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HEALTH CONSULTATION

EXPOSURE INVESTIGATION

OREGON STATE PENITENTIARY
SALEM, MARION COUNTY, OREGON


PUBLIC HEALTH IMPLICATIONS

PCE and TCE exposure doses that are based on the stated exposure scenarios and assumptions are listed in Table 5 along with the most appropriate health guidance values. Information on the toxicology and health effects of exposure to PCE and TCE are included in Appendix 3. Health guidance values provide a basis for evaluating exposures from contaminants in different environmental media (soil, air, water, and food) and depend on the characteristics of the exposed people and the length or duration of the exposure. ATSDR's minimal risk levels (MRL) are defined as estimates of the daily human exposure that are likely to be without an appreciable risk of adverse noncancerous health effects over a specified duration of exposure (acute, <15 days; intermediate, 15-365 days; or chronic, >365 days). EPA's reference doses (RfDs) are an estimate of daily human exposure, including exposure to particularly sensitive people, that are likely to be without appreciable risk of adverse, noncancerous health effects during a lifetime (70 years).

MRL's and RfD's for ingestion are expressed in the same units as the exposure doses (mg/kg/day). These guidance values are derived from experimental data that measure the lowest observed (or no observed) effect levels and then adjusted downward using safety factors to account for the uncertainty in the experimental procedures and laboratory animals used to derive the guidance values. Because the uncertainty factors are used to make the guidance values protective of public health, the health guidance values should not be viewed as strict boundaries between toxic and nontoxic exposures.

Many of the short-term and long-term exposure doses for PCE are greater than the health guidance values listed in Table 5. None of the TCE exposure doses are greater than the health guidance values. Due to the health-protective or conservative nature of the dose calculations and uncertainty factors used to derive the guidance values, the PCE and TCE drinking water exposures to OSP inmates and workers are not likely to produce adverse health effects.

The Toxicological Profile for tetrachloroethylene (PCE; ATSDR, 1997) documents many studies of the health effects of PCE exposure to both humans and laboratory animals. The lowest observed adverse effect level (LOAEL) for short term ingestion of PCE to humans is more than 10 times greater than the highest dose to the OSP population. Similarly, the LOAELs for intermediate and long term ingestion exposures to animals are more than 10 times greater than OSP doses. There were no studies showing adverse health effects for humans within the range of the OSP combined exposure doses for either ingestion or inhalation exposures (ATSDR, 1997). Because no adverse human health effects have been observed in the range of PCE doses estimated for the OSP population (ATSDR, 1997) and doses for which such health effects were listed were more than 10 times greater than OSP doses, OSP exposures are not likely to produce any disease or illness in the OSP population.

The estimated excess cancer risks for PCE (Table 4) are dependent on the duration of the exposure as well as the magnitude of the dose. Excess cancer risks that were calculated using health-protective exposure assumptions ranged from 5.4E-03 to 1.9E-04 for inmates and 5.2E-03 to 7.6E-05 for OSP staff. Staff resident excess risks ranged from 3.5E-04 to 9.7E-05. Based on the maximum inmate residence duration of 9.25 years (SECOR, 2000), a 20 year inmate exposure is very unlikely. However, prison staff may have been employed at OSP for more than 10 years so 20 year exposure durations have been calculated. It is not known how long staff residents may have lived in the on-site residences.

The excess cancer risks represent the expected increase in cancer risk due to exposure to PCE. All of the uncertainties and health-protective exposure assumptions associated with the dose calculations are included in the risk estimation as well as the uncertainty in deriving the cancer slope factor (EPA, 2000). The risk estimates in Table 4 cannot be interpreted as evidence that any member of the OSP population will develop cancer as a result of PCE exposure. Inmates and staff working in the laundry facility may have a moderate increased risk due to estimated PCE inhalation. All other exposure scenarios produce estimates of excess risk fall that are within the range of low to no apparent increased risk (ATSDR, 1991). These low risk estimates combined with the likely over-estimation of exposure doses, indicate that PCE ingestion is not likely to create excess cancers in the OSP population.

