West/Hows Corner Site, Plymouth, Maine
West/Hows Corner Site, Plymouth, Maine
A permeable rock stratum below the earth's surface through which groundwater moves. The aquifer generally is capable of producing water for a well.
Any substance that may produce cancer.
Estimated contaminant concentrations in specific media that are not likely to cause adverse health effects, given a standard daily ingestion rate and standard body weight. The comparison values are calculated from the scientific literature available on exposure and health effects.
The amount of one substance dissolved or contained in a given amount of another substance. For example, sea water contains a higher concentration of salt than fresh water.
Any substance or material that enters a system (the environment, human body, food, etc.) where it is not normally found.
A minimum concentration that must be accurately and precisely measured by the laboratory and/or specified in the quality assurance plan.
The amount of a substance to which a person is exposed. Dose often takes body weight into account.
The presence of hazardous substances in the environment. From the public health perspective, environmental contamination is addressed when it potentially affects the health and quality of life of people living and working near the contamination.
Contact with a chemical by swallowing, by breathing, or by direct contact (such as through the skin or eyes). Exposure may be short term (acute) or long term (chronic).
Water beneath the surface of the ground in a saturated zone.
A response to a specific question or request for information pertaining to a hazardous substance or facility (which includes waste sites). Such a request often includes a time-critical element that necessitates a rapid response; therefore, it is a more limited response than an public health assessment.
The science of analyzing the behavior of water as it occurs beneath the ground surface.
Swallowing (such as eating or drinking) chemicals that have gotten in or on food, drinks, utensils, cigarettes, or hands. After ingestion, chemicals can be absorbed into the blood and distributed throughout the body.
Soil, water, air, plants, animals, or any other parts of the environment that can contain contaminants.
No Apparent Health Hazard
The designation given to sites where human exposure to contaminated media is occurring or has occurred in the past, but where the exposure is below a level of health hazard.
The condition where valid information, usually analytical environmental data, indicates the presence of contaminant(s) of a public health concern in one or more environmental media contacting humans (i.e., air, drinking water, soil, food chain, surface water), and there is evidence that some of those persons have an identified route(s) of exposure (i.e., drinking contaminated water, breathing contaminated air, having contact with contaminated soil, or eating contaminated food).
In risk assessment, the probability that something will cause injury, combined with the potential severity of that injury.
Route of Exposure
The way in which a person may contact a chemical substance. For example, drinking (ingestion) and bathing (skin contact) are two different routes of exposure to contaminants that may be found in water.
Volatile organic compounds (VOCs)
Substances containing carbon and different proportions of other elements such as hydrogen, oxygen, fluorine, chlorine, bromine, sulfur, or nitrogen; these substances easily become vapors or gases. A significant number of the VOCs are commonly used as solvents (paint thinners, lacquer thinner, degreasers, and dry cleaning fluids).
The conclusion that a contaminant exceeds the comparison value or health guideline does not mean that it will cause adverse health effects. Comparison values represent media-specific contaminant concentrations that are used to select contaminants for further evaluation to determine the possibility of adverse public health effects.
Environmental Media Evaluation Guides (EMEGs)
EMEGs are based on ATSDR minimal risk levels (MRLs) and factor in body weight and inhalation rates. An EMEG is an estimate of daily human exposure to a chemical (in ppm) that is likely to be without noncarcinogenic health effects over a specified duration of exposureCacute, intermediate, chronic.
Maximum Contaminant Level (MCL)
The MCL is the drinking water standard established by EPA and enforced by the Maine Department of Environmental Protection. It is the maximum permissible level of a contaminant in water that is delivered to the free-flowing outlet. MCLs are considered protective of human health over a lifetime (70 years) for individuals consuming 2 liters of water per day.
Minimal Risk Level (MRL)
An MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncancer) over a specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration via a given route of exposure. MRLs are based on noncancer health effects only. MRLs can be derived for acute, intermediate, and chronic duration exposures by the inhalation and oral routes.
Reference Dose (RfD)
An RfDis an estimate of a daily exposure (mg/kg/day) to the general public (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime exposure (chronic RfD) or exposure during a limited time interval (subchronic RfD).
