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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. [ABSTRACT FROM AUTHOR]

We reported previously that insecticide exposures were widespread among minority women in New York City during pregnancy and that levels of the organophosphate chlorpyrifos in umbilical cord plasma were inversely associated with birth weight and length. Here we expand analyses to include additional insecticides (the organophosphate diazinon and the carbamate propoxur), a larger sample size (n = 314 mother-newborn pairs), and insecticide measurements in maternal personal air during pregnancy as well as in umbilical cord plasma at delivery. Controlling for potential confounders, we found no association between maternal personal air insecticide levels and birth weight, length, or head circumference. For each log unit increase in cord plasma chlorpyrifos levels, birth weight decreased by 42.6 g [95% confidence interval (CI), -81.8 to -3.8, p = 0.03] and birth length decreased by 0.24 cm (95% CI, -0.47 to -0.01, p = 0.04). Combined measures of (In)cord plasma chlorpyrifos and diazinon (adjusted for relative potency) were also inversely associated with birth weight and length (p < 0.05). Birth weight averaged 186.3 g less (95% CI, -375.2 m -45.5) among newborns with the highest compared with lowest 26% of exposure levels (p = 0.01). Further, the associations between birth weight and length and cord plasma chlorpyrifos and diazinon were highly significant (p ≤ 0.007) among newborns born before the 2000-2001 U.S. Environmental Protection Agency's regulatory actions to phase out residential use of these insecticides. Among newborns born after January 2001, exposure levels were substantially lower, and no association with fetal growth was apparent (p > 0.8). The propoxur metabolite 2-isopropoxyphenol in cord plasma was inversely associated with birth length, a finding of borderline significance (p = 0.05) after controlling for chlurpyrifos and diazinon. Results indicate that prenatal chlorpyrifos exposures have impaired fetal growth among this minority cohort and that diazinon exposures may have contributed to the effects. Findings support recent regulatory action to phase out residential uses of the insecticides. [ABSTRACT FROM AUTHOR]

Discusses the effects of transplacental exposure to environmental pollutants on birth outcomes in a multiethnic population. Association of high prenatal exposure to aromatic hydrocarbons (PAH) with lower birth rate; Explanation of the failure to find significant effect of PAH in the Hispanic subsamples.

Abstract: Exposures to ambient air traffic-related pollutants and their sources have been associated with respiratory and asthma morbidity in children. However, longitudinal investigation of the effects of traffic-related exposures during early childhood is limited. We examined associations of residential proximity and density of traffic and stationary sources of air pollution with wheeze, asthma, and immunoglobulin (Ig) E among New York City children between birth and age 5 years. Subjects included 593 Dominican and African American participants from the Columbia Center for Children''s Environmental Health cohort. Prenatally, through age 5 years, residential and respiratory health data were collected every 3–6 months. At ages 2, 3, and 5 years, serum IgE was measured. Spatial data on the proximity and density of roadways and built environment were collected for a 250m buffer around subjects'' homes. Associations of wheeze, asthma, total IgE, and allergen-specific IgE with prenatal, earlier childhood, and concurrent exposures to air pollution sources were analyzed using generalized estimating equations or logistic regression. In repeated measures analyses, concurrent residential density of four-way intersections was associated significantly with wheeze (odds ratio: 1.26; 95% confidence interval [CI]: 1.01, 1.57). Age 1 exposures also were associated with wheeze at subsequent ages. Concurrent proximity to highway was associated more strongly with total IgE (ratio of the geometric mean levels: 1.25; 95% CI: 1.09, 1.42) than were prenatal or earlier childhood exposures. Positive associations also were observed between percent commercial building area and asthma, wheeze, and IgE and between proximity to stationary sources of air pollution and asthma. Longitudinal investigation suggests that among Dominican and African American children living in Northern Manhattan and South Bronx during ages 0–5 years, residence in neighborhoods with high density of traffic and industrial facilities may contribute to chronic respiratory morbidity, and concurrent, prenatal, and earlier childhood exposures may be important. These findings may have broad implications for other urban populations that commonly have high asthma prevalence and exposure to a high density of traffic and stationary air pollution sources. [Copyright &y& Elsevier]