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Arsenic
Chromium VI Dense Nonaqueous Phase Liquids (DNAPLs) 1,4-Dioxane Mercury MTBE Perchlorate POPs PCBs TCE Other Contaminants
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:
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).
This three-page summary provides data on the carcinogenicity of TCE, its uses, properties, production and exposure.
This profile provides information on human health effects, fate and transport, production, and uses of TCE.
This 153-page draft document is a review of the health affects of TCE.
This web page provides information on human health effects, fate and transport, production, and uses of many chemicals including PCE. |