HEALTH CONSULTATION
Evaluation of PCE and TCE in Residential Indoor Air
PALERMO WELL FIELD GROUND WATER CONTAMINATION
TUMWATER, THURSTON COUNTY, WASHINGTON
BACKGROUND AND STATEMENT OF ISSUES
DOH prepared this health consultation in response to a request from the U.S. Environmental Protection Agency (EPA) to evaluate the results of indoor air samples collected at seven residences located within the Palermo Wellfield Superfund site (site) in Tumwater, Washington. DOH prepares health consultations under a cooperative agreement with the Agency for Toxic Substances and Disease Registry.
The site includes the wellfield and the Palermo neighborhood, both located in the Deschutes River Valley, and the commercial area to the west. The Palermo Wellfield consists of six wells that provide up to 50% of the drinking water for the city of Tumwater. The samples were taken to determine whether residents are being exposed to contaminants believed to have migrated from groundwater into residential indoor air. The health consultation evaluates whether exposures exceed a level of health concern.
In April 1997, the site was added to EPA's 
National Priorities List (NPL) as a result of
trichloroethylene (TCE) detections in several of the city's drinking water supply wells, and later,
TCE and tetrachloroethylene (PCE) detections in soil and groundwater west of the wellfield. The
contamination is believed to have originated from several businesses in the commercial area
upgradient (west) of the wellfield and west of the Palermo neighborhood, near the intersection of
Capitol Boulevard and Trosper Road (Figure 1). Information collected during the Remedial
Investigation (RI) indicate that PCE and TCE are present in two distinct groundwater plumes, which
were believed to have flowed with the groundwater to the base of the Palermo Bluff located above
residences in the Palermo Valley. As the contaminated groundwater surfaced at the base of the Bluff,
it is believed to have collected in low areas and crawl spaces underneath residences along Rainier Avenue (Figure 2).
Computer modeling conducted by EPA indicated that TCE and PCE in surface water beneath homes could move into indoor air and pose a health risk to residents. To eliminate this risk, EPA constructed a subdrain system designed to lower the water table in the vicinity of the affected residences. Although construction of the subdrain has been completed, evaluation of its effectiveness is ongoing.
Since EPA relied upon the results of the air model to assess the potential indoor air health hazard posed by PCE and TCE in crawl space water, residential indoor air sampling was not conducted prior to implementation of the subdrain system. Indoor air sampling was conducted only after implementation of the subdrain system in order to assess the existence and concentration of PCE and TCE.
Air Sampling Methods and Results
Residential indoor air sampling was conducted in late March and late August 2001. Although
attempts were made to collect samples from 15 homes in the Palermo neighborhood, participation
was limited, and only seven homes were tested. Five of these homes are located in the portion of the
neighborhood with the highest groundwater levels and the highest groundwater concentrations of
PCE and TCE. Twenty-four hour samples were collected using flow controllers attached to 6-liter
summa canisters. Samples were collected from the crawl space and living space in five of the homes.
One home had no crawl space, and access to the living space in another home could not be obtained.
As a result, only one air sample was collected from each of these two homes. Background outdoor
air samples were collected during both sampling rounds from the backyard of one of the seven
residences. The sampler was hung from an outdoor lighting fixture positioned approximately head-height.
PCE was detected in the living space of one residence, and in the living space and crawl space of another residence. TCE was detected in the living space and crawl space of one residence. Neither PCE nor TCE were detected above the 1 microgram per cubic meter reporting limit at the background locations.
PCE and TCE concentrations were low in the residences where it was detected, and are discussed in more detail below, relative to their potential health impacts.
Tetrachloroethylene (PCE)
PCE is a manufactured compound widely used for dry cleaning fabrics and as a metal degreaser. It is also used as an intermediate in the manufacturing of other products. It is a nonflammable liquid at room temperature, evaporates easily into the air, and has a sharp, sweet odor. Most people can begin to smell PCE when it is present in the air at or above a level of 100 parts per billion (ppb). Levels of PCE at both Palermo residences where it was detected were over 300 times below this odor level.
