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2004 Progress Report: Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes
EPA Grant Number: R832141C001Subproject: this is subproject number 001 , established and managed by the Center Director under grant R832141
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Columbia Center for Children’s Environmental Health
Center Director: Perera, Frederica P.
Title: Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes
Investigators: Rauh, Virginia , Davidson, Leslie , Greenhill, Larry , Perera, Frederica P. , Whyatt, Robin M.
Current Investigators: Rauh, Virginia
Institution: Columbia University
EPA Project Officer: Fields, Nigel
Project Period: November 1, 2003 through October 31, 2008
Project Period Covered by this Report: November 1, 2003 through October 31, 2004
RFA: Centers for Children's Environmental Health and Disease Prevention Research (2003)
Research Category: Children's Health , Health Effects
Description:
Objective:The objectives of this research project are to: (1) quantify the impact of prenatal and postnatal exposures to air pollutants such as polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and pesticides on neurobehavioral development through 7 years of age, after controlling for the effects of known determinants of child neurodevelopment and potential confounders; (2) refine the measurement of exposure to chronic social stressors in this population for the purpose of assessing the impact of chronic stressors on child neurobehavioral development at 5 and 7 years of age and testing interactions between environmental toxicants and stressors, by which some children are rendered more vulnerable than others to the toxic impact of pollutants; (3) investigate the modifying role of micronutrients and genetic polymorphisms on the association of toxic exposures (PAH and ETS) with fetal growth and neurodevelopment through 7 years of age, as determined in Objective 1; (4) collaborate with the Community Outreach, Translation and Application Core (COTAC) to translate research findings on neurodevelopmental risk associated with toxicant exposures and assist in developing interventions and policies to prevent such exposures; and (5) investigate associations between neurodevelopmental deficits and asthma morbidity at 5 and 7 years of age. We posit that children who exhibit asthma symptoms will be more likely to manifest neurodevelopment deficits as compared to children without symptoms (exploratory).
Progress Summary:Screening and Enrollment
Since December 1998, research workers have screened 992 women who were found eligible and willing to participate in the New York City Mothers and Children Study. Thus far, 589 women have met criteria for complete enrollment (i.e., completed prenatal monitoring, prenatal questionnaire, and maternal or newborn blood sample at delivery), and 492 of these women remain in the study, resulting in a retention rate of 83.5 percent. The cohort has completed 418 12-month, 346 24-month, 283 36-month, and 101 60-month assessments.
Interview
To date, 678 women have completed the 45-minute prenatal interview, including socioeconomic and demographic information, residential history, maternal education level, living conditions during the current pregnancy, history of exposure to active and passive smoking, alcohol, drugs, and consumption of PAH‑containing foods. ETS exposure was measured by questions about timing, frequency, and amount of exposure to cigarette, cigar, and/or pipe smoke in the home. A measure of material hardship assessed the level of unmet basic needs in the areas of food, housing, and clothing. The Psychiatric Epidemiology Research Instrument Demoralization Scale measures maternal nonspecific psychological distress. A follow-up interview is administered at 6, 12, 24, 36, and 60 months. Sociodemographic data show: average maternal age at delivery is 24.9 (± 4.9) years, 65 percent of the women have never been married, 35 percent have not graduated from high school, 90 percent receive Medicaid, and 43 percent have less than $10,000 annual household income. Prenatal ETS exposure was reported by 39.1 percent of women, and postnatal exposure was reported during the first 2 years by 38.7 percent of women. One or more material hardships were reported by 37.7 percent of women during pregnancy. Inadequate or deteriorated housing was reported by 48.1 percent of African American and 38.7 percent of Dominican participants.
Biological Samples/Biomarkers
To date, a blood sample at the time of delivery has been collected from 589 women and/or newborns. In addition to the biomarkers of exposure described in the Exposure Assessment Facility Core progress report, umbilical cord lead levels were analyzed and ranged from nondetectable to 7.6 μg/dL, with a mean of 1.275 μg/dL. Plasma cotinine levels at delivery averaged 1.8 (± 10.6) ng/mL in maternal plasma and 2.3 (± 12.0) ng/mL in newborn blood plasma. Maternal and newborn levels remain highly correlated (r = 0.9, p < 0.001). Almost one-half of mothers and infants had levels of cotinine in maternal or cord blood at the time of delivery (between 0.0250 and 25 ng/mL), indicating that they had been exposed to secondhand smoke within 48 hours. The association between ETS and cotinine levels was significant and of comparable magnitude for both African American (χ2 = 26.89, p < 0.001) and Hispanic women (χ2 = 19.16, p < 0.001).
