Grantee Research Project Results
2013 Progress Report: The Columbia Center for Children’s Environmental Health
EPA Grant Number: R834509Center: The Columbia Center for Children’s Environmental Health
Center Director: Perera, Frederica P.
Title: The Columbia Center for Children’s Environmental Health
Investigators: Perera, Frederica P. , Miller, Rachel L. , Whyatt, Robin M. , Rundle, Andrew , Evans, David , Champagne, Frances , Shepard, Peggy , Rauh, Virginia
Current Investigators: Perera, Frederica P. , Whyatt, Robin M. , Miller, Rachel L. , Evans, David , Rauh, Virginia , Andrews, Howard F. , Champagne, Frances , Rundle, Andrew , Shepard, Peggy
Institution: Columbia University in the City of New York , West Harlem Environmental Action (WE ACT for Environmental Justice) , Columbia University Mailman School of Public Health , Resources for the Future
Current Institution: Columbia University in the City of New York , Resources for the Future , West Harlem Environmental Action (WE ACT for Environmental Justice) , Columbia University Mailman School of Public Health
EPA Project Officer: Callan, Richard
Project Period: September 24, 2009 through September 23, 2014 (Extended to September 23, 2015)
Project Period Covered by this Report: September 24, 2012 through September 23,2013
Project Amount: $3,953,320
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2009) RFA Text | Recipients Lists
Research Category: Children's Health , Human Health
Objective:
RD834509C001: Endocrine Disruptors & Obesity Among Inner-City Children
Aim 1: To test whether prenatal and early-life exposures to the endocrine disruptors PAH and BPA predict body size growth trajectories and childhood obesity at ages 8-12 years. This will be accomplished by following our ongoing birth cohort to ages 8-12 years, measuring height and weight at ages 5, 7, 8-12; body composition at ages 7, 8-10; and metabolic syndrome components at ages 8-12 years. This work takes advantage of a sophisticated geographic information systems-based data on the children’s neighborhoods to control for social (e.g., poverty and socio-demographic composition) and physical factors (e.g., playgrounds, parks, fast-food) likely to predict childhood obesity.
Aim 2: To determine whether differences in the methylation status of key genes involved in adipogenesis (PPARγ2, C/EBPα, C/EBPß, C/EBPδ and DLK1) and appetite control (FTO) mediate the association between xenobiotic exposures and childhood obesity outcomes. Methylation of these genes will be measured in cord white blood cell DNA by pyrosequencing.
RD834509C002: Endocrine Disrupters, Epigenetic Mechanisms & Neurodevelopment
Determine whether:
- prenatal exposures to the endocrine disruptors, PAH and BPA, are associated with adverse neurobehavioral outcomes in peri-pubertal children, as measured by diagnostic assessment of child psychopathology and cognitive functioning;
- prenatal exposure to PAH or BPA is associated with epigenetic changes in candidate genes related to endocrine disruption and immune dysregulation, and whether altered methylation/gene expression in these candidates is associated with the neurobehavioral outcomes; and
- the extent to which neighborhood-level conditions contribute to neurobehavioral outcomes and/or moderate the individual-level associations between exposure to PAH or BPA and child neurodevelopment.
RD834509C003: Molecular/Disease Consequences of Prenatal BPA, PAH Exposure Across Generations
- Examine the consequence of prenatal oral BPA exposure on neurobehavioral, obesity and immune dysfunction in Balb/c mice by determining whether prenatal BPA exposure is associated with abnormal brain cytoarchitecture; impaired social, anxiety-like and cognitive performance; greater adult body weight, body fat composition and organ fat; and immune dysfunction in the adult offspring or grandoffspring.
- Examine the consequence of prenatal oral BPA exposure for tissue-specific molecular modifications in mice by determining prenatal BPA exposure-induced changes in DNA methylation in genes sensitive to endocrine disruption and immune dysregulation in the brain (hippocampus, hypothalamus, cortex), adipocytes and blood of the prenatally BPA-exposed offspring and grandoffspring at gestation day 19 and adulthood (postnatal day [PND]60).
- Examine the consequence of prenatal inhaled PAH exposure at current levels determined to exist in New York City’s Northern Manhattan/South Bronx on neurodevelopment and obesity in Balb/c mice by determining whether prenatal PAH exposure is associated with abnormal brain cytoarchitecture, impaired anxiety-like and cognitive performance, greater body weight through weaning to adulthood, body fat composition and organ fat content in adult offspring and grand offspring.
- Examine the consequence of prenatal inhaled PAH exposure for tissue-specific molecular modifications (DNA methylation) in mice of genes sensitive to endocrine disruption and immune dysregulation in the brain, adipocytes and blood of the prenatally exposed offspring and grandoffspring at gestation day 19 and PND60.
