NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
Prepared by: Rosmarie A. Faust, Ph.D, Chemical Hazard Evaluation Group, Biomedical Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee
Prepared for: Oak Ridge Reservation Environmental Restoration Program.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
Trichloroethene (TCE) is an industrial solvent used primarily in metal degreasing and cleaning operations. TCE can be absorbed through the lungs, mucous membranes, gastrointestinal tract, and the skin. TCE is extensively metabolized in humans to trichloroacetic acid and trichloroethanol, as well as to several minor metabolites, with most of the absorbed dose excreted in urine (ATSDR, 1989; U.S. EPA, 1985).
Human and animal data indicate that exposure to TCE can result in toxic effects on a number of organs and systems, including the liver, kidney, blood, skin, immune system, reproductive system, nervous system, and cardiovascular system. In humans, acute inhalation exposure to TCE causes central nervous system symptoms such as headache, dizziness, nausea, and unconsciousness (U.S. EPA, 1985). Among the reported effects from occupational exposure studies are fatigue, light-headedness, sleepiness, vision distortion, abnormal reflexes, tremors, ataxia, nystagmus, increased respiration, as well as neurobehavioral or psychological changes. Cardiovascular effects include tachycardia, extrasystoles, EKG abnormalities, and precordial pain (Landrigan et al., 1987; Grandjean et al., 1955; Milby, 1968). The use of TCE as an anesthetic has been associated with cardiac arrhythmias (U.S. EPA, 1985).
Cases of severe liver and kidney damage, including necrosis, have been reported in humans following acute exposure to TCE (Defalque, 1961), but these effects generally are not associated with long-term occupational exposures. In animals, TCE has produced liver enlargement with hepatic biochemical and/or histological changes (Nomiyama et al., 1986; Kjellstrand et al., 1981, 1983; Stott et al., 1982; Tucker et al., 1982) and kidney enlargement, renal tubular alterations and/or toxic nephropathy (NTP, 1982, 1986a, 1988). Also observed in animals were hematological effects (Tucker et al., 1982; Mazza and Brancaccio, 1967) and immunosuppression (Sanders et al., 1982). Inhalation studies with rats indicate that TCE is a developmental toxicant causing skeletal ossification anomalies and other effects consistent with delayed maturation (Healy et al., 1982; Dorfmueller et al., 1979). TCE may cause dermatitis and dermographism (U.S. EPA, 1985).
Reference Doses (RfDs) and Reference Concentrations (RfCs) for subchronic and chronic oral and inhalation exposure to TCE are presently under review by EPA (U.S. EPA, 1992a).
Epidemiologic studies have been inadequate to determine if a correlation exists between exposure to TCE and increased cancer risk. Chronic oral exposure to TCE increased the incidences of hepatocellular carcinomas in mice and renal adenocarcinomas and leukemia in rats (NTP, 1988; Maltoni et al., 1986; NTP, 1986a, 1982; NCI, 1976). Chronic inhalation exposure induced lung and liver tumors in mice and testicular Leydig cell tumors in rats (Maltoni et al., 1986, 1988; Fukuda et al., 1983; Bell et al., 1978). Although U.S. EPA's Science Advisory Board recommended a weight-of-evidence classification of C-B2 continuum (C = possible human carcinogen; B2 = probable human carcinogen), the agency has not adopted a current position on the weight-of-evidence classification (U.S. EPA, 1992b). In an earlier evaluation, TCE was assigned to weight-of-evidence Group B2, probable human carcinogen, based on tumorigenic responses in rats and mice for both oral and inhalation exposure and on inadequate data in humans (U.S. EPA, 1987, 1990). Carcinogen slope factors are 1.1E-2 (mg/kg/day)-1 and 6.0E-3 (mg/kg/day)-1 for oral and inhalation exposure, respectively. The corresponding unit risks are 3.2E-7 (µg/L)-1 and 1.7E-6 (µg/m3)-1, respectively (U.S. EPA, 1992b).Retrieve Toxicity Profiles Formal Version
Last Updated 2/13/98