Environmental exposure to organochlorine compounds such as polychlorinated biphenyls (PCBs), 2,2'-bis (p-chlorophenyl)-1, 1, 1-tri-chloroethane (DDT) and its metabolite DDE, and organochloro pesticides has been suggested as a risk factor for breast cancer. The basis for this claim is that some of these are carcinogenic in animals, have estrogenic activity, and are inducers of cytochrome P-450 enzymes that metabolize drugs, hormones, and various xeno-biotics. Some epidemiological studies have suggested an association between this class of compounds and breast cancer risk, but these studies have been contradictory and inconclusive (reviewed in Reference 172).
Because of a purported clustering of breast cancer on Long Island, New York, and a fair amount of political pressure, a $30 million Long Island breast cancer study project was launched to examine the relationship between exposure to environmental agents and breast cancer incidence. The study was carried out under the auspices of the National Cancer Institute and the National Institute of Environmental Health
Sciences. (In fact, the incidence of breast cancer on Long Island is not significantly different from, and in many instances less than, other locales in New York State).173 The published results of this study indicated that there was no association between increased rates of breast cancer and exposure to PCBs, DDT, or pesticides (reviewed in Reference 174). Studies done in other parts of the United States and of the world also show no significant correlation between serum or plasma levels of PCBs or other organochlorine compounds and breast cancer.172,175-177 The only caveat to this is a report from a small cohort study that women living within one mile of hazardous waste sites containing organochlorines had a higher incidence of breast cancer (reviewed in reference 177a). However, when the data were pooled in a combined analysis, there was no association between breast cancer risk and blood levels of PCBs or DDE.177a
An argument has been made that since PCBs and DDTs have been banned since the 1970s, these may not have been the correct chemicals to look at or exposure of female babies in utero may be the key factor here. While there may be some truth to these assumptions since organo-chlorines do persist in the environment and can remain in the body for more than a decade. However, a case-control study based on cohorts of women who donated blood in 1974, 1989, or both and who were matched on age, race, menopausal status, and month and year of blood donation showed that even after 20 years of follow-up after exposure to relatively high concentrations of DDE or PCBs there was no association with an increased risk of breast cancer.178 One might argue that a better way to assess risk is to look at damage to the target in the body to which environmental agents might bind. This was done in a study that looked at polycyclic aromatic hydrocarbon-DNA adduct levels in blood mononuclear cells of women who live on Long Island. Samples from 576 breast cancer cases and 427 age-matched controls were assayed for PAH-DNA adducts by ELISA.179 The levels of PAH-DNA adducts were slightly, though not significantly, higher among cases than controls. Also, there was no consistent association between adduct levels and passive cigarette smoke exposure or consumption of grilled or smoked foods. The authors also concluded that there was not a dose-dependent relationship between exposure and adduct formation, suggesting that there is a threshold effect. This latter point is interesting because there are known polymorphisms in the enzymes that activate and detoxify PAHs, thus a pharmacogenetic analysis could reveal who may be at higher risk.
Finally, it is worth noting that a careful analysis of all risk factors for breast cancer must be done before one can conclude that a "cluster" of breast cancer cases is related to some local environmental factor. For example, a study done in the San Francisco Bay area, involving both Caucasian and African-American women, found that the elevated breast cancer incidence in the Bay area could be completely accounted for by regional differences in known risk factors, e.g., parity, age at first pregnancy, months of breast feeding, and ages at menarche and menopause.180
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