- Engage and expand the Community Advisory and Stakeholder Board;
- Communicate the Center’s research findings through the development of educational materials designed for local residents, community organizations, healthcare providers and other local stakeholders;
- In collaboration with the Center’s Pediatric Health Specialist, facilitate education of public health and clinical professionals working in low-income communities of color;
- Disseminate the Center’s findings using several communication methods;
- Through our partnership with WE ACT, expand the capacity of low-income communities of color to advocate for improved environmental conditions by using the Center’s scientific findings and related findings by other investigators.
Progress Summary:
RD834509C001: Endocrine Disruptors & Obesity Among Inner-City Children
Thus far, 381 cohort children at ages 8 to 12 (African American and Dominican) have been screened for eligibility, and 373 were found to be eligible. Of these 373 children, 342 have been enrolled, 16 have refused enrollment, 11 are pending enrollment and 4 are lost to follow-up. In 2012, we published research in AJE showing that prenatal exposures to PAH were associatied with higher BMI Z-scores at ages 5 and 7 and with higher fat mass at age 7. We are beginning analyses of associations between early childhood exposures to PAH and child body size using in-home air monitoring data.
When data collection at ages 8-12 has been completed, we will test whether prenatal and early-life exposures to PAH predict body size at multiple ages through age 12. In terms of dissemination work on the PAH findings, we sent out a series of coordinated press releases when the paper was published, have made presentations regarding the findings at community forums, and have presented the work in several acadamic forums. Dr. Rundle participated in the NIEHS Virtual Forum: Childhood Obesity and the Environment.
Assays of maternal and child urine samples have been completed for bisphenol A (BPA), and analyses of urinary levels of BPA and child body size to age 7 are ongoing.
Since the launch of our study, there has been growing concern in the academic and lay literature about exposures to phthalates and childhood obesity. We have shown that urinary concentrations of phthalates are correlated with urinary concetrations of BPA, and thus, phthalates have the potential to confound the associations of BPA with the outcomes of concern. Under separate funding, maternal and child urine samples have been analyzed for 9 phthalate metabolites, and Dr. Rundle is overseeing a T32 Medical Fellow in Pediatric Endocrinology, Dr. Michelle Maresca, in analyzing the phthalate metabolite data and child body size.
Pyrosequencing-based analyses of methylation in PPAR Gamma, DLK and FTO are ongoing, and we expect to have complete data at the end of the summer.
RD834509C002: Endocrine Disrupters, Epigenetic Mechanisms and Neurodevelopment
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We previously reported associations between prenatal PAH exposure and child IQ scores at age 5 (Perera 2009) and child behavior at ages 6-8 (Perera 2011, Perera 2012). Briefly, prenatal PAH exposure was associated with lower Full Scale and Verbal IQ at age 5, as well as more behavior problems in the areas of anxiety/depression and attention at ages 6-8. Analyses are ongoing regarding the associations between PAH and further impacts at ages 7 and 9-11, and manuscripts are in preparation.
We previously reported our findings on the association between maternal prenatal BPA exposure (dichotomized into high/low groups at the upper quartile) and child behavior at ages 3-4 (assessed via the CBCL). Briefly, high prenatal BPA exposure was associated with a greater number of problems for boys in the areas of Emotionally Reactive and Aggressive Behavior; in contrast, high BPA exposure was associated with lower scores for Anxious/Depressed and Aggressive Behavior (p < 0.05) for girls (Perera 2012). Analyses of BPA and ages 9-11 outcomes are ongoing.
Results of neurodevelopmental assessments relevant to PAH and BPA will be evaluated in relation to those exposures and to the structural and functional MRI scans currently being conducted under separate funding. To date, 245 scans have been completed.
We previously carried out pyrosequencing assays to assess the methylation of specific CpG sites in a number of candidate genes (cord WBC DNA) as they related to prenatal PAH and BPA exposure. We subsequently added brain-derived neurotrophic factor (BDNF) to our list of candidate genes based on experimental studies in Project 3 (see progress report for Project 3). Our new approach synchronizes our human and animal data to select additional CpG sites of interest, taking advantage of our parallel experimental animal studies that allow us to assess the concordance between CpG-specific methylation related to either PAH or BPA and gene expression in target tissue, which is not accessible in the human cohort. After checking the homology between mice and humans, we map the sequence of interest and identify "indicator" CpG sites located within or around this region that have been assayed using two genome-wide techniques (Infinium 450K and HELP-tagging) in a subset of our cord blood samples from the cohort. Using these indicator CpGs, we can assess the association between methylation and PAH or BPA exposure, as well as neurodevelopmental outcomes. If we identify a signal between either exposure or neurodevelopment at these indicator CpGs and demonstrate that there is sufficient variation in cord blood at these locations for followup analysis, we then develop pyrosequencing assays covering the CpG sites of interest to measure the methylation status of these CpGs in the cord blood samples of the full cohort. This analysis is done on a gene-by-gene basis. We plan to complete data analysis in the coming year.
