Grantee Research Project Results
Final Report: The Columbia Center for Childrens Environmental Health
EPA Grant Number: R836154Center: Southern California Children's Environmental Health Center
Center Director: McConnell, Rob Scot
Title: The Columbia Center for Childrens Environmental Health
Investigators: Perera, Frederica P. , Rauh, Virginia , Rundle, Andrew , Peterson, Bradley S , Shepard, Peggy , Hernandez, Diana
Institution: Columbia University in the City of New York
EPA Project Officer: Callan, Richard
Project Period: September 1, 2015 through August 31, 2019 (Extended to August 31, 2020)
Project Amount: $2,552,707
RFA: Children's Environmental Health and Disease Prevention Research Centers (2014) RFA Text | Recipients Lists
Research Category: Endocrine Disruptors , Human Health , Children's Health
Objective:
The overarching hypothesis of the Columbia Center for Children’s Environmental Health (referred to as the Center or CCCEH hereafter) is that prenatal exposures to combustion-related polycyclic aromatic hydrocarbons (PAH) disrupt early brain development and the process by which the brain matures in childhood; and these disturbances lead to the emergence or persistence of cognitive, emotional and behavioral problems and adiposity in the vulnerable period of adolescence (age 15-17). The Center’s community-based research program in a low-income population of color, has supported the hypothesis by documenting associations between prenatal PAH exposure and long-term effects on children’s neurodevelopment, physical growth, and overall health through adolescence. The research has shown that prenatal and early life PAH exposure is associated with structural and functional changes in brain regions that support cognitive and behavioral functioning. The research has also shown an interaction between social stress and PAH exposure on children’s cognitive, behavioral, and emotional development. These findings on the vulnerability of the prenatal period to these toxic air pollutants indicates that holistic social and environmental policies are needed to prevent serious risks of toxic environmental exposures. Our research has assessed the impacts of New York City (NYC)-based policy interventions on population level indicators to determine the extent to which these initiatives have reduced air pollution and improved health. For more than two decades, we have worked in partnership with We Act for Environmental Justice (WE ACT), our primary community partner, and other community organizations to communicate study findings to policymakers and educate community members about this and other environmental threats. This work has been instrumental in shaping protective evidence-based policies to reduce adverse exposure to air pollutants and other toxic environmental exposures.
Project 1- The Impact of PAH Exposure on Adolescent Neurodevelopment: Disruption of Self-Regulatory Processes
- Aim 1: We will assess the effects of prenatal PAH exposure on neuropsychological performance at 15-17 years of age in a cohort of 350 adolescents who have been followed since the prenatal period
- Aim 2: We will assess the effects of prenatal PAH exposure on clinical outcomes at 15-17 years of age in the same adolescents.
- Aim 3: We will examine the maturational trajectories of neuropsychological and clinical (cognitive, behavioral and emotional) development over time as a function of early PAH exposure.
- Aim 4 (integrative): All 3 projects in this P50 share a common cohort in which we will explore how prenatal PAH exposure dysregulates neurodevelopment (project 1) and physical growth (project 2) via its mediational effects on the brain (
During the project period, we aimed to complete recruitment, scheduling, and assessment activities related to neuropsychological and clinical functioning in the adolescent subjects and their mothers. These objectives are consistent with Specific Aim 1 (to assess the effects of prenatal PAH exposure on neuropsychological performance at 15-17 years of age) and Specific Aim 2 (to assess the effects of prenatal PAH exposure on clinical outcomes at 15-17 years of age in the same adolescents). In addition, we have conducted data cleaning and data entry and prepared for analysis of the neuropsychological and clinical data in relation to PAH exposure levels. We are now poised to conduct tests of the major hypotheses related to Aims 1 and 2. Aim 3 requires the integration of newly acquired with previously collected data to tests hypotheses related to trajectories over time and we are now poised to test these hypotheses using our large body of neuropsychological and clinical outcome data.
Project 2- The Impact of PAH Exposure on Childhood Growth Trajectories and Visceral Adipose Tissue Mass in Adolescence: Linkages to Disrupted Self-Regulatory Processes
- Aim 1: We will follow-up 350 CCCEH cohort children to ages 15 to 17 years old and measure abdominal subcutaneous adipose and visceral adipose tissue mass using MRI and fat mass index (FMI) using bio-impedance and anthropometric outcomes of height, weight, and waist circumference.
