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Toxicology

Halogenated Alkenes

Trichloroethene

Human Health Toxicity

Trichloroethene (TCE) is used as a solvent, degreaser for metals, and as an intermediate in the synthesis of other chemicals. It also is used in the manufacture of electronic equipment and in a range of varnishes, paints, and adhesives. From the 1950s to the 1980s, TCE was used widely in obstetrics and dentistry as an inhalation anesthetic. The general public is exposed to TCE in ambient air, surface water, ground water, and drinking water. A survey conducted between 1981 and 1983 estimated that 401,373 employees were potentially exposed to TCE in the workplace.

The lung and gastrointestinal tract rapidly absorb TCE, and the circulatory system distributes it throughout the body. It concentrates in body fat and organ fat, such as that of the liver and brain. TCE generally metabolizes in the liver but a portion also is exhaled unchanged following both oral and inhalation exposure. As a lipophilic compound, TCE is predicted to be in breast milk where it could present a potential source of exposure to nursing infants.

Long-term animal studies employing dermal and inhalation routes of exposure indicate that among the non-cancer effects of the compound, the central nervous system is most sensitive to TCE. However, the liver and kidney are also affected.

Epidemiological studies indicate that the children of women exposed to TCE (and other degreasing solvents) have elevated risks for cardiac abnormalities. Neural tube defects also have been reported as a result of exposure to solvents (including TCE) in the workplace and in drinking water. Animal drinking water studies on the developmental effects of TCE indicate that TCE or its metabolites cause both cardiac and eye malformations. Other studies suggest that TCE affects the developing brain in rats. Several studies indicate that TCE may have a potentially adverse effect on the reproductive and endocrine systems of the human male.

TCE does not appear to be a potent genotoxicant, and in a number of standard tests, it has shown negative results for genotoxicity. However, the compound has produced some positive results, so it is not possible to completely rule out the possibility of genotoxicity.

The National Toxicology Program (NTP) concludes that TCE is "reasonably expected to be a human carcinogen" based on limited evidence of carcinogenicity from studies in humans and sufficient evidence of carcinogenicity from studies in experimental animals. The International Agency for Research on Cancer (IARC) classifies TCE as a "probable human carcinogen" based on limited evidence of carcinogenicity in human studies and sufficient evidence in animal studies. Animal studies indicate that TCE induces tumors of the liver, lung, and kidney. Tumors develop in TCE-exposed experimental animals at several sites that also develop tumors in humans.


Adapted from:

Adobe PDF LogoToxicological Profile for Trichloroethylene (TCE)
Agency for Toxic Substances and Disease Registry (ATSDR)
Department of Health and Human Services, Atlanta, GA, 1997

Adobe PDF LogoPublic Health Goal for Trichloroethylene in Drinking Water
Office of Environmental Health Hazard Assessment
California Environmental Protection Agency (CalEPA), 1999

Adobe PDF LogoReport on Carcinogens, Eleventh Edition
National Toxicology Program (NTP)
U.S. Department of Health and Human Services, 2002

Adobe PDF LogoTrichloroethylene Health Risk Assessment: Synthesis and Characterization. External Review Draft
Office of Research and Development
U.S. EPA, EPA/600/P-01/002A, 2001


Jump to
Ecological Toxicity | Human Health References | Ecological References

Ecological Toxicity

Although numerous studies exist on the effects of TCE in laboratory animals, no studies were located for terrestrial species of mammals, birds, or reptiles.

Some acute toxicity data are available for aquatic species. Median lethal concentrations (LC50) values have been reported for grass shrimp (96 hr LC50 2 mg/L), medaka (24 hr LC50 440–730 mg/L), medaka (48 hr LC50 1.9 mg/L), sheepshead minnow (96 hr LC50 20 mg/L), bluegill sunfish (96 hr LC50 44.7 mg/L), fathead minnow (96 hr LC50 40.7 mg/L), and clawed toad 21-28 days after hatching (48 hr LC50 45 mg/L).

Human Health References

Adobe PDF LogoPublic Health Goal for Trichloroethylene in Drinking Water
Office of Environmental Health Hazard Assessment
California Environmental Protection Agency (CalEPA), 1999

Adobe PDF LogoReport on Carcinogens, Eleventh Edition
National Toxicology Program (NTP)
U.S. Department of Health and Human Services, 2002

This three-page summary provides data on the carcinogenicity of TCE, its uses, properties, production and exposure.

Adobe PDF LogoToxicological Profile for Trichloroethylene (TCE)
Agency for Toxic Substances and Disease Registry (ATSDR)
Department of Health and Human Services, Atlanta, GA, 1997

This profile provides information on human health effects, fate and transport, production, and uses of TCE.

Adobe PDF LogoTrichloroethylene Health Risk Assessment: Synthesis and Characterization. External Review Draft
Office of Research and Development
U.S. EPA, EPA/600/P-01/002A, 2001

This 153-page draft document is a review of the health affects of TCE.

Ecological References

Adobe PDF LogoEnvironmental Contaminants Encyclopedia
Irwin, R.J., et al.
National Park Service, Water Resources Division, Fort Collins, CO, 1998

This web page provides information on human health effects, fate and transport, production, and uses of many chemicals including PCE.



Other DNAPLs Toxicology Topics:


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