In an analysis involving environmental PAH exposure, neighborhood-level characteristics and cognitive development at age 5, we found a significant association between high PAH exposure and decreased IQ scores based on the Wechsler Preschool and Primary Scale of Intelligence-Revised (WPPSI-R). Children with high prenatal PAH exposure (defined as above the median level of 2.26 ng/m3) were predicted to score 3.45 points lower on the full-scale outcome than those in the low prenatal PAH exposure group. Comparable results were observed for the verbal and performance subscales at 3.90 and 1.67 points, respectively, although the decrease in the performance subscale measurement was not statistically significant. Similar results were also seen in the verbal performance scale when adjusting for housing and neighborhood variables (Lovasi 2013). Further analyses using neighborhood-level data and GIS software are ongoing with respect to developmental outcomes at older ages.
Aims 1 & 2: Cohorts of Balb/c mice have been exposed prenatally to low-dose BPA (2 μg/kg, 20 μg/kg, 200 μg/kg or tocopherol-stripped corn oil control). Our findings of sex-specific and dose-dependent effects of BPA-induced changes in estrogen receptor and DNA methyltransferase gene expression, DNA methylation and social/anxiety behavior were recently published in PNAS. These findings indicate that postnatal maternal care provided by BPA-exposed mothers alters offspring brain gene expression independent of BPA-induced effects and can, in some cases, mediate or moderate the effect of prenatal BPA exposure on offspring outcomes. In the past year, we have complemented these results with finding that BPA induces changes in object recognition memory and the expression and DNA methylation of genes involved in cognition. We have also found changes in gene expression within the placenta following gestational BPA exposure.
Aims 3 & 4: Offspring and grandoffspring mice are being assessed for effects on weight, growth trajectories, adiposity and neurobehavioral outcomes following prenatal PAH exposure. Tools for the later include open field behavioral studies and measures of mobility, distance travel and fecal boli. These experiments are concomitant with tests for altered relevant gene expression and DNA methylation in the brain and adipose tissue following prenatal PAH exposure.
Community Outreach and Translation Core
- CASB Development: In collaboration with WE ACT, CCCEH expanded the CASB to include active members from the community and governmental agencies engaged in advocacy and community awareness of environmental health issues—emphasizing the significance of endocrine-disrupting chemicals and child development. The current list of CASB members includes representatives from Autism Speaks; Bronx Borough President’s Office; Community Health Worker Network of NY State; Dominican Medical Association; East Harlem Asthma Center of Excellence (NYC Department of Health and Mental Hygiene); A.I.R. Harlem; Isabella Geriatric Center; New York-Presbyterian Hospital WIC Program; Northern Manhattan Perinatal Partnership; Nos Quedamos; and Urban Health Plan, Inc. Active engagement of the CASB has been maintained through quarterly meetings and incorporation of their feedback into the Center's education and outreach strategies.
- Health Education: COTC staff and the CASB have continued development of a holistic educational campaign promoting environmental health. Six main themes have been identified, and content has been collaboratively developed with the CASB. As a part of this campaign, the Center created a children’s activity book which incorporates the six holistic themes into imaging and activities intended to engage both child and parent. COTC staff has used the educational messaging to develop workshops. Three workshops have been completed: two for CASB member organizations (NYC Department of Health and the Isabella Geriatric Center) and one for Columbia University staff. In September 2012, COTC staff started creating monthly tips which offer guidance on limiting exposures to environmental harms. Monthly tips are disseminated through the Center website and social media (Facebook and Twitter). Other Center educational materials have been disseminated to the community through multiple avenues, including distribution of materials at local farmers markets, health fairs and partner community organization.
- Education for Public Health and Clinical Professionals: On October 2, 2012, the Center and WE ACT held a second community briefing series. Dr. Frederica Perera discussed neurodevelopmental health risks associated with bisphenol-A (BPA); Dr. Andrew Rundle spoke about his work linking obesity with polycyclic aromatic hydrocarbons (PAHs); and WE ACT’s Executive Director, Ms. Peggy Shepard, presented on the current state of policy reform regarding endocrine-disrupting exposures at the local, state and national levels. There were over 60 attendees at the event, more than double the number from last year’s briefing. Some attendees included the NYC Department of Health, the New York State Office of the Attorney General, the Environmental Protections Agency, the Center for Health, Environment & Justice, as well as other health and community organizations. Throughout the year, Center staff translated our findings to scientific, public health and clinical groups. WE ACT’s Peggy Shepard discussed the partnership with the Center in her presentation “Working Against the Clock: Protecting Children’s Health, Safety and their Futures” at the 2012 APHA Annual Meeting. Center investigators, including Drs. Perera, Miller, Rauh, Rundle and Herbstman, made 28 presentations on our research during the year at grand rounds, online forums and conferences.
