||Carcinogenicity of the Chlorinated Acetic Acids.
DeAngelo, A. B. ;
McMillan, L. P. ;
||Health Effects Research Lab., Research Triangle Park, NC.
Liver neoplasms ;
Chlorine organic compounds ;
Laboratory animals ;
Acetic acid/dichloro ;
Acetic acid/trichloro ;
Toxic substances ;
||Some EPA libraries have a fiche copy filed under the call number shown.
Dichloroacetic Acid (DCAA) and trichloroacetic acid (TCAA) comprise a major fraction of the reaction products formed when water containing a variety of precursor humic materials is chlorinated. Both DCAA and TCAA administered in the drinking water increased the incidence of hepatocellular carcinomas in mice. DCAA was more potent than TCAA in increasing the tumor incidence and the number of tumors per liver. The acids appear to act as complete carcinogens since prior initiation with ethylnitrosourea was not required. However, DCAA and TCAA would not appear to be direct genotoxic carcinogens since they have tested negative in short term tests. Both acids induce hepatic peroxisome proliferation (PP) in mice. The peroxisome proliferator chemicals are postulated to comprise a novel class of non-mutagenic hepatocarcinogens. PP may not account fully for the tumorigenic activity of DCAA and TCAA since the former is a relatively weak peroxisome proliferator and a strong carcinogen, while the latter is a strong peroxisome proliferator and a relatively weak carcinogen.