In a birth cohort study, we have assessed the dose-response relationship between individual measurements of prenatal airborne 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 polycyclic aromatic hydrocarbons (PAH) 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. While cord blood PAH-DNA adducts were significantly associated with the B[a]P exposure categorized by tertiles (nonparametric 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/m3. The calculated fetal/maternal blood adducts ratio (FMR) linearly increased with the B[a]P exposure (z = 1.99, p = 0.047) and was highest at B[a]P concentrations exceeding 5.70 ng/m3.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 health of children and help in establishing new protective guidelines for newborns.
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机译：在一项出生队列研究中，我们评估了针对产前空气传播的PAH暴露的个体测量值和针对母体血液加合物和出生季节调整的脐带血中特定PAH-DNA加合物的剂量反应关系。该研究使用了克拉科夫一个较早建立的儿童出生队列的数据。最终分析包括362名孕妇，这些孕妇分娩了足月婴儿，并在妊娠中期掌握了包括苯并[a] py（B [a] P）在内的八种空气中多环芳烃（PAH）的个人暴露的完整数据，如下：母血和脐带血中的DNA加合物。脐带血PAH-DNA加合物与空气中产前PAH暴露之间的关系是非线性的。虽然脐血PAH-DNA加合物与三分位数分类的B [a] P暴露显着相关（非参数趋势z = 3.50，p <0.001），但B [a] P与母体血液加合物之间的关系微不足道（z = 1.63，p ＝ 0.103）。基于多变量线性回归模型，我们估算了产前空气传播的B [a] P对脐带血加合物水平的影响。总体而言，脐带血加合物的14.8％归因于母体加合物的水平，而3％归因于产前B [a]暴露高于5.70 ng / m 3 。随着B [a] P暴露，计算出的胎儿/母体血液加合物比率（FMR）线性增加（z = 1.99，p = 0.047），并且在B [a] P浓度超过5.70 ng / m <3时最高总之，结果支持其他发现，即胎盘经母体吸入暴露于B [a [P]后会在发育中的胎儿中造成DNA损伤。这也证实了胎儿对产前PAH暴露的敏感性增加，这应该是公共卫生关注的问题，尤其是在高污染地区，因为DNA加合物代表DNA的致癌性改变。这项出生队列研究的继续将评估可能的健康影响。 DNA对儿童健康的损害，并有助于建立新生儿的新保护准则。
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