Department of Epidemiology and Preventive Medicine, Jagiellonian University Medical College, Krakow, Poland.
J Expo Sci Environ Epidemiol. 2013 Jul;23(4):371-7. doi: 10.1038/jes.2012.117. Epub 2013 Jan 9.
In a birth cohort study, we have assessed the dose-response relationship between individual measurements of prenatal airborne polycyclic aromatic hydrocarbon (PAH) exposure and specific PAH-DNA adducts in cord blood adjusted for maternal blood adducts and season of birth. The study uses data from an earlier established birth cohort of children in Krakow. The final analysis included 362 pregnant women who gave birth to term babies and had complete data on personal exposure in the second trimester of pregnancy to eight airborne PAHs including benzo[a]pyrene (B[a]P), as well as DNA adducts, both in maternal and cord blood. The relation between cord blood PAH-DNA adducts and airborne prenatal PAH exposure was non-linear. Although cord blood PAH-DNA adducts were significantly associated with the B[a]P exposure categorized by tertiles (non-parametric trend z=3.50, P<0.001), the relationship between B[a]P and maternal blood adducts was insignificant (z=1.63, P=0.103). Based on the multivariable linear regression model, we estimated the effect of the prenatal airborne B[a]P on the level of cord blood adducts. In total, 14.8% of cord blood adducts variance was attributed to the level of maternal adducts and 3% to a higher prenatal B[a] exposure above 5.70 ng/m(3). The calculated fetal/maternal blood adduct ratio (FMR) linearly increased with B[a]P exposure (z=1.99, P=0.047) and was highest at B[a]P concentrations exceeding 5.70 ng/m(3). In conclusion, the results support other findings that transplacental exposure to B[a]P from maternal inhalation produces DNA damage in the developing fetus. It also confirms the heightened fetal susceptibility to prenatal PAH exposure that should be a matter of public health concern, particularly in the highly polluted areas, because DNA adducts represent a pro-carcinogenic alteration in DNA. The continuation of this birth cohort study will assess the possible health effects of fetal DNA damage on the health of children and help in establishing new protective guidelines for newborns.
在一项出生队列研究中，我们评估了个体产前空气中多环芳烃（PAH）暴露测量值与脐带血中特定 PAH-DNA 加合物之间的剂量反应关系，同时调整了母体血液加合物和出生季节因素。该研究使用了来自克拉科夫一个早期建立的儿童出生队列的数据。最终分析纳入了 362 名足月分娩的孕妇，这些孕妇在妊娠中期个人暴露于包括苯并[a]芘（B[a]P）在内的 8 种空气中 PAH 的情况以及母血和脐血中的 DNA 加合物数据完整。脐带血 PAH-DNA 加合物与产前空气 PAH 暴露之间的关系是非线性的。尽管脐带血 PAH-DNA 加合物与 B[a]P 暴露呈三分位（非参数趋势 z=3.50，P<0.001）显著相关，但 B[a]P 与母体血液加合物之间的关系并不显著（z=1.63，P=0.103）。基于多变量线性回归模型，我们估计了产前空气中 B[a]P 对脐带血加合物水平的影响。总的来说，14.8%的脐带血加合物变异归因于母体加合物水平，3%归因于高于 5.70ng/m(3)的产前 B[a]P 暴露。计算得出的胎儿/母体血液加合物比值（FMR）与 B[a]P 暴露呈线性关系（z=1.99，P=0.047），在 B[a]P 浓度超过 5.70ng/m(3)时最高。总之，这些结果支持其他研究发现，母体吸入 B[a]P 会导致胎儿发生 DNA 损伤。它还证实了胎儿对产前 PAH 暴露的敏感性增加，这应该是公共卫生关注的问题，特别是在污染严重的地区，因为 DNA 加合物代表 DNA 中促癌的改变。该出生队列研究的延续将评估胎儿 DNA 损伤对儿童健康的潜在影响，并有助于为新生儿制定新的保护指南。
