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Carcinogenesis Humans

Ashby, ]., Brady, A., Elcombe, C.R., Elliott, B.M., Ishmael, J., Odum, Tugwood, J.D., Kettle, S. and Purchase, I.F.H. (1994) Mechanistically-bas human hazard assessment of peroxisome proliferator-induced hepato-carcinogenesis. Human and Experimental Toxicology, 13, Supplement 2. [Pg.510]

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]

Toxicology and Carcinogenesis Studies of Feny I Alcohol, National Toxicology Program, U.S. Department of Health and Human Services, Washington, D.C., May 1989. [Pg.63]

Symposium on Toxicology, Carcinogenesis, and Human Health Effects of 1,3-Butadiene (265). Detailed comparisons of various personal monitoring devices are available (266), and control of occupational exposure to 1,3-butadiene has been reviewed (267). ... [Pg.349]

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]

Experimental animal studies have played a key role in the understanding of the mechanisms of chemical carcinogenesis. The duration of development of a cancer in humans may be several decades, and the development probably includes several steps. Furthermore, individual susceptibility is also important for the disease. Therefore, it has been extremely difficult to make the required observations in exposed individuals. [Pg.318]

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]

KALL M A, VANG o and CLAUSEN J (1996) Effects of dietary broccoli on human in vivo drug metabolising enzymes Evaluation of caffeine, oestrone and chloroxazone metabolism. Carcinogenesis 17 793-9. [Pg.237]

PALOZZA P, SERINI S, MAGGIANO N, ANGELINI M, BONINSEGNA A, DI NICUOLO F, RANELLETTI F O and CALVIELLO G (2002) Induction of cell cycle arrest and apoptosis in human colon adenocarcinoma cell lines by P-carotene through down-regulation of cyclin A and Bcl-2 family proteins , Carcinogenesis, 23, 11-18. [Pg.278]

The N-nitroso compounds are a potential source of carcinogenesis in humans. N-nltroso compounds appear to be ubiquitous in our environment, being present in low levels in foods, cosmetics, drugs, atmosphere, etc., and also appear to be formed endogenously in vivo. [Pg.201]


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Carcinogenesis

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