1,2-DCA mainly by breathing it in air or by drinking it in 1,2-DCA-contaminated water. However, if drinking-water supplies contain more than 6 ppb of 1,2-DCA, exposure by ingestion is expected to be more significant than inhalation (81). Because of the high vapor pressure of 1,2-DCA, it rapidly volatilizes thereby making dermal contact less significant than the inhalation route of exposure for residents east of Letterkenny (64, 81, 82). Studies of Letterkenny indicate that most of the 1,2-DCA in Letterkenny groundwater results from the breakdown of 1,1,1-TCA.

A maximum concentration of 2.5 µg/L of 1,2-DCA was detected in wells east of the SE Area. Little information exists about the development of cancer in people who have experienced long-term exposure to 1,2-DCA. Using animal studies, however, EPA has classified 1,2-DCA as a probable human carcinogen (Group B2) from both ingestion and inhalation routes (76, 82, 83). Prior to 1982, ingestion and inhalation of 1,2-DCA at the maximum detected level would not have resulted in an increased cancer risk; however, it is not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. Assuming the inhalation dose and dermal dose is about equal to the estimated ingestion dose (0.16 µg/kg/day for children and 0.07 µg/kg/day for adults) associated with the contaminated water, the total estimated dose would be three times those estimated ingestion dose which would correspond to respectively 0.48 and 0.21 µg/kg/day for children and adults. Those doses are below the NOAEL of 189 µg/kg/day in people for a study that investigated adverse liver effects in mice (84). Therefore, adverse noncancerous effects are not expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

The potential for cancerous adverse health effects were evaluated for five years of exposure via inhalation and dermal contact. From 1982 until 1987, ingestion and inhalation of 1,2-DCA at the maximum detected level would not have resulted in an increased cancer risk; however, it is not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to.

There are no health guidelines for noncancerous health effects caused by chronic exposure via ingestion and inhalation of or dermal contact with 1,2-DCA. However, in a study of the health effects of intermediate exposures (84), mice were given 1,2-DCA-contaminated water for approximately 90 days. The results showed 189,000 µg/kg/day to be the NOAEL for adverse liver effects in mice. Applying an uncertainty factor of 1000, accounting for animal-human variability, sensitive individuals, and duration variability, would correspond to 189 µg/kg/day in people. Using the maximum concentration of 2.5 µg/L detected for 1,2-DCA, the daily estimated ingestion dose for children and adults east of Letterkenny would have been 0.16 µg/kg/day and 0.07 µg/kg/day, respectively. Assuming the inhalation and dermal dose is approximately equal to the estimated ingestion dose, noncancerous effects to the liver are not expected from past exposure. The total dose for children and adults (0.32 and 0.14 µg/kg/day, respectively, which is two times the estimated ingestion doses above) is below the NOAEL of 189 µg/kg/day in people.

1,2-DCA is a clear, synthetic liquid used primarily to make vinyl chloride and several solvents that remove grease, glue, and dirt. It is also added to leaded gasoline to remove excess lead. In the past, it was a component of some cleaning solutions and pesticides; some adhesives, such as those used to glue wallpaper or carpeting; and some paint, varnish, and finish removers (82). Automobile and heavy equipment mechanics, machinists, janitors, and registered nurses are frequently exposed to 1,2-DCA in the workplace (82). The National Occupational Exposure Survey conducted by the National Institute of Occupational Safety and Health notes that workers are exposed to 1,2-DCA when it is used as a fumigant, solvent, or diluent in open-system operations (82). People who have 1,2-DCA-contaminated well water east of Letterkenny may have additional exposures to 1,2-DCA if they were employed in the occupations or industries discussed here.

Persons who were exposed to 1,2-DCA-contaminated wells and were taking the medications, disulfiram or phenobarbital, used to treat alcoholism and seizures respectively, may have been highly sensitive to the effects of 1,2-DCA (82). Those drugs may alter a person's metabolism, resulting in increased levels of the active metabolites of 1,2-DCA. Reduced hepatic glutathione (GSH) also may alter the excretion of active metabolites. GSH plays a protective role in the liver by helping the body excrete active metabolites of 1,2-DCA. Reduced nutritional intake, such as fasting, can result in lowered GSH levels, which, as shown in animal studies, may dramatically slow the excretion of 1,2-DCA (82).

