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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 effectsthat may result from exposures to environmental contaminants,available health outcome data, public health concerns. TheToxicologic Evaluation section will assess the toxicologic andcarcinogenic effects of exposure to contaminants that are abovecomparison values relative to the complete and potential exposurepathways. The Health Outcome Data Evaluation section evaluatesavailable community health information to determine whetheradverse health effects have occurred. The Community HealthConcerns Evaluation section discusses public health concernsvoiced by the community about possible exposure to contaminantsrelative to documented exposures and potential health effects.

B. Toxicologic Evaluation

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

In order to understand health effects that may be caused by aspecific chemical, it is helpful to review factors related to howthe human body processes the chemical after exposure. Thosefactors include the exposure concentration (how much), theduration of exposure (how long), the route of exposure(breathing, eating, drinking, or skin contact), and themultiplicity of exposure (combination of contaminants). Onceexposure occurs, individual characteristics such as age, sex,nutritional status, health status, lifestyle, and geneticsinfluence how the chemical is absorbed, distributed, metabolized(processed), and excreted (eliminated). Together, those factorsdetermine potential health effects that exposed people may have.

To determine the possible health effects of specific chemicals,ATSDR researches scientific literature. The resultinginformation is compiled and published in a series of chemical-specific ATSDR documents called Toxicological Profiles. Toxicological Profiles are references that describe adversehealth effects that could be associated with exposure to aspecific chemical in the environment. In addition, they includehealth guidelines such as ATSDR's minimal risk levels (MRLs) andEPA's reference doses (RfDs), reference concentrations (RfCs),and cancer slope factors (CSFs). When RfDs, RfCs, and MRLs arenot available, a no observed adverse effect level (NOAEL) orlowest observed adverse effect level (LOAEL) may be used toestimate levels below which no adverse health effects(noncancerous) are expected.

ATSDR compares a variety of health guidelines to contaminantconcentrations 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 ofcontaminants is likely to cause an increased risk of developingcancer and/or noncancerous adverse health effects. ATSDR's MRLis an estimate of daily human exposure to a chemical not likelyto cause an appreciable risk of harmful effects (noncancerous)over a specified duration of exposure. MRLs are based on humanand animal studies and are reported for acute (less than or equalto 14 days), intermediate (15-364 days), and chronic (greaterthan or equal to 365 days) exposures. If a person's dailyexposure is below the MRL, adverse health effects are notexpected. An RfD is EPA's estimate of the daily oral (ingestion)exposure not likely to cause appreciable risk of harmfulnoncancerous effects during a persons's lifetime (70 years). Likewise, an RfC is EPA's estimate of the daily inhalationexposure not likely to cause appreciable risk of harmfulnoncancerous effects during a person's lifetime (70 years). Boththe RfD and RfC take into account sensitive subpopulations.

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

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

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

The maximum contaminant concentration detected in a particularmedium is used to estimate exposure doses. Using the maximumconcentration to evaluate exposure results in an evaluationprotective of public health, because without historical exposuredata, contaminants may have been greater or lower than thepreviously detected concentrations.

Off-site residents, adjacent to the SE Area, may have beenexposed to multiple chemicals by ingestion of, skin contact with,and inhalation of VOC-contaminated well water. Most of the wellsbelonged to residents, but a few of them belonged to businesses. Data are very limited, however, on the health effects of multiplechemical exposures by oral, dermal, and inhalation routes. Effects of specific contaminants detected in multiple media maybe additive, synergistic, or antagonistic. Although some studiesindicate that simultaneous exposure to contaminants that areknown or probable human carcinogens might increase the risk ofdeveloping cancer and/or noncancerous health effects, the levelsat which those effects may occur are unknown (100-105). Currentresearch involving complex chemical mixtures will eventually addnew information that will be used in future evaluations.

Past Completed Pathway - Groundwater From Private Wells

Private well water contamination in neighborhoods east (adjacentto the SE Area) of Letterkenny Army Depot represent a past-completed exposure pathway for residents who used the water fordrinking and other household purposes (such as cooking, bathing,mopping, and showering). Contaminants detected in those privatewells (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 apotable water supply when contamination above MCLs was detectedin 1982. Primary exposure points for the SE Area surfacewater/groundwater pathway were off-site private wells andsprings. The main contamination source has been identified asthe former industrial lagoon. Water from contaminated wells werereplaced with bottled drinking-water. Those residences, and afew businesses, were later connected to the Guilford WaterAuthority System. Conversion to a centralized water-supplysystem began in October 1982 and was completed in 1987. Exposureto contaminated groundwater between 1982 and 1987 was throughshowering, bathing, mopping, washing cars, etc. It's unlikelythat ingestion would account for exposure in those persons, sincewells with VOCs exceeding MCLs were replaced with bottled water(109). Inhalation of and dermal contact with VOCs would haveaccounted 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 atthe lagoon area in 1954, until 1982, when VOCs greater than MCLswere detected in off-site private wells. However, it is veryunlikely that exposure could have occurred for that length oftime. The actual duration of exposure during the 33-yearinterval is unknown, and it would be difficult to reasonablypredict the length of time that exposure could have occurred. Periodic monitoring of off-site wells/springs has indicated thatcontaminant concentrations have decreased since VOCs above MCLswere first discovered in 1982 (41, 42, 106).

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

The following paragraphs evaluate potential health effects fromcontaminant exposure via inhalation of and dermal contact withspecific, individual chemicals (VOCS) (Figure 4). For purposesof this assessment, the inhalation dose is considered to beapproximately equal to the estimated ingestion dose, and thedermal dose is estimated to be about equal to the estimatedingestion dose. Evaluation of potential risk for cancerousadverse health effects is based on the maximum concentrationdetected in private wells and EPA Cancer Slope Factors (CSFs), ifavailable 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 fromcontaminated wells east of the SE Area boundary (Figure 4). Allthree exposure routes are believed to be equally significant withregard to absorption of 1,1-DCE based on reports in theliterature (51).

