Abstract

In their report on exposures of green monkeys to bisphenol A (BPA) Leranth et al. (1) represent their study as the evaluation of an exposure at the Environmental Protection Agency (EPA) oral reference dose (RfD) of 50 μg per kilogram of body weight per day. The EPA oral RfD (which can be found at www.epa.gov/ncea/iris/subst/0356.htm) is intended to apply to chronic oral exposures, not subcutaneous continuous-release exposures as used in the study. It is incorrect to suggest that this exposure paradigm results in potential physiological levels of BPA comparable to those after ingestion exposures by primates. It is well known that ingested BPA undergoes rapid first-pass conjugation in the liver of humans and other primates (2). The result of these metabolic events is that actual tissue exposures to BPA at sites distal to the liver, after ingestion exposures, is only a fraction of the amount ingested. Thus, the exposure route used in the Leranth et al. study (1) does not result in potential target organ exposures that might result from ingestion of BPA at the EPA oral RfD. The intent to link the unconventional exposure route to human risk was stated explicitly in a report of the study by The Washington Post (3). The toxicological evaluation of potential human exposures to environmental chemicals is difficult under the best circumstances, so it is important that the relevance of exposure routes be understood and explicitly recognized in studies such as the one reported by Leranth et al. (1).

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