The goal of the etiologic study is to examine the influence of selected ambient and indoor pollutants (polycyclic aromatic hydrocarbons and environmental tobacco smoke) on fetal growth and early childhood development (at 6,7,12, and 24 months) in a cohort of inner-city, minority children. The study is undertaken because of growing concern that exposures to this widespread environmental toxicants, disproportionately concentrated in low-income urban areas, have particularly adverse effects on fetal and early childhood development. We combine expertise in molecular epidemiology, state of the art ambient and indoor pollutant monitoring techniques, use of geographical information system, attention to the role of nutrient status in toxicant susceptibility (essential fatty acids and antioxidants), and a framework for assessment of child growth and developmental effects within the context of the social environment. Exposure data (from personal indoor and ambient air monitoring, and questionnaire) will be collected from 480 pregnant women residing in low- income areas of norther Manhattan. Blood samples will be collected at delivery (umbilical cord blood and maternal blood) and at 24 months (infant blood). Biomarkers (PAH-DNA adducts, cotinine, lead antioxidants, and essential fatty acids) will be analyzed in those samples. Fetal outcomes include birthweight, length, head circumference, and size for gestational age. Developmental outcomes will be assessed at 6,7, 12, and 24 months, using the Fagan Test and the Bayley Scales. A questionnaire (administered prenatally, 6,12 and 24 months) collects information on environmental exposure on environmental exposure, social disadvantage, daily activities, infant feeding practices, health status, and level of maternal distress. An observational measure of he quality of physical stimulation and mother-child interaction is conducted in the home at 24 months. Collectively, these measures permit control for poverty-related confounders of the association between toxicant exposures and growth/developmental outcomes, improving our estimates of the proportion of development deficit/delay that can be attributed to the toxic study factors. We will also provide data to the Data Management Statistics and Community Impact Modeling Core for multi-level analysis of whether or not the strength of the associations between toxic exposures and individual developmental child outcomes varies as a function of broader social conditions.
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