Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children

Environmental Science and Pollution Research, Sep 2014

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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Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children

Wiesaw A. Jedrychowski 0 1 2 3 4 5 Frederica P. Perera 0 1 2 3 4 5 David Camann 0 1 2 3 4 5 John Spengler 0 1 2 3 4 5 Maria Butscher 0 1 2 3 4 5 Elzbieta Mroz 0 1 2 3 4 5 Renata Majewska 0 1 2 3 4 5 Elbieta Flak 0 1 2 3 4 5 Ryszard Jacek 0 1 2 3 4 5 Agata Sowa 0 1 2 3 4 5 0 F. P. Perera Columbia Center for Children's Environmental Health, Mailman School Public Health, Columbia University , New York, NY 10027, USA 1 W. A. Jedrychowski ( 2 Responsible editor: Philippe Garrigues 3 M. Butscher Polish-American Institute of Pediatrics, Jagiellonian University Medical College , Krakow, Poland 4 J. Spengler Harvard School of Public Health, Harvard University , Boston, MA 02138, USA 5 D. Camann Department of Analytical and Environmental Chemistry, Southwest Research Institute , San Antonio, TX 78238, USA 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 i m p a c t s o f PA H c o m p o u n d s o n f e t a l g r o w t h a n d 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 PAHDNA 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 (childs 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 PAHDNA 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) 1.36.8). 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 0.10.9). 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. Early cognitive development is vital for an individuals ability to learn, adjust, and take advantage of the opportunities available in various environments (Deary 2010; Hunter 1986; Moffitt et al. 1981). It has been demonstrated that individuals scoring higher on intelligence tests in early childhood are more likely to achieve higher education levels and socioeconomic status and have greater success in professional careers (McCall 1977). Attention to the impact on childrens cognitive dysfunction of ambient air pollutants such as tobacco smoke (Bauman et al. 1991; Eskenazi and Castorina 1999; Johnson et al. 1999; Weitzman et al. 2002; Yolton et al. 2005), diesel exhaust pollutants (Wang et al. 2009), or exposure to polycyclic aromatic hydrocarbons (PAHs) (Perera et al. 2011) has recently increased (Brown et al. 2005), and our previous study in the present cohort reported that prenatal PAH was associated with lower intelligence scores at age 5 (Edwards et al. 2010). PAHs belong to a group of chemical compounds formed during the incomplete combustion of organic material; the best known member of this class of compounds is benzo[a]pyrene (BaP). The PAH compounds are ubiquitous and have been found in polluted air in occupational and urban environments, tobacco smoke, and broiled foods (IARC 2010; Lijinsky 1991; Phillips 1999; US EPA 2005; WHO 2001). They readily cross the placenta (Castano-Vinyals et al. 2004; Godschalk et al. 2003; Kihlstrom 1986; Schulte and Perera 1993;); however, the estimated transplacental dose of PAH is about ten times lower than the dose to maternal tissues (Perera et al. 2005). Transplacental exposure to PAH leads to the formation of DNA adducts in the fetus (Neubert and Tapken 1988; Srivastava et al. 1986), which are considered a molecular dosimeter of PAH absorbed over the prenatal period. PAHDNA adducts reflect individual differences in exposure, absorption, and distribution o (...truncated)


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Wiesław A. Jedrychowski, Frederica P. Perera, David Camann, John Spengler, Maria Butscher, Elzbieta Mroz, Renata Majewska, Elżbieta Flak, Ryszard Jacek, Agata Sowa. Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children, Environmental Science and Pollution Research, 2015, pp. 3631-3639, Volume 22, Issue 5, DOI: 10.1007/s11356-014-3627-8