Grantee Research Project Results
2014 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
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, 2013 through September 23,2014
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:
R834509C001: Endocrine Disruptors and 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, and 8-12; body composition at ages 7, and 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, socio-demographic composition) and physical factors (e.g., play grounds, 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) mediates the association between xenobiotic exposures and childhood obesity outcomes. Methylation of these genes will be measured in cord white blood cell DNA by pyrosequencing.
R834509C002: Endocrine Disrupters, Epigenetic Mechanisms and 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.
- Determine whether prenatal exposure to PAH or BPA is associated with epigenetic changes (DNA methylation measured by pyrosequencing and validated by gene expression) in candidate genes, is associated with endocrine disruption and immune dysregulation known to be critical in fetal brain development, and whether altered methylation/gene expression in these candidates is associated with the neurobehavioral outcomes.
- Using GIS, determine 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.
R834509C003: Molecular/Disease Consequences of Prenatal BPA and 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 day19 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 prenatally exposed offspring and grandoffspring at gestation day19 and PND60.
Community Outreach and Translation Core
- 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 and Obesity Among Inner-City Children
We have completed study subject enrollment with 400 cohort children having been followed-up through ages 8.5 to 12 years of age. Children provided fasting blood samples and took part in a clinical examination to assess blood lipids; blood glucose; insulin levels; blood pressure; pubertal development; and height, weight and waist circumference.
Following up on our 2012 AJE publication showing that prenatal exposures to PAH were associated with higher BMI z-scores at ages 5 and 7 and with higher fat mass at age 7, we have completed repeated measures analyses of BMI z-scores and body composition at ages 5, 7, 9 and 11. We are also analyzing data on the children’s exposures to airborne PAH at age 5 and subsequent obesity risk. We find that prenatal higher PAH exposure predicts higher fat mass index through age 11; however, child exposure to PAH at age 5 does not predict anthropometric outcomes. We are writing these results up for submission for publication.
Our analyses of maternal urinary bisphenol A (BPA) levels during pregnancy and child urinary levels of BPA show that they are not associated with child anthropometric outcomes through age 7. This work was presented at the 2014 ISEE conference in Seattle.
We have completed analyses of methylation status for eight CpG sites in the promoter of PPAR Gamma in cord white blood cell DNA and find no associations between exposures to PAH, BPA or phthalates and methylation status. In addition, methylation status does not predict child anthropometric outcomes. We have completed the lab work for DLK, and data analyses are ongoing.
We have completed analyses of urinary phthalate concentrations in maternal and child (ages 3 and 5) urine samples and child anthropometric outcomes at ages 5 and 7. Child anthropometric outcomes are not associated with child urinary metabolite concentrations. However, higher concentrations of non-DEHP metabolites in maternal urine are associated with lower BMI z-scores at ages 5 and 7 and with lower fat mass index and waist circumference at age 7 among boys only. A paper describing the results of these analyses is under review at Environmental Health Perspectives.
We have also completed analyses of child anthropometric outcomes and maternal use of antibiotics during pregnancy and mode of delivery and find that C-section birth and antibiotic use are associated with higher BMI z-scores at age 7. A paper describing these results was published in International Journal of Obesity. We have also completed analyses showing that excessive weight gain during pregnancy is associated with higher BMI z-scores and fat mass in the child at ages 5 and 7. A paper describing these results is under peer review and the results were presented at the 2014 SER conference.
R834509C002: Endocrine Disrupters, Epigenetic Mechanisms and Neurodevelopment
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 have now been completed regarding the associations between prenatal or postnatal PAH exposure and various neurodevelopmental outcomes at ages 7-11; and manuscripts are either accepted, in revision, in review or submitted. A manuscript showing the effects of high PAH as measured by PAH-DNA adducts in maternal blood on attention deficit hyperactivity problems in children at age 9 has been accepted to PLOS One. High maternal adducts were significantly associated with increased hyperactive-impulsive and inattentive symptoms measured on the DSM-IV subscales of the Conners’ Parent Rating Scale (CPRS) in addition to increased scores on the Conners’ ADHD Global Index. These analyses were adjusted for important potential variables, including characteristics of the home environment, maternal ADHD and comorbid anxiety/depression in the children (Perera et al., in press). Additionally, a manuscript on the interaction between maternal material hardship and PAH exposure (as measured by PAH-DNA adducts in umbilical cord blood) on child IQ at age 7 is currently under review. Analyses focusing on the impacts of PAH-DNA adducts, measured in maternal blood at delivery, on deficient emotional self-regulation (DESR) and social responsiveness are ongoing; a manuscript is 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 3-5 (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). A paper updating these analyses of BPA and behavioral outcomes at ages 7-9 has been reviewed, and revisions are now being completed.
During this no-cost extension year, results of remaining 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, 305 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 the 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 and these indicator CpGs and demonstrate that there is sufficient variation in cord blood at these locations for follow-up 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 under the no-cost extension.
It is widely recognized that because DNA methylation is cell-specific, failure to account for cell distribution when examining methylation in a mixed cell population can confound hypothesized exposure-to-methylation associations, leading to spurious results or failure to detect true relationships. Methods have been developed using the regression calibration approach to adjust for cellular mixture requiring reference methylation data. Currently, two reference datasets are now available, both derived from adult blood. Cells represented in these datasets may not reflect the most prevalent cellular components of cord blood, leading some to question whether they are optimal when applied to cord blood. We have generated a 450K reference dataset using cord blood samples and are currently evaluating whether this reference dataset works better at adjusting for cell mixture in a cord blood matrix than the reference datasets from adult blood. This work was presented at the PPTOX meeting, and a manuscript is currently in preparation.