- Aim 2: We will characterize growth and adiposity trajectories from childhood into adolescence.
- Aim 3: We will apply cluster analysis to the anthropometric, eating behavior, physical activity and neurodevelopment and behavioral outcomes data collected at ages 15 to 17
- Aim 4 (integrative): All 3 projects in this P50 share a common cohort in which we will explore how prenatal PAH exposure dysregulates neurodevelopment (project 1) and physical growth (project 2) via its mediational effects on the brain (project 3).
Project 3: An MRI Study of the Effects of Prenatal and Early Childhood PAH Exposure on Brain Maturation and Its Mediating Influences on Adverse Adolescent Outcomes
- Aim 1: We will assess the effects of prenatal and early childhood postnatal exposure to PAH (hereafter, “early PAH exposure”) on the structure, function, and metabolism of self-regulatory systems (frontal, parietal, and mesial temporal cortices, and subcortical nuclei) in the brains of 350 cohort children who have undergone MRI scanning at 9-12 years of age.
- Aim 2: We will assess whether PAH-related brain disturbances at 9-12 years of age (identified in Aim 1) mediate the association between prenatal PAH exposure and adverse CEBA outcomes at 15-17 years
- Aim 3: We will acquire anatomical MRI scans at 15-17 years in 350 children with previous imaging at 9-12 years to assess how prenatal and early childhood exposures to PAH alter the trajectory of brain development throughout adolescence, and whether such alterations predict CEBA problems.
Administrative Core
- Aim 1: Provide oversight and coordination of the Center’s projects and cores.
- Aim 2: Manage the formation and involvement of the External Advisory Committee (EAC).
- Aim 3: Facilitate career development of the career development investigator (CDI) and training of future environmental and public health professionals at the graduate and post-graduate levels.
- Aim 4: Coordinate with the COTC and the Center’s Pediatric Health Specialists to facilitate the translation of scientific findings and dissemination to key stakeholders.
Community Outreach and Translation Core (COTC): Engaging community on mobile environmental applications, air pollution policy impacts, and dissemination of Center findings
- Aim 1: Working together with We Act for Environmental Justice (WE ACT), our primary community partner, and our active Community Advisory and Stakeholder Board (CASB), we assessed community residents’ preferences for environmental health information, their current use of mobile applications to obtain it, and identified and promoted the use of mobile applications that meet community preferences and needs. The purpose of this aim was to help community residents learn to use mobile technology to identify and reduce toxic exposures to air pollution and other contaminants that have adverse effects on health.
- Aim 2: Working closely with WE ACT and the NYC Dept. of Health and Mental Hygiene (NYCDOHMH), we will determine the extent to which New York City policies have reduced air pollution and improved health, and communicate this information to community environmental organizations, policy-makers and the public.
- Aim 3: Working with WE ACT and our CASB, we will translate the Center’s findings to key target populations using a variety of communications strategies. The purpose of this aim is to educate residents, other stakeholders, and policy-makers about how Center research findings can help them reduce exposure, improve health, and take policy relevant action.
Summary/Accomplishments (Outputs/Outcomes):
Project 1- The Impact of PAH Exposure on Adolescent Neurodevelopment: Disruption of Self-Regulatory Processes
During the NCE period, we completed recruitment, scheduling, and assessment activities related to neuropsychological and clinical functioning in the adolescent subjects and their mothers. We continued to work closely with the DMC on data entry, data security, and distributing data to study investigators, and continued to monitor the protocol, using a checklist. We have continued to use the decision rules from the protocol for detection of high-risk scores on psychosocial domains for: (1) immediate action or (2) mental health referral. To date, N=322 neuropsychological batteries have been completed, and 6 additional batteries have been scheduled.
Finally, building on Dr. Pagliaccio’s work on behavioral outcomes associated with stress by PAH, Dr. Margolis submitted an R01 application submitted in response to a call for proposals to study effects of neurotoxicants on mental health outcomes. Reviews were enthusiastic, calling the work “the holy grail of all studies focused on very early, including prenatal, influences on behavior.”