Non-cancer toxicity:
Since the maximum concentration of PCE detected in indoor air was over 100 times lower than ATSDR's non-cancer health comparison value (i.e., 272 micrograms per cubic meter chronic EMEG), exposures to the levels detected are not expected to result in noncarcinogenic health effects.
Cancer toxicity:
The carcinogenicity characterization has a long history. A July 1985 Health Assessment document for PCE classified it as a Group C (possible human) carcinogen, but indicated that it would be reevaluated based on new information. An April 1987 addendum to the Health Assessment document proposed that it be classified as a B2 (probable human) carcinogen, and provided a revised inhalation risk estimate. A February 1991 document discussed newer data relative to weight-of-evidence classification. The EPA's Science Advisory Board has determined that these documents are technically adequate, and offered an opinion that the weight-of-evidence is on C-B2 continuum (possible human carcinogen/probable human carcinogen). Currently, the Agency has not adopted a final position on the weight-of-evidence classification. The International Agency for Research on Cancer (IARC) considers PCE as a Class 2A carcinogen (probably carcinogenic to humans, based on limited human evidence and sufficient evidence in animals). The U.S. Department of Health and Human Services determined that it may reasonably be anticipated to be carcinogenic to humans.
Although a number of human studies (primarily epidemiology studies of dry-cleaning workers) suggest the possibility of increased cancer incidences from exposure to PCE, particularly esophageal and bladder cancers, it has not been shown to definitively cause cancer in humans. Other cancers suspected of being associated with exposures to high levels of PCE (thousands of times higher than levels measured in Palermo residences) include intestinal, pancreatic, lung, kidney, skin, colon, and lymphatic/hematopoietic cancer. Following inhalation exposure to PCE, mononuclear cell leukemia was observed in rats and hepatic tumors were observed in mice. However, because both mononuclear cell leukemia and hepatic tumors are common in rats and mice, respectively, the relevance of these tumors to humans is not clear.
The concentrations of PCE in indoor air detected in the two Palermo residences were from over 300,000 to over 600,000 times lower than the cancer effect levels (CEL) derived in the rodent studies discussed above. Although the cancer slope factor for PCE has been removed pending the reassessment, the previous slope factor can be used to estimate cancer risk. The estimated increased chance of developing cancer from chronic exposure to the maximum detected concentration of PCE in indoor air is insignificant, approximately one additional cancer in a population of ten million persons exposed. Some or all of this estimated risk can be attributed to background levels of PCE commonly found in the indoor air of urban residences (Table 3).
Trichloroethylene (TCE)
TCE is primarily used as a metal degreaser. The primary users of this compound are the automotive and metals industries. It is also found in some household products, such as typewriter correction fluid, paint removers, adhesives, and spot removers. Most people can begin to smell TCE in air at or above 100,000 parts per billion. Levels of PCE in the single Palermo residence where it was detected were about 100,000 times below this odor level.
The National Center for Environmental Assessment (NCEA) is currently finishing a revised human health risk assessment on TCE. This assessment will present EPA's most current evaluation of the potential health risks from exposure to TCE. TCE exposure is associated with a number of adverse health effects, including neurotoxicity, immunotoxicity, developmental toxicity, liver toxicity, kidney toxicity, endocrine effects, and several forms of cancer. The mechanistic information suggests some risk factors that may make some populations more sensitive, and that TCE could affect children and adults differently.
Non-cancer toxicity:
Although a chronic-duration inhalation health comparison value (MRL, or minimal risk level) is currently not available, ATSDR has derived an intermediate-duration MRL of 537 g/m3 (100 ppb) for inhalation exposure to TCE. The MRL is based on neurological effects on rats observed in a 1994 study. An EPA inhalation reference concentration (RfC) of 40 g/m3 has also been derived, and is based on critical effects in the central nervous system, liver, and endocrine system. TCE concentrations measured in indoor air at the single residence where it was detected were 100 to 170 times lower than the MRL, and seven to 13 times lower than the RfC, indicating that neurological or other non-carcinogenic health effects would not be expected.