Birth Outcomes
Birth weight, length, and head circumference were abstracted from the medical record following delivery. The mean birth weight for the cohort is 3388.9 (± 479.5) g and 39.3 (± 1.5) weeks gestational age. A significant inverse correlation was seen between PAH levels in maternal personal air samples and both birth weight (p = 0.003) and head circumference (p = 0.01) among the African American newborns but not Dominicans. Self-reported ETS exposure was associated with smaller head circumference (ß = -0.01, p = 0.04) after adjusting for potential confounders. Cotinine was significantly associated with birth length (ß = -0.01, p = 0.05). Benzo[a]pyrene (B[a]P)-DNA alone was not significantly associated with any birth outcome; however, the interaction between high/low adducts and ETS was significant using either adduct variable. There was a 233 g (6.8%) reduction in birth weight and 1 cm (2.9%) reduction in head circumference among the high B[a]P-DNA/ETS+ compared with the low B[a]P-DNA/ETS- correlated (rs > 0.9, p < 0.001). Of those who self-reported moderate or high ETS exposure (125 or 38.8 percent of those with cotinine values), 91 (72.8%) screened positive for the detectable group. Prenatal pesticide exposure also reduced fetal growth. Among newborns born before January 1, 2001 (prior to the U.S. Environmental Protection Agency ban), an inverse and highly significant association was seen between (ln)cord plasma chlorpyrifos levels and both birth weight (B = -67.3 g/unit, p = 0.008) and birth length (B = -0.43 cm/unit, p = 0.004). Among newborns born after January 1, 2001, the relationships were no longer significant (p > 0.5). Similarly, among newborns born prior to January 1, 2001, a significant inverse association (p < 0.01) was seen between the (ln) combined levels of cord plasma chlorpyrifos and diazion (in chloryrifos-equivalents) and both birth weight and length. Birth weight averaged 215.1 g less among those with the highest compared to lowest 26 percent of exposure levels (p = 0.03). Among newborns born after 2001, the magnitude of the effect was no longer significant (p > 0.8).
Neurodevelopmental Outcomes
Data entry has been completed for 426 Denver II Developmental Tests, 385 Fagan Tests of Infant Intelligence at 6 months, 418 Bayley Scales of Infant Development at 12 months, 346 Bayley Scales at 24 months, 283 Bayley Scales at 36 months, and 101 Wechsler Preschool and Primary Scale of Intelligence Tests at 60 months. At 6 months, 11 percent of infants scored in the “suspect” range for developmental delay on the Denver and 19.9 percent were in the “at risk” range on the Fagan. At 12 months, 15-16 percent were in the mildly delayed range for cognitive and motor development and 1-2 percent in the moderately delayed range. At 24 months, 39.4 percent were mildly delayed and 11.9 percent moderately delayed for cognitive development. Twelve percent were mildly delayed and 2.6 percent moderately delayed for motor development. At 36 months, 38.3 percent were mildly delayed and 9.6 percent moderately delayed for cognitive development. Also, 13.8 percent were mildly delayed and 6.4 percent moderately delayed for motor development. The overall mean 24-month Mental Development Index (MDI) Bayley score was 84.31 (sd = 12.91), and African American children had significantly higher mean MDI scores (mean = 87.55; sd = 12.31) than Dominican children (mean = 82.77; sd = 12.68; p < .01). Lower scores on the Bayley Scales by Dominican children largely were a function of failed language items, possibly related to bilingual practices in the home. The proportion of children with significant delay (MDI < 80) was 32.3 percent overall (27.3% of African Americans and 36.1% of Dominicans). The mean unadjusted 2-year cognitive development score of children who were exposed to prenatal ETS (mean = 82.02; sd = 13.01) was significantly lower than the mean score for children who were not exposed (mean = 86.61; sd = 12.30) (F = 7.41, p = .007). Prenatal residential ETS exposure was associated with a 5-point adjusted mean decrement in 24-month cognitive development score (Bayley MDI), and this 5-point decrement resulted in a twofold risk of developmental delay (< 80) on the Bayley MDI, after adjustment for maternal education, blood lead level, marital status, ethnicity, sex, and age