neoFroxx® Trichloroacetic Acid (TCA) pure EP (pharma grade), CAS: 76-03-9

Used as a medication (peeling agent to remove wrinkles) and in organic synthesis; Generated in chlorinated water that contains organic matter; The sodium salt of TCA is used as a pre- and post-emergent herbicide; [ACGIH]

ACGIH - Documentation of the TLVs and BEIs, 7th Ed. Cincinnati: ACGIH Worldwide, 2020.

Haz-Map, Information on Hazardous Chemicals and Occupational Diseases

Trichloroethylene may act as a promoter, because it inhibits intercellular communication in vitro. It is converted to trichloroacetic acid (TCA) in mice, but not much in rats. TCA acts as a peroxisome proliferator, and the neoplasm in the liver of mice may arise through this mechanism. These chemicals are conjugated with GSH, yielding products that are converted to the reactive metabolites in the kidneys through the action of beta-lyase. These steps occur to a greater extent in rats than in mice, and account for the pronounced nephrotoxicity, involving alpha-2-microglobin accumulation, probably a key reaction. The nephrotoxicity explains the low but definite yield of kidney neoplasms.

Amdur, M.O., J. Doull, C.D. Klaasen (eds). Casarett and Doull's Toxicology. 4th ed. New York, NY: Pergamon Press, 1991., p. 193

Hazardous Substances Data Bank (HSDB)

Induction of peroxisome proliferation has been repeatedly associated with the chronic toxicity and carcinogenicity of trichloroacetic acid to the liver It can induce peroxisome proliferation in the livers of both mice and rats, as indicated by increased activities of palmitoyl-coenzyme A oxidase and carnitine acetyl transferase, the appearance of peroxisome proliferation associated protein and increased volume density of peroxisomes after exposure to trichloroacetic acid for 14 days. The compound induced peroxisome proliferation in mouse but not in rat kidney, and it induced peroxisome proliferation in primary cultures of hepatocytes from rats and mice but not in those from humans.

IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V63 302 (1995)

Hazardous Substances Data Bank (HSDB)

A linear dose response relation /was found/ between TCA induced hepatocellular nodules and proliferative lesions in male mice given the compound in their drinking water at 1000 to 2000 ppm for 1 year. Hepatocellular hypertrophy with intracellular glycogen and a marked accumulation of lipofuscin (indicative of massive intracellular lipid peroxidation) developed. These data suggest that TCA induced hepatotoxicity in mice was related to the generation of free radicals during its in vivo biotransformation. Neither necrosis nor hyperplasia were seen in TCA exposed mice.

American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1602

Hazardous Substances Data Bank (HSDB)