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). We are using the results from the GIS work to inform our future analyses of the associations between endocrine disruptors and neurobehavioral outcomes. These neighborhood-level factors are potential effect modifiers and confounders, and our previous results allow us to build the most accurate models possible.
R834509C003: Molecular/Disease Consequences of Prenatal BPA, PAH Exposure Across Generations
Aims 1 and 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. These findings have recently been accepted for publication at PNAS. We have also found changes in gene expression within the placenta following gestational BPA exposure.
Aims 3 and 4: Greater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in offspring and grandoffspring mice. Preliminary findings suggests evidence of hyper-reactivity. Effects of a high folate diet are being examined.
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. Active engagement of the CASB has been maintained through quarterly meetings and incorporation of their feedback into the Center's education and outreach strategies. During the past year, the CASB has been actively involved in disseminating the materials which they collaboratively developed for the Healthy Homes, Healthy Child (HHHC) educational campaign.
- Health Education: In July 2013, the Center completed a set of six bilingual educational materials aimed at women and children in Northern Manhattan and the South Bronx. These materials utilize the Center’s new focus on providing holistic strategies to reduce exposure to a range of environmental toxicants rather than focusing on one chemical or health outcome. Over the past year, we have actively distributed these materials to the Northern Manhattan and South Bronx community through our CASB members, local nonprofit organizations and direct outreach. Since September 2013, the Center has distributed over 11,000 HHHC holistic campaign brochures. Additionally, we have developed a system for tracking the number of brochures distributed, what organizations make the request, and their intended use. This system allows us to better understand the reach of our materials and how they are being utilized in the community. Organizations to which we have distributed the HHHC materials include WE ACT for Environmental Justice; the New York Presbyterian Hospital Women, Infant, and Children (WIC) Program; the Harlem Health Promotion Center; and the NYC Department of Health and Mental Hygiene. On April 26, 2014, the Center, WE ACT and the Community League of the Heights (CLOTH)’s Community Health Academy cohosted an environmental health fair. The 2014 Green Kids Health Fair provided information about environmental health, as well as gave children and adults a place to be physically active while promoting the messaging of the HHHC campaign. The event brought together community organizations to provide information to residents, including lead testing by Microecologies, lead education and resources from WE ACT, Corbin Hill Farms, and the NYC Department of Emergency Management. Other highlights included Zumba, yoga for kids and physical activity games.
- Education for Public Health and Clinical Professionals: On October 23, 2013, the Center and WE ACT organized its third annual briefing to stakeholders at Columbia’s main campus. The event was open to community leaders, elected officials and policymakers to engage in dialogue about our research findings and to discuss how these organizations can be further involved with the Center and WE ACT. The briefing focused on clean air and included presentations from Center director Dr. Frederica Perera, Columbia University professor Dr. Diana Hernandez, and WE ACT federal policy analyst Dr. Jalonne White Newsome. There were 65 attendees from a variety of organizations, such as the NYC Department of Health and Mental Hygiene, Environmental Defense Fund, and Northern Manhattan Improvement Corporation. As in past years, the event received very positive feedback from the participants. Throughout the year, Center staff translated our findings to scientific, public health and clinical groups. The successful partnership between the Center and WE ACT has been highlighted by WE ACT’s Peggy Shepard at the 2014 EPA/NIEHS Children’s Centers Webinar Series as well as COTC co-director Dr. David Evans and WE ACT’s Ogonanya Dotson-Newman at a conference, "Bridging the Expertise of Communities and Academia", hosted by the Irving Institute of Clinical and Translational Research. Center investigators, including Drs. Perera, Miller, Rauh, Rundle and Herbstman, made over 40 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 have been featured in over 60 online media outlets, including TIME, Bloomberg News, Scientific American, the Guardian and On Earth Magazine. 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 redesigned website.
- Capacity Building & Informing Policy: During the year, Dr. Perera testified about the impact of research on the environmental causes of disease and neurodevelopmental disorders in children at a congressional briefing. Ms. Peggy Shepard and Dr. Perera testified at the New York City Council Committee on Environmental Protection oversight hearing about air quality impacts, measures and mitigation in environmental justice communities. Additionally, Dr. Perera served as expert consultant on the effects of climate change on children's health to the Subcommittee on Climate Change of the President's Task Force on Children's Environmental Health Risks and Safety Risks to Children in Washington, D.C.
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.
R834509C002: Endocrine Disrupters, Epigenetic Mechanisms and Neurodevelopment
We plan to complete our aims and submit manuscripts reporting new results as described above in the coming year.
R834509C003: Molecular/Disease Consequences of Prenatal BPA, PAH Exposure Across Generations
BPA (Aims 1 and 2): Assessment of fetal brain and placenta gene expression and analyses of growth/weight gain data. PAH (Aims 3 and 4): Completion of ongoing experiments and analyses related to the behavioral outcomes.
Community Outreach and Translation Core
COTC staff and the CASB will continue mass dissemination of the HHHC educational campaign through distribution of materials and presentations to community groups as well as developing new educational strategies. 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.). |
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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. |
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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. |
R834509 (2011) R834509 (Final) R827027 (2002) R832141 (2007) R832141 (Final) |
Exit Exit Exit |
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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. |
R834509 (2014) R834509 (Final) R834509C002 (Final) R832141 (Final) |
Exit |
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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. |
R834509 (2011) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (Final) |
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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. |
R834509 (2012) R834509 (2013) R834509 (2014) R834509 (Final) R834509C002 (2012) R834509C002 (Final) |
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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) |
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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) |
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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) |
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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, miceRelevant Websites:
Columbia Center for Children’s Environmental 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.