Cancer toxicity:
Mechanistic research indicates that TCE-induced carcinogenesis is complex, involving multiple carcinogenic metabolites acting through multiple modes of action. In 1985, EPA classified TCE as a probable human carcinogen. Three years later EPA reviewed information suggesting the weight-of-evidence was on a possible human carcinogen - probable human carcinogen continuum. Under EPA's proposed (1996, 1999) cancer guidelines, TCE can be characterized as "highly likely to produce cancer in humans." These findings are consistent with those of the International Agency on Research of Cancer (IARC, 1995) and the National Toxicology Program (NTP, 2000). As a result of the reassessment, EPA withdrew the inhalation and oral unit risk values.
In experimental rodent studies, high doses of TCE administered to mice resulted in tumors of the lungs, liver, and testes. Other possible cancers associated with exposure to high levels of TCE include cancer of the bladder, stomach, prostate, kidney, and pulmonary system.
TCE cancer effects levels (CELs), which were derived from lowest observed adverse effects levels (LOAELs) in chronic-duration studies on rats and mice, ranged from 100,000 ppb to 600,000 ppb. The levels of TCE measured in Palermo residential indoor air samples were from 100,000 to 600,000 times lower than these CELs.
In order to estimate cancer risk for persons assumed to be chronically exposed to the detected levels of TCE in indoor air, the previous EPA inhalation slope factor was used. The estimated increased cancer risk was slight, approximately one additional cancer in a population of one million persons exposed over many years. As with PCE, some or all of this estimated risk can be attributed to background levels of TCE commonly found in the indoor air of urban residences (Table 3).
Background Levels of PCE and TCE in Indoor Air:
PCE and TCE concentrations measured in Palermo residential indoor air were at levels consistent with those often found in indoor urban environments.
The presence of contaminants in ambient and indoor air in urban areas has been well established. It is also clear that levels of VOCs in indoor air are consistently higher than those found in ambient air. Table 3 and Table 4 below shows the maximum concentrations of PCE and TCE measured at Palermo residences, compared to background indoor and outdoor air concentration ranges, based on various U.S. studies.
Based on the small number of Palermo residences where PCE and/or TCE was detected and tested (three out of seven residences tested), it is impossible to definitively ascertain the source of these contaminants. Although the contaminated groundwater may be the source, the levels of PCE and TCE detected in Palermo residential indoor air are also similar to those expected in a typical, urban indoor-air environment (i.e., background).
Table 1. PCE and TCE indoor air concentrations
(in micrograms/cubic meter)
Palermo Valley residences, Tumwater, Washington
|
House 1 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | 2.1 (= 0.31 ppb) | Living Space | PCE | 1.8 (= 0.27 ppb) |
| TCE | ND | TCE | ND | ||
| Crawlspace | PCE | ND | Crawlspace | PCE | ND |
| TCE | ND | TCE | ND | ||
|
House 2 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | Not tested | Living Space | PCE | Not tested |
| TCE | Not tested | TCE | Not tested | ||
| Crawlspace | PCE | ND | Crawlspace | PCE | ND |
| TCE | ND | TCE | ND | ||
|
House 3 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | ND | Living Space | PCE | Not tested |
| TCE | ND | TCE | Not tested | ||
| Crawlspace | PCE | Not tested (no crawlspace) | Crawlspace | PCE | Not tested |
| TCE | Not tested (no crawlspace) | TCE | Not tested | ||
|
House 4 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | ND | Living Space | PCE | ND |
| TCE | 3.1 (= 0.58 ppb) | TCE | 2.2 (= 0.41 ppb) | ||
