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December 6, 2006

Toxicology

Bisphenol A May Trigger Human Breast Cancer

Study in rats provides strongest case yet against common environmental chemical

Bette Hileman

A new study finds the strongest evidence yet for the hypothesis that widespread environmental exposure to bisphenol A during fetal life causes breast cancer in adult women. The research, led by Ana M. Soto, professor of anatomy and cellular biology at Tufts University School of Medicine, in Boston, was published Dec. 6 in the online edition of Reproductive Toxicology (DOI: 10.1016/j.reprotox.2006.10.002).

Soto and her colleagues exposed pregnant rats to bisphenol A at doses ranging from 2.5 to 1,000 µg per kg of body weight per day. By the time the pups exposed at the lowest dose reached the equivalent of puberty (50 days old), about 25% of their mammary ducts had precancerous lesions, a proportion three to four times higher than among the nonexposed controls. Mammary ducts from all other exposure groups showed elevated levels of lesions. Cancerous lesions were found in the mammary glands of one-third of the rats exposed to 250 µg/kg/day.

Bisphenol A, a known estrogenic compound, is ubiquitous in the environment. Many people receive exposures of about 2.5 µg/kg/day, and mammary gland development in rats and humans is very similar. Therefore, Soto says, "bisphenol A could be one factor causing the increase in breast cancer incidence over the past 50 years."

Bisphenol A is used in the manufacture of polycarbonate plastics and epoxy resins. It is found in many food and beverage containers, including baby bottles. It is also found in canned food linings and dental composites, and it leaches from all of these products. In one study, Soto notes, urine samples from 95% of the human subjects contained the chemical.

According to Soto, a large body of previous research suggests bisphenol A might cause breast cancer. One study shows that the daughters of women who took the potent synthetic nonsteroidal estrogen diethylstilbestrol (DES) during their pregnancies between 1948 and 1971 have 2.5 times the normal incidence of breast cancer. Bisphenol A, which is structurally similar to DES, may act by a similar mechanism, she explains.

"What is important to note is that Soto's research is not a one-shot finding," says Frederick vom Saal, professor of biology at the University of Missouri. "It follows five years of research demonstrating precancerous changes in the mammary glands of mice with prenatal bisphenol A exposure. Now, Soto has switched to the rat, which is considered a much better animal model for studying human carcinogenesis."

The Environmental Protection Agency has set a safe human intake dose of 50 µg/kg/day for bisphenol A. "On the basis of the effects observed in recent studies, this seems to be an unsafe level," Soto says.

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