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2006 Progress Report: Growth and Development Research Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes

EPA Grant Number: R832141C001
Subproject: 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
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, 2005 through October 31,2006
RFA: Centers for Children's Environmental Health and Disease Prevention Research (2003)
Research Category: Children's Health , Health Effects

Description:

Objective:

The specific aims of the project are to: (1) quantify impact of pre-/postnatal exposures to polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and 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 and 7, and interactive effects between environmental toxicants and sociodemographic conditions; (3) investigate the modifying role of micronutrients and genetic polymorphisms on the association of PAHs and ETS with fetal growth and neurodevelopment through age 7, as determined in Aim 1; (4) collaborate with the Community Translation and Application Core (COTAC) to translate and apply findings to education initiatives; and (5) investigate associations between neurodevelopmental deficits and asthma morbidity at ages 5 and 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 December 1998, research workers have screened 1,188 willing and eligible women for the study. To date, 725 are fully enrolled (completed prenatal monitoring, prenatal questionnaire, and maternal or newborn blood sample at delivery); 586 currently remain in the study. The retention rate is 81 percent. Assessments completed thus far include: 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). The average maternal age at delivery is 25 + 4.9 years; 35.1 percent are African-American; 64.9 percent are Dominican; 65.6 percent have never been married; 35.8 percent have not graduated from high school; 41.6 percent receive public assistance; and 90.8 percent 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 percent of personal air samples collected during pregnancy (range 0.1-344.8 ng/m3, n = 394) and 64 percent of cord blood samples (range 0.3-63 pg/g, n = 341). Maternal and cord plasma levels were similar and highly correlated (r = 0.79, p < 0.001), indicating that pesticides are readily transferred from mother to developing fetus. A total of 19.7 percent of women were in the highest quartile of chlorpyrifos exposure during pregnancy. Urinary PAH metabolites analyzed by the Centers for Disease Control and Prevention (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-hydroxyprene (1-OHP) (183.5 ng/g, non log-transformed) was higher than that reported by the National Health and Nutrition Examination Survey (NHANES) for children ages 6-11 (2001-2002) (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, and head circumference among African-Americans, after controlling for the effects of ETS, CPF, and other known physical, biologic, and toxic determinants of fetal growth. Among African-Americans, prenatal exposure to PAHs was associated with lower birth weight (average decrement 264.48 gms, p = 0.003) and smaller head circumference (average 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 and 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 benzo(a)pyrene (BaP) is a representative PAH, BaP-DNA adducts were measured by high-performance liquid chromatography (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 approximately 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 approximately 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 (BSID-II) (12-, 24-, 36-month), and 264 Wechsler Preschool and Primary Scale of Intelligence (60-month). Among 183 3-year-olds who had annual developmental assessments using the BSID-II, we evaluated effects on mental and psychomotor development of high prenatal exposure to airborne PAHs (upper quartile PAHs versus 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-Followup

Overall loss-to-followup in the study is 19 percent.

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 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:

http://www.mailman.hs.columbia.edu/ccceh/ exit EPA

Progress and Final Reports:
2004 Progress Report
2005 Progress Report
Original Abstract


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

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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.

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