Table 5. Calculated Exposure Doses and Health Guidance Values

Exposure Scenario Exposure Dose
mg/kg/day
Health Guidance Value
mg/kg/day

PCE


30 day

Inmate 6.9e-02

5.0e-02 [1]

uncertainty factor- 100

endpoint- developmental effects

Inmate laundry bldg. 9.2e+00
Staff 2.0e-02
Staff shower area 6.7e-02
Staff laundry bldg. 9.2e+00
Staff residents adult 1.2e-01
Staff residents child 5.1e-01

PCE


10 yr

Inmate 1.8e-02

1.0e-02 [2]

uncertainty factor- 1000

endpoint- liver toxicity in mice;

weight gain in rats

Inmate laundry bldg. 9.2e+00
Staff 5.1e-03
Staff shower area 1.7e-02
Staff laundry bldg. 9.1e+00
Staff resident adult 3.1e-02
Staff resident child 1.3e-01

TCE


30 day

Inmate 2.5e-03

2.0E-1 [3]

uncertainty factor- 300

endpoint- developmental effects

Inmate laundry bldg. 2.5e-03
Staff 7.1e-04
Staff shower area 5.7e-03
Staff laundry bldg. 7.1e-04
Staff resident adult 3.3e-03
Staff resident child 1.3e-02

TCE


10 year

Inmate 7.0e-04

Not Available [4]

Inmate laundry bldg. 7.0e-04
Staff 2.0e-04
Staff shower area 1.6e-03
Staff laundry bldg. 2.0e-04
Staff resident adult 9.4e-04
Staff resident child 3.8e-03
Table 5. (Continued)
[1] Acute, oral ingestion MRL; (ATSDR, 2000)
[2] Chronic, oral ingestion RfD; (EPA, 2000b).
[3] Acute, oral ingestion MRL; (ATSDR, 2000).
[4] TCE guidance values for long term exposure have been withdrawn by EPA and ATSDR. However, calculated doses are more than 10,000 times lower than doses that have produced adverse health effects in long term animal studies (ATSDR, 1997).

With the possible exception of the laundry facility inhalation doses, the calculated exposure doses in Table 4 probably over-estimate the exposure doses because they are based on very protective, but standard, exposure assumptions listed in Table 3 and the maximum OSP supply well concentrations listed in Table 1. Because these calculated exposure doses use maximum measured concentrations and protective exposure assumptions, it is unlikely that any exposure doses based on the water concentrations are greater than those listed in Table 4.

All of the exposure doses and cancer risk estimates based on ingestion of contaminated groundwater are low, and by themselves, unlikely to produce adverse health effects. However, those inmates and staff working in the laundry facility were probably exposed to significantly higher PCE doses via inhalation from the dry cleaning process. ATSDR has received very limited information related to the OSP dry cleaning facility, the number of inmates or officers employed there, or the specific types of cleaning or air handling equipment used there. Based on average air concentrations for other dry cleaning facilities, inhalation exposure doses may have been 100 times greater than the ingestion dose from the OSP water supply wells.

Epidemiologic studies of occupational PCE inhalation exposures among dry cleaning workers have indicated a number of significant health effects including renal, neurologic, hepatic, and excess cancers of the lung, cervix, esophagus, kidney, skin, and liver (ATSDR, 1997). Direct interpretation of health effects from PCE exposures in those studies are complicated by exposures to other contaminants, smoking and lifestyle behaviors, and socioeconomic factors.

There are several studies which indicate that humans do not have the same PCE metabolic pathways as rats and using such animal models may significantly over-estimate human cancer risk (Volkel, et.al., 1998; Pahler, et.al., 1999). Additionally, Beyer, et.al. (1999) state that PCE classification as human carcinogen is primarily based on positive findings in rat and mouse cancer bioassays, but that human epidemiology studies do not show consistent excess cancers and that PCE is not likely to be a human carcinogen.

These potential health effects from PCE inhalation exposure have been addressed with the development of occupational exposure limits by the National Institute of Occupational Safety and Health and by the Occupational Health and Safety Administration. Because ATSDR has no information on the dry cleaning operations at OSP, it is not currently possible to determine if the occupational exposure limits have been exceeded or to calculate specific exposure doses for those inhalation exposures. However, in light of the potential occupational inhalation exposures to some OSP inmates and workers, combined with the ingestion exposures from the OSP water supply wells, additional evaluation of the occupational exposure scenario should be conducted.


CONCLUSIONS AND RECOMMENDATIONS

Two water supply wells at the OSP contained measurable concentrations of PCE and TCE. Inmates and workers at the OSP were exposed to these contaminants through ingestion of drinking water and inhalation of the PCE and TCE that volatilized from the water into air. Exposure doses to inmates and prison workers were calculated from measured maximum contaminant concentrations and health-protective exposure assumptions for both short term (30 day) and long term (10 year) exposure durations.