Chlorobenzene

Exposure Prior to 1982
Residents east of the SE Area were exposed to chlorobenzene by inhalation, ingestion, and dermal absorption of contaminated groundwater from residential wells. People were exposed to chlorobenzene mainly by breathing it from volatilization in showers or by drinking it in chlorobenzene-contaminated water. Dermal contact with chlorobenzene is considered to be an insignificant route of exposure for residents east of Letterkenny (85), compared to inhalation and ingestion.

In a study of chronic oral exposure to chlorobenzene, rats and mice did not contract cancer (86). Because of no data and inadequate evidence of carcinogenicity in humans and animals, EPA has classified chlorobenzene as a Class D carcinogen (87). Therefore, at this time, chlorobenzene is not believed to be a probable human carcinogen.

A maximum concentration of 0.8 µg/L of chlorobenzene was detected in wells east of the SE Area. Children and adults exposed to 0.8 µg/L of chlorobenzene would have estimated ingestion exposures of 0.05 µg/kg/day and 0.02 µg/kg/day, respectively. Adverse health effects to the liver and kidneys (88) are not expected, because estimated ingestion exposures are below the chronic oral RfD of 20 µg/kg/day.

Noncancerous adverse health effects are not expected when multiple exposure routes (ingestion, inhalation and dermal contact) are evaluated. There are no health guidelines (RfCs, MRLs, etc.) for chronic inhalation of or dermal contact with chlorobenzene. However, assuming the inhalation and dermal dose are approximately equal to the estimated ingestion dose, the total dose for children and adults (0.15 and 0.06 µg/kg/day, respectively, which is three times the estimated ingestion doses above) is below the chronic oral RfD of 20 µg/kg/day.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses are provided since they are being compared to inhalation and dermal exposure doses.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation and dermal contact) are evaluated. There are no health guidelines (RfCs, MRLs, etc.) for chronic inhalation of or dermal contact with chlorobenzene. However, assuming the inhalation dose and dermal dose are approximately equal to the estimated ingestion dose, the total dose for children and adults (0.10 and 0.04 µg/kg/day, respectively, which is two times the estimated ingestion doses above), is below the chronic oral RfD of 20 µg/kg/day.

Populations who may be unusually sensitive to adverse health effects from chlorobenzene exposure have not been found (85). However, because chlorobenzene has been associated with adverse effects to the liver and kidneys, persons who have compromised function of the liver and kidneys may be more susceptible to chlorobenzene exposure.

By 1987, the production of chlorobenzene in the United States declined by nearly 60%. That decline is mainly attributed to the replacement of chlorobenzene by another chemical (cumen) in phenol production and the end of DDT production in the United States. Since no major new uses have been found for chlorobenzene in recent years, its decline is expected to continue (89, 90, 91). Current primary uses of chlorobenzene are as a solvent for pesticide formulations, diisocyanate manufacture, degreasing automobile parts, and for the production of nitrochlorobenzene (85). Therefore, residents east of the installation who were employed by industries that used chlorobenzene during the time of exposure could have had additional exposures to chlorobenzene other than those exposures from using contaminated water from private wells.

Summary - Past Completed Pathway - Groundwater From Private Wells

Exposure Prior to 1982
Off-site residents east of the SE Area of Letterkenny were exposed to eight different VOCs by way of ingestion and inhalation of and dermal contact with VOC-contaminated water from their private wells. Prior exposure to several VOCs which are probable carcinogens at the maximum detected level may have resulted in a slight increased cancer risk, if those levels or higher were continuously present in private wells for a chronic exposure period. However, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to. Noncancerous adverse health effects from ingestion and inhalation of and dermal contact with the eight VOCs are not likely. Because of the lack of both exposure duration information and published data on health effects stemming from low-level, chronic exposure to multiple chemicals, potential adverse health effects associated with multiple-chemical exposure is at the time unknown.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private well contamination above MCLs, significant exposure via ingestion of VOCs was eliminated. Although only inhalation and dermal contact are evaluated for adverse health effects, estimated ingestion doses were provided since they were compared to inhalation and dermal exposure doses in that evaluation. Prior exposure to several VOCs which are probable carcinogens at the maximum detected level may have resulted in a slight increased cancer risk, if those levels or higher were continuously present in private wells for a chronic exposure period. However, it not possible to adequately address the potential for cancerous adverse health effects, because we do not know how long persons were actually exposed or what concentrations they were exposed to. Noncancerous adverse health effects from inhalation of and dermal contact with the eight chemicals are not likely.