| Crawlspace | PCE | ND | Crawlspace | PCE | ND |
| TCE | 5.6 (= 1 ppb) | TCE | 4.6 (= 0.86 ppb) | ||
|
House 5 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | ND | Living Space | PCE | ND |
| TCE | ND | TCE | ND | ||
| Crawlspace | PCE | ND | Crawlspace | PCE | ND |
| TCE | ND | TCE | ND | ||
|
House 6 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | ND | Living Space | PCE | ND |
| TCE | ND | TCE | ND | ||
| Crawlspace | PCE | ND | Crawlspace | PCE | ND |
| TCE | ND | TCE | ND | ||
|
House 7 |
|||||
|
March 28, 2001 |
August 22, 2001 |
||||
| Living Space | PCE | Not tested | Living Space | PCE | 1.8 (= 0.27 ppb) |
| TCE | Not tested | TCE | ND | ||
| Crawlspace | PCE | Not tested | Crawlspace | PCE | 2.1 (= 0.31 ppb) |
| TCE | Not tested | TCE | ND | ||
|
Background (outdoor) air sampling results |
|||||
|
March 28, 2001: 5003 Rainier Ave. (ND)
August 22, 2001: 5003 Rainier Ave. (ND)
|
|||||
Table 2. PCE and TCE health comparison values
(in micrograms per cubic meter)
| Chemical | Maximum indoor air concentration | Non cancer health comparison value | Cancer comparison values | Cancer risk at maximum concentration |
| PCE | 2.1 (living space sample) | 272 (chronic EMEG/MRL) | 4.38 (MTCA B, CLARC II update) 3.1 (EPA Region 3) |
1 x 10-7 |
| TCE | 5.6 (crawlspace sample) 3.1 (living space sample) |
537 (Intermediate EMEG/MRL) 40 (Inhalation RfC) |
1.46 (MTCA B, CLARC II update) 1.0 (EPA Region 3) |
1 x 10-6 7 x 10-7 |
EMEG = ATSDR Environmental media evaluation guide
MRL = ATSDR Minimal risk level
MTCA = Washington State Model Toxics Control Act
CLARC = Department of Ecology Cleanup Levels and Risk Calculations
Inhalation RfC = EPA Inhalation Reference Concentration
Table 3. Contaminants of concern detected
in indoor air, Palermo residences, Tumwater, Washington
(in micrograms per cubic meter)
| Contaminant | Maximum Detected Concentration | Indoor Air Background
Level Ranges (based on various studies) |
Source of Indoor Air Background Level Ranges |
| Tetrachloroethylene (PCE) | 2.1 | 0.4 - 9 | Shah/Pellizzari |
| Trichloroethylene (TCE) | 5.6 | 0.075 - 7 | Shah/Pellizzari |
Table 4. Background levels of PCE and TCE
measured in outdoor air, Palermo neighborhood, Tumwater, Washington
(in micrograms per cubic meter)
| Contaminant | Palermo Background (Outdoor) Air Concentration | Outdoor Air Background Level Ranges (based on various studies) |
Source of National Outdoor Air Background Level Ranges |
| Tetrachloroethylene (PCE) | Not detected | 0.31 - 0.66 | Shah/Wallace |
| Trichloroethylene (TCE) | Not detected | 0.2 - 0.7 | Shah/Wallace |
ATSDR's Child Health Initiative recognizes that the unique vulnerabilities of infants and children deserve special emphasis with regard to exposures to environmental contaminants. Infants, young children, and the unborn may be at greater risk than adults from exposure to particular contaminants. Exposure during key periods of growth and development may lead to malformation of organs (teratogenesis), disruption of function, and even premature death. In certain instances, maternal exposure, via the placenta, could adversely effect the fetus. After birth, children may receive greater exposures to environmental contaminants than adults. Children are often more likely to be exposed to contaminants from playing outdoors, ingesting food that has come into contact with hazardous substances, or breathing soil and dust. Pound-for-pound of body weight, children drink more water, eat more food, and breathe more air than adults. For example, in the United States, children in the first 6 months of life drink seven times as much water per pound as the average adult. The implication for environmental health is that, by virtue of children's lower body weight, given the same exposures, they can receive significantly higher relative contaminant doses than adults.