Many of the resulting PCE exposure doses are greater than applicable health guidance values, but because of the safety factors built into the guidance values and the health-protective exposure assumptions that probably over-estimate exposure doses, it is unlikely that ingestion of drinking water would produce adverse public health effects for the OSP population. However, in addition to the OSP-wide drinking water exposures, inmates and staff at the dry cleaning facility, which was the original PCE source, may have been exposed to significant doses of PCE via inhalation.

TCE exposure doses did not exceed health guidance values and were not likely to produce adverse health effects. TCE present in the groundwater is presumed to be a degradation product produced in the groundwater aquifer and was not present at the dry cleaning facility.

ATSDR recommends additional evaluation of the occupational inhalation exposures that may have occurred at OSP to determine whether occupational exposures were within regulatory limits. This evaluation should also include a determination of the PCE air concentrations in the laundry building, the number and frequency of people employed at the facility, and the cleaning and air handling equipment in use at the facility.



Prepared by:

Mark W. Evans, Ph.D.
Environmental Geologist
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation

Reviewed by:

John E. Abraham, Ph.D.
Branch Chief
Exposure Investigations and Consultations Branch
Division of Health Assessment and Consultation

Susan Moore
Section Chief
Exposure Investigations and Consultations Branch
Division of Health Assessment and Consultation

Robert Johnson, M.D.
Medical Officer
Exposure Investigations and Consultations Branch
Division of Health Assessment and Consultation


REFERENCES

ATSDR, 2000. Minimal Risk Levels for Hazardous Substances. Agency for Toxic Substances and Disease Registry. United States Public Health Service. August, 2000. http://www.atsdr.cdc.gov/mrls.html

ATSDR, 1997. Toxicological Profile for Tetrachloroethylene. Agency for Toxic Substances and Disease Registry, United States Public Health Service. Atlanta, GA, September, 1997.

ATSDR, 1997. Toxicological Profile for Trichloroethylene. Agency for Toxic Substances and Disease Registry, United States Public Health Service. Atlanta, GA, 1997.

ATSDR, 1991. Decision Statement TOX.14. Draft QAA-27. Agency for Toxic Substances and Disease Registry, United States Public Health Service. Atlanta, GA, revised 1991.

ATSDR, 1990. Public Health Statement Tetrachloroethylene. Agency for Toxic Substances and Disease Registry, United States Public Health Service. Atlanta, GA, 1990.

ATSDR, 1989. Public Health Statement Trichloroethylene. Agency for Toxic Substances and Disease Registry, United States Public Health Service. Atlanta, GA, 1989.

Andelman, B.J., et.al., 1989. Exposure to volatile chemicals from indoor uses of water. Proceeding of Total Exposure Methodology: A New Horizon. Las Vegas, NV, November 27-30, 1989.

Beyer, L.A., et.al., 1999. Is Perchloroethylene (Perc) a probable carcinogen in humans? The Toxicologist, V.48 (1-S), Oxford University Press, March 1999.

EPA, 2000. Draft Risk Assessment Issue Paper for: Carcinogenicity Information for Tetrachloroethylene. Unpublished Issue Paper, Environmental Protection Agency, Superfund Technical Support Center, Cincinnati, OH, August 2000.

EPA, 2000b. Integrated Risk Information System. Environmental Protection Agency, August, 2000. http://www.epa.gov/ngispgm3/iris/index.html

EPA, 1990. Exposure Factors Handbook. Environmental Protection Agency Office of Health and Environmental Assessment, Washington, D.C., EPA/600/8-89/043, March 1990.

Foster, S.A. and Chrostowski, P.C., 1986. Integrated household exposure model for use of tap water contaminated with volatile organic chemicals. Presented at the79th Annual Meeting of the Air Pollution Control Association, Minneapolis MN, June 22-27, 1986.

GIT, 2000. Contaminant transport analysis for the Oregon State Penitentiary, Salem, Oregon. Georgia Institute of Technology, Multimedia Environmental Simulations Laboratory, Atlanta, GA, April 2000.

Grimm, M.W., 1989. Letter from M.W. Grimm, Regional Engineer, Drinking Water Program (State of Oregon) to J. Boydston, P.E., Manager, Drinking Water Program concerning VOC analysis at the Oregon State Penitentiary, October 24, 1989.