A maximum concentration of 8.6 µg/L of 1,1-DCE was detected incontaminated private well water. Children and adults exposed to8.6 µg/L of 1,1-DCE would have estimated ingestion exposures of0.54 µg/kg/day and 0.25 µg/kg/day, respectively. Since theevidence for carcinogenicity in animals is restricted to twostudies, addressing inhalation and dermal contact, respectively,of 1,1-DCE in mice (83, 99), and since information from humans isinconclusive (51), 1,1-DCE has been classified as a possiblehuman carcinogen (Group C) by the EPA for both oral andinhalation exposure routes. (Group C is used by EPA tocategorize chemicals for which there is limited evidence ofcarcinogenicity in animals, but inadequate evidence or no datafrom epidemiologic studies in people.) Prior to 1982, ingestionand inhalation of 1,1-DCE at the maximum detected level may haveresulted in an increased cancer risk; however, it not possible toadequately address the potential for cancerous adverse healtheffects, because we do not know how long persons were actuallyexposed or what concentrations they were exposed to.

Adverse noncancerous effects are not expected to result fromingestion of 1,1-DCE because the levels detected in private wellseast of the SE Area would result in estimated exposure dosesbelow the minimal risk level (MRL) of 9 µg/kg/day. The MRL isthe estimated level below which adverse noncancerous effects arenot expected.

For 1,1-DCE, ATSDR has calculated a chronic inhalation MRL of 30ppb, which is approximately equal to estimated doses of 2.34 and0.82 µg/kg/day in children and adults, respectively. Assumingthe estimated exposures from inhalation of volatilized 1,1-DCEfrom showers and cooking are approximately equal to estimatedingestion exposures, no adverse noncancerous health effects wouldbe expected from inhalation of volatilized 1,1-DCE from pastcontaminated well water east of Letterkenny.

Although it is recognized that dermal contact with 1,1-DCE alsois a significant route of exposure (51), guidelines such as MRLs,RfDs, and NOAELS have not been established for dermal contact to1,1-DCE. However, assuming all three exposure routes (ingestion,inhalation, and dermal contact) are equally significant withregard to absorption of 1,1-DCE and assuming the estimatedexposures from ingestion of 1,1-DCE in well water would beapproximately equal to estimated dermal exposures, no adversehealth effects are expected from past dermal contact of 1,1-DCEcontaminated water used for showering or other householdactivities such as mopping, washing dishes, and washing cars.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation, ingestion, and dermalcontact) are evaluated. Assuming that the inhalation dose anddermal dose are approximately equal to the ingestion dose, therespective estimated doses for children and adults would be threetimes the ingestion dose. The total dose for children and adultswould be 1.62 and 0.75 µg/kg/day, respectively. Those totaldoses are below doses at which adverse health effects would beexpected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand 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 and0.25 µg/kg/day for children and adults, respectively. From 1982until 1987, ingestion and inhalation of 1,1-DCE at the maximumdetected level may have resulted in an increased cancer risk;however, it not possible to adequately address the potential forcancerous adverse health effects, because we do not know how longpersons were actually exposed or what concentrations they wereexposed to.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation and dermal contact) areevaluated. Assuming that the inhalation dose and dermal dose maybe approximately equal to the estimated ingestion dose, therespective estimated doses for children and adults would be threetimes the ingestion dose. Those total doses are below aconcentration expected to cause adverse health effects.

Also known as vinylidene chloride, 1,1-DCE is used to makevarious plastics, such as packaging materials (flexible films,e.g., plastic food wraps) and flame-retardant fabrics (51). Anational survey conducted by NIOSH (54), estimated that thelargest numbers of workers potentially exposed to DCE in theworkplace were special trade contractors or workers in thefabricated metal products or wholesale trade industries. Theoccupational groups with the largest numbers of exposed workerswere carpenters, warehousemen (not otherwise classified) andmiscellaneous 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 privatewell water.

Although information about populations that may be especiallysensitive to 1,1-DCE is from animal studies, the following groupsmay have been particularly susceptible to the chemical's toxiceffects 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, certaincentral nervous system dysfunctions, and people who are fasting(51). Increased susceptibility to 1,1-DCE toxicity is largelycaused by the formation of toxic intermediates during itsmetabolism (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 theyingested, inhaled, and dermally contacted T-1,2-DCE-contaminatedwater from their private wells. Although dermal exposure waspossible, dermal absorption of T-1,2-DCE is likely to be minimalcompared to inhalation, because it rapidly evaporates into theair (55). Studies of Letterkenny indicate that most of thecis/trans 1,2-dichloroethene (1,2-DCE) in Letterkenny groundwaterresults from the breakdown of trichloroethene (TCE) used in SEArea operations (106).

The literature showed no exposure studies of animals or peoplethat investigate the possible carcinogenicity of T-1,2-DCE,although one study is currently investigating the potential forcancerous effects of 1,2-DCEs following acute oral exposure (55,56, 57). Prior to 1982, exposure occurred via ingestion andinhalation 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 possiblecarcinogenicity of T-1,2-DCE are available, ATSDR can address thepotential for cancerous adverse health effects from T-1,2-DCEexposure. At this time, T-1,2-DCE is not believed to be aprobable human carcinogen.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation and dermal contact) areevaluated. Assuming that the inhalation dose and dermal dose maybe approximately equal to the estimated ingestion dose, therespective estimated doses for children and adults would be threetimes the ingestion dose. Those total doses are below thechronic ingestion RfD of 20 µg/kg/day for T-1,2-DCE. The RfD isthe estimated level below which adverse noncancerous effects arenot expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand dermal exposure doses.

A maximum concentration of 66 µg/L was detected in residentialwells east of the Letterkenny. The estimated daily exposuresfrom ingestion of 66 µg/L of T-1,2-DCE would have been 4.13µg/kg/day for children and 1.89 µg/kg/day for adults. Thoseestimated doses are below the T-1,2-DCE chronic RfD of 20µg/kg/day. The RfD is the estimated level below which adversenoncancerous effects are not expected. For T-1,2-DCE, no healthguidelines, 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 expectedwhen multiple exposure routes (inhalation and dermal contact) areevaluated. Assuming that the inhalation dose and dermal dose maybe approximately equal to the estimated ingestion dose, the totaldose would be two times the ingestion dose. The total dosesbelow the chronic ingestion RfD of 20 µg/kg/day for T-1,2-DCE. The RfD is the estimated level below which adverse noncancerouseffects are not expected.

