International Agency for Research on Cancer (IARC) - Summaries & Evaluations

(Group 3)

For definition of Groups, see Preamble Evaluation.

VOL.: 63 (1995) (p. 291)
CAS No.: 76-03-9
Chem. Abstr. Name: Trichloroacetic acid

5. Summary and Evaluation

5.1 Exposure data

Trichloroacetic acid is produced commercially in small amounts by chlorination of acetic or chloroacetic acid. It is used principally in the form of the sodium salt, as a herbicide. Most human exposure to trichloroacetic acid occurs because of its metabolic formation from tetrachloroethylene, trichloroethylene, 1,1,1-trichloroethane, 1,1,2,2-tetrachloroethane and chloral hydrate. Trichloroacetic acid can also be formed during the chlorination of drinking-water.

5.2 Human carcinogenicity data

The available data were too limited to form the basis for an evaluation of the carcinogenicity of trichloroacetic acid to humans.

5.3 Animal carcinogenicity data

Trichloroacetic acid was tested by oral administration in the drinking-water in two studies in males of one strain of mice. In both studies, the incidence of hepatocellular adenomas and carcinomas was increased.

5.4 Other relevant data

Trichloroacetic acid has a longer plasma half-life in humans than in rodents, presumably because there is more binding to plasma proteins in humans. Much of an administered dose of trichloroacetic acid is excreted unchanged in the urine of rats and mice. Reductive dechlorination and glutathione conjugation are involved in the formation of the urinary metabolites, oxalate and thiodiacetic acid.

Little is known about the toxicity of this compound to humans. Single doses of high concentrations of trichloroacetic acid induce lipid peroxidation in the livers of rats and mice. Trichloroacetic acid causes hepatic peroxisome proliferation in both rats and mice in vivo and in cultured hepatocytes from mice and rats, but not from humans. Short-term, repeated administrations of trichloroacetic acid induced cell proliferation in the livers of mice but reduced cell proliferation in the livers of rats.

No data were available on the effects of trichloroacetic acid on human reproduction. In rats, fetotoxicity was observed at doses that are maternally toxic.

Trichloroacetic acid induced chromosomal aberrations and abnormal sperm in mice in one study. The results of studies on the induction of DNA strand breaks and micronuclei were inconclusive.

Trichloroacetic acid did not induce chromosomal aberrations in a single study or DNA strand breaks in cultured mammalian cells. Inhibition of intercellular communication has been reported. It was not mutagenic to bacteria.

5.5 Evaluation

There is inadequate evidence in humans for the carcinogenicity of trichloroacetic acid.

There is limited evidence in experimental animals for the carcinogenicity of trichloroacetic acid.

Overall evaluation

Trichloroacetic acid is not classifiable as to its carcinogenicity to humans (Group 3).

For definition of the italicized terms, see Preamble Evaluation.


Last updated 05/27/1997

    See Also:
       Toxicological Abbreviations
       Trichloroacetic acid (ICSC)
       Trichloroacetic acid (SIDS)
       Trichloroacetic acid (IARC Summary & Evaluation, Volume 84, 2004)