Past, Present, and Future Completed Pathways - Groundwater From Private Wells

Sampling of off-post residential well water during July 1991 detected carbon tetrachloride, aluminum, and lead at maximum concentrations of respectively, 0.81, 2310, and 54.4 µg/L (41). Those maximum concentrations are above comparison values (Table 6). Only one well (near the SE Area) was detected to have carbon tetrachloride and it was connected to municipal water by May 1992 (92). That exposure pathway has been eliminated. Lead was detected in six wells at concentrations above the EPA action level of 15 µg/L: 54.4 (near the PDO Area), 43.3 (near the SE Area), 31.9 (near the SE Area), 24 (near the PDO Area), 17.2 (near the SE Area), and 15.8 (near the SE Area) µg/L. Aluminum was detected in three wells at concentrations above 50 µg/L, the EPA Secondary Maximum Contaminant Level (SMCL): 2,310 (near the SE Area), 405 (near the PDO Area), and 187 (near the SE Area) µg/L. Of those wells, both aluminum and lead were detected in two wells (41). Those six wells with lead and aluminum detections remain in service, and the past contamination represents a past, present, and future completed exposure pathway. It is unknown how long those chemicals were present in the off-site wells. The contaminant concentrations are evaluated for potential adverse health effects since they were detected above ATSDR's environmental comparison values.

Carbon Tetrachloride

One well has been detected with carbon tetrachloride and, consequently, it was connected to municipal water by May 1992 (92); exposure has stopped. The exposure duration was for approximately one year, according to sampling data, but it may have been longer. The following paragraphs evaluate that past exposure.

Residents with the carbon-tetrachloride-contaminated well were exposed to carbon tetrachloride by inhalation, ingestion, and dermal absorption of contaminated groundwater. Based on reports in the literature, all three exposure routes are believed to be equally significant with regard to absorption of carbon tetrachloride (93).

A maximum concentration of 0.81 µg/L of carbon tetrachloride was detected in one well east of the SE Area. Children and adults exposed to 0.81 µg/L of carbon tetrachloride would have estimated ingestion exposures of 0.05 µg/kg/day and 0.02 µg/kg/day, respectively. The EPA has classified carbon tetrachloride as a probable (Group B2) carcinogen by both ingestion and inhalation routes. Ingestion and inhalation of carbon tetrachloride at the maximum detected level would not have resulted in an increased cancer risk.

Noncancerous adverse health effects are not expected when multiple exposure routes (inhalation, ingestion, and dermal contact) are evaluated. Assuming the inhalation dose and dermal dose are approximately equal the estimated ingestion exposure dose (0.05 and 0.02 µg/kg/day for children and adults, respectively), the total estimated dose would be three times those estimated ingestion dose which would correspond to respectively 0.15 and 0.06 µg/kg/day for children and adults. Noncancerous adverse health effects are not expected, because the total doses are below the chronic oral RfD of 0.70 µg/kg/day.

In the past, carbon tetrachloride was widely used as a cleaning fluid. In industry, it has been used as a degreasing agent, and in the household, it has been used as a spot remover from clothing, furniture, and carpeting. Until 1986, it was used as a fumigant to kill insects in grain and as a cleaning fluid in the home (93). Because of the toxicity of carbon tetrachloride, those consumer uses have been discontinued, and only industrial uses remain. The major current use of carbon tetrachloride is in the production of chloroflurocarbons, such as dichlorodifluoromethane (F-12) and trichlorofluoromethane (F-11), that are primarily used as refrigerants (16) in industries. Residents east of the installation who were employed by such industries during the time of exposure (July 1991 until May 1992) may have had additional exposures to carbon tetrachloride other than those from their contaminated well water.

