Bisphenol A, a chemical used in many consumer products, is much in the news and the topic of considerable debate. BPA has estrogenic properties and has been linked with a number of health effects, primarily in animal studies. Some adverse impacts in people are suggested by preliminary investigations. Concerns are justified since more than 90% of Americans have detectable levels of BPA in their urine.
We suspect that much of the exposure is coming from contaminated food and beverages since polycarbonate plastic food and beverage containers leach BPA into their contents and BPA-containing resin lines the inside of many metal food and beverage cans. On November 7, New York Times columnist Nicholas Kristof wrote about bisphenol A, bringing the topic to an even larger audience. Kristof interviewed me, among a number of others, while preparing his column.
Today’s journalists often invite comments on their columns to be posted on a blog, and Kristof’s Nov. 7 website was especially active. One commenter to the blog raised the important issue of BPA metabolism, claiming that all BPA is glucuronidated (an enzyme-linked metabolic process that facilitates excretion of BPA and other chemicals) in the intestine and that people are therefore not likely to be exposed to any free (active) BPA. He writes, “The most important fact about BPA is that at concentrations to which we are exposed to BPA in the diet, all of BPA is metabolized to the BPA-glucuronide (Chem. Res. Toxicol., 2002, 15(10):1281-1287). Further studies have shown that this metabolism occurs in the intestine, so humans are essentially not exposed to BPA.” The commenter notes that glucuronidated BPA has zero estrogenic activity.
To a limited extent, this has been studied. In 6 adults given 25 micrograms of BPA by mouth, low levels of free (active) BPA were identified in the urine of 2 of them. (Volkel, Drug Metab and Deposition; 33(11); 2005). In that same study, no free BPA was identified in the urine of adult participants who had not been given any BPA.
But, of greater concern, free (active) BPA has been measured in human amniotic fluid. These studies show us that the developing fetus is exposed to higher concentrations of free (active) BPA than adults–not surprising since a fetus has not yet developed mature enzymatic detoxifying capabilities. (Ikezuki; Human Reprod; 17(11); 2002)
Another study showed similar levels of free BPA in the blood of neonatal rodents, whether given BPA by injection or by mouth. (Taylor; Reprod Toxicol; 25; 2008)
Numerous animal studies show that the developing fetus is particularly sensitive to health effects of low levels of BPA exposure. Some of these impacts carry life-long consequences. The combination of increased vulnerability during fetal/infant development and reduced capacity to metabolize BPA into its inactive form creates considerable concern.
Public health professionals and policy makers must decide when evidence is sufficient to act. In this case, safer alternatives are available for virtually all applications that are likely to result in contaminating food and beverages with this chemical. Despite remaining uncertainties, at SEHN we believe that fetuses and infants should be given the benefit of the doubt….not chemical and product manufacturers.