Grantee Research Project Results
2006 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: Water Environment and Reuse Foundation's National Center for Resource Recovery and Nutrient Management
Center Director: Olabode, Lola
Title: Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes
Investigators: Rauh, Virginia
Current Investigators: Rauh, Virginia , Whyatt, Robin M. , Perera, Frederica P. , Greenhill, Larry , Davidson, Leslie
Institution: Columbia University in the City of New York
EPA Project Officer: Callan, Richard
Project Period: November 1, 2003 through October 31, 2008 (Extended to October 31, 2010)
Project Period Covered by this Report: November 1, 2005 through October 31,2006
RFA: Centers for Children's Environmental Health and Disease Prevention Research (2003) RFA Text | Recipients Lists
Research Category: Children's Health , Human Health
Objective:
The specific aims of the project are to: 1) Quantify impact of pre-/postnatal exposures to PAH, ETS & pesticides on neurobehavioral development through age 7; 2) Refine measurement of exposure to chronic social stressors to assess their impact on child neurobehavioral development at ages 5 & 7, & interactive effects between environmental toxicants & sociodemographic conditions; 3) Investigate modifying role of micronutrients & genetic polymorphisms on the association of PAHs & ETS with fetal growth and neurodevelopment through age 7, as determined in Aim 1; 4) Collaborate with COTAC to translate & apply findings to education initiatives; and 5) Investigate associations between neurodevelopmental deficits & asthma morbidity at ages 5 & 7. Explore if children exhibiting asthma symptoms are more likely to manifest neurodevelopment deficits as compared to children without symptoms.
Progress Summary:
Screening and Enrollment
Since 12/98, research workers have screened 1188 willing & eligible women for the study. To date, 725 are fully enrolled (completed prenatal monitoring, prenatal questionnaire, & maternal or newborn blood sample at delivery); 586 currently remain in the study. The retention rate is 81%. Assessments completed thus far: 538 12-month, 432 24-month, 379 36-month, 226 48-month, 279 60-month, and 143 72-month.
Interview and Demographics
To date, 838 women have completed the prenatal interview (contents reported previously). Average maternal age at delivery is 25 + 4.9 years; 35.1% are African American; 64.9% are Dominican; 65.6% have never been married; 35.8% have not graduated from high school; 41.6% receive public assistance; and 90.8% are currently on Medicaid.
Biological Samples/Biomarkers
To date, a blood sample at delivery has been collected from 725 women and/or newborns. In addition to the Exposure Assessment Core progress report’s biomarkers of exposure, chlorpyrifos (CPF) was detected in 99.7% of personal air samples collected during pregnancy (range 0.1-344.8 ng/m3, n=394) and 64% of cord blood samples (range 0.3-63 pg/g, n=341). Maternal & cord plasma levels were similar & highly correlated (r=0.79, p<0.001), indicating that pesticides are readily transferred from mother to developing fetus. 19.7% of women were in the highest quartile of chlorpyrifos exposure during pregnancy. Urinary PAH metabolites analyzed by CDC in a cohort subset of 48 5-year olds demonstrate common and highly variable exposure among cohort children. Samples were tested for 24 PAHs of which 11 were above the limit of detection. Concentrations of metabolites were creatinine-corrected (ng/g); the mean level of 1-OHP (183.5 ng/g, non log transformed) was higher than that reported by NHANES for children ages 6-11 (2001-2) (66.8 ng/m3, non log transformed).
