Organochlorine Residues and Risk of Breast Cancer

Abstract

Considerable attention has recently been focused on the possible role of estrogenic compounds as etiologic agents in the development of human breast cancer. This review summarizes data from relevant laboratory and epidemiological studies to assess the hypothesis that exposure to organochlo-rines, and specifically 2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane (DDT), increases breast cancer risk. Organochlorine compounds, including pesticides such as DDT and industrial compounds such as the polychlorinated biphenyls (PCBs), have had a long history of use. In general, these compounds are characterized by their high lipophilicity and environmental persistence. DDT was widely used in agriculture and public health programs from 1943 to 1972, when it was removed from use in the Western world. DDT is still used, however, in many developing nations. The International Agency for Research on Cancer concluded that there was adequate evidence that DDT was carcinogenic in laboratory animals, yet epidemiological evidence has not been compelling. The estrogenic activity of o, p'-DDT has been well characterized; however, the affinity of estrogen receptors for this compound is very weak and reported to be 1/2,000–1/10,000 that of 17β-estradiol. Epidemiologically, some investigators have reported elevated levels of 1,1-dichloro-2,2-bis(p-chloro-phenyl)ethylene, a DDT metabolite, and PCBs in breast adipose tissue and blood serum taken from breast cancer patients when compared with controls, while others have reported the absence of such an association. While the etiology of breast cancer is not fully understood, it is generally recognized that estrogenic compounds may increase the risk of disease. Contemporary human exposure to DDT and other organochlorines is very limited and would likely play an insignificant role when compared with other sources of exposure, such as estrogen replacement therapy and phytoestrogens in food.