Impact: This R01 will integrate advanced pattern recognition methods, a cognitive neuroscience approach and state-of-the-art fMRI techniques to identify brain pathways through which prenatal exposures alter behavior later in adolescence. We will identify circuit-based changes in brain function that likely mediate associations between prenatal exposure profiles and symptoms of psychiatric disorders that typically emerge and co-occur in adolescence. By simultaneously studying mixtures of chemical and social stressors as well as profiles of co-occurring symptoms, we will greatly enhance our ability to comprehensively characterize the complex impacts of prenatal environmental exposures on behavioral symptoms in adolescence. Our findings will allow public health interventions to improve the quality of children’s perinatal environment and the development of novel circuit-specific intervention tools.
Project 2- The Impact of PAH Exposure on Childhood Growth Trajectories and Visceral Adipose Tissue Mass in Adolescence: Linkages to Disrupted Self-Regulatory Processes
During the NCE period, we completed enrollment and evaluations of 300 cohort participants at ages 15 to 18. This includes the completion of data collection on physical activity, hedonic eating, food insecurity, height, weight, waist circumference, % body fat, and blood pressure from the teens and their mothers. We have also collected data on weight cycling, weight loss practices and weight loss surgery from the mothers, and resting heart rate and heart rate recovery after a step test from the teens. Furthermore, the teens have all taken part in MRI scans of the abdomen to measure visceral abdominal fat and we have completed image analysis of the MRI scans and estimated adipose tissue volumes.
We are updating and finalizing analyses in the full sample (n=300) of predictors of differences in visceral abdominal adipose tissue that we previously reported on, for the first half of the enrollees (n=140) in our previous progress reports. As predictors of abdominal adipose tissue volume we are analyzing data on: 1) prenatal exposures to PAH and PM2.5; 2) trajectories of development of emotional self-regulation from age 3-5 to age 11; 3) excessive gestational weight gain; 4) food insecurity; and 5) prenatal exposures to phthalates and Bis-phenol A.
We have completed and published analyses of prenatal exposure to PAH and BMI Z-score trajectories from age 5 to age 14 (Aim 2) [Rundle et al., Environmental Research, Environ Res. 2019 Oct;177]. We found that at age 5, BMI Z-scores were significantly greater for children in the third tertile of exposure relative to the first tertile (0.35 Z-score units, 95% CI 0.09, 0.61, p = 0.007) and were non-significantly higher for the second tertile of exposure compared to the first tertile (0.25 Z-score units, 95% CI -0.02, 0.52, P = 0.075). The trajectories of BMI Z-scores by tertiles of exposure converged as the children aged, such that by age 11 years the estimated mean BMI Z-scores associated with each tertile of exposure were not different. The data indicated that highly exposed children spend a greater proportion of their childhood with higher BMI Z-scores, thus in an oxidative state.
Dr. Peterson will soon begin analyzing MRI data collected age 9-11 on brain structure and function in relation to anthropometric data collected at the same time point (Aim 4). In support of these analyses, Drs. Rundle and Goldsmith identified possible relevant confounding variables for the analyses of the anthropometric data, assessed missing covariate data and implemented a multiple imputation strategy using Multiple Imputation by Chained Equations (MICE) to impute missing covariate values. Five sets of data with anthropometric data and covariate data, with imputed values for missing covariate data, were created and sent to Dr. Peterson for analyses with the MRI scan data.
Dr. Eliza Kinsey, a post-doctoral scholar in the Department of Epidemiology, was awarded a K99R00 Career Development Application to study food insecurity and child obesity and neurodevelopment outcomes in the cohort. She has since co-authored three papers on childhood obesity and food insecurity within the context of COVID-19.
Project 3: An MRI Study of the Effects of Prenatal and Early Childhood PAH Exposure on Brain Maturation and Its Mediating Influences on Adverse Adolescent Outcomes
During the NCE period, we focused on the following objectives:
(1) Statistical analysis of Magnetic Resonance Imaging (MRI) data for ages 9-12 years in our cohort. We have done this especially for anatomical MRI, Arterial Spin Labeling (ASL) perfusion, DRI, and Magnetic Resonance Spectroscopy (MRS) data (Specific Aims 1 and 2);
(2) Integration of these MRI data with the demographic, behavioral, and cognitive data acquired at ages 9-12 years, particularly in continuing analyses of the ways in which prenatal PAH exposure levels moderate the association of MRI with cognitive and behavioral measures (Specific Aims 1 and 2);
(3) Completed processing of newly acquired anatomical brain imaging data (Specific Aim 3).
