Effect of Prenatal Exposure to Airborne Pollutants on Inner-City Kids
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.

The impact of environmental toxicants on children's health is increasingly recognized as significant (Faustman 2000; Greater Boston Physicians for Social Responsibility 2000; Landrigan et al. 1999; Perera et al. 2002). Human and experimental studies indicate that the fetus and infant are more sensitive than adults to diverse environmental toxicants, including lead, mercury, environmental tobacco smoke (ETS), polycyclic aromatic hydrocarbons (PAHs), and pesticides (National Research Council 1993; Neri et al. 2006; Perera et al. 2005b; Whyatt and Perera 1995; World Health Organization 1986). Urban minority populations represent high-risk groups for adverse health and developmental outcomes (Claudio et al. 1999; Federico and Liu 2003; New York City Department of Health 1998; Perera et al. 2002). Although urban air pollution crosses geographic and socioeconomic boundaries, these same populations are likely to be more heavily exposed to indoor and outdoor air pollution and pesticides (Breysse et al. 2005; Olden and Poje 1995; Perera et al. 2002). As reported previously, the present study cohort has had substantial although variable exposure to multiple contaminants during pregnancy, with 100% of subjects having exposure to PAHs and pesticides in the air during pregnancy and 40% reporting ETS exposure (Perera et al. 2003; Rauh et al. 2004; Whyatt et al. 2002). PAH exposure in this urban cohort of nonsmokers is largely due to traffic sources and ETS (which was controlled for in analyses).

To our knowledge, there have been no prior human studies of the effect of prenatal exposure to airborne PAHs on child development. However, prenatal exposure to ETS has been associated with reduced fetal growth and cognitive functioning (Martinez et al. 1994; Rauh et al. 2004; Schuster and Ludwig 1994; Sexton et al. 1990; Windham et al. 1999; Yolton et al. 2005). Associations have been observed between prenatal exposure to the pesticide chlorpyrifos (CPF) and neurodevelopmental outcomes in experimental systems (Aldridge et al. 2005). Lead and mercury are known developmental toxicants affecting fetal development (Agency for Toxic Substances and Disease Registry 1999; Canfield et al. 2003; Grandjean et al. 1997; Lanphear et al. 2000).

In addition to being genotoxic and carcinogenic, PAHs such as benzo[a]pyrene (BaP) are endocrine disruptors (Bostrom et al. 2002; Bui et al. 1986; Kazeto et al. 2004). Prior laboratory and human studies in Central Europe and in our New York City cohort indicate that transplacental exposure to PAHs is associated with adverse birth outcomes (Barbieri et al. 1986; Bui et al. 1986; Dejmek et al. 2000; Legraverend et al. 1984; Perera et al. 1998, 2005a). In the present analysis, we evaluated the effects of prenatal exposure to airborne PAHs, estimated by personal air sampling of the mother during pregnancy, on mental and psychomotor development of children through 36 months of age, controlling for physical, biologic, and psychosocial determinants of these outcomes.