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

Chloroform

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

A maximum concentration of 2.8 µg/L of chloroform was detected incontaminated private well water. Children and adults exposed to2.8 µg/L of chloroform would have estimated ingestion exposuresof 0.18 and 0.08 µg/kg/day for children and adults, respectively. Little information exists about the development of cancer inpeople who have been chronically exposed to chloroform. However,using animal studies, EPA has classified chloroform as a probablehuman carcinogen (Group B2) when ingested and inhaled (59). Theterm "Group B2" is used by EPA to categorize chemicals for whichthere is sufficient evidence of carcinogenicity in animals, butinadequate evidence or no data from epidemiologic studies inpeople (60, 61). Prior to 1982, ingestion and inhalation ofchloroform at the maximum detected level would not have resultedin an increased cancer risk. It is not known how long personswere actually exposed or what concentrations they were exposedto.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation, ingestion, and dermalcontact) are evaluated. Assuming the estimated exposures frominhalation of volatilized chloroform from showers and cooking areapproximately equal to the estimated ingestion exposure dose andassuming the dermal exposure approximates the estimated ingestiondose, the total estimated dose would be three times the estimatedingestion dose. Those doses are below the chronic oral RfD of 10µg/kg/day for chloroform. Therefore, no adverse noncanceroushealth effects would be expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand dermal exposure doses.

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

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation and dermal contact) areevaluated. Assuming the inhalation and dermal doses areapproximately equal to the estimated ingestion exposure dose, thetotal estimated dose would be two times the estimated ingestiondose. Those doses are below the chronic oral RfD of 10 µg/kg/dayfor chloroform. Therefore, no adverse noncancerous healtheffects would be expected.

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

Chloroform was previously used as an anesthetic, but it has beenreplaced by safer and more versatile materials (62). Chloroform,also known as trichloromethane, enters the environment fromchemical companies, paper mills, waste water from sewagetreatment plants, and drinking water that contains chlorine. Chlorine is added to most drinking water and many waste waters todestroy bacteria. Those who work in industries that usechloroform can be exposed to higher than normal amounts ofchloroform (59). Residents east of the SE Area who were employedby such industries may have had work-related exposures tochloroform in addition to exposures from using private wellwater.

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 theyingested 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) orpeople that have conclusively shown 1,1,1-TCA to be a carcinogenfollowing ingestion of 1,1,1-TCA. One study (Quast et al 1988)demonstrated no evidence of carcinogenicity by the inhalationroute (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 inoff-site water wells east of Letterkenny. The estimated dailyexposures from ingesting 92 µg/L would be 5.75 g/kg/day forchildren and 2.63 µg/kg/day for adults. Health guidelines havenot been established for noncancerous health effects in peoplewho inhale or ingest, or have dermal contact with 1,1,1-TCA. Guidelines are needed to determine what levels of 1,1,1-TCA couldbe associated with those exposure routes.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation, ingestion, and dermalcontact) are evaluated. One long-term occupational study foundthat central nervous system effects ranged from 200,000 - 900,000ppb of 1,1,1-TCA (67). The study focused on inhalation exposureswith an average duration of 6.7 years per study group. Theresults from that study was used to approximate inhalation dosesfor children and adults to be 214 µg/kg/day for children and 75µg/kg/day for adults. Assuming the inhalation and dermal dosesare about equal to the estimated ingestion dose, adversenoncancerous effects via inhalation, ingestion, and dermalcontact are not expected. The total doses are below levels atwhich adverse health effects are expected to occur.

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

A maximum concentration of 92 µg/L was detected in off-site waterwells east of Letterkenny. The estimated daily exposures fromingesting 92 µg/L of 1,1,1-TCA would have been 5.75 µg/kg/day forchildren and 2.63 µg/kg/day for adults. Health guidelines havenot been established for noncancerous health effects in peoplewho inhale or ingest, or have dermal contact with 1,1,1-TCA. Guidelines are needed to determine what levels of TCA could beassociated with those exposure routes.

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

Animal studies show that nicotine enhances the harmful effects of1,1,1-TCA (69), suggesting that simultaneous exposure to nicotineand 1,1,1-TCA could pose an increased health risk in people. Therefore, smokers exposed to 1,1,1-TCA could have an increasedrisk of health effects compared with nonsmokers. Low doses ofethanol also enhances the harmful effects of 1,1,1-TCA (70),suggesting that increased health risks may be associated withsimultaneous exposure to those two chemicals. Phenobarbital,which is prescribed for certain cases of epilepsy, reportedlyenhances the hepatotoxicity of 1,1,1-TCA in rats (71). Thus, anincreased risk of hepatotoxicity may be associated withsimultaneous exposure to that drug and 1,1,1-TCA. The literaturesuggests that people who have cardiac arrhythmias also may bemore susceptible to the health effects of 1,1,1-TCA (65). Persons belonging to groups previously described and who alsowere exposed to 1,1,1-TCA in contaminated well water east ofLetterkenny may have been more susceptible to the health effectsfrom 1,1,1-TCA exposure.

1,1,1-TCA, is a synthetic chemical with many industrial andhousehold uses. It is often used as a solvent to dissolve othersubstances, e.g., glue and paint. In industry, it is widely usedto remove oil and/or grease from manufactured metal parts. Italso may be in household products such as spot cleaners, glues,and aerosol sprays (65). Thus, residents east of the SE Area whowere employed by those industries may have had other exposures to1,1,1-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 theyingested contaminated private well water. Ingestion, inhalation,and dermal contact were the routes of exposure to contaminatedwater. Dermal contact appears to be a more significant route ofexposure if large amounts are applied on the skin, which would bemore likely to happen in an occupational setting (72, 73, 74). Therefore, dermal contact is not as significant (but isevaluated) as the inhalation route of exposure to residents whoused contaminated well water for household purposes.