(4) In addition, we have conducted many of the same analyses in each MRI modality using geospatial modeling-based estimates of prenatal PM2.5 exposure, covarying for prenatal PAH exposure and other potential confounders, to understand how PM2.5 and PAH separately affect brain development.
Administrative Core
Aim 1: Over the past year the Administrative Core (AC) has continued to provide oversight and coordination of the Center’s projects and cores by facilitating communication through Project and Executive Council (EC) meetings, maintaining fiscal oversight through weekly contact with the financial coordinator, assisting with the ordering of supplies, maintaining the project IRB, and circulating data requests and manuscripts. We have continued to hold regular project meetings with research staff, investigators, and coordinators of all projects to review grant progress, discuss challenges or obstacles, and adjust activities accordingly. Additionally, the EC, consisting of all project and core leaders, continues to meet regularly to discuss updates and plans for data analysis, discuss any financial updates, and review the progress according to the project aims. The AC maintains regular contact with the financial coordinator, Raquel Sotelo, to review the spending on the grant, assist with the personnel changes that have occurred, and work on any agency requests. The AC acts as a central location for the ordering of supplies related to the project, including updated manuals for the neuropsychiatric battery, heart rate monitors and measurement devices used for the obesity project. The AC is also responsible for circulating any data requests and manuscripts to the EC to keep them abreast of analyses occurring and allow for their feedback and input.
Aim 2: The EAC meeting for the fifth year took place on June 26, 2019 and was a half day meeting, where we shared our progress and updates with our EAC. In her summary report, the EAC Chair, Dr. Jerilynn Radcliffe, stated: “The work has progressed very well and is an important contribution to the field. Keep going, we are looking forward to hearing what comes next.” Since Dr. Ali Hamade, Assistant Commissioner of Health in the Bureau of Environmental Disease and Injury Prevention at the NYC DOH has left his position, per his recommendation, Dr. Maureen Little has replaced him in his previous DOH advisory role for the Center. Dr. Maureen Little currently has a position in the office of Environmental Health Assessment and Communication. She also has a long history in Environmental Public Health practice and research and is a Diplomat of the American Board of Toxicology.
Aim 3: Dr. David Pagliaccio continued to be the CDI. As described above, the CDI award allowed him to develop new expertise in environmental epidemiology in order to link environmental exposures with neurodevelopmental and mental health outcomes. Dr. Pagliaccio’s recent paper published in the Journal of Child Psychology and Psychiatry received considerable attention in the scientific community
Aim 4: CCCEH researchers have presented findings at the Society for Epidemiologic Research, International Society for Children’s Health and the Environment, International Society for Environmental Epidemiology, the International Society for Exposure Science, Society of Toxicology, America Psychiatric Association, International Conference on Urban Health, International Society for Environmental Epidemiology (ISEE), Environmental Mutagenesis and Genomics Society (EMGS), American Meteorological Society (AMS) and other conferences.
Community Outreach and Translation Core (COTC): Engaging community on mobile environmental applications, air pollution policy impacts, and dissemination of Center findings
During the NCE period, we had several changes in personnel and leadership in our Center’s COTC. Diana Hernández, PhD replaced Dr. David Evans when he retired in May 2019 as the director of the Center’s COTC. Dr. Diana Hernández is an Associate Professor of Sociomedical Sciences at Columbia University's Mailman School of Public Health. Her research focuses on the social determinants of health and the impact of policy and structural interventions on health and socioeconomic wellbeing of vulnerable populations. She actively engages in a variety of translational activities through consulting, board service and social entrepreneurship in real estate in her native South Bronx neighborhood.
Last year, Kimberly Burke, former COTC Coordinator, transitioned into a new role as an Operations Manager at the Herbert Irving Comprehensive Cancer Center but continues to provide guidance as needed. Maricela Ureño, MPH, has replaced Kim in her role as COTC Coordinator. She is trained as a community organizer and has extensive experience working on community outreach programs in the US and internationally. In her previous role as the Program Manager with our partner organization, Columbia University Head Start, a CASB member, she regularly disseminated the Center’s environmental health findings to community members and relevant stakeholders.