Reproductive Health Effects
Adverse reproductive health effects in women have been reported to be associated with occupational exposures to PCE in the dry cleaning industry. These effects included menstrual disorders and spontaneous abortions. However, limitations of these studies precluded a definitive association between PCE exposure and these health effects. Levels of PCE and TCE detected in indoor air were well below levels at which reproductive effects were observed in the relevant animal studies. As a result, adverse reproductive health effects would not be expected.
Developmental Health Effects
The developing fetus, children, and especially the developing nervous system may be particularly susceptible to the toxic effects of PCE. Animal studies suggest that PCE can cross the placenta and that TCA, a metabolite of both PCE and TCE, concentrates in the fetus. Unmetabolized PCE has been excreted in breast milk, and in one health study, was detected in an exposed infant with liver damage. Rats that were given oral doses of PCE when they were very young, while their brains were still developing, were hyperactive when they became adults. It is not known whether PCE may have similar effects on the developing brain in human babies.
In Woburn, Massachusetts, studies of residents exposed to drinking water contaminated with solvents, including PCE, suggest the possible association of exposure to PCE and eye/ear anomalies and central nervous system/chromosomal/oral cleft anomalies. However, it is unclear whether other confounding factors might have influenced these health outcomes.
Under certain conditions of exposure, TCE is also believed to affect the developing fetus. Children have also been identified as a potentially susceptible population. The levels of PCE and TCE detected in indoor air were well below levels which caused developmental health effects in these studies. As a result, adverse developmental health effects would not be expected.
1) PCE was detected at low levels in indoor air at two of the seven residences tested, while TCE was detected at low levels in indoor air at one of the seven residences tested.
2) The levels of PCE and TCE detected in residential indoor air do not pose a non-cancer health hazard. A slight increased cancer risk was estimated for residents assumed to be exposed to the maximum detected level of TCE continuously over many years. However, this risk is similar to that expected to result from background exposure to TCE and PCE. Exposures to the detected levels of PCE and TCE in indoor air pose no apparent public health hazard.
3) Studies have shown that VOCs (such as PCE and TCE) are usually present at low levels in outdoor and indoor air in urban areas. Outdoor sources include automobile exhaust and industrial emissions, while indoor air contaminants often come from household cleaners, paints, carpeting, and building materials.As a result, background levels of VOCs in indoor and outdoor air are a source of exposure for residents living in urban environments. Health risks associated with background exposure can be similar to or higher than risks from localized hazardous waste releases to the environment. Based on the limited number of Palermo residences tested, it is not clear whether the source of the indoor air detections is the contaminated groundwater, or other unrelated background source(s).
1) Copies of this health consultation will be provided to residents whose homes were tested, EPA, and Ecology. Additional copies will be available upon request.
2) Follow up with residents' whose homes were tested should be conducted by EPA and DOH to explain the results of the indoor air analysis.
3) DOH should be notified if groundwater and/or surface water chemical concentrations increase, posing an increased potential health hazard to residences at the base of the Palermo bluff..
Paul Marchant
Washington State Department of Health
Office of Environmental Health Assessments
Site Assessment Section
Designated Reviewer
Robert Duff, Manager
Washington State Department of Health
Office of Environmental Health Assessments
Site Assessment Section
Technical Project Officer
Debra Gable
Technical Project Officer
SPS, SSAB, DHAC
ATSDR
Figure 1. Project Area Location Map
Figure 2. Project Area Plan View
This Health Consultation was prepared by the Washington State Department of Health under a cooperative agreement with the Agency for Toxic Substances and Disease Registry (ATSDR). It is in accordance with approved methodology and procedures existing at the time the health consultation was begun.
Debra Gable
Technical Project Officer
SPS, SSAB, DHAC
ATSDR
The Division of Health Assessment and Consultation, ATSDR, has reviewed this public health consultation and concurs with the findings.
Richard Gillig
Branch Chief
SSAB, DHAC
ATSDR
