Elevation tumor incidence

In a novel experiment, Ip et al. (1999) demonstrated that rats fed a RA-enriched butter had reduced mammary epithelial mass, decreased size of the TEB population, suppressed proliferation of TEB cells, and inhibition of mammary tumor incidence and tumor number similar to animals fed an equivalent quantity of mixed CLA isomers. There was a consistently higher level of RA in the liver, mammary fat pad, peritoneal fat, and blood plasma of rats fed RA-enriched butter compared to CLA-fed rats. The elevated RA levels resulted, no doubt, from endogenous A9-desaturation of VA, which was concurrently increased in the RA-enriched butter. 

Intermediate-duration topical application of benz[a]anthracene to the backs of mice for 30 weeks resulted in a slightly elevated (2.6%) (but not statistically significant) skin tumor incidence. No definitive conclusions can be drawn from this study since only one dose was employed and no statistical analysis was performed. 

Skin of hairless mice subjected to chronic low levels of UV displayed increased epoxide at 4 weeks and maximum levels at 10 weeks (69>70). Subsequently, it was shown a-epoxide hydrase increased starting at 8 and peaking at 15 weeks and that its elevation coincided with a decline in epoxide but also a rapid increase in tumor incidence (70,71). Dietary intake of ascorbate, butylated hydroxytoluene (BUT), dl-a-tocopherol and reduced glutathione decreased levels of a-epoxide by 50% and suppressed tumor formation induced by UV light (72,73). 

P>[a P has been carcinogenic in all animal species tested to date, including mouse, rat, hamster, rabbit, guinea pig, duck, newt, dog, monkey, and fish. Intratracheal instillation and inhalation studies in a number of species have resulted in elevated incidences of respiratory tract and upper digestive tract tumors, and intraperitoneal and subcutaneous injections... 

Repeated oral administration of 300mg/kg daily to both sexes of two strains of mice for 80 weeks induced a significant elevated incidence of tumors, mostly hepatomas. Four other limited studies in rats and mice using oral gavage, subcutaneous or intraperitoneal injection, and skin painting failed to confirm these findings. The lARC has determined that there is limited evidence in animals and inadequate evidence in humans for the carcinogenicity of dichloroethyl ether." ... 

Cancer. There is no specific evidence from epidemiological studies that diazinon causes cancer in humans. Several studies have reported an increased incidence of cancers (brain tumors, Hodgkin s lymphoma, multiple myelomas) in humans who were concurrently or sequentially exposed to a number of insecticides, including diazinon (Cantor et al. 1992 Davis et al. 1993 Morris et al. 1986). However, it is not possible to attribute the increase in cancer incidence exclusively to diazinon exposure. Consequently, while the findings in these studies suggest an elevated risk for the cancers from high exposure to insecticides, in general, the data are far too limited to be used to evaluate the potential for diazinon to cause cancer in humans. 

Neoplastic effects in the NTP (1986) bioassay included increased incidences of neoplastic nodules in the liver in the male and female rats and hepatocellular adenoma or carcinoma (combined) in the male mice. Slightly elevated incidences of thyroid gland follicular cell tumors were additionally observed in exposed male mice, although the increases were equivocal. No exposure-related neoplastic changes were found in the chronic study of the 77.4% decaBDE mixture (Kociba et al. 1975 Norris et al. 1975a), but the power of this study to detect carcinogenic effects is limited by the very low dose levels in comparison to those tested in the NTP bioassay. 

An elevated incidence of breast cancer has also been observed in the female patients in this group (14 cases versus 4.1 to 6.1 expected). Eight of these cases occurred among those injected as children, whereas only 0.6 to 0.9 were expected. In patients injected as adults, the 6 observed cases are not significantly different from the 3.5 to 5.2 cases expected (Spiess et al. 1989). This suggests that exposure to radium-224 during childhood poses a much greater risk for the induction of breast tumors than does exposure as an adult. 

Studies of occupational exposures to sulfur mustard indicate an elevated risk of respiratory tract and skin tumors following long-term exposure to acutely toxic concentrations. Overall, several factors are important regarding the assessment of the carcinogenicity of sulfur mustard. Increased cancer incidence in humans appears to be associated only with exposures that caused severe acute effects, and occupational exposures tended to involve repeated exposures and repeated injury of the same tissues. Because the therapeutic use of the sulfur mustard analog nitrogen mustard is associated with an increased incidence of CML, the reports of CML in HD-exposed individuals appear to be relevant to the eareinogenicity of sulfur mustard. 

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