Grantee Research Project Results
2007 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 , 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, 2006 through October 31, 2007
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 and 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:
As previously reported, prenatal exposure to PAHs reduced birth weight and head circumference in African-American babies born to women who were more highly exposed to the air pollutants. (Perera et al., 2003). Prenatal exposure to two household pesticides, chlorpyrifos and diazinon, which transfer easily from the mother to her fetus, reduced birth weight by an average of 6.6 ounces – the equivalent of weight reduction seen in babies born to women who smoked (Whyatt et al., 2004). Furthermore, children prenatally exposed to secondhand smoke – especially children experiencing material hardship (unmet basic needs food, clothing and housing) – were found to have significantly reduced scores on tests of cognitive development at two years of age (Rauh et al., 2004).
Screening and Enrollment
Since December 1998, research workers have screened 1188 willing & eligible women for the study. Enrollment is now complete, with 725 fully enrolled (completed prenatal monitoring, prenatal questionnaire, & maternal or newborn blood sample at delivery); 586 currently remain in the study. Developmental assessments completed thus far: 538 12-month, 432 24-month, 379 36-month, 279 60-month, and 143 72-month.
Interview and Demographics
To date, 838 women have completed the prenatal interview (contents reported previously). Demographic characteristics of the sample remain stable since the last progress report. Average maternal age at delivery is approximately 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. PAHs were detected in 100% of air samples (mean 3.4 + 6.6 ng/m3) Urinary PAH metabolites analyzed by CDC in an initial subset of 48 5-year olds demonstrate common and highly variable exposure in the cohort. Samples were tested for 24 PAH 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
Building on the finding of reduced birth weight in response to prenatal exposure to chlorpyrifos (CPF) among inner-city pregnant women (Whyatt et al., 2004), we differentiated subtypes of growth restriction in utero. High CPF-exposed infants were significantly more likely to be born small-for-gestational age (<10th %) (p=0.02), with lower mean birth weight, smaller head circumference, and shorter birth length than comparable infants with lower exposure. This suggests growth-restriction in early pregnancy, curtailing the rate of cell division/organ size, resulting in symmetrically small infants, similar to effects of maternal antenatal smoking. No significant differences in ponderal index [birth weight in kg/(birth length in m)3], a measure of thinness, suggest proportionate growth restriction with adequate deposition of subcutaneous fat, and no microcephaly [birth head circumference in cm/(birth length in m)3]. Constitutional smallness was controlled by inclusion of nonpathological maternal determinants of infant size in regression models. Highly exposed children (lower birth weight) remain marginally lighter at 5 years of age, regardless of SGA at birth, and SGA children have smaller heads at ages 1-5, regardless of CPF exposure. Children with CPF-associated SGA show an accelerated increase in BMI between 3 and 5 years, but it is too soon to draw conclusions (Rauh et al., 2007). In addition, 1 ln-unit increase in prenatal PAH exposure was associated with a 2-fold increase in both risk of being born small for gestational age (95% CI = 1.088 – 3.472) among African-Americans, but not among Dominicans after controlling for likely confounders. A log-unit increase in prenatal PAH exposure was associated with a 5-fold increase in risk of being born preterm for African-Americans (95% CI, 1.839 – 11.886, p-value = 0.001), but not among Dominican newborns. No significant reduction in Ponderal Index was observed for either ethnic group (Hyunok et al., 2007).
Neurodevelopmental Outcomes
Neurotoxic effects of prenatal exposure to CPF have been evaluated in 254 children through the first 3 years of life (Rauh, et al. 2006). A previous report showed widespread prenatal CPF exposure and significant adverse impacts on birth weight and birth length. This report examined cognitive and motor development at 12, 24, and 36 months on the Bayley Scales of Infant Development as a function of CPF levels in umbilical cord plasma collected from the newborns at delivery. Models were adjusted for race/ethnicity, sex, length of gestation, maternal education, maternal IQ, prenatal secondhand smoke exposure, and quality of the home environment. Using clinically defined cut-points for developmental delay, we found that children prenatally exposed to high CPF levels, greater than 6.17 picograms/gram (pg/g) plasma, were significantly more likely than children exposed to low levels of CPF to experience delay in both psycho-motor (p=0.002) and cognitive (p=0.024) development at 36 months of age. In addition, highly exposed children were significantly more likely than less exposed children to manifest attention problems (p=0.009), symptoms of attention deficit/hyperactivity disorder (ADHD) (p=0.046), and symptoms of pervasive developmental problems (p=0.025) at 3 years of age, based on parental report using the Child Behavior Checklist.
Similarly, prenatal PAH exposure was associated with significantly lower mental development index (MDI) scores and delayed metal development at age 3, after adjusting for potential confounders (Perera, et al 2006).
Loss to Follow-up
The retention rate for the full cohort was 72.68% at the five-year follow-up.
Significance
The study is providing much needed data on the effects of PAH, ETS, and pesticide exposures. As the cohort matures, trajectories of growth and neurodevelopment are being evaluated, providing the opportunity to monitor long-term effects of selected exposures.
Future Activities:
Enrollment, data collection, and analyses will continue as planned through children’s 9th birthday.
Journal Articles:
No journal articles submitted with this report: View all 3 publications for this subprojectSupplemental Keywords:
RFA, Scientific Discipline, Health, 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 exposureProgress 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