- Communications: COTC staff continues to work closely with the Mailman School of Public Health in the development and dissemination of press releases about Center findings. The Center’s recent findings linking BPA exposure and asthma were featured in over 50 online media outlets, including TIME, CNN and Scientific American. COTC staff helped to coordinate on-air interviews, including spots on CBS This Morning highlighting Dr. Herbstman and a NY1 interview with Dr. Robin Whyatt about BPA. Other media coverage included a highlight in the Mailman School of Public Health magazine about the Center’s air pollution research and stories in NY Times, PBS, Chicago Tribune, Bloomberg, Huffington Post, and others. Center findings continue to be distributed through “Center Updates” to our listserv of over 1,200 subscribers, posts on our Facebook and Twitter accounts, and highlights on our newly redesigned website.
- Capacity Building & Informing Policy: During the year, Dr. Julie Herbstman testified regarding the use and effectiveness of flame retardants in children’s products to the New York State Assembly Standing Committees on Environmental Conservation and Health. WE ACT Executive Director Peggy Shepard and other staff members continue to utilize Center research findings in their advocacy efforts for policy change. Drs. Perera and Perzanowski presented findings on air pollution for WE ACT’s West Harlem Clean Heat Council. Additionally, Drs. Perera and Rundle discussed Center findings at the WE ACT Researcher Roundtable, a forum for updating WE ACT staff on recent research.
Future Activities:
RD834509C001: Endocrine Disruptors & Obesity among Inner-City Children
The research is on schedule, and we plan to continue as described in our grant application.
RD834509C002: Endocrine Disrupters, Epigenetic Mechanisms and Neurodevelopment
We plan to complete the research and submit manuscripts reporting results in the coming year.
RD834509C003: Molecular/Disease Consequences of Prenatal BPA, PAH Exposure Across Generations
BPA (aims 1,2): Analysis of epigenetic changes within cognition-related genes in brain and blood, assessment of fetal brain and placenta gene expression/DNA methylation, analyses of growth/weight gain data, and F2 offspring analyses. PAH (aims 3,4): Completion of ongoing experiments, especially organ-specific gene expression and DNA methylation. Assessments of differences in phenotype and gene expression in F2 mice will continue. Community Outreach and Translation Core
COTC staff and the CASB will develop additional materials for the holistic educational campaign and will continue to make educational presentations to community groups. COTC staff will continue translating Center research findings and increase its reach through the Center’s communications platforms, including social media, press releases, and our new website.
Journal Articles: 60 Displayed | Download in RIS Format
| Other center views: | All 104 publications | 62 publications in selected types | All 60 journal articles |
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Albert DA, Begg MD, Andrews HF, Williams SZ, Ward A, Conicella ML, Rauh V, Thompson JL, Papapanou PN. An examination of periodontal treatment, dental care, and pregnancy outcomes in an insured population in the United States. American Journal of Public Health 2011;101(1):151-156. |
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Buckley JP, Engel SM, Braun JM, Whyatt RM, Daniels JL, Mendez MA, Richardson DB, Xu Y, Calafat AM, Wolff MS, Lanphear BP, Herring AH, Rundle AG. Prenatal phthalate exposures and body mass index among 4- to 7-year-old children: a pooled analysis. Epidemiology 2016;27(3):449-458. |
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Choi H, Wang L, Lin X, Spengler JD, Perera FP. Fetal window of vulnerability to airborne polycyclic aromatic hydrocarbons on proportional intrauterine growth restriction. PLoS One 2012;7(4):e35464 (11 pp.). |
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Choi H, Perera FP. Sources of greater fetal vulnerability to airborne polycyclic aromatic hydrocarbons among African Americans. Journal of Epidemiology and Community Health 2012;66(2):121-126. |
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Durham T, Guo J, Cowell W, Riley K, Wang S, Tang D, Perera F, Herbstman J. Prenatal PM2.5 Exposure in Relation to Maternal and Newborn Telomere Length at Delivery. Toxics 23;10(1):13. |
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Genkinger JM, Stigter L, Jedrychowski W, Huang T-J, Wang S, Roen EL, Majewska R, Kieltyka A, Mroz E, Perera FP. Prenatal polycyclic aromatic hydrocarbon (PAH) exposure, antioxidant levels and behavioral development of children ages 6-9. Environmental Research 2015;140:136-144. |