Appendix C: Estimates of Human Exposure Doses and Evaluation of Health Effects Based on Toxicity Information for PCE at the West/Hows Corners Superfund Site
I. Estimates of Human Exposure Dose and Determination of Health Effects
ATSDR estimated human exposure doses for the following pathways: 1) ingestion of residential well water (1968 to 1988), 2) ingestion of residential well water (1994 to 1996), and 3) water vapor inhalation from residential well water (1994 to 1996). The estimated exposure doses were used to evaluate potential noncancer (noncarcinogenic) and cancer (carcinogenic) effects associated with PCE.
Dose Estimates: Deriving human exposure doses requires incorporating information about the amount of environmental media consumed or inhaled and the duration and frequency of the exposure. In the absence of exposure-specific information (and as a prudent public health practice), ATSDR applies several conservative exposure assumptions to define site-specific exposures as accurately as possible. The assumptions used in estimating the exposure doses are presented below in Section II of this appendix.
When evaluating noncancer effects, ATSDR uses standard health guideline values, including ATSDR's Minimal Risk Levels (MRLs) and EPA's Reference Doses (RfDs), to determine whether adverse effects are likely to occur. The MRLs and RfDs are estimates of daily human exposure to a substance that are likely to be without appreciable risk of adverse noncancer health effects over a specified duration. The MRLs and RfDs are conservative values because they are based on the levels of exposure reported in the literature which represent no-observed-adverse-effect levels (NOAELs) or lowest-adverse-effect-levels (LOAELs) for the most sensitive outcome for a given route of exposure (e.g., ingestion, inhalation). In addition, uncertainty (safety) factors are applied to the NOAELs or LOAELs to account for variation in the human population and uncertainty involved in extrapolating information relevant to humans from animal studies. MRLs are developed for acute, intermediate, and chronic exposure intervals. Only an acute (14 days' exposure or less) MRL is available for PCE. The acute oral MRL for PCE (0.05 mg/kg/day) is based on a study on examining behavioral/nervous system effects in mice (ATSDR, 1997). The chronic RfD for PCE (0.01 mg/kg/day) considers liver effects in rodents: no adverse effects were observed in the animals at doses below 14 mg/kg/day a safety factor of 1,000 was applied to this "NOAEL" to derive the RfD (IRIS, 1997).
II. Exposure Pathways Evaluated
A. Ingestion of PCE-Contaminated Groundwater
ATSDR used the following equation to estimate exposure doses for ingestion of groundwater:
Estimated exposure dose (chronic) = Conc. x IR x EF x ED
BW x AT
Conc. = Maximum concentration in private drinking water wells (mg/L or ppm)
IR = Ingestion rate: 2 liters/day (adult); 1 liter/day (child)
EF = Exposure frequency or number of exposure events per year of exposure:350 days/year
ED = Exposure duration or the duration over which exposure occurs: 20 years (1968 to 1988) and 2 years (1994 to 1996)
BW = Body weight (kg): adult = 70 kg; child = 16 kg
AT = Averaging time or the time period over which cumulative exposures are averaged (ED x 365 days/year for noncancer and 70 x 365 days/year for cancer)
Additional Assumptions for Estimating Human Exposure Doses and Human Health Effects
Using the above equation, ATSDR estimated exposure doses for ingestion of PCE in residential well water for two time periods of possible exposure.
Possible Exposures from 1968 to 1988:
- These exposure dose estimates were derived assuming daily exposure to the average level (760 ppb) detected in the most contaminated private well being used between 1968 and 1988. No data were available for this period of time, but it is expected that the average concentration measured over five years of sampling (1988 to 1993) is a reasonable estimate of conditions for the previous 20 years. Furthermore, only 12 of the approximately 180 private well water samples available exceeded this level.
Possible Exposures from 1994 to 1996:
- These exposure dose estimates were derived assuming daily exposure to maximum levels detected during recent sampling events in private wells being used between 1994 and 1996 (150 ppb). No data were available for this period of time, but it is expected that the maximum detected concentration measured in 1996 is a reasonable estimate of conditions in the previous two years. Furthermore, no other private wells in use in the area for which samples are available had PCE detected as high as this.
Evaluation of Human Health Effects
Possible Exposures from 1968 to 1988:
- Based on ATSDR's dose estimates, adults and children could have been exposed in the past to PCE at doses (0.02 and 0.05 mg/kg/day, respectively), assuming they were exposed to the average contamination (760 ppb PCE) detected in the most contaminated private well being used between 1968 and 1988.
