PAH Exposure

A 140 volume 117 | number 4 | April 2009 • Environmental Health Perspectives PAH Exposure doi:10.1289/ehp.0800445 We were very interested to read the article by Choi et al. (2008). The difference between maternal exposure and our own data on actual concentrations of poly cyclic aromatic hydro carbons (PAHs) in the human male fetal liver (Fowler et al. 2008) was striking. Eight of the PAH exposures meas ured by Choi et al. were also on our list of PAHs measured in the human fetal liver during the second trimester. Assuming that the 48‐hr samples of air‐ borne PAH exposure used by Choi et al. (2008) truly reflect longer‐term exposure more relevant to the outcomes under con‐ sideration (which is contentious because the measurements may either over estimate or under estimate true exposure), then we can approximate a comparison between the two studies. Therefore, we calculated the fold‐ difference between the maximal second tri‐ mester exposures (nanograms per cubic meter) reported by Choi et al. in their Table 2 and the mean male fetal liver values presented in our Table 3 [(Fowler et al. 2008), corrected to nanograms per kilogram dry weight]. We calculated values separately for fetuses from mothers who smoked cigarettes and for those who did not (Table 1). The smallest differ‐ ence was 5‐fold for benzo[a]pyrene (BaP), whereas the largest difference was 8,340‐fold for benz[a]anthracene (BaA), in all cases representing accumulation in the fetal liver considerably above personal maternal expo‐ sure to airborne PAHs. Of course there are other sources of exposure to PAHs, such as air pollution and occupational sources, but these data very clearly suggest that large quantities of PAHs are crossing the placenta and accumulating in the fetus. Perhaps even more interesting was the very different rela‐ tive proportions of these eight PAHs in the air compared with in fetal livers: BaA com‐ prised 11% in air but 94–96% in the livers, whereas pyrene was 17% in the air but below detection in the livers. This suggests that very different proportions of PAHs are accumulat‐ ing in fetal tissues and it also underscores the fundamental principle that to really under‐ stand health risks we cannot afford to ignore the actual tissue levels in favor of exposure estimates alone. The authors declare they have no competing financial interests. Paul A. Fowler Centre for Reproductive Biology & Medicine Institute for Medical Sciences University of Aberdeen Aberdeen, United Kingdom E‐mail: [email protected]