From water samples collected from private drinking water wellsnear the SE Area, a maximum concentration of 48 µg/L of TCE wasdetected. The estimated daily exposures of children and adultswho would have ingested a concentration of 48 µg/L of TCE fromwell water are 3 µg/kg/day and 1.37 µg/kg/day, respectively. Thecarcinogenicity 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, ingestionand inhalation of TCE at the maximum detected level may haveresulted in an increased cancer risk; however, it not possible toadequately address the potential for cancerous adverse healtheffects, because we do not know how long persons were actuallyexposed or what concentrations they were exposed to.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation, ingestion, and dermalcontact) are evaluated. Assuming the estimated exposures frominhalation of and dermal contact with TCE are approximately equalto the estimated ingestion exposure dose, the total estimateddose would be three times the estimated ingestion dose. Thetotal dose is below the chronic intermediate MRL of 100 µg/kg/dayfor ingestion of TCE. Therefore, no adverse noncancerous healtheffects would be expected.

Exposure During 1982 and 1987
Since bottled water was provided to persons with private wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand dermal exposure doses.

The potential for cancerous adverse health effects were evaluatedfor five years of exposure via inhalation and dermal contact. From 1982 until 1987, ingestion and inhalation of TCE at themaximum detected level may have resulted in an increased cancerrisk; however, it not possible to adequately address thepotential for cancerous adverse health effects, because we do notknow how long persons were actually exposed or whatconcentrations they were exposed to.

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

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation and dermal exposure) areevaluated. Assuming the inhalation dose and dermal dose mayapproximate the ingestion dose, the respective estimated dosesfor children and adults would be two times the estimatedingestion dose. Those total doses are below doses at whichnoncancerous adverse health effects would be expected.

Persons particularly susceptible to TCE exposures are chronicconsumers of alcohol, people with heart disease, people takingdisulfiram (a medication used to treat alcoholism), and peopletaking the anticoagulant warfarin (72). Those medicationsincrease the toxicity of TCE in the liver by interfering with itsnormal metabolism. Thus, residents who used contaminated wellseast of the SE Area and belonged to the above groups may havebeen more susceptible to health effects from TCE exposure.

According to the literature, TCE exposure usually occurs inoccupational settings where the chemical is used as a solvent toremove grease from metal parts (72). Products that may containTCE are some types of typewriter correction fluids, paints andpaint removers, glue, spot removers, rug-cleaning fluids, andmetal cleaners (72). Thus, residents east of the installationwho were employed by those industries or used those householdproducts may have been exposed to TCE in addition to contaminatedwater 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, inhalationof, and dermal contact with 1,1,2,2-PCA-contaminated water fromcontaminated wells east of the SE Area boundary. Based onreports in the literature, all three exposure routes are believedto be equally significant with regard to absorption of PCA (75).

Water samples collected from private drinking-water wells east ofLetterkenny contained a maximum concentration of 13 µg/L of1,1,2,2-PCA. The estimated daily exposures of children andadults who would have ingested a concentration of 13 µg/L of1,1,2,2-PCA are 0.81 µg/kg/day and 0.37 µg/kg/day, respectively. Since the evidence for carcinogenicity in animals is restrictedto two studies in mice (76, 77), and since information fromhumans is inconclusive (78), 1,1,2,2-PCA has been classified as apossible human carcinogen (Group C) by the EPA for both oral andinhalation exposure routes (79). Prior to 1982, ingestion andinhalation of 1,1,2,2-PCA at the maximum detected level may haveresulted in a slight increased cancer risk; however, it notpossible to adequately address the potential for cancerousadverse health effects, because we do not know how long personswere actually exposed or concentrations they were exposed to.

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

Exposure During 1982 and 1987
Since bottled water was provided to persons with private wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand dermal exposure doses.

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

There are no health guidelines for noncancerous health effectscaused by chronic exposure from ingestion and inhalation of ordermal contact with 1,1,2,2-PCA. However, workers in India'sbangle (ornamental bracelet or anklet) industry who dipped theirhands in 1,1,2,2-PCA, as well as inhaled it, had tremors,headaches, and dizziness in addition to gastric pains during 3 to6 months of exposure (80). Specific exposure levels are notknown, but air concentrations were detected to be between 9 and98 ppm (or between 9,000 ppb and 98,000 ppb for the LOAEL). Using the results from that study and assuming the inhalation andingestion doses to be approximately equal, adverse noncancerouseffects are not expected.

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

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation and dermal contact) areevaluated. Assuming the inhalation dose is approximately equalto the estimated ingestion dose associated with the contaminatedwater and assuming the dermal exposure dose is about equal theingestion exposure dose (0.81 µg/kg/day and 0.37 µg/kg/day forchildren and adults, respectively), the total estimated dosewould be two times those estimated ingestion dose which wouldcorrespond to respectively 1.62 and 0.74 µg/kg/day for childrenand adults). Those doses are below levels expected to result inadverse health effects.

1,1,2,2-PCA has been used in large amounts to produce otherchemicals and as an industrial solvent. It is also used toseparate other substances, to clean and degrease metals, and inpaints and pesticides. However, worker exposure to highconcentrations of 1,1,2,2-PCA is not likely, because it isgenerally used to produce other chemicals. That process takesplace in automatic systems, in which there is no human contactwith the product (75). Therefore, residents east of theinstallation who were employed by industries that use 1,1,2,2-PCAare not expected to have had additional exposures to 1,1,2,2-PCAother 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 byinhalation, ingestion, and dermal absorption of contaminatedgroundwater 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 containmore than 6 ppb of 1,2-DCA, exposure by ingestion is expected tobe more significant than inhalation (81). Because of the highvapor pressure of 1,2-DCA, it rapidly volatilizes thereby makingdermal contact less significant than the inhalation route ofexposure for residents east of Letterkenny (64, 81, 82). Studiesof Letterkenny indicate that most of the 1,2-DCA in Letterkennygroundwater results from the breakdown of 1,1,1-TCA.