at testing. This ETS effect on early neurodevelopment is smaller than reported active smoking effects and comparable to the effect of prenatal low-level lead exposure (range from 3.4 to 6.6 points). Joint exposure to prenatal ETS in the context of chronic material hardship (unmet basic needs) was associated with a 7-point decrement in 24-month MDI, suggesting that the neurotoxic effects of ETS are exacerbated under conditions of deprivation. The effect size of the ETS-material hardship interaction is comparable to lead-socioeconomic status interaction effects and cocaine-socioeconomic status interaction effects. There were no other significant interactions of exposure variables with sociodemographic factors nor were there any significant interactions among exposure variables. Because PAH is one of the constituents of ETS, the finding that airborne PAH is not significant in the model suggests that the ETS effect on cognitive development is not explained by the contribution of PAH.
Loss to Followup
Followup assessments at 12 months have been completed on 422 out of 525 (80%) of fully enrolled infants who have reached 12 months of age. Followup assessments at 24 months have been completed on 344 out of 477 (72%) of fully enrolled infants who have reached their second birthday. Followup assessments at 36 months have been completed on 284 out of 392 (72%) of fully enrolled infants who have reached their third birthday and at 60 months on 114 out of 145 (79%) of infants who have reached their fifth birthday. Loss-to-followup in the study is 16.5 percent.
Significance
This study is one of the first to measure the internal or molecular dose and biologic effects of a comprehensive battery of common environmental pollutants on a range of neurodevelopmental domains from birth through 7 years of age in a cohort of inner-city children, thus providing much needed data on the effects of cumulative exposures. This also is one of the first studies to assess the social context of environmental pollution for the purpose of investigating how social conditions/stressors render some children more susceptible than others to the adverse effects of toxic exposures.
Future Activities:We will continue enrollment, monitoring, interviewing, medical record abstraction, and analysis of pollutants in air samples and biologic markers in maternal/infant blood samples. Analyses of the associations between exposures, biomarkers, infant growth, and neurocognitive development are ongoing, and will continue through the children’s seventh year. We currently are initiating the first behavioral assessments at 4-5 years of age, and plan to test for learning/attentional disorders and more subtle indications of autonomic regulatory dysfunction.
Journal Articles:No journal articles submitted with this report: View all 3 publications for this subproject
Supplemental Keywords:children’s health, children’s environmental health, genetics, health effects, health risk assessment, air pollutants, exposure assessment, national exposure, pesticides, PAHs, ETS, tobacco smoke,
,
HUMAN HEALTH, ENVIRONMENTAL MANAGEMENT, INTERNATIONAL COOPERATION, Scientific Discipline, Health, RFA, Health Effects, Risk Assessment, Health Risk Assessment, Epidemiology, Children's Health, Biochemistry, Environmental Policy, Genetics, exposure assessment, genetic risk factors, children's environmental health, diesel exhaust, assessment of exposure, prenatal exposure, genetic susceptibility, maternal exposure, nutritional risk factors, genetic mechanisms, environmental risks, asthma
Relevant Websites:
Progress and Final Reports:
Original Abstract
2005 Progress Report
2006 Progress Report
Main Center Abstract and Reports:
R832141 Columbia Center for Children’s Environmental Health
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R832141C001 Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes
R832141C002 Research Project on Asthma: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
R832141C003 Mechanistic Research Project
R832141C004 Community-Based Intervention Project: Reduction of Exposure and Risk from Pesticides and Allergens
R832141C005 Community Translation and Application Core (COTAC)
R832141C006 Exposure Assessment Facility Core
R832141C007 Data Management, Statistics and Community Impact Modeling Core
R832141C008 Administrative Core