Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children
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Date
2014
Author(s)
Jedrychowski, Wiesław A.
Perera, Frederica P.
Camann, David
Spengler, John
Butscher, Maria
Mroz, Elzbieta
Majewska, Renata
Flak, Elżbieta
Jacek, Ryszard
Sowa, Agata
Publisher
Springer Berlin Heidelberg
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Citation
Jedrychowski, Wiesław A., Frederica P. Perera, David Camann, John Spengler, Maria Butscher, Elzbieta Mroz, Renata Majewska, Elżbieta Flak, Ryszard Jacek, and Agata Sowa. 2014. “Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children.” Environmental Science and Pollution Research International 22 (5): 3631-3639. doi:10.1007/s11356-014-3627-8. http://dx.doi.org/10.1007/s11356-014-3627-8.
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced by combustion of fossil fuel and other organic materials. Both experimental animal and human studies have reported the harmful impacts of PAH compounds on fetal growth and neurodevelopment, including verbal IQ of children. Here, we have assessed the association between cognitive function of children and prenatal PAH exposures. The study is part of an ongoing, longitudinal investigation of the health effects of prenatal exposure to air pollution on infants and children in Krakow, Poland. The subjects in this report included 170 children whose mothers were enrolled to the study in the first or second trimester of pregnancy whose cord blood were tested for PAH–DNA adducts and who were assessed at age 7 using the Wechsler Intelligence Scale for Children-Revised (WISC-R). The outcome of a priori interest was depressed verbal IQ index (DepVIQ), which is the difference between WISC-R performance and verbal IQ scores. Prenatal PAH exposure was measured by cord blood PAH–DNA adducts, an individual dosimeter, integrating exposure from various sources of exposure over the gestational period. The estimated effect of prenatal PAH exposure on cognitive function was adjusted in multivariable regression for a set of potential confounders (child’s gender, parity, maternal education, breastfeeding practice, environmental tobacco smoke (ETS), and postnatal PAH exposure). The prevalence of DepVIQ was significantly higher in children with detectable PAH–DNA adducts compared to those with undetectable adducts (13.7 vs. 4.4 %,). Binary multivariable regression documented that the relative risk of DepVIQ increased threefold with a ln-unit increase in cord blood adducts (relative risk (RR) = 3.0, 95 % confidence interval (CI) 1.3–6.8). Postnatal PAH exposure also increased the risk of DepVIQ (RR = 1.6, 95 % CI 1.1–2.5). Long-term exclusive breastfeeding (at least 6 months) showed a protective effect (RR = 0.3, 95 % CI 0.1–0.9). In conclusion, these results provide further evidence that PAHs are harmful to the developing fetal brain with effects extending through childhood, with implications for the academic success of the children.
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