Toxicity Profiles
Condensed Toxicity Summary for 1,1,2,2-TETRACHLOROETHANE
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 J.C.Norris,Ph.D., Chemical Hazard Evaluation Group in the Biomedical and Environmental Information Analysis Section, Health Sciences Research Division, Oak Ridge National Laboratory*.
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
1,1,2,2-Tetrachloroethane (CAS No. 79-34-5) is a two-carbon chain molecule with two chlorine atoms on each carbon atom. Uses of 1,1,2,2-tetrachloroethane have been as a chemical intermediate, industrial solvent, and extractant. 1,1,2,2-Tetrachloroethane was found on at least 278 of the hazardous waste sites on the United States Environmental Protection Agency's National Priorities List. Chemical degradation occurs by the loss of chlorine atoms, and the half-life of 1,1,2,2-tetrachloroethane in air is about 2 months and in groundwater 1 to 3 months. Bioaccumulation of 1,1,2,2-tetrachloroethane in fish and other aquatic organisms is not expected to be significant (ATSDR;1994).
Two human studies suggested that between 50 and 97% of inspired 1,1,2,2-tetrachloroethane was retained (Lehman and Schmidt-Kehl 1936, Morgan et al. 1970). Mouse and rat gavage studies indicated that 100% of 1,1,2,2-tetrachloroethane was absorbed (Dow Chemical Company 1988). Animal metabolites were trichloroethane, trichloroacetic acid, dichloroacetic acid, glyoxylic acid, and oxalic acid (Ikeda and Ohtsuji 1972, Mitoma et al. 1985, Yllner 1971). Vinyl chloride is another possible metabolite (Hallen et al. 1986). Human and animal studies indicate that the majority of 1,1,2,2-tetrachloroethane is metabolized (ATSDR 1994). Ten percent or less of the parent compound is exhaled in humans and animals.
Humans acutely exposed by the oral route had clinical signs inclusive of pulmonary congestion and edema (Hepple 1927, Mant 1953), lung collapse (Mant 1953) shallow breathing during unconsciousness, low blood pressure, a faint pulse (Sherman 1953, Ward 1955), and epicardial and endocardial anoxic hemorrhage (Mant 1953). Acute inhalation exposure studies of humans to concentrations ranging from 116 to 262 ppm for 10 to 30 minutes resulted in mucosal irritation, nausea and vomiting, eye mucosal irritation, and dizziness (Lehman and Schmidt-Kehl 1936).
A man died after cleaning a spill of 1,1,2,2-tetrachloroethane with his bare hands. His spleen was found to be enlarged with nodular areas on the surface (Coyer 1944). Chronic exposures in humans have resulted in reports of headache, tremors, dizziness, numbness, drowsiness, gastrointestinal distress, liver destruction, fatty degeneration in the liver (Hamilton 1917, Koelsch 1915, Lobo-Mendonca 1963, Minot and Smith 1921, Willcox et al. 1915). Jaundice and enlarged livers have also been reported in exposed workers (Coyer 1944, Horiguchi et al. 1964, Jeney et al. 1957, Koelsch;1915).
Acute oral lethal concentrations in rats range from 200 to 330 mg/kg (ATSDR 1994). Centrilobular swelling was observed in mice after an oral dose of 75 mg/kg/day given for 4 days (Dow Chemical Company 1988). Body weight loss and central nervous system depression and debilitation occurred in 16% of the rats receiving 300 mg/kg/day for 3 to 4 days (Dow Chemical Company 1988). Rats orally administered a single dose of 100 mg/kg displayed necrosis and fatty degeneration of the liver, increased serum leucine aminopeptidase, increased liver ascorbic acid, and increased liver triglyceride levels (Schmidt et al. 1980a). Rats orally treated for 17 weeks with a dose of 3.2;mg/kg/day exhibited chronic inflammation of the kidney (Gohlke et al. 1977). Rats had a body weight loss of 38% for the males and 24% for the females after 6 weeks of 178 mg/kg/day but apparently recovered by the end of the 78-week treatment regiment (NCI 1978). At the 280 mg/kg/day dosage, rats died after 70 weeks. At the end of the 78 weeks of 284 mg/kg/day, male mice died of tubular nephrosis and female mice demonstrated hydronephrosis (NCI 1978). [These NCI (1978)dosages were time-weighted averages of the different doses given.] An oral reference dose (RfD) is under review by the United States Environmental Protection Agency (EPA 1995a).
Lethal exposure concentrations and exposure times for rats were approximately 1000 ppm after 4 to 6 hours (Carpenter et al. 1949, Deguchi 1972, Schmidt et al. 1980b, Smyth et al. 1969) and 5100;ppm after 30 minutes (Price et al. 1978). One of 10 rats exposed to 6300 ppm for 30 minutes exhibited myocardial damage (Price et al. 1978). Mice exposed to 600 ppm for 3 hours developed fatty changes in the liver (Tomokuni 1969, 1970; Hayrack et al. 1962). Exposure of rats to 130 ppm for 15 weeks resulted in increased liver weights, granulation and vacuolization of the liver, and liver hyperplasia (Truffert et al. 1977). Rabbits exposed to 15 ppm for 7 to 11 months exhibited signs of liver degeneration (Navrotskiy et al. 1971). One monkey exposed to a time-weighted average of 1974;ppm for 2 hours/day, 6 days/week for 9 months (no control) had transient diarrhea, anorexia, centrilobular vacuolization, and fatty degeneration of the liver (Hayrack et al. 1962). An inhalation reference concentration (RfC) has not been derived.
The dermal LD50 value in rabbits was determined to be 6.36 g/kg (Smyth et al. 1969). Thickening of the cellular nucleus and pseudoeosinophilic infiltration was observed after dermal application of 514 mg/cm2 for 16 hours on guinea pigs (Kronevi et al. 1981).
Army workers exposed to 1,1,2,2-tetrachloroethane vapor in a clothing processing plant had a very slight increase in death due to genital cancers, leukemia, or other lymphomas than workers not employed in a clothing plant (Norman et al. 1981). Male and female mice orally administered 142 and 284 mg/kg/day for 78 weeks had an increase in hepatocellular carcinomas (NCI 1978). Based on these results, 1,1,2,2-tetrachloroethane has been classified as Group C, possible human carcinogen (EPA;1995b). For oral exposures, the slope factor is 0.2 (mg/kg/day)-1, and the unit risk is 5.8E-06;(g/L)-1 (EPA 1995a). For inhalation exposures, the slope factor is 0.2 (mg/kg/day)-1 (EPA;1995b), and the unit risk is 5.8E-05 (g/m3)-1 (EPA 1995a).
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Last Updated 2/13/98