Birth Outcomes
Analysis of effects of prenatal exposure to airborne PAHs (based on personal air monitoring) showed significant associations with reduced birth weight, length, & head circumference among African-Americans, after controlling for the effects of ETS, CPF, and other known physical, biologic, & toxic determinants of fetal growth. Among African Americans, prenatal exposure to PAHs was associated with lower birth weight (avg decrement 264.48 gms, p=0.003) & smaller head circumference (avg decrement 0.79 cm, p=0.01), after adjusting for potential confounders. This decrement in birth weight is similar to that reported for active maternal smoking. After adjusting for CPF, the relationships between PAHs & birth outcomes among African Americans were unchanged (p=0.02 birth weight; p=0.06 head circumference). PAHs and CPF appear to be significant independent determinants of birth outcomes. After adjustment for other PAH sources (dietary PAHs; ETS measured by cotinine), the associations between monitored PAHs and birth outcomes remained significant (p=0.02 birth weight; p=0.04 head circumference among African Americans). The absence of a significant effect among Dominican infants is consistent with reports of a healthy immigrant effect. Our analyses of later health outcomes do not show ethnic differences. Because BaP is a representative PAH, BaP-DNA adducts were measured by HPLC fluorescence as a proxy for PAH-DNA adducts in mother-newborn pairs from the cohort. Mean levels of adducts in cord blood (0.24 per 108 nucleotides, n=268) and maternal blood at delivery (0.22 per 108 nucleotides, n=268) were comparable, despite the 10-fold lower estimated transplacental dose of PAHs, suggesting the fetus is ~10-fold more sensitive to DNA damage from PAHs. Using adducts as a continuous or dichotomous measure and controlling for potential confounders, we observed a significant adverse interaction between adducts and ETS on birth weight (p=0.05) and head circumference (p=<0.03). In contrast to the analysis with PAHs in air, as the exposure variable, the effect was seen in both ethnic groups. Among an initial 314 newborns, CPF levels in cord blood were significantly inversely associated with infant birth weight and length after controlling for potential confounders. Birth weight of infants in the highest quartile of CPF exposure was ~152 gms lower than among infants with CPF exposures in the low exposure group. This effect size is in the range of that for active maternal smoking.
Neurodevelopmental Outcomes
Data entry is complete for 587 Denver II Developmental Tests, Fagan Tests of Infant Intelligence (6-month), Bayley Scales of Infant Development II (12,24,36-month), 264 WPPSI (60-month). Among 183 3-year-olds who had annual developmental assessments using the Bayley (BSID-II), we evaluated effects on mental & psychomotor development of high prenatal exposure to airborne PAHs (upper quartile PAHs vs. others), adjusting for known risk factors and potential confounders. Subjects with cotinine levels indicative of maternal active smoking were excluded. Behavioral development was assessed by the Child Behavior Checklist. No association existed between PAHs, psychomotor development index (PDI) or behavioral problems; however, high prenatal PAH exposure was associated with lower mental development index (MDI) at age 3 (beta=5.69, p<0.01) and greater chance of developmental delay (OR=2.89 95% CI=1.33, 6.25, p=0.01). Moderate delay on the BSID is a criterion for early intervention services eligibility. These preliminary results suggest that environmental PAHs at recent NYC air levels may adversely affect children’s cognitive development at age 3. Three-year-olds prenatally exposed to the highest levels of CPF (highest quartile>6.17 picograms/gm in cord blood plasma) scored, on average, 6.5 points lower on BSID-II motor development (p=0.003) and 3.3 points lower on cognitive development, (p=0.06) compared to those with lower levels of exposure. The odds of developmentally delayed children (scores <85) in the highly exposed group were 5 times higher than in the low exposed group on the PDI and 2.4 times greater on the MDI. Children prenatally exposed to high levels of pesticides were 11.6, 6.3, and 5.6 times more likely to score in the clinical symptom range for attentional problems, attentional problems with hyperactivity, and pervasive developmental disorder, respectively, than children with low levels of CPF exposure.
Loss to Follow-up
Overall loss-to-follow up in the study is 19%.
Significance
The study is providing much needed data on the effects of cumulative exposures. It is one of the first to measure molecular dose and biologic effects of a comprehensive set of common environmental pollutants on a range of neurodevelopmental domains from birth through age 7 in a cohort of inner-city children and assesses interactive effects of material deprivation with toxic environmental exposures.
Future Activities:
Enrollment, data collection, and analyses will continue as planned through children’s 7th birthdays.
Journal Articles:
No journal articles submitted with this report: View all 3 publications for this subprojectSupplemental 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,, RFA, Health, Scientific Discipline, INTERNATIONAL COOPERATION, ENVIRONMENTAL MANAGEMENT, HUMAN HEALTH, Genetics, Health Risk Assessment, Epidemiology, Biochemistry, Health Effects, Children's Health, Environmental Policy, Risk Assessment, asthma, prenatal exposure, environmental risks, genetic mechanisms, Human Health Risk Assessment, diesel exhaust, assessment of exposure, genetic risk factors, children's environmental health, exposure assessment, genetic susceptibility, maternal exposureRelevant Websites:
http://www.mailman.hs.columbia.edu/ccceh/ Exit
Progress and Final Reports:
Original AbstractMain Center Abstract and Reports:
R832141 Water Environment and Reuse Foundation's National Center for Resource Recovery and Nutrient Management 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
The perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.
Project Research Results
3 journal articles for this subproject
Main Center: R832141
172 publications for this center
157 journal articles for this center