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Cancer animal studies

Hawrylewicz, E.J., Zapata, J.J. and Blair, W.H. (1995). Soy and experimental cancer animal studies, J. Nutr., 125, 698S-708S. [Pg.106]

T (with its contaminant TCDD), might increase their risk of adverse health effects, particularly various forms of cancer. Animal studies do not support the notion that 2,4,5-T itself is carcinogenic. Chronic feeding studies in rats did not produce an increased mmor incidence, even at doses of 30mg/l /day, which produced toxic effects. The lARC has determined that there is inadequate evidence for carcinogenicity of 2,4,5-T in animals and that... [Pg.702]

Chromium and cancer Several studies have shown that chrominm (VI) compounds can increase the risk of lung cancer. Animal studies have also shown an increased risk of cancer. The WHO has determined that chromium (VI) is a human carcinogen. The DHHS has observed that certain chromium (VI) compounds are known to cause cancer in humans. The U.S. EPA has reported that chrominm (VI) in air is a human carcinogen. ... [Pg.90]

Certain chemicals are known to cause skin cancer. Animal studies show that topical applications of substances, such as polynuclear aromatic hydrocarbons, can induce skin cancer. Coal tar, soots, shale oils, and many arsenical compounds can induce skin tumor. [Pg.33]

In 1971 the OSHA standard for benzene (20 CFR, Part 1910.0000) adopted a permissible exposure limit (PEL) of 10 ppm benzene measured as an 8-h TWA. In October of 1976 NIOSH updated its earlier criteria document on benzene and recommended that OSHA lower the benzene exposure standard from 10 to 1 ppm. This proposed implementation was blocked by the United States Supreme Court iu 1980 on the basis of iusufficient evidence linking benzene to cancer deaths. By the mid-1980s convincing evidence of the carciuogenicity of benzene appeared through animal studies which justified reconsideration of the 1 ppm PEL (130). [Pg.48]

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]

Industries that burn wood, gas, oil or coal contribute most of the rest of airborne B(a)P. Studies on animals have shown that contact with BaP and PAH can cause skin cancer, but the effects of breathing or ingesting them are not yet well enough studied to draw a conclusion as to other cancers. Animal tests have shown that exposure to BaP may cause reproduction difficulty. The U.S. government considers BaP a human carcinogen. [Pg.251]

Animal studies show effects of methyl parathion similar to those seen in people. In addition, short-term high exposure of animals to methyl parathion caused decreased heart rate. This may be the result of methyl parathion s effects on the nerves that control the heart. Methyl parathion decreased the ability of animals to fight infections in some studies, but not in others. It is not known whether any of these effects occur in people. It is not known whether methyl parathion affects the ability of animals to reproduce. Studies in animals have not shown that methyl parathion causes cancer. [Pg.25]

From the limited data on the kinetics and distribution of liposomes in man (Zonneveld and Crommelin, 1988) it can be concluded that the overall behavior of liposomes in man is similar to that observed in animals. Studies in cancer patients showed predominant lirer and spleen uptake of technetium-labeled liposomes (Richardson et al.,... [Pg.283]

The lowest concentrations resulting in cancer in reliable animal studies are indicated as cancer effect levels (CELs) in Table 2-1 and Figure 2-1. [Pg.62]

Comparative Toxicokinetics. In humans, the targets for trichloroethylene toxicity are the liver, kidney, cardiovascular system, and nervous system. Experimental animal studies support this conclusion, although the susceptibilities of some targets, such as the liver, appear to differ between rats and mice. The fact that these two species could exhibit such different effects allows us to question which species is an appropriate model for humans. A similar situation occurred in the cancer studies, where results in rats and mice had different outcomes. The critical issue appears to be differences in metabolism of trichloroethylene across species (Andersen et al. 1980 Buben and O Flaherty 1985 Filser and Bolt 1979 Prout et al. 1985 Stott et al. 1982). Further studies relating the metabolism of humans to those of rats and mice are needed to confirm the basis for differences in species and sex susceptibility to trichloroethylene s toxic effects and in estimating human heath effects from animal data. Development and validation of PBPK models is one approach to interspecies comparisons of data. [Pg.191]

Children s Susceptibility. No studies were located in which comparisons were made between the sensitivity of children and adults to the toxicity of americium. Animal studies indicate that juvenile dogs are less susceptible than adults to americium-induced bone cancer (Lloyd et al. 1999). No direct evidence was located to indicate that the pharmacokinetics of americium in children may be different from that in adults. Based on dosimetric considerations related to differences in the parameters of available models, as well as studies in animals, it seems likely that children may be more susceptible to americium toxicity than are adults by virtue of age-related differences in pharmacokinetics. Absorption of ingested americium may be as much as 200 times greater in neonatal animals than in adults. (Bomford and Harrison 1986 David and Harrison 1984 Sullivan et al. 1985). [Pg.124]

We have no proof that lead causes cancer in humans. Kidney tumors have developed in rats and mice given large doses of lead. The animal studies have been criticized because of the very high doses used, among other things. The results of high-dose studies should not be used to predict whether lead may cause cancer in humans. The Department of Health and Human Services (DHHS) has determined that lead acetate and lead phosphate may reasonably be expected to be... [Pg.24]


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See also in sourсe #XX -- [ Pg.234 , Pg.235 ]




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