Prenatal Airborne Polycyclic Aromatic Hydrocarbon Exposure and Child IQ at Age 5 Years

Abstract

OBJECTIVE-This study evaluated the relationship between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) and child intelligence. METHODS-Children of nonsmoking black or Dominican-American women residing in New YorkCity were monitored from in utero to 5 years of age, with determination of prenatal PAH exposure through personal air monitoring for the mothers during pregnancy. At 5 years of age, intelligence was assessed for 249 children by using the Wechsler Preschool and Primary Scale of IntelligenceRevised. Multivariate linear regression models were used to estimate and to test the associations between prenatal PAH exposure and IQ.RESULTS-After adjustment for maternal intelligence, quality of the home caretaking environment, environmental tobacco smoke exposure, and other potentially confounding factors, high PAH levels (above the median of 2.26 ng/m 3 ) were inversely associated with full-scale IQ (P = .007) and verbal IQ (P = .003) scores. Children in the high-exposure group had full-scale and verbal IQ scores that were 4.31 and 4.67 points lower, respectively, than those of less-exposed children (≤2.26 ng/m 3 ). The associations between logarithmically transformed, continuous, PAH levels and these IQ measures also were significant (full-scale IQ: β = −3.00; P = .009; verbal IQ: β = −3.53; P = .002). Exposures during the prenatal and early postnatal stages are of particular concern because of the heightened susceptibility of fetuses and infants to diverse environmental pollutants, including PAHs. [8][9][10][11][12] In addition to their more-immediate health effects, certain prenatal exposures may critically affect epigenetic programming and immune, metabolic, and neurologic functions, with consequences manifesting throughout the life span. [13][14][15][16] Increased susceptibility during early stages of development is attributed to higher cell proliferation rates, lower immunologic competence, and decreased ability to detoxify chemicals and to repair DNA damage. [8][9][10] Laboratory experiments have indicated that the fetal brain and nervous system may be particularly sensitive to PAHs. [16][17][18][19] For example, in utero exposure to diesel exhaust, which contains a variety of PAHs, was associated with significant reductions in performance on the passive avoidance learning test for both male and female mice and affected the emotional behaviors associated with the serotonergic and dopaminergic systems in the mouse brain. 19 In addition, transplacental exposure of rats to benzo [a]pyrene depressed the levels of N-methyl-D-aspartate receptor subunit 1 within the hippocampus significantly and, after birth, impaired long-term potentiation, a marker of long-term memory and learning. 20 A number of PAHs, such as benzo [a]pyrene, were shown to be reproductive and developmental toxicants in experimental studies involving prenatal exposure. 17,20,21 In epidemiological studies, transplacental PAH exposure was associated with fetal growth reduction, including reduced birth weight and birth...

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).…”

DOHaD

“…Cependant, dans une autre étude, l'exposition aux PM 10 entre 2 et 8 ans n'était pas significativement associée à la fonction ventilatoire mesurée à 8 ans [45]. Concernant le neurodé-veloppement, deux études rapportent que l'exposition prénatale au dioxyde d'azote, au benzène et aux hydrocarbures aromatiques polycycliques, pourrait altérer le développement cognitif évalué à 14 mois et à 5 ans [46,47]. Dans ce type d'étude, la prise en compte de l'exposition postnatale, afin de dissocier les effets des expositions pré-et postnatales, reste un défi méthodologique encore peu pris en compte.…”

Decoding Neurodevelopment: Findings on Environmental Exposures and Synaptic Plasticity

“…They have linked autistic behaviors with prenatal exposures to the organophosphate insecticide chlorpyrifos (Eskenazi et al 2007) and also with prenatal exposures to phthalates . Additional prospective studies have linked loss of cognition (IQ), dyslexia, and ADHD to lead (Jusko et al 2008), methyl mercury (Oken et al 2008), organophosphate insecticides (London et al 2012), organo chlorine insecticides (Eskenazi et al 2008), polychlorinated biphenyls (Winneke 2011), arsenic (Wasserman et al 2007), manganese (Khan et al 2011), polycyclic aromatic hydrocarbons (Perera et al 2009), bisphenol A (Braun et al 2011), brominated flame retardants (Herbstman et al 2010), and perfluorinated compounds (Stein and Savitz 2011).…”