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Carcinogens/carcinogenesis

De Eloea S (2000) Threshold mechanisms and site specificity in chromium(VI) carcinogenesis. Carcinogen 21 533-541. [Pg.451]

A toxic component of braken fern, perhaps either quercetin (105) or ptaquiloside, a glucoside (106), has a mixed history of carcinogenicity. It is sometimes impHcated in an increased incidence of bladder cancer in animals and esophageal cancer in humans. Multiple other dietary components seem to either promote or interfere with its action, and the significance of braken fern in human carcinogenesis remains unproven. [Pg.481]

Cobalt compounds can be classified as relatively nontoxic (33). There have been few health problems associated with workplace exposure to cobalt. The primary workplace problems from cobalt exposure are fibrosis, also known as hard metal disease (34,35), asthma, and dermatitis (36). Finely powdered cobalt can cause siUcosis. There is Htfle evidence to suggest that cobalt is a carcinogen in animals and no epidemiological evidence of carcinogenesis in humans. The LD q (rat) for cobalt powder is 1500 mg/kg. The oral LD q (rat) for cobalt(II) acetate, chloride, nitrate, oxide, and sulfate are 194, 133, 198, 1700, 5000, and 279 mg/kg, respectively the intraperitoneal LD q (rat) for cobalt(III) oxide is 5000 mg/kg (37). [Pg.379]

A2 - Suspected human carcinogens. Chemical substances, or substances associated with industrial process, which are suspect of inducing cancer, based on their limited epidemiological evidence or demonstration of carcinogenesis in one or more animal species by appropriate methods. [Pg.177]

Ashby, J., and D. Paton (1993). The Influence of Chemical Structure on the Extent and Sites of Carcinogenesis for 522 Rodent Carcinogens and 55 Different Human Carcinogen Estytosurts."Mutation Research 286, 3-74. [Pg.145]

I 97. Efarris, C. C. (1989). Interindividual variation. among humans in carcinogen metabolism, DNA adduct formation and DNA repair. Carcinogenesis 10, 1563-1566. [Pg.344]

A scientifically evaluated and fully referenced data bank, developed and maintained by the National Cancer Institute (NCI). It contains some 8,000 chemical records with carcinogenicity, mutagenicity, tumor promotion, and tumor inhibition test results. Data are derived from studies cited in primaiy journals, current awareness tools, NCI reports, and other special sources. Test results have been reviewed by experts in carcinogenesis and mutagenesis. [Pg.304]

NCI. 1979. Bioassay of methyl parathion for possible carcinogenicity. Bethesda, MD U.S. Department of Health, Education, and Welfare, National Institutes of Health, National Cancer Institute, Carcinogenesis Testing Program. DHEW (NIH) Publication No. 79-1713 NCI-CG-TR-157, 112. [Pg.224]

NCI. 1978. Bioassay of endosulfan for possible carcinogenicity. Carcinogenesis Testing Program,... [Pg.308]

Third, reactions of activated species of chemical carcinogens with DNA are thought to be of great importance in chemical carcinogenesis. Some chemicals (eg, benzojajpyrene) require activation by monooxygenases... [Pg.631]

NCI. 1976. Carcinogenesis bioassay of trichloroethylene (CAS No. 79-01-6). Bethesda, MD National Cancer Institute, Division of Cancer Cause and Prevention, Carcinogenesis Program, Carcinogen Bioassay and Program Resources Branch. NCI-CG-TR-2, DHEW Publ. No. (NIH) 76-802. [Pg.281]


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See also in sourсe #XX -- [ Pg.631 ]




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