A maximum concentration of 2.5 µg/L of 1,2-DCA was detected inwells east of the SE Area. Little information exists about thedevelopment of cancer in people who have experienced long-termexposure to 1,2-DCA. Using animal studies, however, EPA hasclassified 1,2-DCA as a probable human carcinogen (Group B2) fromboth ingestion and inhalation routes (76, 82, 83). Prior to1982, ingestion and inhalation of 1,2-DCA at the maximum detectedlevel would not have resulted in an increased cancer risk;however, it is not possible to adequately address the potentialfor cancerous adverse health effects, because we do not know howlong persons were actually exposed or what concentrations theywere exposed to.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation, ingestion, and dermalcontact) are evaluated. Assuming the inhalation dose and dermaldose is about equal to the estimated ingestion dose (0.16µg/kg/day for children and 0.07 µg/kg/day for adults) associatedwith the contaminated water, the total estimated dose would bethree times those estimated ingestion dose which would correspondto 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 astudy 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 wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand dermal exposure doses.

The potential for cancerous adverse health effects were evaluatedfor five years of exposure via inhalation and dermal contact. From 1982 until 1987, ingestion and inhalation of 1,2-DCA at themaximum detected level would not have resulted in an increasedcancer risk; however, it is not possible to adequately addressthe potential for cancerous adverse health effects, because we donot know how long persons were actually exposed or whatconcentrations they were exposed to.

There are no health guidelines for noncancerous health effectscaused by chronic exposure via ingestion and inhalation of ordermal contact with 1,2-DCA. However, in a study of the healtheffects of intermediate exposures (84), mice were given 1,2-DCA-contaminated water for approximately 90 days. The results showed189,000 µg/kg/day to be the NOAEL for adverse liver effects inmice. Applying an uncertainty factor of 1000, accounting foranimal-human variability, sensitive individuals, and durationvariability, would correspond to 189 µg/kg/day in people. Usingthe maximum concentration of 2.5 µg/L detected for 1,2-DCA, thedaily estimated ingestion dose for children and adults east ofLetterkenny would have been 0.16 µg/kg/day and 0.07 µg/kg/day,respectively. Assuming the inhalation and dermal dose isapproximately equal to the estimated ingestion dose, noncancerouseffects to the liver are not expected from past exposure. Thetotal dose for children and adults (0.32 and 0.14 µg/kg/day,respectively, which is two times the estimated ingestion dosesabove) is below the NOAEL of 189 µg/kg/day in people.

1,2-DCA is a clear, synthetic liquid used primarily to make vinylchloride and several solvents that remove grease, glue, and dirt. It is also added to leaded gasoline to remove excess lead. Inthe past, it was a component of some cleaning solutions andpesticides; some adhesives, such as those used to glue wallpaperor 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 theworkplace (82). The National Occupational Exposure Surveyconducted by the National Institute of Occupational Safety andHealth notes that workers are exposed to 1,2-DCA when it is usedas a fumigant, solvent, or diluent in open-system operations(82). People who have 1,2-DCA-contaminated well water east ofLetterkenny may have additional exposures to 1,2-DCA if they wereemployed in the occupations or industries discussed here.

Persons who were exposed to 1,2-DCA-contaminated wells and weretaking the medications, disulfiram or phenobarbital, used totreat alcoholism and seizures respectively, may have been highlysensitive to the effects of 1,2-DCA (82). Those drugs may altera person's metabolism, resulting in increased levels of theactive metabolites of 1,2-DCA. Reduced hepatic glutathione (GSH)also may alter the excretion of active metabolites. GSH plays aprotective role in the liver by helping the body excrete activemetabolites of 1,2-DCA. Reduced nutritional intake, such asfasting, can result in lowered GSH levels, which, as shown inanimal 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 byinhalation, ingestion, and dermal absorption of contaminatedgroundwater from residential wells. People were exposed tochlorobenzene mainly by breathing it from volatilization inshowers or by drinking it in chlorobenzene-contaminated water. Dermal contact with chlorobenzene is considered to be aninsignificant route of exposure for residents east of Letterkenny(85), compared to inhalation and ingestion.

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

A maximum concentration of 0.8 µg/L of chlorobenzene was detectedin wells east of the SE Area. Children and adults exposed to 0.8µg/L of chlorobenzene would have estimated ingestion exposures of0.05 µg/kg/day and 0.02 µg/kg/day, respectively. Adverse healtheffects to the liver and kidneys (88) are not expected, becauseestimated ingestion exposures are below the chronic oral RfD of20 µg/kg/day.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (ingestion, inhalation and dermalcontact) are evaluated. There are no health guidelines (RfCs,MRLs, etc.) for chronic inhalation of or dermal contact withchlorobenzene. However, assuming the inhalation and dermal doseare approximately equal to the estimated ingestion dose, thetotal dose for children and adults (0.15 and 0.06 µg/kg/day,respectively, which is three times the estimated ingestion dosesabove) 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 wellcontamination above MCLs, significant exposure via ingestion ofVOCs was eliminated. Although only inhalation and dermal contactare evaluated for adverse health effects, estimated ingestiondoses are provided since they are being compared to inhalationand dermal exposure doses.

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

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

By 1987, the production of chlorobenzene in the United Statesdeclined by nearly 60%. That decline is mainly attributed to thereplacement of chlorobenzene by another chemical (cumen) inphenol production and the end of DDT production in the UnitedStates. Since no major new uses have been found forchlorobenzene in recent years, its decline is expected tocontinue (89, 90, 91). Current primary uses of chlorobenzene are as a solvent for pesticide formulations, diisocyanatemanufacture, degreasing automobile parts, and for the productionof nitrochlorobenzene (85). Therefore, residents east of theinstallation who were employed by industries that usedchlorobenzene during the time of exposure could have hadadditional exposures to chlorobenzene other than those exposuresfrom 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 wereexposed to eight different VOCs by way of ingestion andinhalation of and dermal contact with VOC-contaminated water fromtheir private wells. Prior exposure to several VOCs which areprobable carcinogens at the maximum detected level may haveresulted in a slight increased cancer risk, if those levels orhigher were continuously present in private wells for a chronicexposure period. However, it not possible to adequately addressthe potential for cancerous adverse health effects, because we donot know how long persons were actually exposed or whatconcentrations they were exposed to. Noncancerous adverse healtheffects from ingestion and inhalation of and dermal contact withthe eight VOCs are not likely. Because of the lack of bothexposure duration information and published data on healtheffects stemming from low-level, chronic exposure to multiplechemicals, potential adverse health effects associated withmultiple-chemical exposure is at the time unknown.