Persons who were exposed to carbon tetrachloride-contaminated well water and were taking the following medications or were members of the groups discussed in the following paragraphs may have been highly sensitive to the effects of carbon tetrachloride (93) during the time of exposure. Some drugs and other chemicals have been detected to significantly increase the toxicity of carbon tetrachloride; some of the effects have only been observed in animals but they include: phenobarbital, pentobarbital, phenylbutazone, TCE, and substances with alcohols and ketones. In addition, a variety of conditions may predispose certain segments of the population to carbon tetrachloride toxicity. Persons with alcoholic cirrhosis, or other liver diseases which have significantly reduced the function of the liver, have a diminished ability to tolerate carbon tetrachloride-induced toxicity. The same is true for carbon tetrachloride-induced toxicity of the kidneys in people with significant renal dysfunction from other causes. According to animal studies, diabetics and people who are fasting may also be more susceptible to carbon tetrachloride toxicity (93).

Aluminum

Residents were exposed to aluminum when they ingested contaminated water from their private wells. Aluminum, like most metals, is very poorly absorbed through the skin and is not a volatile compound (94). Thus, ingestion is the only route of exposure to residents with aluminum-contaminated wells.

A review of the literature detected no exposure studies in animals or people that have found aluminum to be a carcinogen. In fact, aluminum is used to make antacids and antiperspirants and used for the treatment of drinking water. Also, studies of interactions of aluminum and other materials that may be detected at hazardous waste sites show that aluminum has a protective effect against the toxic effects of other chemicals (94).

Despite the widespread occurrence of aluminum in foods and drinking water, there is little indication that it is toxic by this route. The FDA considers aluminum utensils, cookware, and packaging to be nontoxic, along with aluminum-containing antacids, food additives, and baking powder (94).

A maximum concentration of 2,310 µg/L of aluminum was detected in a residential well near the SE Area, east of Letterkenny. Other concentrations that were detected are the following: 405 (near the PDO Area) and 187.0 (near the SE Area) µg/L of aluminum. All of those were detected in off-site private wells near the SE Area, with the exception of 54.4 and 24.0 which were detected in off-site private wells near the PDO Area. The estimated daily exposures from ingestion of 2,310 µg/L of aluminum would be 2.31 mg/day for children and 4.62 mg/day for adults. Reports available on normal dietary levels of aluminum suggest that 20 mg/day may be an acceptable representation (94). Also, antacids and buffered aspirin, which are often taken in multiple daily doses for prolonged periods, contain 4 - 562 mg/kg of aluminum. When large oral loads of aluminum (1,000 - 4,000 mg/day) in the form of antacids are ingested, some of this excess aluminum is absorbed, with an aluminum retention rate of 0.3 - 10% (94). Therefore, adverse health effects from ingestion of aluminum in drinking water wells are not likely to occur.

Patients who have Alzheimer's disease may be more vulnerable to the effects of aluminum than other people. A number of factors other than aluminum are known to be associated with Alzheimer's and other neurodegenerative diseases, including genetic factors, viral infections, and immune system dysfunction (94). Although exposure to low levels of aluminum in the drinking water and food is unlikely to alter the clinical course of the disease in those persons, ingestion of large amounts, such as in multiple daily doses of antacids, should be avoided (96). Some studies show that people with Alzheimer's disease have more aluminum than usual in their brains. We do not know for certain whether aluminum accumulation is a result of the disease or its cause (95). Persons with Alzheimer's who were also exposed to aluminum-contaminated well water may be more sensitive to the health effects.

Aluminum metal has a wide variety of uses; the majority is as a structural material in the construction, automotive, and aircraft industries. Workers in the aluminum industry often work in potrooms where hot aluminum metal is recovered from the ore and they are thus exposed to aluminum dust. They can get more aluminum dust than normal into their lungs (94). Persons who were employed by those industries and using wells that contained aluminum may have had additional exposures to aluminum in the workplace.

