Health risk assessment of environmental exposure to trichloroethylene

• Published in: Regulatory toxicology and pharmacology Vol. 11; no. 1; p. 24
• Main Authors: Brown, L P, Farrar, D G, de Rooij, C G
• Format: Journal Article
• Language: English
• Published: Netherlands 01.02.1990
• Subjects: Animals; Environmental Pollutants - toxicity; Humans; Risk; Trichloroethylene - toxicity
• ISSN: 0273-2300; 1096-0295
• DOI: 10.1016/0273-2300(90)90005-V

A review of the animal data showed trichloroethylene (TRI) to be of low acute toxicity. Repeated exposure showed that the target organs were the liver, and to a lesser extent, the kidney. TRI is not mutagenic or only marginally mutagenic. There is no evidence of fetotoxicity or teratogenicity. TRI is judged not to exhibit chronic neurotoxicity. Lifetime bioassays resulted in tumors in both the mouse and the rat. However, because of qualitative and quantitative metabolic differences between rodent and human, no one suitable tumor site can be chosen for human health risk assessment. In addition, of the several epidemiology studies, none has demonstrated a positive association for increased tumor incidence. A review of the health effects in humans shows TRI to be of low acute toxicity and, following chronic high doses, to be hepatotoxic. Environmental exposure to TRI is mainly via the atmosphere, while the contribution from exposure to drinking water and foodstuffs is negligible. The total body burden was calculated as 22 micrograms/day. The safety margin approach based on human health effects showed that TRI levels are well within the safety margin for the human no-observable-effect level (10,000 times lower). The total body burden represents a risk of 1.4 X 10(-5) by linearized multistage modeling. Therefore, by either methodological approach to risk assessment, the environmental occurrence of TRI does not represent a significant health risk to the general population or to the population in areas close to industrial activities.