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

Past, Present, and Future Completed Pathways - Groundwater FromPrivate Wells

Sampling of off-post residential well water during July 1991detected carbon tetrachloride, aluminum, and lead at maximumconcentrations of respectively, 0.81, 2310, and 54.4 µg/L (41). Those maximum concentrations are above comparison values (Table6). Only one well (near the SE Area) was detected to have carbontetrachloride and it was connected to municipal water by May 1992(92). That exposure pathway has been eliminated. Lead wasdetected in six wells at concentrations above the EPA actionlevel of 15 µg/L: 54.4 (near the PDO Area), 43.3 (near the SEArea), 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. Aluminumwas detected in three wells at concentrations above 50 µg/L, theEPA Secondary Maximum Contaminant Level (SMCL): 2,310 (near theSE Area), 405 (near the PDO Area), and 187 (near the SE Area)µg/L. Of those wells, both aluminum and lead were detected intwo wells (41). Those six wells with lead and aluminumdetections remain in service, and the past contaminationrepresents a past, present, and future completed exposurepathway. It is unknown how long those chemicals were present inthe off-site wells. The contaminant concentrations are evaluatedfor potential adverse health effects since they were detectedabove 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 forapproximately one year, according to sampling data, but it mayhave been longer. The following paragraphs evaluate that pastexposure.

Residents with the carbon-tetrachloride-contaminated well wereexposed to carbon tetrachloride by inhalation, ingestion, anddermal absorption of contaminated groundwater. Based on reportsin the literature, all three exposure routes are believed to beequally significant with regard to absorption of carbontetrachloride (93).

A maximum concentration of 0.81 µg/L of carbon tetrachloride wasdetected in one well east of the SE Area. Children and adultsexposed to 0.81 µg/L of carbon tetrachloride would have estimatedingestion exposures of 0.05 µg/kg/day and 0.02 µg/kg/day,respectively. The EPA has classified carbon tetrachloride as aprobable (Group B2) carcinogen by both ingestion and inhalationroutes. Ingestion and inhalation of carbon tetrachloride at themaximum detected level would not have resulted in an increasedcancer risk.

Noncancerous adverse health effects are not expected whenmultiple exposure routes (inhalation, ingestion, and dermalcontact) are evaluated. Assuming the inhalation dose and dermaldose are approximately equal the estimated ingestion exposuredose (0.05 and 0.02 µg/kg/day for children and adults,respectively), the total estimated dose would be three timesthose estimated ingestion dose which would correspond torespectively 0.15 and 0.06 µg/kg/day for children and adults. Noncancerous adverse health effects are not expected, because thetotal doses are below the chronic oral RfD of 0.70 µg/kg/day.

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

Persons who were exposed to carbon tetrachloride-contaminatedwell water and were taking the following medications or weremembers of the groups discussed in the following paragraphs mayhave been highly sensitive to the effects of carbon tetrachloride(93) during the time of exposure. Some drugs and other chemicalshave been detected to significantly increase the toxicity ofcarbon tetrachloride; some of the effects have only been observedin animals but they include: phenobarbital, pentobarbital,phenylbutazone, TCE, and substances with alcohols and ketones. In addition, a variety of conditions may predispose certainsegments of the population to carbon tetrachloride toxicity. Persons with alcoholic cirrhosis, or other liver diseases whichhave significantly reduced the function of the liver, have adiminished ability to tolerate carbon tetrachloride-inducedtoxicity. The same is true for carbon tetrachloride-inducedtoxicity of the kidneys in people with significant renaldysfunction from other causes. According to animal studies,diabetics and people who are fasting may also be more susceptibleto carbon tetrachloride toxicity (93).

Aluminum

Residents were exposed to aluminum when they ingestedcontaminated water from their private wells. Aluminum, like mostmetals, is very poorly absorbed through the skin and is not avolatile 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 inanimals or people that have found aluminum to be a carcinogen. In fact, aluminum is used to make antacids and antiperspirantsand used for the treatment of drinking water. Also, studies ofinteractions of aluminum and other materials that may be detectedat hazardous waste sites show that aluminum has a protectiveeffect against the toxic effects of other chemicals (94).

Despite the widespread occurrence of aluminum in foods anddrinking water, there is little indication that it is toxic bythis route. The FDA considers aluminum utensils, cookware, andpackaging to be nontoxic, along with aluminum-containingantacids, food additives, and baking powder (94).

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

Patients who have Alzheimer's disease may be more vulnerable tothe effects of aluminum than other people. A number of factorsother than aluminum are known to be associated with Alzheimer'sand other neurodegenerative diseases, including genetic factors,viral infections, and immune system dysfunction (94). Althoughexposure to low levels of aluminum in the drinking water and foodis unlikely to alter the clinical course of the disease in thosepersons, ingestion of large amounts, such as in multiple dailydoses of antacids, should be avoided (96). Some studies showthat people with Alzheimer's disease have more aluminum thanusual in their brains. We do not know for certain whetheraluminum accumulation is a result of the disease or its cause(95). Persons with Alzheimer's who were also exposed toaluminum-contaminated well water may be more sensitive to thehealth effects.

Aluminum metal has a wide variety of uses; the majority is as astructural material in the construction, automotive, and aircraftindustries. Workers in the aluminum industry often work inpotrooms where hot aluminum metal is recovered from the ore andthey are thus exposed to aluminum dust. They can get morealuminum dust than normal into their lungs (94). Persons whowere employed by those industries and using wells that containedaluminum may have had additional exposures to aluminum in theworkplace.

Lead

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

The EPA has concluded that human data is inadequate to determinethe potential carcinogenicity of lead exposure. However, basedon animal studies, the EPA has classified lead as a probablehuman carcinogen (Group B2) via ingestion. Exposure to leadsalts has resulted in kidney tumor development in laboratoryanimals. Case reports have implicated lead as a potential renalcarcinogen in humans (97). However, at this time, no healthguidelines are available to evaluate the potentialcarcinogenicity of lead exposure in adults and children.

