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Pure Appl. Chem., Vol. 70, No. 9, pp. 1713-1723, 1998 Natural and anthropogenic environmental
oestrogens: Breast cancer: evidence for xeno-oestrogen involvement in altering its incidence and risk J.J. Li1 and S.A. Li Abstract: This review specifically addresses whether environmental estrogen xenobiotics increase breast cancer risk, and thus contribute to the gradual and persistent rise in breast cancer incidence since 1940. Xenoestrogens are a structurally diverse group of chemicals that includes organochlorine pesticides, herbicides, pollutants, industrial chemicals, and metabolites of potent carcinogens. They possess estrogenic activity, and when compared to that of 17b-oestradiol, their estrogenic potency ranges from weak (10-3) to extremely weak (10-6), using a variety of in-vivo and in-vitro endpoints. It is evident that the sequestering of xenoestrogens in mammalian adipose tissue and their gradual release may not be a property of all xenoestrogens. Long-term animal carcinogenicity studies of individual xenoestrogens [e.g., dichlorodiphenyl trichloroethane (DDT), dichlorodiphenyl dichloroethane (DDE), dieldrin, aldrin, polychlorinated biphenyls (PCBs), phthalates] are revealing. Only atrazine has been shown to have the mammary gland as a marginal target site for cancer. A number of xenoestrogens (DDT, DDE, PCBs) induce tumors in the liver, lung, and lymphomas in various murine species. Human neoplasms induced by individual xenoestrogens largely reflect those induced in animal studies, with possible additional associations of pancreatic and hematologic cancers. Earlier small case-control studies lent credence to an association of xenoestrogens and breast cancer. Subsequent larger prospective case-control studies from the USA, Europe, and Mexico, however, do not support this relationship. It is concluded from the evidence presented that xenoestrogens do not play a significant role in human breast cancer etiology, its subsequent development, or in the gradual rise in breast cancer incidence.
Page last modified 21 May 1999.
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