Life Systems, Inc., 1989. Guidelines for incorporation of inhalation and dermal exposures from drinking water in the calculation of health advisory and DWEL values. Submitted to U.S. Environmental Protection Agency, Office of Drinking Water, Contract No. 68-CB-0033, December 1989.

Pahler, A., et.al., 1999. Dose-Dependent Protein Adduct Formation in Kidney, Liver, and Blood of Rats and in Human Blood after Perchloroethene Inhalation. Toxicological Sciences V. 48:.5-13, 1999.

SECOR, 2000. Baseline Human Health Risk Assessment, Oregon State Penitentiary. By SECOR, Inter. Inc., for the Oregon State Department of Corrections, Salem, OR, May 2000.

SECOR, 1998. Remedial Investigation Report, Oregon State Penitentiary. By SECOR, Inter. Inc., for the Oregon State Department of Corrections, Salem, OR, June 1998.

SECOR, 1994. Phase II Site Investigation Report, Oregon State Penitentiary. By SECOR, Inter. Inc., for the Oregon State Department of Corrections, Salem, OR, February 1994.

Trewartha, M., 2000. Personal communication (e-mail) to Mark W. Evans. August 9, 2000.

Volkel, W., et.al., 1998. Biotransformation of Perchloroethene: Dose-Dependent Excretion of Trichloroacetic Acid, Dichloroacetic Acid, and N-acetyl-S-(trichlorovinyl)-L-Cysteine in Rats and Humans after Inhalation. Toxicology and Applied Pharmocology, V. 153: 20-27, 1998.

Wan, Jo K., Weisel, C.P., and Lioy, J.P., 1990. Chloroform exposure and the health risk associated with multiple uses of chlorinated tap water. Risk Analysis, 1990, v.10(4):581-5.


APPENDIX 1

A. Estimation of Air Concentration in Shower (from, Life Systems, Inc., 1989).

Ca(shower) = f x (Cw/2) x [(Rws)(1-ebt)]/[(RvsVs) + (OwaRws)]

where
Ca = concentration in air
1.79e-05
mg/L
0.017859 mg/m-3
Cw = concentration in water
2.10e-02
mg/L
f = factor for non-attainment of equilibrium
5.00e-01
(unitless)
default
Rws = rate of water use in shower
4.80e+02
L/min
default
t = duration of shower (average)
1.50e+01
min
90th percentile
Rvs = rate of ventilation in shower
3.00e-02
/min
default
Vs = volume of shower enclosure (stall)
1.70e+06
L
default
Owa = Ostwald water/air partition coef.
1.33e+00
unitless
chemical specific
b = (RwsOwa + VsRvs)/Vs

3.04e-02

/min


Calculation of Ostwald water/air coefficient
Owa = RT/H
where
H = Henry's Law constant

1.80E-02 atm*m3/mole for PCE (ATSDR, 1990)

RT = gas constant x temp

2.40E-02 atm*m3/mole at 20 C


B. Estimation of Air Concentration in Whole House (from, Life Systems, Inc., 1989).

Ca(house) = f x Cw x Rw/(RvVh + OwaRw)

where
Ca = concentration in air
1.30e+00
ug/m3

5.09e-01

Ca = concentration in air
1.30e-06
mg/L
1.31e-03
Cw = concentration in water
6.20e-02
mg/L
 
f = factor for non-attainment of equilibrium
5.00e-01
(unitless)
default
Rw = rate of water use
5.00e+01
L/person/day
default
Rv = rate of ventilation of household ventilation
1.20e+01
/day
default
Vh = volume of home
9.90e+04
L/person
default
Owa = Ostwald water/air partition coefficient
1.20e+00
unitless
chemical specific


Calculation of Ostwald water/air coefficient
Owa = RT/H
where
H = Henry's Law constant

2.00e-02

atm*m3/mole
(TCE)
RT=gas constantxtemp

2.40e-02

atm*m3/mole at 20 C


APPENDIX 2(A): Route specific and combined PCE exposure doses and cancer risk for OSP population.