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Herbstman JB, Tang D, Zhu D, Qu L, Sjodin A, Li Z, Camann D, Perera FP. Prenatal exposure to polycyclic aromatic hydrocarbons, benzo[a]pyrene-DNA adducts, and genomic DNA methylation in cord blood. Environmental Health Perspectives 2012;120(5):733-738. |
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Herbstman JB, Wang S, Perera FP, Lederman SA, Vishnevetsky J, Rundle AG, Hoepner LA, Qu L, Tang D. Predictors and consequences of global DNA methylation in cord blood and at three years. PLoS One 2013;8(9):e72824 (10 pp.). |
R834509 (2014) R834509 (Final) R834509C002 (Final) |
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Hoepner LA, Whyatt RM, Just AC, Calafat AM, Perera FP, Rundle AG. Urinary concentrations of bisphenol A in an urban minority birth cohort in New York City, prenatal through age 7 years. Environmental Research 2013;122:38-44. |
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Hoepner LA, Whyatt RM, Widen EM, Hassoun A, Oberfield SE, Mueller NT, Diaz D, Calafat AM, Perera FP, Rundle AG. Bisphenol A and adiposity in an inner-city birth cohort. Environmental Health Perspectives 2016;124(10):1644-1650. |
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Iyer S, Perera F, Zhang B, Chanock S, Wang S, Tang D. Significant interactions between maternal PAH exposure and haplotypes in candidate genes on B[a]P-DNA adducts in a NYC cohort of non-smoking African-American and Dominican mothers and newborns. Carcinogenesis 2014;35(1):69-75. |
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Jung KH, Bernabe K, Moors K, Yan B, Chillrud SN, Whyatt R, Camann D, Kinney PL, Perera FP, Miller RL. Effects of floor level and building type on residential levels of outdoor and indoor polycyclic aromatic hydrocarbons, black carbon, and particulate matter in New York City. Atmosphere 2011;2(2):96-109. |
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Jung KH, Perzanowski M, Rundle A, Moors K, Yan B, Chillrud SN, Whyatt R, Camann D, Perera FP, Miller RL. Polycyclic aromatic hydrocarbon exposure, obesity and childhood asthma in an urban cohort. Environmental Research 2014;128:35-41. |
R834509 (2014) |
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Jung KH, Liu B, Lovinsky-Desir S, Yan B, Camann D, Sjodin A, Li Z, Perera F, Kinney P, Chillrud S, Miller RL. Time trends of polycyclic aromatic hydrocarbon exposure in New York City from 2001 to 2012: assessed by repeat air and urine samples. Environmental Research 2014;131:95-103. |
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Jung K, Goowin K, Perzanowski M, Chillrud S, Perera F, Miller R, Lovinsky-Desir S. Personal Exposure to Black Carbon at School and Levels of Fractional Exhaled Nitric Oxide in New York City. Environmental Health Prespectives 2021;129(9). |
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Kundakovic M, Champagne FA. Epigenetic perspective on the developmental effects of bisphenol A. Brain, Behavior, and Immunity 2011;25(6):1084-1093. |
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Kundakovic M, Gudsnuk K, Franks B, Madrid J, Miller RL, Perera FA. Champagne FA. Sex-specific epigenetic disruption and behavioral changes following low-dose in utero bisphenol A exposure. Proceedings of the National Academy of Sciences of the United States of America 2013;110(24):9956-9961. |
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Kundakovic M, Gudsnuk K, Herbstman JB, Tang D, Perera FP, Champagne FA. DNA methylation of BDNF as a biomarker of early-life adversity. Proceedings of the National Academy of Sciences of the United States of America 2015;112(22):6807-6813. |
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Lovasi GS, Quinn JW, Rauh VA, Perera FP, Andrews HF, Garfinkel R, Hoepner L, Whyatt R, Rundle A. Chlorpyrifos exposure and urban residential environment characteristics as determinants of early childhood neurodevelopment. American Journal of Public Health 2011;101(1):63-70. |
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Lovasi GS, O’Neil-Dunne JPM, Lu JWT, Sheehan D, Perzanowski MS, MacFaden SW, King KL, Matte T, Miller RL, Hoepner LA, Perera FP, Rundle A. Urban tree canopy and asthma, wheeze, rhinitis, and allergic sensitization to tree pollen in a New York City birth cohort. Environmental Health Perspectives 2013;121(4):494-500. |
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Lovasi GS, Eldred-Skemp N, Quinn JW, Chang HW, Rauh VA, Rundle A, Orjuela MA, Perera FP. Neighborhood social context and individual polycyclic aromatic hydrocarbon exposures associated with child cognitive test scores. Journal of Child and Family Studies 2014;23(5):785-799. |