Lead

Residents were exposed to lead when they ingested contaminated water from their private wells. Lead, like most metals, is very poorly absorbed through the skin and is not a volatile compound (97). Thus, ingestion is the only route of exposure to residents with lead-contaminated wells.

The EPA has concluded that human data is inadequate to determine the potential carcinogenicity of lead exposure. However, based on animal studies, the EPA has classified lead as a probable human carcinogen (Group B2) via ingestion. Exposure to lead salts has resulted in kidney tumor development in laboratory animals. Case reports have implicated lead as a potential renal carcinogen in humans (97). However, at this time, no health guidelines are available to evaluate the potential carcinogenicity of lead exposure in adults and children.

A maximum concentration of 54.4 µg/L of lead was detected in residential wells in July 1991; other concentrations that were detected are the following: 43.3, 31.9, 24.0, 17.2, and 15.8 µg/L of lead. All of those were detected in off-site private wells near the SE Area, with the exception of 54.4 and 24.0 which were detected in off-site private wells near the PDO Area. The EPA Office of Drinking Water has established 15 µg/L as an action level for lead in drinking water (43). The estimated daily exposures from ingestion of 54.4 µg/L of lead is 3.40 µg/kg/day for children and 1.55 µg/kg/day for adults.

The National Academy of Science has established 3,000 g/week (or 6.12 µg/kg/day) for adults as the Acceptable Daily Intake (ADI) for lead (97). The ADI is an estimate of the daily exposure dose that is likely to be without harmful effects even if continued exposure occurs over a lifetime. The daily estimated ingestion exposure from ingestion of lead in off-site private wells would be about 1.55 µg/kg/day for adults, or about 25% of the ADI. The actual exposure would be lower because 100% absorption is unlikely (97). Therefore, adverse noncancerous health effects are not expected from adults off-site of Letterkenny who ingested lead in private well water.

Most adverse health effects that have been observed in people are based on blood-lead levels. Children are especially sensitive to lead toxicity. Because lead is ubiquitous in the environment, many children have elevated blood-lead concentrations approaching those believed to cause adverse health effects (10 µg/dL) (19, 97). As a result, any additional exposure to lead may be potentially harmful.

The National Academy of Science has established < 3,000 µg/week (or < 26.79 µg/kg/day) for children as the Acceptable Daily Intake (ADI) for lead (97). The daily estimated ingestion exposure from ingestion of lead in off-site private wells would be about 3.40 µg/kg/day for children, or about 13% of the ADI. Absorption of lead in children is not 100%, but it is expected to be above 50%. Lead exposure in children could increase the blood-lead levels of children and adults since lead is present in the ambient environment. Lead concentrations of 15.8 µg/l may increase the blood-lead level in children to an estimated 1.10 µg of lead/dL of blood. Lead concentrations of 54.4 µg/l may increase the blood-lead level in children to an estimated 3.90 µg of lead/dL of blood. Since these are estimates, the increases in blood-lead levels may be slightly higher or lower. Those increases in blood-lead levels may add to the body burden of lead in children off-site of Letterkenny. Residents with lead detected above the EPA action level of 15 µg/l have been notified of their private well sampling results and referred to a health professional at the Pennsylvania Department of Health. Residents have also been advised of corrective measures that can be taken to reduce lead levels in their water, if the source of lead is the residential piping system. However, persons with lead detected in their water, especially those with levels above the EPA action level of 15 µg/l, need to be reminded to take precautions (such as flushing the water lines) to reduce the amount of lead in their water.

The most sensitive target of lead poisoning is the nervous system. The developing nervous system in children can be adversely affected at blood-lead levels of less than 10 µg/dL. Effects of lead exposure in children include deficits in IQ score, cognitive function, psychometric intelligence scores, speech and language processing, attention span, hearing acuity, motor skills, reaction time, and hand-eye coordination (19, 97). Because of those findings and the lack of health guidelines established for ingestion of lead, continued exposure to lead at levels above the EPA action level of 15 µg/l in drinking water is not recommended.

