Effect of Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbonson Neurodevelopment in the First 3 Years of Life among Inner-City Children

Abstract

Our prospective cohort study of nonsmoking African-American and Dominican mothers and children in New York City is evaluating the role of prenatal exposure to urban pollutants, including polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and pesticides, in the pathogenesis of neurobehavioral disorders. We used the Bayley Scales of Infant Development to evaluate the effects on child mental and psychomotor development of prenatal exposure to airborne PAHs monitored during pregnancy by personal air sampling. Behavioral development was assessed by the Child Behavior Checklist. We adjusted for potential confounders including sociodemographic factors and prenatal exposure to ETS and chlorpyrifos. Prenatal exposure to PAHs was not associated with psychomotor development index or behavioral problems. However, high prenatal exposure to PAHs (upper quartile) was associated with lower mental development index at age 3 [β= –5.69; 95% confidence interval (CI), –9.05 to –2.33; p < 0.01]. The odds of cognitive developmental delay were also significantly greater for children with high prenatal exposure (odds ratio = 2.89; 95% CI, 1.33 to 6.25; p = 0.01). General estimated equation analysis showed a significant age × PAH effect on mental development (p = 0.01), confirming the age-specific regression findings. Further adjustment for lead did not alter the relationships. There were no differences in effect sizes by ethnicity. The results require confirmation but suggest that environmental PAHs at levels recently encountered in New York City air may adversely affect children’s cognitive development at 3 years of age, with implications for school performance.

Fruit and vegetable intake influences the association between exposure to polycyclic aromatic hydrocarbons and a marker of oxidative stress in pregnant women

“…It has been reported that the estimated exposure to carcinogenic PAHs in early gestation and the levels of PAH-DNA adducts in cord blood are associated with intrauterine growth retardation (Dejmek et al, 2000), lower birth weight, reduced length and head circumference (Perera et al, 1998;Choi and Perera, 2011). In addition, a prospective cohort study involving residents of New York City found that prenatal exposure to airborne PAHs was associated with reduced Mental Developmental Index scores at 3 years of age (Perera et al, 2006) and IQ at 5 years of age (Perera et al, 2009). These adverse effects of PAH exposure during pregnancy may appear because PAHs can cause oxidative stress through the formation of quinone metabolites of PAHs, which can induce reactive oxygen species via redox cycling (Flowers et al, 1997;Bolton et al, 2000;Singh et al, 2007).…”

“…Exposure to PAHs during pregnancy is known to increase the risk of adverse pregnancy outcomes, such as preeclampsia (Wu et al, 2009) and fetal growth retardation (Dejmek et al, 2000). There is now also evidence that prenatal PAH exposure is associated with a reduction in physical growth at birth (Perera et al, 1998(Perera et al, , 2003 and in the child's subsequent cognitive development (Perera et al, 2006(Perera et al, , 2009Tang et al, 2008).…”

Down-regulation of early ionotrophic glutamate receptor subunit developmental expression as a mechanism for observed plasticity deficits following gestational exposure to benzo(a)pyrene

“…The study provides evidence that environmental contaminants at levels currently encountered in New York City adversely affect fetal development. (Perera et al, 2003) A more recent prospective epidemiological study in support of the deleterious effects of gestational exposure to PAH's on cognitive functioning was reported recently by Perera et al, (2006). An effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3-years of life among inner-city children was identified.…”

“…These previous studies have also revealed that brain to body weight ratios are greater in exposed offspring relative to controls indicative of intrauterine growth retardation which has been shown to manifest as low birth weight in offspring. Recent epidemiological studies have identified an effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 Years of life among inner-city children (Perera et al, 2006). The present study utilizes a well-characterized animal model to test the hypothesis that gestational exposure to B(a)P causes dysregulation of developmental ionotropic glutamate receptor subunit expression, namely the N-methyl-D-aspartate receptor (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptor (AMPAR) both critical to the expression of synaptic plasticity mechanisms.…”

Quantitative Assessment of Polycyclic Aromatic Hydrocarbons and Heavy Metals in Fish Roasted with Firewood, Waste Tyres and Polyethylene Materials

“…These diolepoxides covalently binds to DNA base pair, forming a stable depurinating adduct through electrophilic cabonium ions. This blocks polymerase replication activity and perturbs the double helix DNA structure [25]. These biochemical processes can disrupt proper DNA copying, increase DNA damage and reduce repair activities.…”