There now is evidence that many of the synthetic chemicals released into the environment can impact on the function of the endocrine system of many organisms. One group of chemicals, the alkylphenols, used in paints, pesticides, herbicides, detergents, and plastics, has been found to have the ability to bind estrogen receptors. This estrogenic property makes these compounds potentially hazardous to the developing reproductive system and neuroendocrine brain. In this study we deter- mined the effects of exposure to the environmental toxins 4-nonylphenol (NP) and 4-tert-octylphenol (OP) and to synthetic estrogen diethylstilbesterol (DES) during the early postnatal period (d 0-10) on the development of reproductive function. The day of vaginal opening, ovulation, prepubertal LH levels, LH response to estradiol, estrous cyclicity, and ovarian histology were determined. In the OP- and DES-treated groups, the vaginal opening was observed to have occurred several days prior to that of the control group. The NP-treated group showed vaginal opening at ages similar to those of the control group. Treatment with OP prevented ovulation in a significant number of animals, as well as in all animals treated with DES, whereas the control and NP-treated animals ovulated normally. Animals treated with DES and OP had significantly lower ovarian weights and higher uterine weights than either control animals or NP-treated animals. Higher basal LH levels, as well as the absence of the prepubertal LH surge, were observed in both DES- and OP-treated animals. A significant number of OP-treated animals showed no LH response to the estradiol-17beta challenge. NP-treated animals responded positively to the estradiol-17beta challenge. Persistent estrus was also apparent in both OP- and DES-treated animals. Upon histological examination, the ovaries in OP-treated animals were found to have a decreased number of corpora lutea and an increased number of preantral and atretic follicles. These data suggest that exposure to OP during the critical period of sexual brain differentiation affects the onset of puberty and reproductive development.