Certain subgroups of the population may be more susceptible to the harmful effects of lead exposure. Those groups include preschool age children (<6 years old), pregnant women, the elderly, smokers, alcoholics, and people with genetic diseases affecting heme synthesis (a component of the blood), nutritional deficiencies, and neurological or kidney dysfunction (97). Therefore, people who either are currently being exposed or were exposed to lead-contaminated water and belong to the groups previously discussed may be more susceptible to the harmful effects of lead.

Lead has been used for many different purposes. The major sources of lead released to water are lead plumbing and solder in houses, schools, and public buildings (19, 97). It has been used in the production of some types of batteries in industrial settings, and in the production of ammunition and some kinds of metal products (such as sheet lead, solder, and pipes). For older wells, the most common use of lead has been in the construction of such wells and associated piping. Some chemicals containing lead, such as tetraethyl lead and tetramethyl lead, are used as gasoline additives. However, the use of these lead-containing chemicals in gasoline is much less than it used to be, because these additives are being phased out. Other chemicals containing lead are used in paint. The amount of lead added to paints and ceramic products, roofing, caulking, ammunition, gasoline additives, and solder has been reduced in recent years because of lead's harmful effects in humans and animals. Currently, workers may be exposed to lead in a wide variety of occupations including smelting and refining industries, steel welding and cutting operations, battery manufacturing plants, gasoline stations, and radiator repair shops (97). Persons who were employed by lead industries and have wells with lead detected above the EPA action level may have additional workplace exposures.

Summary - Past, Present, and Future Completed Pathways - Groundwater From Private Wells

Off-site residents have been exposed to carbon tetrachloride, aluminum, and lead for approximately one year, possibly longer for aluminum and lead. Exposure to carbon tetrachloride was stopped when the residence was connected to municipal water in May of 1992, and no adverse health effects are expected from past exposures to carbon tetrachloride and aluminum. However, continued chronic exposure to lead above the EPA action level of 15 µg/L may result in adverse health effects in children over time; exposure to lead concentrations greater than the action level is not recommended.

Past, Present, and Future Completed Pathways - Surface Water - SE Area

Four contaminants were detected above comparison values in surface water emanating from the SE Area. Those contaminants include 1,1,1-trichloroethane, trans-1,2-dichloroethene, trichloroethene, and tetrachlorethane (Table 6, Appendix 3). The contaminants were detected off-site in Conochocheague Creek, Rowe Run, and Rowe Run Spring. Because those surface water bodies are shallow, swimming in them is not possible, and no fish were observed (20). Possible routes of exposure would be accidental ingestion, dermal contact, and inhalation of volatilized VOCs. The potential receptor population for the SE surface water/groundwater pathway would be those persons who use those surface waters for recreational activities, such as wading, or for watering farm animals (farmers). However, if accidental exposure to emerging groundwater or surface waters were to occur, the SE groundwater/surface water pathway would be complete on an intermittent basis. Human exposure to the previously detected concentrations of VOCs in this open area is not expected to result in adverse health effects because of the limited duration of exposure.

Past, Present, and Future Completed Pathways - Surface Water - PDO Area

In surface waters of Rocky Spring Creek and Lake of the PDO Area, ten contaminants were detected above comparison values; they include trichloroethene, 1,1,1-trichloroethane, trans-1,2-dichloroethene, chloroform, 1,1-dichloroethene, 1,1-dichloroethane, methylene chloride, 1,1-dichloroethane, tetrachlorethane, and chlorobenzene (Table 5). The Rocky Spring Lake/Creek system is not used as a water supply. Swimming in the lake is prohibited and thus the possible routes of exposure would be accidental ingestion, dermal contact, and inhalation of volatilized VOCs.

The potential receptor population for the PDO surface/groundwater pathway is limited to installation personnel, their dependents, and guests who use the Rocky Spring Lake/Creek system for recreational activities and maintenance/remedial workers who work with monitoring wells. As long as maintenance/remedial workers use personal protective equipment and follow appropriate procedures during maintenance and remedial activities, exposure to contaminants will be diminished. However, if accidental exposure to groundwater or surface waters of the Rocky Spring Creek/Lake system does occur, the PDO Area surface water/groundwater pathway would be complete on an intermittent basis. Human exposure to the previously detected concentrations of VOCs in the open area is not expected to result in adverse health effects because of the limited duration of exposure.