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

The National Academy of Science has established 3,000 g/week (or6.12 µg/kg/day) for adults as the Acceptable Daily Intake (ADI)for lead (97). The ADI is an estimate of the daily exposure dosethat is likely to be without harmful effects even if continuedexposure occurs over a lifetime. The daily estimated ingestionexposure from ingestion of lead in off-site private wells wouldbe about 1.55 µg/kg/day for adults, or about 25% of the ADI. Theactual exposure would be lower because 100% absorption isunlikely (97). Therefore, adverse noncancerous health effectsare not expected from adults off-site of Letterkenny who ingestedlead in private well water.

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

The National Academy of Science has established < 3,000 µg/week(or < 26.79 µg/kg/day) for children as the Acceptable DailyIntake (ADI) for lead (97). The daily estimated ingestionexposure from ingestion of lead in off-site private wells wouldbe 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 tobe above 50%. Lead exposure in children could increase theblood-lead levels of children and adults since lead is present inthe ambient environment. Lead concentrations of 15.8 µg/l mayincrease the blood-lead level in children to an estimated 1.10 µgof lead/dL of blood. Lead concentrations of 54.4 µg/l mayincrease the blood-lead level in children to an estimated 3.90 µgof lead/dL of blood. Since these are estimates, the increases inblood-lead levels may be slightly higher or lower. Thoseincreases in blood-lead levels may add to the body burden of leadin children off-site of Letterkenny. Residents with leaddetected above the EPA action level of 15 µg/l have been notifiedof their private well sampling results and referred to a healthprofessional at the Pennsylvania Department of Health. Residentshave also been advised of corrective measures that can be takento reduce lead levels in their water, if the source of lead isthe residential piping system. However, persons with leaddetected in their water, especially those with levels above theEPA action level of 15 µg/l, need to be reminded to takeprecautions (such as flushing the water lines) to reduce theamount of lead in their water.

The most sensitive target of lead poisoning is the nervoussystem. The developing nervous system in children can beadversely affected at blood-lead levels of less than 10 µg/dL. Effects of lead exposure in children include deficits in IQscore, 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 guidelinesestablished for ingestion of lead, continued exposure to lead atlevels above the EPA action level of 15 µg/l in drinking water isnot recommended.

Certain subgroups of the population may be more susceptible tothe harmful effects of lead exposure. Those groups includepreschool age children (<6 years old), pregnant women, theelderly, smokers, alcoholics, and people with genetic diseasesaffecting heme synthesis (a component of the blood), nutritionaldeficiencies, and neurological or kidney dysfunction (97). Therefore, people who either are currently being exposed or wereexposed to lead-contaminated water and belong to the groupspreviously discussed may be more susceptible to the harmfuleffects of lead.

Lead has been used for many different purposes. The majorsources of lead released to water are lead plumbing and solder inhouses, schools, and public buildings (19, 97). It has been usedin the production of some types of batteries in industrialsettings, and in the production of ammunition and some kinds ofmetal products (such as sheet lead, solder, and pipes). Forolder wells, the most common use of lead has been in theconstruction of such wells and associated piping. Some chemicalscontaining 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 chemicalscontaining lead are used in paint. The amount of lead added topaints and ceramic products, roofing, caulking, ammunition,gasoline additives, and solder has been reduced in recent yearsbecause of lead's harmful effects in humans and animals. Currently, workers may be exposed to lead in a wide variety ofoccupations including smelting and refining industries, steelwelding and cutting operations, battery manufacturing plants,gasoline stations, and radiator repair shops (97). Persons whowere employed by lead industries and have wells with leaddetected above the EPA action level may have additional workplaceexposures.

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 longerfor aluminum and lead. Exposure to carbon tetrachloride wasstopped when the residence was connected to municipal water inMay of 1992, and no adverse health effects are expected from pastexposures to carbon tetrachloride and aluminum. However,continued chronic exposure to lead above the EPA action level of15 µg/L may result in adverse health effects in children overtime; exposure to lead concentrations greater than the actionlevel is not recommended.

Past, Present, and Future Completed Pathways - Surface Water - SEArea

Four contaminants were detected above comparison values insurface water emanating from the SE Area. Those contaminantsinclude 1,1,1-trichloroethane, trans-1,2-dichloroethene,trichloroethene, and tetrachlorethane (Table 6, Appendix 3). Thecontaminants were detected off-site in Conochocheague Creek, RoweRun, and Rowe Run Spring. Because those surface water bodies areshallow, swimming in them is not possible, and no fish wereobserved (20). Possible routes of exposure would be accidentalingestion, dermal contact, and inhalation of volatilized VOCs. The potential receptor population for the SE surfacewater/groundwater pathway would be those persons who use thosesurface waters for recreational activities, such as wading, orfor watering farm animals (farmers). However, if accidentalexposure to emerging groundwater or surface waters were to occur,the SE groundwater/surface water pathway would be complete on anintermittent basis. Human exposure to the previously detectedconcentrations of VOCs in this open area is not expected toresult in adverse health effects because of the limited durationof 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; theyinclude 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 SpringLake/Creek system is not used as a water supply. Swimming in thelake is prohibited and thus the possible routes of exposure wouldbe accidental ingestion, dermal contact, and inhalation ofvolatilized VOCs.

The potential receptor population for the PDO surface/groundwaterpathway is limited to installation personnel, their dependents,and guests who use the Rocky Spring Lake/Creek system forrecreational activities and maintenance/remedial workers who workwith monitoring wells. As long as maintenance/remedial workersuse personal protective equipment and follow appropriateprocedures during maintenance and remedial activities, exposureto contaminants will be diminished. However, if accidentalexposure to groundwater or surface waters of the Rocky SpringCreek/Lake system does occur, the PDO Area surfacewater/groundwater pathway would be complete on an intermittentbasis. Human exposure to the previously detected concentrationsof VOCs in the open area is not expected to result in adversehealth effects because of the limited duration of exposure.

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

Off-site food crops irrigated and farm animals (and associatedproducts) watered with contaminated water are completed exposurepathways. Primarily TCE and other VOCs have been detected inoff-site springs/wells near the SE Area that may be used forthose uses (Table 6). However, volatilization during theirrigation process removes up to 97 percent of trichloroethene(27). Additionally, TCE (and most VOCs) are not readily taken upby plants (27) so food crop consumption probably does notrepresent a significant exposure. Dairy cows drink from thecontaminated springs and creeks and consumption of their milk mayrepresent a chronic exposure. Most VOCs are lipophilic so thatVOC concentrations in milk may be greater than whole animalconcentrations (25). No data are available to estimatecontaminant concentrations or doses with respect to the foodchain/biota pathway. Biota studies are planned during 1993.