- These doses are below or equal to the acute MRL of 0.05 mg/kg/day; therefore, adverse noncancer effects are not expected to be associated with any short-term drinking water exposures.
- These doses slightly exceed the chronic RfD for PCE (0.01 mg/kg/day). Because the increase is so marginal (a factor of 2 and 5, respectively) no adverse health effects are expected. As mentioned previously, the RfD is based on a study that considers liver effects in rodents. No adverse health effects were observed in the animals at doses below 14 mg/kg/day. Because conservative uncertainty factors have been applied to derive the RfD value for human health effects and other animal studies do not show effects at this low level, adverse effects would not be expected at the doses estimated for possible past exposures to 760 ppb PCE in drinking water.
Possible Exposures from 1994 to 1996:
- Based on ATSDR's dose estimates, adults and children could have been exposed in the past to PCE at doses (0.004 and 0.009 mg/kg/day, respectively) that are below the acute MRL of 0.05 mg/kg/day and the chronic RfD of 0.01 mg/kg/day, assuming they were exposed to the maximum contamination (150 ppb PCE) detected in residential wells being used between 1994 and 1996.
- ATSDR assumes no present or potential future health hazards exist because recent sampling reveals that groundwater from residential wells in use in the vicinity of the site meets drinking water standards.
B. Inhalation of PCE-Contaminated Groundwater While Using a Vaporizer
ATSDR evaluated the health effects associated with PCE in air that might result from using a vaporizer. Because no measured air data were available, ATSDR used a conservative model to estimate indoor air concentrations of PCE while using a vaporizer. While ATSDR prefers using actual data over modeled data, using a conservative model like that described below allowed ATSDR to consider a worst-case screening scenario. If no health effects are shown to be associated with this scenario, no health effects would be expected to be associated with lower concentrations more likely to have actually been in indoor air, if PCE was present at all.
The model equations and assumptions are presented below.
(1) Emission Rate = Concentration of PCE in water x flow rate of vaporizer x CF1
(2) Vapor Concentration = Emission Rate x Duration of vaporizer use x CF2
Volume of Air in Room
- The equation used to estimate vapor concentrations does not account for clean or new air that is typically introduced/exchanged within a room. If air exchange rates were factored into the equation, vapor concentration estimates would be even lower.
- Both of these equations assume that the PCE emitted by the vaporizer is immediately mixed in the indoor air and all PCE in water is emitted into the air.
- The indoor air concentrations only account for the period when the vaporizer is operating (8 hours/day).
PCE concentrations in indoor air in a typical bedroom were estimated using the above equation (according to the parameters outlined in Table C-1). The estimated concentration of PCE in a room over an 8 hour period is 0.005 ppm.
|Parameter||Value used for Vaporizer|
Concentration of PCE in residential well water (assumed maximum concentration in residential well water being used between 1994 and 1996.)
Flow rate of vaporizer
Duration of vaporizer use per day
Volume of Air in Room (Small bedroom) (GEOMET, 1982)
Conversion Factor (CF1)
Conversion Factor (CF2)
*Based on vaporizer flow rate of 4 gallons/day.
Key: PCE = tetrachloroethylene; ppb = parts per billion; m3 = cubic meters
Evaluation of Human Health Effects
- The estimated air concentration of 0.005 ppm is below the acute (short-term) and chronic (long-term) MRLs of 0.2 ppm and 0.04 ppm, respectively. Adverse noncancer health effects are, therefore, not likely for any exposures that may have occurred between 1994 and 1996.
- ATSDR assumes no present or potential future health hazards exist because recent sampling reveals that PCE contamination in groundwater from residential wells in use in the vicinity of the site is below drinking water health-based comparison values.
PCE is a chlorinated hydrocarbon primarily used as a dry-cleaning solvent, vapor-degreasing solvent, and drying agent for metals. PCE does not readily adhere to soils so when this chemical is spilled on the ground it is likely to pass through the soil and reach the groundwater. People may become exposed to PCE by drinking contaminated groundwater or breathing it if it is released during normal household use of the water. Another common way for people to become exposed to PCE in the home is from clothing that have been to the dry cleaners. In addition, some commercial products contain PCE.
