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Safety assessment of endocrine-disrupting chemicals (EDCs) is now an important issue because of fear of human exposure. Bisphenol A (BPA), a compound initially synthesized as a chemical oestrogen, is now used as a monomer for the production of polycarbonate plastic products such as baby bottles. In the present experiment, toxicity and effects of BPA administration to maternal rats and response of their offspring to N-nitrosobis(2-hydroxypropyl)amine (BHP) treatment were studied. Growth retardation was observed in maternal rats throughout the period of BPA exposure (total dose of 21 ± 3 grams per rat). Serum TSH was elevated in maternal rats receiving a soybean-devoid diet and offspring of maternal rats with or without BPA but this was not thought to be caused by BPA. Histopathologically, no significant organ toxicity was observed in BPA-treated maternal rats. Examination of cleavage of the balanopreputial gland in males and opening of the vagina in females performed on 5 to 7-week-aged offspring, demonstrated no abnormal differentiation or growth retardation. BPA exposure did not affect BHP-induced carcinogenesis in the thyroid, lung, thymus, esophagus, and liver, location, incidences, and numbers of tumors not differing in offspring born from maternal rats with or without BPA administration. These results indicate that BPA does not induce any tissue injury for maternal or offspring rats, with no effects on target organ carcinogenesis of BHP in offspring.

Lack of Effects of Bisphenol A in Maternal Rats or Treatment on Response of Their Offspring to N-Nitrosobis (2-hydroxypropyl)amine.