Past, Present, and Future Completed Pathways - Off-Site Biota and Food Crops - Near the SE Area

Off-site food crops irrigated and farm animals (and associated products) watered with contaminated water are completed exposure pathways. Primarily TCE and other VOCs have been detected in off-site springs/wells near the SE Area that may be used for those uses (Table 6). However, volatilization during the irrigation process removes up to 97 percent of trichloroethene (27). Additionally, TCE (and most VOCs) are not readily taken up by plants (27) so food crop consumption probably does not represent a significant exposure. Dairy cows drink from the contaminated springs and creeks and consumption of their milk may represent a chronic exposure. Most VOCs are lipophilic so that VOC concentrations in milk may be greater than whole animal concentrations (25). No data are available to estimate contaminant concentrations or doses with respect to the food chain/biota pathway. Biota studies are planned during 1993.

Past, Present, and Future Completed Pathways - Fish From Rocky Spring Lake

Rocky Spring Lake has been stocked primarily with rainbow trout, but the lake is also inhabited by brown trout, brook trout, large-mouth bass, crappie, catfish, and bluegills. Fish consumed from Rocky Spring Lake are a point of exposure to contaminants in the PDO surface/groundwater pathway (Table 8). The receptor populations are the installation personnel, their dependents, guests, and anyone else who consumes the fish. Thus far, mercury, pesticides, and VOCs have been detected at levels below the U.S. Food and Drug Administration threshold levels for fish consumption (41) and the EPA's Acceptable Risk-Based Concentrations (44). From limited sampling conducted thus far, the levels of substances detected in fish tissue at Rocky Spring Lake are not expected to result in adverse health effects. Additional sampling in 1992 of fish tissue, algae, and surface water detected no mercury concentrations above federal standards; however, the results have not yet been released. Samples of fish tissue, algae, and surface water will again be collected and analyzed for mercury during April through September of 1993.

C. Health Outcome Data Evaluation

Health outcome data have been evaluated because past exposures have occurred to some compounds that are potential or probable carcinogens and because the community is concerned about possible health effects associated with using contaminated groundwater. County-level health outcome data were available for review. Knowledge of the duration exposure together with site-specific health outcome data are necessary to determine possible adverse health effects from site-related exposures.

Letterkenny Army Depot borders three townships. The Pennsylvania Department of Health provided cancer mortality data and census information for the state of Pennsylvania and for the three townships (Greene, Hamilton, and Letterkenny) that Letterkenny borders. Data included age-sex specific distribution of the populations of the townships and average annual sex-specific death rates of Pennsylvania, 1979-1981. After reviewing the data, ATSDR found no elevated rates of cancer for the townships that Letterkenny Army Depot occupies (Tables 1-3, Appendix 3).

The Riggans Mortality Tapes, a database of cancer mortality maintained by EPA and NCI, were also reviewed. The database includes virtually all cancer death records for 1950-1979. The cancer mortality rates are reported by county for each of the three decades 1950-1959, 1960-1969, and 1970-1979. In addition, the percent change from 1950-59 to 1970-79 is included in the data. Data from death certificates were obtained from the National Center for Health Statistics and the Bureau of the Census. The cause of death is coded by the International Classification of Disease (ICD) codes. The information is provided for four sex-race groups: white male, white female, nonwhite male, and nonwhite female (49).

Analysis of three decades of data from the Riggans Mortality Tapes did not indicate a pattern of elevated cancer mortality rates for the race/sex groups of Franklin County. Although Pennsylvania's cancer mortality rates are slightly higher than the national average, the rates for Franklin County were not elevated across any of the race/sex groups.