Following exposures, PCE readily gets into the blood (i.e., it is absorbed). Once absorbed, it is dispersed throughout the body. Because of the characteristics of PCE, some of it goes to fatty areas of the body, a small amount of the chemical is changed to other chemicals (metabolites) by the liver which are in turn eventually eliminated from the body in the urine, and most of the rest of the chemical is eliminated through the breath. The amount (or dose) of chemical (or its metabolites) that reach critical organs is largely dependent on the manner in which people are exposed and particularly on the amount, frequency, and duration of exposure.
Most of the health effects information on PCE comes from experimental animal studies or epidemiologic investigations in which workers were occupationally exposed to PCE, primarily through inhalation exposures. A limited number of studies exist, however, that examine the relationship between PCE in drinking water supplies and various health effects. Evidence from animal studies indicate that the organs most sensitive to toxic levels of PCE are the central nervous system (CNS), the liver, and the kidneys (ATSDR, 1997).
Results from several animal studies show that liver cancers occur in mice and leukemia occurs in rats following the administration of high doses over the lifetime (ATSDR, 1997). Data from human studies, however, are inadequate to establish a definitive link between PCE and cancer in humans.
In the animal experiments in which cancers were produced in animals breathing PCE, the concentrations in air were 100 parts per million (ppm) in mice and 200 ppm in rats. In the studies in which mice received PCE (mixed in corn oil) through a stomach tube (i.e., by gavage) once daily, the lowest dose that produced cancers was 368 mg/kg/day. Rats receiving similar doses by gavage did not develop tumors (ATSDR, 1997). Because the induction of cancers in rodents required extremely high doses and because the chemical was given in a manner (i.e., single daily gavage dose in corn oil) not consistent with expected human exposure (drinking water throughout the course of the day), a direct comparison of exposure doses for animals and humans may not be entirely appropriate. Furthermore, there is some evidence that elements of rodent biology not shared by humans may have played a role in the development of cancers seen in mice and rats in the experimental studies.
Epidemiologic studies pertaining to PCE and cancer have methodological limitations and are, therefore, largely inconclusive. Some studies of dry-cleaning and laundry workers have suggested a possible association between long-term (years) of PCE exposure (inhalation) and increased cancer risk. Several studies have suggested an association between PCE and leukemia in populations drinking PCE-contaminated groundwater. A study of PCE and TCE in groundwater in Woburn, Massachusetts suggested a weak association between PCE and TCE and the development of leukemia in children of households using contaminated well water. A follow-up study recently completed by the Massachusetts Department of Public Health (MDPH) suggests that children whose mothers drank water from the reportedly contaminated wells from two years before conception to birth were at higher risk of leukemia (MDPH, 1996). The magnitude of this association, however, remains unclear and definitive causation is not possible. No other associations between consumption of VOC-contaminated water and cancer were identified in the study. As noted above, however, these studies suffer from design problems often typical in these types of studies (e.g., small study size and/or inability to clearly document whether or not exposures occurred, and to whom and at what levels).
The relevance of laboratory animal data to humans and available human data are being closely examined by scientists and government agencies. EPA, for example, is currently reviewing the scientific literature pertaining to the carcinogenicity of PCE to determine how it should be classified (e.g., as a probable or possible human carcinogen). Considering the ongoing controversy about the relevance of cancers induced in animals under extreme conditions of exposure (lifetime gavage administration of very high doses), and the recent evidence on differences in the manner in which the chemical is handled by animals and humans, the only thing that can be said is that PCE may be carcinogenic to humans. As such, ATSDR evaluates possible cancer outcomes when reviewing site-specific PCE exposures.
Epidemiologic studies suggest a weak association between exposure to PCE-contaminated water and noncancer effects including immunological abnormalities, birth defects, and effects on behavior. Overall, however, these studies have been largely inconclusive. A study of residents consuming water from several wells contaminated with a variety of solvents in Woburn, Massachusetts, including PCE (21 ppb) and TCE (267 ppb), revealed some immunological abnormalities in 23 adults (Lagakos et al., 1986). Some developmental effects were observed in this same population, but scientists could not establish a clear association with exposures to PCE or other solvents present in the water. In addition, a study of VOCs in a New Jersey water supply showed an association between VOC exposure and birth defects (Bove et al., 1995). Exposure to multiple chemicals in the water and numerous confounding factors (i.e., multiple exposures) prevented making any definitive conclusions about an association between health effects and PCE and/or TCE exposure in these studies.