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Lovinsky-Desir S, Miller RL. Epigenetics, asthma, and allergic diseases:a review of latest advancements. Current Allergy and Asthma Reports 2012;12(3):211-220. |
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Maresca MM, Hoepner LA, Hassoun A, Oberfield SE, Mooney SJ, Calafat AM, Ramirez J, Freyer G, Perera FP, Whyatt RM, Rundle AG. Prenatal exposure to phthalates and childhood body size in an urban cohort. Environmental Health Perspectives 2015 June 12 [Epub ahead of print], doi:10.1289/ehp.1408750. |
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Maresca MM, Hoepner LA, Hassoun A, Oberfield SE, Mooney SJ, Calafat AM, Ramirez J, Freyer G, Perera FP, Whyatt RM, Rundle AG. Prenatal exposure to phthalates and childhood body size in an urban cohort. Environmental Health Perspectives 2016;124(4):514-520. |
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Margolis AE, Herbstman JB, Davis KS, Thomas VK, Tang D, Wang Y, Wang S, Perera FP, Peterson BS, Rauh VA. Longitudinal effects of prenatal exposure to air pollutants on self-regulatory capacities and social competence. Journal of Child Psychology and Psychiatry 2016;57(7):851-860. |
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Miller RL, Garfinkel R, Lendor C, Hoepner L, Li Z, Romanoff L, Sjodin A, Needham L, Perera FP, Whyatt RM. Polycyclic aromatic hydrocarbon metabolite levels and pediatric allergy and asthma in an inner-city cohort. Pediatric Allergy and Immunology 2010;21(2 Pt 1):260-267. |
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Mueller NT, Whyatt R, Hoepner L, Oberfield S, Dominguez-Bello MG, Widen EM, Hassoun A, Perera F, Rundle A. Prenatal exposure to antibiotics, cesarean section and risk of childhood obesity. International Journal of Obesity 2015;39(4):665-670. |
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Nobel KG, Fifer WP, Rauh VA, Nomura Y, Andrews HF. Academic achievement varies with gestational age among children born at term. Pediatrics 2012;130(2):e257-e264. |
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Orjuela MA, Liu X, Warburton D, Siebert AL, Cujar C, Tang D, Jobanputra V, Perera FP. Prenatal PAH exposure is associated with chromosome-specific aberrations in cord blood. Mutation Research 2010;703(2):108-114. |
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Orjuela MA, Liu X, Miller RL, Warburton D, Tang D, Jobanputra V, Hoepner L, Suen IH, Diaz-Carreno S, Li Z, Sjodin A, Perera FP. Urinary naphthol metabolites and chromosomal aberrations in 5-year-old children. Cancer Epidemiology, Biomarkers & Prevention 2012;21(7):1191-1202. |
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Patel MM, Hoepner L, Garfinkel R, Chillrud S, Reyes A, Quinn JW, Perera F, Miller RL. Ambient metals, elemental carbon, and wheeze and cough in New York City children through 24 months of age. American Journal of Respiratory and Critical Care Medicine 2009;180(11):1107-1113. |
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Perera FP, Li Z, Whyatt R, Hoepner L, Wang S, Camann D, Rauh V. Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age 5 years. Pediatrics 2009;124(2):e195-e202. |
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Perera FP, Wang S, Vishnevetsky J, Zhang B, Cole KJ, Tang D, Rauh V, Phillips DH. Polycyclic aromatic hydrocarbons-aromatic DNA adducts in cord blood and behavior scores in New York City children. Environmental Health Perspectives 2011;119(8):1176-1181. |
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Perera FP, Tang D, Wang S, Vishnevetsky J, Zhang B, Diaz D, Camann D, Rauh V. Prenatal polycyclic aromatic hydrocarbon (PAH) exposure and child behavior at age 6-7 years. Environmental Health Perspectives 2012;120(6):921-926. |
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Perera FP, Chang HW, Tang D, Roen EL, Herbstman J, Margolis A, Huang TJ, Miller RL, Wang S, Rauh V. Early-life exposure to polycyclic aromatic hydrocarbons and ADHD behavior problems. PLoS One 2014;9(11):e111670 (9 pp.). |
R834509 (2014) R834509 (Final) R834509C002 (Final) R832096 (Final) |
Exit Exit |
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Perera F, Herbstman J. Prenatal environmental exposures, epigenetics, and disease. Reproductive Toxicology 2011;31(3):363-373. |
R834509 (2011) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (Final) |
Exit Exit Exit |
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Perera F, Vishnevetsky J, Herbstman JB, Calafat AM, Xiong W, Rauh V, Wang S. Prenatal bisphenol A exposure and child behavior in an inner-city cohort. Environmental Health Perspectives 2012;120(8):1190-1194. |