 

PCE_30 day:W-3

PCE 30day:W-1 PCE_Annual CSF 10 yr risk 20 yr risk
Inmates- General Population

mg/kg-day

mg/kg-day mg/kg-day 1/(mg/kg-day)    
inhalation from showers

1.5E-03

1.8E-05 3.7E-04 2.00E-03 1.07E-07 2.13E-07
inhalation from sink in cell

1.9E-02

2.4E-04 4.9E-03 2.00E-03 1.39E-06 2.79E-06
ingestion

4.9E-02

6.0E-04 1.2E-02 5.20E-02 9.13E-05 1.83E-04
Combined Dose

6.9E-02

8.6E-04 1.8E-02   9.28E-05 1.86E-04
Inmates- Laundry Workers            
inhalation inside building

9.1E+00

9.1E+00 9.1E+00 2.00E-03 2.61E-03 5.22E-03
inhalation from showers

1.5E-03

1.8E-05 3.7E-04 2.00E-03 1.07E-07 2.13E-07
inhalation from sink in cell

1.9E-02

2.4E-04 4.9E-03 2.00E-03 1.39E-06 2.79E-06
ingestion

4.9E-02

6.0E-04 1.2E-02 5.20E-02 9.13E-05 1.83E-04
combined dose

9.2E+00

9.1E+00 9.2E+00   2.71E-03 5.41E-03
Prison Staff- General Population            
ingestion

2.0E-02

2.5E-04 5.1E-03 5.20E-02 3.80E-05 7.61E-05
Prison Staff- Laundry Bldg.            
ingestion

2.0E-02

2.5E-04 5.1E-03 5.20E-02 1.46E-06 2.93E-06
Inhalation inside bldg.

9.1E+00

9.1E+00 9.1E+00 2.00E-03 2.61E-03 5.22E-03
combined dose

9.2E+00

9.1E+00 9.1E+00   2.61E-03 5.23E-03
Prison Staff- Shower Area            
inhalation from shower area

4.7E-02

5.9E-04 1.2E-02 2.00E-03 3.41E-06 6.82E-06
ingestion

2.0E-02

2.5E-04 5.1E-03 5.20E-02 3.80E-05 7.61E-05
combined dose

6.7E-02

8.4E-04 1.7E-02   4.15E-05 8.29E-05
OSP Onsite Staff Residences            
adult-ingestion

4.9E-02

6.0E-04 1.2E-02 5.20E-02 9.13E-05 1.83E-04
adult-inhalation from showers

3.3E-02

4.0E-04 8.2E-03 2.00E-03 2.36E-06 4.71E-06
adult- whole house inhalation

4.3E-02

5.2E-04 1.1E-02 2.00E-03 3.12E-06 6.25E-06
adult- combined dose

1.2E-01

1.5E-03 3.1E-02   9.68E-05 1.94E-04
child- ingestion

1.7E-01

2.1E-03 4.3E-02 5.20E-02 3.20E-04 6.39E-04
child- inhalation from showers

1.5E-01

1.8E-03 3.8E-02 2.00E-03 1.07E-05 2.14E-05
child- inhalation whole house

2.0E-01

2.4E-03 5.0E-02 2.00E-03 1.42E-05 2.84E-05
child- combined dose

5.1E-01

6.3E-03 1.3E-01   3.45E-04 6.89E-04


APPENDIX 2(B): Route specific and combined TCE exposure doses to OSP population.

 

TCE_30 day:W-3

TCE 30day:W-1 TCE_Annual
Inmates- General Population

mg/kg-day

mg/kg-day mg/kg-day
inhalation from showers

5.4E-05

7.0E-06 1.5E-05
inhalation from sink in cell

6.9E-04

9.3E-05 1.9E-04
ingestion

1.7E-03

2.3E-04 4.9E-04
Combined Dose

2.5E-03

3.3E-04 7.0E-04
Inmates- Laundry Workers      
inhalation inside building

0.0E+00

0.0E+00 0.0E+00
inhalation from showers

5.4E-05

7.0E-06 1.5E-05
inhalation from sink in cell

6.9E-04

9.3E-05 1.9E-04
ingestion

1.7E-03

2.3E-04 4.9E-04
combined dose

2.5E-03

3.3E-04 7.0E-04
Prison Staff- General Population      
ingestion

7.1E-04

9.5E-05 2.0E-04
Prison Staff- Laundry Bldg.      
ingestion

7.1E-04

9.5E-05 2.0E-04
Inhalation inside bldg.

