ABSTRACT
Perinatal estrogen exposure serves as a model for assessing the potential toxicity of a broad range of chemicals that have estrogenic activity-that is, actions mimicking that of estrogen (for reviews see Bern, 1992a, b; Iguchi, 1992). These chemicals, which are widespread in the environment, include some chlorinated organic compounds, polycyclic aromatic hydrocarbons, herbicides, and pharmaceutical agents (for reviews see Colborn and Clement, 1992; Colborn et al., 1993; Guillette, 1995). It has been hypothesized that such chemicals may contribute directly or indirectly to the increasing rate of breast cancer (Davis and Bradlow, 1995) and disorders of the male reproductive tract (Peterson et al., 1992). Several of these chemicals, including dichlorodiphenyltrichloroethane (DDT), 2, 3, 7, 8-tetrachlorodibenzo-pdioxin (TCDD, dioxin), and methoxychlor (an estrogenic pesticide currently used as a substitute for DDT) have reproductive effects similar to those of DES after in utero exposure in rodents (Cooke and Eroschenko, 1990; Roman et al., 1995).
