Trichloroethylene is a colourless liquid with a characteristic, slightly sweet odour. It is used as a solvent in a variety of applications. Environmental transport and distribution: Contamination of water has been reported but, with the exception of contamination of water supplies through accidental spillage, levels have been very low. Trichloroethylene is probably widely distributed in the environment, but usually only at fairly low levels, i.e., in the ug/kg range in sediments, in the low ug/litre range in natural waters, in the low ug/m3 range in air, and in the ug/kg range in aquatic biota. Trichloroethylene has a low bioaccumulation and biomagnification potential. BCF for fish was 17 and for animals higher up in the food chain BCF was around 100. The limited toxicity data available show LC50 values for aquatic biota in the mg/litre range (fish, 96-h LC50 = 16-67 mg/l, Crustacean nanplins, 46-h LC50 = 20 mg/l and algae, EC50 = 8 mg/l). Trichloroethylene is degraded in biological and abiotic systems; in air (where most environmental trichloroethylene is expected to occur), its lifetime is about 10 days. It seems unlikely that the present rate of release of trichloroethylene into the environment would contribute significantly to depletion of the stratospheric ozone layer. Effects on experimental animals: Trichloroethylene is a moderately toxic substance. In terms of acute toxicity, LC50 values in rodent test species range from 45 to 260 mg/m , and oral LD50 values range from 2400 to 4920 mg/kg body weight. The toxic effects of exposure are related to a depressant action on the central nervous system. Central nervous system depression can lead to coma and death. Liquid trichloroethylene has an irritant effect on the skin and eyes; trichloroethylene vapour is irritant to the respiratory tract. Toxic effects on the kidneys are produced in rats by long-term oral administration. Minimal changes in the kidneys can occur after oral administration of 100 mg/kg body weight per day for 13 weeks and nephrotic changes can be found following oral administra- tion of 500 mg/kg body weight per day, for 2 years. In mice, toxic effects on the kidney occur after oral administration of 3000 mg/kg per day, for 13 weeks, and mild nephrotic changes following 1000 mg/kg per day, for 2 years. Also, in mice, oral administration of 6000 mg/kg body weight per day for 13 weeks produced necrotic changes in the liver. Continuous exposure of mice by inhalation to 810 mg/m3 trichloroethylene for 2 days resulted in an increased relative liver weight, which decreased following cessation of exposure. Some immunological changes have been observed in rodents exposed to trichloroethylene by inhalation at concentrations between 10 and 1000 mg/m3 for several weeks and also in those given trichloroethylene in their drinking-water (0.1 5 g/litre) for a similar period. Trichloroethylene does not cause any biologically significant embryotoxic or teratogenic effects. The evidence for mutagenic effects is inconclusive. There is clear evidence that trichloroethylene is carcinogenic in mice with lifetime (2-year) exposures 1620 mg/m3 by inhalation or oral administration of 700 - 1200 mg/m3 body weight per day. There is some evidence that trichloroethylene causes tumours in rats; a low incidence of renal tumours occurred in rats exposed for 2 years to levels of 3240 mg/m3 by inhalation or 500 - 1000 mg/kg per day by the oral route. There are species and strain differences in carcinogenic response and the purity of the trichloroethylene and the nature of any additives affect the outcome. Effects on man: The signs and symptoms of over-exposure in human beings are mainly related to the central nervous system; for example, headache, drowsiness, hyperhydrosis, tachycardia, and, in more severe cases, stupor and coma. Trichloroethylene is analgesic and anaesthetic; inhalation of concentrations between 27 000 mg/m3 (5000 ppm) and 108 000 mg/m3 (20 000 ppm) have been used in anaesthetic procedures. Fatalities have been reported through accidental or suicidal over-exposure to trichloroethylene. In general, the lethal oral dose for an adult is of the order of 7000 mg/kg body weight, but a death has occurred following a single dose of 50 ml (75 g). Deaths have been reported following inhalation of trichloroethylene, including a number that have occurred during anaesthetic procedures. While respiratory depression cannot be excluded, it is more likely that cardiac arrest, related to the arrhythmic properties of trichloroethylene, was the cause of death. In laboratory and work-place studies, demonstrable psychomotor impairment was found following inhalation exposure to 5400 mg/m3 (1000 ppm) for 2 h, and reaction time was increased by exposure to a concentration of 1320 mg/m3 (245 ppm), under work-place conditions. Effects on the respiratory and gastrointestinal tracts are related to the irritant properties of trichloroethylene. Irritation of mucous membranes occurs with exposure to trichloroethylene vapour at concentrations of 810 - 3510 mg/m3 (150 - 650 ppm). At autopsy, following fatal ingestion, lesions of the gastrointestinal tract have been found. Liquid trichloroethylene and its vapour at anaesthetic concentrations (27 500 - 108 000 mg/m3) cause eye irritation and superficial corneal damage, which normally recovers completely. Liquid trichloroethylene is mildly irritating to the skin but, if it is held in contact for any length of time, for example, by clothing or footwear, it can produce marked skin irritation with blistering. Repeated contact produces defatting of the skin and dermatitis. High oral doses (200 - 300 ml or more), taken suicidally or through misuse, have produced toxic effects on the liver and kidneys. Hepatic necrosis and nephropathy have been found at autopsy. The use of trichloroethylene in a confined unventilated space for 3 - 4 h has also resulted in liver and kidney damage. Addiction to trichloroethylene ("vapour sniffing") has produced liver and kidney damage, and deaths have occurred. Chronic neurotoxic effects may occur, and a "psychoorganic syndrome", with lassitude and depression, has been described but has not been found consistently in studies on groups of trichloroethylene workers. It is probable that many of the effects described were due to the metabolites of trichloroethylene. Degeneration of cranial nerves has occurred following short-term exposures to high levels of trichloroethylene, generally in enclosed spaces. However, it is considered that the cranial neuropathy is probably due to breakdown products, mainly dichloroacetylene, rather than to trichloroethylene itself. Polyneuropathies have been reported following long-term exposure. Data from epidemiological studies on carcinogenicity in occupationally exposed groups are inconclusive.