Bisphenol A and carcinogenesis

Regarding "A Ban on Estrogenics?"1 we must be wary also about a possible cancer risk from long-term exposure to bisphenol A (BP-A) and other estrogenic endocrine disruptors as well. Steroidal/non-steroidal and postmenopausal estrogens and diethylstilbestrol (DES) as examples at low doses are long-known human carcinogens.2 In 1980, the National Toxicology Program in public session reported on the carcinogenicity of BP-A.3 With renewed emphasis on endocrine disruptors,4 we decided our bioassay fin

James Huff(huff1@niehs.nih.gov)
Sep 11, 2005

Regarding "A Ban on Estrogenics?"1 we must be wary also about a possible cancer risk from long-term exposure to bisphenol A (BP-A) and other estrogenic endocrine disruptors as well. Steroidal/non-steroidal and postmenopausal estrogens and diethylstilbestrol (DES) as examples at low doses are long-known human carcinogens.2 In 1980, the National Toxicology Program in public session reported on the carcinogenicity of BP-A.3 With renewed emphasis on endocrine disruptors,4 we decided our bioassay findings should be made more widely available.5

Overall, the NTP concluded that while the evidence of carcinogenicity was not fully convincing, marginal increases in leukemias in male and female rats, along with increases in the combined incidence of lymphomas and leukemias in male mice, suggest that BP-A may be associated with increased cancers of the hematopoietic system. Increases in interstitial-cell tumors of the testes in rats were also evidence of carcinogenesis, as was the unusual occurrence of mammary gland fibroadenomas in male rats.

We know however that hormonally active carcinogens would be better evaluated for carcinogenesis using different design strategies: 1) begin exposures either before or shortly after conception, continuing through gestation, lactation, and weaning, and 2) for an exposure period longer than 104 weeks that is the "standard" bioassay, extending to 120 weeks or lifetime,67 With this modest design alteration, carcinogenesis results of the NTP shorter studies of BP-A would certainly be substantiated and strengthened.

For DES, the strongest evidence for carcinogenicity comes from epidemiological studies of women exposed to DES in utero. Thus, exposures to these hormonal chemicals should be greatly reduced or eliminated, especially for pregnant women, embryos/fetuses, and children.

James Huff, PhD National Institute of Environmental Health Sciences Research Triangle Park, NC huff1@niehs.nih.gov