Polycyclic aromatic hydrocarbons (PAHs) as determinants of various anthropometric measures of birth outcome

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants that are known to induce oxidative stress. There have been several reports about the link between PAH exposure and complications in pregnancy. This cross-sectional study was conducted to: (1) measure the levels of benzo(a)anthracene (BaA), chrysene (Ch), benzo(b)fluoranthene (BbF), benzo(a)pyrene (BaP), and dibenzo(a,h)anthracene (DBahA) in placentas and maternal and -umbilical cord blood obtained at delivery from 1578 women between June 2005 and 2006 in the area of Al-Kharj, Saudi Arabia; (2) assess their influence on various anthropometric measures of birth outcome taking into consideration the carcinogenic properties of these PAHs; and (3) determine the degree of PAH-related oxidative DNA damage and birth outcome. Among the five tested PAHs, only BaP was carcinogenic; therefore, the levels of the other four probable or possible carcinogenic PAHs (BaA, Ch, BaF, and DBahA) were summed as ∑4-PAHs. Levels of 1-hydroxypyrene (1-HP) were determined in maternal urine samples as a biomarker of PAH internal dose. Urinary cotinine (COT) was measured as an index of smoking. The following markers of oxidative stress were selected: malondialdehyde (MDA) in cord (C-MDA) and maternal (M-MDA) serum and 8-hydroxy-2-deoxyguanosine (8-OHdG) in maternal urine. None of the tested PAHs was found in maternal or cord blood. However, all five PAH compounds were detected in placentas; Ch was the highest (6.582 μg/kg dry wt.), and BaA was the lowest (0.236 μg/kg dry wt.). The mean concentration of urinary 1-HP found in this study was 0.216 ± 0.856 μg/g Cr. After adjusting for gestational age and other confounding variables, regression models revealed an inverse relationship between placental weight, cord length and placental BaP. A similar trend was observed between cord length and ∑4-PAHs in placental tissues. Urinary 1-HP, though, cannot be used as an unequivocal biomarker of PAH exposure, but it can be an appropriate indicator of exposure to environmental tobacco smoke (ETS). The data demonstrate that ETS exposure (as measured by urinary COT) may adversely affect birth outcome as shown by reduced head circumference, birth weight, and birth length, as well as increased cephalization index. The positive relationship between 8-OHdG levels and 1-HP in urine provides evidence of an oxidative stress mechanism. Although this study provides no direct evidence of an association between PAH exposure and DNA damage, increased oxidative stress in the form of lipid peroxidation significantly affected various birth measures. Therefore, there is a need for studies regarding PAH exposure and its associated biological effects to determine the extent of potential fetal damage as well as possible long-term effects, such as cancer.