Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children

• Published in: Environmental science and pollution research international 2015-03, Vol.22 (5), p.3631-3639
• Main Authors: Jedrychowski, Wiesław A, Perera, Frederica P, Camann, David, Spengler, John, Butscher, Maria, Mroz, Elzbieta, Majewska, Renata, Flak, Elżbieta, Jacek, Ryszard, Sowa, Agata
• Format: Article
• Language: English
• Subjects: academic achievement; Adducts; Age; Air Pollutants - analysis; Air Pollutants - toxicity; Air pollution; Animals; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Blood; brain; Breast Feeding; Breastfeeding & lactation; Child; Child, Preschool; childhood; Children; Children & youth; cognition; Cognition & reasoning; Cognition Disorders - chemically induced; Cognition Disorders - epidemiology; Cognitive ability; combustion; confidence interval; Deoxyribonucleic acid; DNA; DNA Adducts - analysis; DNA Adducts - toxicity; Drug dosages; Earth and Environmental Science; Ecotoxicology; Education; Environment; Environmental Chemistry; Environmental Health; Environmental science; Epidemiology; Exposure; Female; fetal development; fossil fuels; gender; Health care; Human exposure; Humans; Infant; infants; Intelligence; Intelligence tests; Longitudinal Studies; Male; Maternal Exposure; mothers; Multivariate analysis; neurodevelopment; Outdoor air quality; Parent educational background; Passive smoking; Poland - epidemiology; Pollutants; Pollution; Polyallylamine hydrochloride; Polycyclic aromatic hydrocarbons; Polycyclic Aromatic Hydrocarbons - analysis; Polycyclic Aromatic Hydrocarbons - toxicity; Postpartum period; Pregnancy; Prenatal development; Prenatal exposure; Prenatal Exposure Delayed Effects - epidemiology; Preventive medicine; protective effect; Public health; Regression Analysis; relative risk; Research Article; Risk; Rope; Sex Factors; smoking (habit); Studies; Tobacco smoke; Tobacco Smoke Pollution; Waste Water Technology; Water Management; Water Pollution Control; Wechsler Scales; Womens health
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-014-3627-8

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.