D. Community Health Concerns Evaluation

This section will evaluate health-related community concerns that were introduced in the Community Health Concerns section. The following health concerns were voiced by the community and are addressed below:

1. What are the potential long-term health effects from ingesting contaminated well water?

The private well contamination in the neighborhoods east of the SE Area boundary (Figure 4) of Letterkenny resulted in past exposures for residents who used the water for drinking and other household purposes. However, the actual duration of the past exposures is unknown. Exposures stopped when the 41 wells, primarily at off-site residences and a few businesses, with VOCs detected above MCLs were replaced with municipal water. Possible health effects associated with past use of water containing a mixture of VOCs are unknown, largely because of the lack of exposure duration information and published data on health effects stemming from low-level, chronic exposure to multiple contaminants. Past exposure to some of the individual VOCs may have resulted in an increased risk of developing cancer, based on continuous exposure to the maximum concentrations detected. For that reason, health outcome data were evaluated. Evaluation of the health outcome data from 1959 to 1979 and 1979 to 1981 (one database was from mortality rates from 1950 to 1979 and the other database was from 1979 to 1981) found no elevated cancer mortality rates for men or women of Franklin County.

Different wells at other off-site residences were detected with carbon tetrachloride, aluminum, and lead. Those homeowners were advised of the sampling results and referred to a health professional at the Pennsylvania Department of Health. Exposure to carbon tetrachloride was stopped when that one residence was supplied an alternate water source in May 1992; that exposure is not expected to result in adverse health effects. Exposure to aluminum is not expected to result in adverse health effects. However, continued chronic exposure to lead above the EPA action level of 15 µg/L may result in adverse health effects in children. Persons with lead detections above the EPA action level should be reminded of the corrective actions they can take to reduce the amount of lead in their wells. The current data is based on one sampling event; therefore, those wells should be resampled both at the wellhead and at the tap to verify those present levels. Additional sampling of those wells and a hydrogeological study will be performed during 1993.

2. Will well water will be safe to use again in the future?

Two types of remediation are being used to reduce the amount of contamination that is present in the SE Area soils in the lagoon area. (The SE Area soils in the lagoon area were determined to be the main contaminant source for 41 off-site wells which were detected with VOCS exceeding appropriate drinking water standards during 1982 to 1987.) Remediation of the soils and groundwater in that area have occurred in an attempt to prevent further contamination migration from soils into the groundwater. Letterkenny is currently using a groundwater treatment system to reduce VOCs in the groundwater and has been operating since 1989. Likewise, low thermal treatment was begun in January of 1992 to treat the lagoon soils. The process involved excavating down to the bedrock, treating the soils (the contamination source) of the SE Area with a low thermal temperature treatment, and returning them to the same area after treatment. The lagoon area was capped upon the return of the treated soils to the excavated area. Lagoon closure operations were completed in November of 1992 with lagoon closure certification to follow in early 1993 (106). The K Area soils in the SE Area will also be remediated with low thermal temperature treatment during 1993.

It would be very difficult to predict if or when the off-site private well water will be safe to consume again; monitoring is the only way to guarantee the water is safe. Residents who are using municipal water for drinking and other household uses are not being exposed to contaminated well water. However, some of those off-site private wells are still being used to water food crops and farm animals and could be used for household purposes, such as washing cars; therefore, accidental ingestion of private well water, inhalation of vapors, and food chain exposures are still possible. Additional biota and environmental characterization off-site near the SE Area is planned for 1993 and may delineate those potential exposure pathways.

3. Is the incidence of cancer on my neighbor's street unusually high and is it related to the contaminants from Letterkenny Army Depot?

Analysis of available health outcome data found no elevated cancer mortality rates for neither men nor women of Franklin County. ATSDR evaluates health outcome data for adverse health affects in areas adjacent to hazardous waste sites on the NPL. Health outcome data have been evaluated because past exposures have occurred to some compounds that are potential or probable carcinogens and because the community is concerned about possible health effects associated with using contaminated groundwater. Health outcome data is not exposure specific; therefore, cancer deaths cannot be connected to any specific cause. County-level health outcome data were available for review. A more thorough review requires a knowledge of exposure duration and site-specific health outcome data at the community level.

Additional environmental sampling currently being performed both on- and off-site will be evaluated to determine the potential for contaminant exposure to result in noncancerous and/or cancerous health effects.

Next Section          Table of Contents


Agency for Toxic Substances and Disease Registry, 1825 Century Blvd, Atlanta, GA 30345
Contact CDC: 800-232-4636 / TTY: 888-232-6348
 
USA.gov: The U.S. Government's Official Web Portal