Past, Present, and Future Completed Pathways - Fish From RockySpring 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 consumedfrom Rocky Spring Lake are a point of exposure to contaminants inthe PDO surface/groundwater pathway (Table 8). The receptorpopulations 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 fishconsumption (41) and the EPA's Acceptable Risk-BasedConcentrations (44). From limited sampling conducted thus far,the levels of substances detected in fish tissue at Rocky SpringLake are not expected to result in adverse health effects. Additional sampling in 1992 of fish tissue, algae, and surfacewater detected no mercury concentrations above federal standards;however, the results have not yet been released. Samples of fishtissue, algae, and surface water will again be collected andanalyzed for mercury during April through September of 1993.

C. Health Outcome Data Evaluation

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

Letterkenny Army Depot borders three townships. The PennsylvaniaDepartment of Health provided cancer mortality data and censusinformation for the state of Pennsylvania and for the threetownships (Greene, Hamilton, and Letterkenny) that Letterkennyborders. Data included age-sex specific distribution of thepopulations of the townships and average annual sex-specificdeath rates of Pennsylvania, 1979-1981. After reviewing thedata, ATSDR found no elevated rates of cancer for the townshipsthat Letterkenny Army Depot occupies (Tables 1-3, Appendix 3).

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

Analysis of three decades of data from the Riggans MortalityTapes did not indicate a pattern of elevated cancer mortalityrates for the race/sex groups of Franklin County. AlthoughPennsylvania's cancer mortality rates are slightly higher thanthe national average, the rates for Franklin County were notelevated across any of the race/sex groups.

D. Community Health Concerns Evaluation

This section will evaluate health-related community concerns thatwere introduced in the Community Health Concerns section. Thefollowing health concerns were voiced by the community and areaddressed below:

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

The private well contamination in the neighborhoods east of theSE Area boundary (Figure 4) of Letterkenny resulted in pastexposures for residents who used the water for drinking and otherhousehold purposes. However, the actual duration of the pastexposures is unknown. Exposures stopped when the 41 wells,primarily at off-site residences and a few businesses, with VOCsdetected above MCLs were replaced with municipal water. Possiblehealth effects associated with past use of water containing amixture of VOCs are unknown, largely because of the lack ofexposure duration information and published data on healtheffects stemming from low-level, chronic exposure to multiplecontaminants. Past exposure to some of the individual VOCs mayhave resulted in an increased risk of developing cancer, based oncontinuous exposure to the maximum concentrations detected. Forthat reason, health outcome data were evaluated. Evaluation ofthe health outcome data from 1959 to 1979 and 1979 to 1981 (onedatabase was from mortality rates from 1950 to 1979 and the otherdatabase was from 1979 to 1981) found no elevated cancermortality rates for men or women of Franklin County.

Different wells at other off-site residences were detected withcarbon tetrachloride, aluminum, and lead. Those homeowners wereadvised of the sampling results and referred to a healthprofessional at the Pennsylvania Department of Health. Exposureto carbon tetrachloride was stopped when that one residence wassupplied an alternate water source in May 1992; that exposure isnot expected to result in adverse health effects. Exposure toaluminum is not expected to result in adverse health effects. However, continued chronic exposure to lead above the EPA actionlevel of 15 µg/L may result in adverse health effects inchildren. Persons with lead detections above the EPA actionlevel should be reminded of the corrective actions they can taketo reduce the amount of lead in their wells. The current data isbased on one sampling event; therefore, those wells should beresampled both at the wellhead and at the tap to verify thosepresent levels. Additional sampling of those wells and ahydrogeological 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 ofcontamination that is present in the SE Area soils in the lagoonarea. (The SE Area soils in the lagoon area were determined tobe the main contaminant source for 41 off-site wells which weredetected with VOCS exceeding appropriate drinking water standardsduring 1982 to 1987.) Remediation of the soils and groundwaterin that area have occurred in an attempt to prevent furthercontamination migration from soils into the groundwater. Letterkenny is currently using a groundwater treatment system toreduce VOCs in the groundwater and has been operating since 1989. Likewise, low thermal treatment was begun in January of 1992 totreat the lagoon soils. The process involved excavating down tothe bedrock, treating the soils (the contamination source) of theSE Area with a low thermal temperature treatment, and returningthem to the same area after treatment. The lagoon area wascapped upon the return of the treated soils to the excavatedarea. Lagoon closure operations were completed in November of1992 with lagoon closure certification to follow in early 1993(106). The K Area soils in the SE Area will also be remediatedwith low thermal temperature treatment during 1993.

It would be very difficult to predict if or when the off-siteprivate well water will be safe to consume again; monitoring isthe only way to guarantee the water is safe. Residents who areusing municipal water for drinking and other household uses arenot being exposed to contaminated well water. However, some ofthose off-site private wells are still being used to water foodcrops and farm animals and could be used for household purposes,such as washing cars; therefore, accidental ingestion of privatewell water, inhalation of vapors, and food chain exposures arestill possible. Additional biota and environmentalcharacterization off-site near the SE Area is planned for 1993and 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 elevatedcancer mortality rates for neither men nor women of FranklinCounty. ATSDR evaluates health outcome data for adverse healthaffects in areas adjacent to hazardous waste sites on the NPL. Health outcome data have been evaluated because past exposureshave occurred to some compounds that are potential or probablecarcinogens and because the community is concerned about possiblehealth effects associated with using contaminated groundwater. Health outcome data is not exposure specific; therefore, cancerdeaths cannot be connected to any specific cause. County-levelhealth outcome data were available for review. A more thoroughreview requires a knowledge of exposure duration and site-specific health outcome data at the community level.

Additional environmental sampling currently being performed bothon- and off-site will be evaluated to determine the potential forcontaminant exposure to result in noncancerous and/or canceroushealth effects.


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