Determinants of serum PCAHs are well documented in newborns and young children (7, 8).
Briefly, the method involved n-hexane extraction of the sample and removal of acid-labile matrix components, fat, and nonstable PCAHs by passage through a silica column containing concentrated [H.
We identified determinants of the serum concentration of PCAHs by single regression and subsequently by stepwise regression procedures in which we set the p-value at 0.
Hence, taking adolescents as study populations has advantages for studying secular trends in the serum concentration of PCAHs and for monitoring the effectiveness of environmental hygiene strategies aiming at the reduction of exposure to these compounds.
Because PCAHs are persistent in the environment, people may be exposed to them through their diet.
Throughout life, PCAHs accumulate in the mother's body.
In 1993, Sharpe and Skakkebaek (8) hypothesized that xenoestrogens such as PCAHs may interfere with the development of Sertoli and Leydig cells during fetal development (Figure 3A).
Our hypothesis of an excessive maternal exposure to PCAHs during pregnancy is plausible.
Moreover, we cannot exclude the possibility that an unknown toxic compound emitted along with PCAHs (e.
We did not find an inverse correlation between the serum testosterone concentration and the biomarkers of exposure to PCAHs.
The possible effects of PCAHs on sexual differentiation and maturation are less documented in females than in males.
In conclusion, our findings suggest that, in line with the concept of endocrine disruption and Sharpe and Skakkebaek's hypothesis (8), environmental exposure to PCAHs may adversely interfere with the sexual maturation during the fetal and pubertal stages of development.