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 and Communication Program, Biomedical and 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.
1,1-Dichloroethylene (CAS No. 75-35-4), also known as 1,1-dichloroethene and vinylidine chloride, is a colorless liquid that is used primarily in the production of polyvinylidine chloride (PVC) copolymers and as an intermediate for synthesis of organic chemicals. The major application for PVC copolymers is the production of flexible films for food packaging such as Saran® wrap (ATSDR, 1993).
1,1-Dichloroethylene does not occur naturally (IARC, 1986) but is found in the environment due to releases associated with its production and transport and with the production of its polymers. Because of its high volatility, releases to the atmosphere are the greatest source of ambient 1,1-dichloroethylene. Smaller amounts are released to surface waters and soils (ATSDR, 1993). Loss of 1,1-dichloroethylene from water and soils is primarily due to volatilization. In the atmosphere, reaction with photochemically generated hydroxyl radicals is expected to be the predominant removal mechanism (EPA, 1987). Human exposure to 1,1-dichloroethylene is potentially highest in workplace settings and in the vicinity of hazardous waste sites where the compound may contaminate environmental media (ATSDR, 1993).
The primary effect of acute exposure to high concentrations (approximately 4000 ppm) of 1,1-dichloroethylene vapor in humans is central nervous system (CNS) depression which may progress to unconsciousness (Gosselin et al., 1984). Occupational exposure has been reported to cause liver dysfunction in workers (Tierney et al., 1979). 1,1-Dichloroethylene is irritating when applied to the skin and prolonged contact can cause first degree burns (Tierney et al., 1979). Direct contact with the eyes may cause conjunctivitis and transient corneal injury (IARC, 1986).
In experimental animals, the liver and kidneys are target organs for the toxic effects of 1,1-dichloroethylene. Subchronic oral exposure for 90 days to 1,1-dichloroethylene in drinking water produced slight hepatotoxic effects at 200 ppm (Rampy et al., 1977), and chronic oral exposure to drinking water for 2 years produced hepatocellular changes in males at >=100 ppm and in females at >=50 ppm (Quast et al., 1983). Gavage administration of 10 mg/kg/day, 5 days/week for 2 years produced chronic inflammation of the kidney in male and female rats and liver necrosis in male and female mice (NTP, 1982). Exposure by inhalation to 55 ppm 1,1-dichloroethylene, 6 hours/day, 5 days/week for up to 1 year produced fatty liver changes in rats and focal degeneration and necrosis in mice (Lee et al., 1977).
In a three-generation study, no treatment-related effects on reproduction or neonatal development were seen in male and female Sprague-Dawley rats administered up to 200 ppm of 1,1-dichloroethylene in the drinking water (Nitschke et al., 1983). However, inhalation exposure during gestation produced increased resorptions and minor skeletal alterations in rodents at concentrations that caused maternal toxicity. These effects were reported in rats and mice at >=15 ppm (Short et al., 1977a) and in rats and rabbits at >=80 ppm and >=160 ppm, respectively (Murray et al., 1979).
An oral Reference Dose (RfD) of 9E-3 mg/kg/day was derived for chronic exposure (EPA, 1994a) and subchronic exposure to 1,1-dichloroethylene (EPA, 1994b), based on liver lesions seen in rats in a 2-year drinking water study (Quast et al., 1983). The oral RfD is currently under review and may be subject to change. An inhalation Reference Concentration (RfC) for 1,1-dichloroethylene is under review (EPA, 1994a).
An epidemiology study using a small cohort found no association between the occurrence of cancer or cancer mortality and exposure to 1,1-dichloroethylene (Ott et al., 1976). Oral carcinogenicity bioassays (drinking water or gavage exposures) with experimental animals gave generally negative results (NTP, 1982; Quast et al., 1983; Maltoni et al., 1984, 1985). In one inhalation study (Maltoni et al., 1985), statistically significant increases in renal adenocarcinomas were noted in male Swiss mice exposed to 25 ppm for 12 months. Also observed were statistically significant increases in mammary gland carcinomas in females and lung tumors in both sexes. Results of other inhalation studies with rats, mice, and hamsters have been negative (Hong et al., 1981; Maltoni et al., 1984; Quast et al., 1986).
Based on EPA guidelines, 1,1-dichloroethylene was assigned to weight-of-evidence group C, possible human carcinogen. For oral exposure, the slope factor is 6E-1 (mg/kg/day)-1 and the unit risk is 1.7E-5 (ug/L)-1 (EPA, 1994a). The inhalation slope factor and unit risk are 1.2E+0 (mg/kg/day)-1 and 5.0E-5 (ug/m3)-1 (EPA, 1994a), respectively. Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97