R834509 (2012) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (2012) R834509C002 (Final) |
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Perera F, Weiland K, Neidell M, Wang S. Prenatal exposure to airborne polycyclic aromatic hydrocarbons and IQ:estimated benefit of pollution reduction. Journal of Public Health Policy 2014;35(3):327-336. |
R834509 (2014) R834509 (Final) R834509C002 (Final) |
Exit |
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Perera F, Phillips DH, Wang Y, Roen E, Herbstman J, Rauh V, Wang S, Tang D. Prenatal exposure to polycyclic aromatic hydrocarbons/aromatics, BDNF and child development. Environmental Research 2015;142:602-608. |
R834509 (Final) R834509C002 (Final) |
Exit Exit Exit |
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Peterson BS, Rauh VA, Bansal R, Hao X, Toth Z, Nati G, Walsh K, Miller RL, Arias F, Semanek D, Perera F. Effects of prenatal exposure to air pollutants (polycyclic aromatic hydrocarbons) on the development of brain white matter, cognition, and behavior in later childhood. JAMA Psychiatry 2015;72(6):531-540. |
R834509 (Final) R834509C002 (Final) R832096 (Final) |
Exit |
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Rauh VA, Horton MK, Miller RL, Whyatt RM, Perera F. Neonatology and the environment:impact of early exposure to airborne environmental toxicants on infant and child neurodevelopment. Neoreviews 2010;11(7):363-369. |
R834509 (2011) R834509 (2012) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (Final) R834509C003 (2012) R834509C003 (Final) |
Exit Exit |
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Roen EL, Wang Y, Calafat AM, Wang S, Margolis A, Herbstman J, Hoepner LA, Rauh V, Perera FP. Bisphenol A exposure and behavioral problems among inner city children at 7-9 years of age. Environmental Research 2015;142:739-745. |
R834509 (2014) R834509 (Final) R834509C002 (Final) |
Exit Exit Exit |
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Rundle AG, Gallagher D, Herbstman JB, Goldsmith J, Holmes D, Hassoun A, Oberfield S, Miller RL, Andrews H, Widen EM, Hoepner LA. Prenatal exposure to airborne polycyclic aromatic hydrocarbons and childhood growth trajectories from age 5-14 years. Environmental research 2019;177:108595. |
R834509 (Final) R827027 (2002) R832141 (Final) |
Exit Exit |
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Rundle A, Hoepner L, Hassoun A, Oberfield S, Freyer G, Holmes D, Reyes M, Quinn J, Camann D, Perera F, Whyatt R. Association of childhood obesity with maternal exposure to ambient air polycyclic aromatic hydrocarbons during pregnancy. American Journal of Epidemiology 2012;175(11):1163-1172. |
R834509 (2012) R834509 (2013) R834509 (2014) R834509 (Final) R834509C001 (2012) R834509C001 (Final) |
Exit Exit Exit |
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Rundle A, Rauh VA, Quinn J, Lovasi G, Transande L, Susser E, Andrews HF. Use of community-level data in the National Children’s Study to establish the representativeness of segment selection in the Queens Vanguard Site. International Journal of Health Geographics 2012;11:18 (11 pp.). |
R834509 (Final) |
Exit Exit |
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Tang WY, Levin L, Talaska G, Cheung YY, Herbstman J, Tang D, Miller RL, Perera F, Ho SM. Maternal exposure to polycyclic aromatic hydrocarbons and 5'-CpG methylation of interferon-γ in cord white blood cells. Environmental Health Perspectives 2012;120(8):1195-1200. |
R834509 (2012) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (2012) R834509C002 (Final) |
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Vishnevetsky J, Tang D, Chang HW, Roen EL, Wang Y, Rauh V, Wang S, Miller RL, Herbstman J, Perera FP. Combined effects of prenatal polycyclic aromatic hydrocarbons and material hardship on child IQ. Neurotoxicology and Teratology 2015;49:74-80. |
R834509 (2014) R834509 (Final) R834509C002 (Final) R832096 (Final) |
Exit Exit Exit |
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Wang S, Chanock S, Tang D, Li Z, Edwards S, Jedrychowski W, Perera FP. Effect of gene-environment interactions on mental development in African American, Dominican, and Caucasian mothers and newborns. Annals of Human Genetics 2010;74(1):46-56. |
R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (Final) R832141 (2007) R832141 (Final) |
Exit Exit Exit |
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Wang S, Yu Z, Miller RL, Tang D, Perera FP. Methods for detecting interactions between imprinted genes and environmental exposures using birth cohort designs with mother-offspring pairs. Human Heredity 2011;71(3):196-208. |