0.0E+00

0.0E+00 0.0E+00
combined dose

7.1E-04

9.5E-05 2.0E-04
Prison Staff- Shower Area      
inhalation from shower area

5.0E-03

6.5E-04 1.4E-03
ingestion

7.1E-04

9.5E-05 2.0E-04
combined dose

5.7E-03

7.5E-04 1.6E-03
OSP Onsite Staff Residences      
adult-ingestion

1.7E-03

2.3E-04 4.9E-04
adult-inhalation from showers

1.2E-03

1.5E-04 3.4E-04
adult- whole house inhalation

4.0E-04

5.2E-05 1.1E-04
adult- combined dose

3.3E-03

4.4E-04 9.4E-04
child- ingestion

6.0E-03

8.0E-04 1.7E-03
child- inhalation from showers

5.5E-03

7.0E-04 1.5E-03
child- inhalation whole house

1.8E-03

2.4E-04 5.2E-04
child- combined dose

1.3E-02

1.7E-03 3.8E-03


APPENDIX 3: Toxicological Information and Health Effects from PCE and TCE

1. Tetrachloroethylene

PCE is a synthetic chemical that is widely used for dry cleaning fabrics and for metal-degreasing operations. It enters the body mainly through inhalation and ingestion. If PCE is placed directly on the skin, there is some dermal absorption. Very little PCE in the air can be absorbed dermally.

Most PCE leaves the body through exhalation. This is true regardless of the route of entry. A small amount is metabolized into other chemicals that are removed from the body in urine. One of these chemicals, trichloroacetic acid (TCA), is also thought to be harmful. Most of the changed PCE leaves the body in a few days. Some of the PCE remains in the body and is found in the blood and other tissues, especially body fat. Part of the PCE that is stored in fat may stay in the body for several days or weeks before it is eliminated.

Neurological effects (impaired memory, numbness of extremities, peripheral neuropathy, and impaired vision) and cardio-respiratory effects (irregular heartbeat, asthma) have mainly been noted in inhalation exposures at fairly high levels.

Results of animal studies, conducted with amounts much higher than those that most people are exposed to, show that PCE can cause liver and kidney damage and liver and kidney cancers. Although it has not been shown to cause cancer in people, the U. S. Department of Health and Human Services has determined that PCE may reasonably be anticipated to be a carcinogen. The International Agency for Research on Cancer has determined that PCE is possibly carcinogenic to humans. PCE can be toxic to unborn animals in a laboratory setting. How PCE may affect the developing brain in human babies is not known.

The federal government develops regulations and recommendations to protect public health. EPA has recommended limits on how much PCE can be present in drinking water. EPA recommends that there should not be more than 5 parts per billion (ppb) in the drinking water.

2. Trichloroethylene

TCE is now mainly used as a solvent to remove grease from metal parts. It enters the body mainly through inhalation and ingestion. It can also enter the body by dermal absorption. About half of inhaled TCE will be absorbed; the rest is immediately exhaled. Ingested TCE is mostly absorbed. Dermal absorption takes place to a modest degree.

Once absorbed, the liver metabolizes much of the TCE. The majority of the metabolites leave the body in the urine within a day. Some of the TCE or its metabolites can be stored in body fat for a brief period, and thus may accumulate if exposure continues.

Neurological effects (fatigue, headache, memory loss, decreased appetite, irritability, euphoria or depression) have mainly been noted in inhalation exposures at fairly high levels.

It is uncertain whether people who breathe air or drink water containing TCE are at higher risk of cancer or if their children have more birth defects. At a site in Woburn, Massachusetts, people who used water for several years from two wells that had high levels of TCE may have had a higher incidence of childhood leukemia than other people. Increased numbers of children were reported to be born with cardiac abnormalities, a finding which is supported by data from some animal studies showing developmental effects of TCE on the heart. However, other chemicals were also in the water from this well. We do not have any clear evidence that TCE alone can cause leukemia or any other type of cancer in humans.

As part of the National Exposure Registry, the Agency for Toxic Substances and Disease Registry (ATSDR) compiled data on 4,280 residents of three states (Michigan, Illinois, and Indiana) who had environmental exposure to TCE. It found no definitive evidence for an excess of cancers from TCE exposure. In studies using high doses of TCE in rats and mice, tumors in the lungs, liver, and testes were found, providing some evidence that high doses of TCE can cause cancer in experimental animals. We do not know if TCE affects human reproduction.

The federal government develops regulations and recommendations to protect public health. EPA has set a drinking water standard of 5 parts of TCE per one billion parts of water (ppb).

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