The continuation proposed here extends a prospective cohort study using biomarkers to examine the effects of in utero and postnatal exposure to environmental pollutants on the health of African American and Latina children in NYC. That study is now following subjects for 2 years postnatally to assess the relationship between exposure to ambient and indoor pollutants (PAR, particulate matter, environmental tobacco smoke/ETS, allergens) and risk of developmental impairment, asthma and cancer. The continuation has important new components: (1) an extension of the follow-up period from the currently funded 2 years to 5 years: (2) the measurement of maternal and infant exposure to non-persistent pesticides (NPP): (3) the measurement of infant and child exposure to endotoxins; 4) the evaluation of biomarkers of genetic susceptibility to the toxicants studied; (5) the assessment of cognitive development, behavioral adjustment, asthma and genetic damage through age 5; and (6) the recruitment of additional subjects so that a cohort of 400 mother/child pairs will remain in the study for the full five years, ensuring us adequate power to test our main hypotheses. AU of these new analyses will be done on the full cohort, as the relevant samples from the initial cohort have been processed and stored appropriately. The extended follow up allows periodic reassessment of health, development, and behavioral functioning in order to track cascading effects and identify damage that might become manifest only after age 2, when more complex physical and developmental demands arise. Moreover, follow up of children through age 5 permits definitive clinical diagnosis of health outcomes such as attention-deficit/hyperactivity disorder (ADHD) and asthma, not possible in younger children. Primary aims are: 1) to quantify the impact of prenatal and/or postnatal exposures to indoor and outdoor air pollutants on fetal and child growth and neurobehavioral development through 5 years of age, controlling for known physical and psychosocial confounders; 2) to assess the degree to which prenatal and/or postnatal exposure to air pollutants and home allergens contribute to risk of childhood asthma from birth through five years of age, controlling for known confounders; and 3) to quantify associations between prenatal and/or postnatal exposures to PAH/aromatic pollutants and ETS on procarcinogenic genetic damage (PAH/aromatic-DNA and 4-ABP-Hb adducts) in umbilical cord and child?s blood cells.
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