R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (Final) |
Exit Exit |
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Wang S, Xiong W, Ma W, Chanock S, Jedrychowski W, Wu R, Perera FP. Gene-environment interactions on growth trajectories. Genetic Epidemiology 2012;36(3):206-213. |
R834509 (2012) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (2012) R834509C002 (Final) |
Exit Exit |
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Wang Y, Perera F, Guo J, Riley K, Durham T, Ross Z, Ananth C, Baccarelli A, Wang S, Herbstman J. A methodological pipeline to generate an epigenetic marker of prenatal exposure to air pollution indicators. Epigenetics 2021;1-9. |
R834509 (Final) R827027 (2002) R832141 (Final) |
Exit |
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Weiland K, Neidell M, Rauh V, Perera F. Cost of developmental delay from prenatal exposure to airborne polycyclic aromatic hydrocarbons. Journal of Health Care for the Poor and Underserved 2011;22(1):320-329. |
R834509 (2011) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (Final) |
Exit Exit |
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Widen EM, Whyatt RM, Hoepner LA, Ramirez-Carvey J, Oberfield SE, Hassoun A, Perera FP, Gallagher D, Rundle AG. Excessive gestational weight gain is associated with long-term body fat and weight retention at 7 y postpartum in African American and Dominican mothers with underweight, normal, and overweight prepregnancy BMI. American Journal of Clinical Nutrition 2015;102(6):1460-1467. |
R834509 (Final) R834509C001 (Final) |
Exit Exit |
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Widen EM, Whyatt RM, Hoepner LA, Mueller NT, Ramirez-Carvey J, Oberfield SE, Hassoun A, Perera FP, Gallagher D, Rundle AG. Gestational weight gain and obesity, adiposity and body size in African-American and Dominican children in the Bronx and Northern Manhattan. Maternal and Child Nutrition 2016;12(4):918-928. |
R834509 (Final) |
Exit Exit |
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Widen E, Burns N, Daniels M, Backlund G, Rickman R, Foster S, Nichols A, Hoepner L, Kinsey E, Ramireaz-Carvey J. Gestational weight change and childhood body composition trajectories from pregnancy to early adolescence. Obesity 10;. |
R834509 (Final) R827027 (2002) R832141 (Final) |
Exit Exit |
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Widen E, Nichols A, Kahn L, Factor-Livak P, Insel B, Hoepner L, Dube S, Rauh V, Perera F, Rundel A. Prepregnancy obesity is associated with cognitive outcomes in boys in a low-income, multiethnic birth cohort. BMC Pediatrics 2019;19(1):507. |
R834509 (Final) R827027 (2002) |
Exit Exit |
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Witherspoon NO, Trousdale K, Bearer CF, Miller RL. The public health and policy implications of epigenetics and pediatric health research. Environmental Health Perspectives 2012;120(10):a380-a381. |
R834509 (2012) R834509 (2013) R834509C003 (2012) |
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Yan Z, Zhang H, Maher C, Arteaga-Solis E, Champagne FA, Wu L, McDonald JD, Yan B, Schwartz GJ, Miller RL. Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice. PLoS One 2014;9(10):e110706 (15 pp.). |
R834509 (2014) R834509 (Final) R834509C003 (Final) |
Exit Exit |
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Zeinomar N, Grant-Alfieri A, Burke K, de Hoz M, Tehranifar P, Walker D, Morton T, Shepard P, Herbstman J, Miller R, Pera F, Terry M. Cancer Risk Reduction Through Education of Adolescents:Development of a Tailored Cancer Risk-Reduction Educational Tool. Journal of Cancer Education 2021;. |
R834509 (Final) R827027 (2002) R832141 (Final) |
Exit Exit |
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Widen EM, Whyatt RM, Hoepner LA, Mueller NT, Ramirez‐Carvey J, Oberfield SE, Hassoun A, Perera FP, Gallagher D, Rundle AG. Gestational weight gain and obesity, adiposity and body size in African-American and Dominican children in the Bronx and Northern Manhattan. Maternal & Child Nutrition 2016;12(4):918-928. |
R834509C001 (Final) R836154 (2017) |
Exit |
Supplemental Keywords:
Bisphenol A, polycyclic aromatic hydrocarbons, obesity, neurodevelopment, children, epigenetics, mice;Relevant Websites:
Columbia Center for Children's Health Exit
Progress and Final Reports:
Original Abstract Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R834509C001 The Role of Endocrine Disruptors in Childhood Obesity
R834509C002 The Role of Endocrine Disruptors in Neurodevelopmental Disorders
R834509C003 The Mechanisms of Endocrine Disruptors in Laboratory Mice
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.