Additionally, Anabel Cole, MPH, has joined the COTC team to help meet outreach and research translation needs, including running our newly formed Youth Advisory Council, collaborating with our community partners, and helping to coordinate other outreach activities within the Center’s cohorts. Anabel, a lifelong resident of the Northern Manhattan community, has worked at the Center since 2012. Both Maricela and Anabel are bilingual, native Spanish speakers.
Translate Center’s Findings :
- Host stakeholder briefing
- Continue Healthy Home, Healthy Child campaign
- Disseminating key research findings through communication activities and the media
Conclusions:
Project 1- The Impact of PAH Exposure on Adolescent Neurodevelopment: Disruption of Self-Regulatory Processes
We have previously reported our findings related to Specific Aim 1 (to assess the effects of prenatal PAH exposure on neuropsychological performance at 15-17 years of age) and Specific Aim 2 (to assess the effects of prenatal PAH exposure on clinical outcomes at 15-17 years of age in the same adolescents). In relation to Specific Aim 3, our preliminary analysis has shown significant inverse effects of PAH air concentrations on a measure of inhibitory control at 12-14 years of age, as measured by the NEPSY-II, which assesses neuropsychological development, with no association or interaction with early life stress (see below for composite index of stress). The association with PAH remains significant controlling for environmental tobacco smoke (ETS), sex, gestational age, maternal IQ, maternal education, HOME caretaking, heating season, ethnicity, cotinine, lead, and chlorpyrifos. Now that the MRIs are almost completed, the investigators will be working with Dr. Peterson to determine whether or not there is any mediation by the brain parameters. For Specific Aim 4, we are now addressing the cross-study integrative questions, having resolved questions related to outliers and covariates.
Dr. David Pagliaccio, CDI, has continued to work with Drs. Rauh and Margolis to develop hypotheses for analyses and publication. Dr. Pagliaccio is interested in pursuing questions regarding anxiety, depression, allostatic load, and stressful experiences, and how environmental exposures may moderate effects of early life adversity on emotional development and brain connectivity. He created an early life stress composite measure, using 5-year data. On this measure, greater early life stress predicts greater CBCL symptomology (internalizing and externalizing) at age 11 and is moderated by PAH exposure, such that the positive association between early life stress and symptoms is stronger among those with more PAH exposure. This holds up when controlling for ETS, sex, gestational age, maternal IQ, maternal education, HOME caretaking, heating season, ethnicity, cotinine, lead, and chlorpyrifos
Under separate funding, Dr. Rauh and co-investigators will continue to work with the statistician, Dr. Jeff Goldsmith on data analyses involving the integration of PAH exposure, behavioral, neuro-psychological and clinical data with MRI modalities.
Project 2- The Impact of PAH Exposure on Childhood Growth Trajectories and Visceral Adipose Tissue Mass in Adolescence: Linkages to Disrupted Self-Regulatory Processes
We have completed analyses of prenatal PAH exposure and growth trajectories from age 5 to 14 (Aim 2). We find that, compared to the first tertile of prenatal PAH exposure concentrations (lowest exposure group), child BMI z-score is higher at age 5 for those exposed at the higher level (second and third tertiles) of prenatal exposure. However, the children in the first and second tertiles of exposure have steeper gains in BMI z-scores from age 5 to 11 than those in the highest exposure group, such that the trajectories have converged by age 11. Overall however, children in the higher exposure groups (second and third tertiles) of prenatal PAH exposure concentrations spend a greater portion of their childhood at higher BMI, hence in an inflammatory oxidative state.
We have also completed the analyses of phthalate metabolites measured in maternal urine and child and BMI Z-score trajectories from age 5 to 14. Consistent with our prior publication on data through age 7, our new analyses show that non-DEHP metabolites are associated with lower BMI Z-score trajectories from age 5 to 14 among girls.
In developing these trajectory analyses we established a series of methodological procedures that will be applied to trajectory analyses across health outcomes in the cohort. These procedures include: multiple imputation to account for missing covariate data; analyses using inverse probability weights for varying follow-up across follow-up periods; and analyses that account for clinical referrals made as part of the cohort follow-up.
We have completed group- based latent growth analyses of trajectories of DESR scale scores from age 3-5 years to age 11 years and have identified two underlying trajectory typologies, one of which represents a poorer development of emotional self-regulation and accounts for 18% of the participants (Aim 4). We have completed analyses of associations between membership in these two trajectory typologies and diet data collected at age 8.5 to 12 years. We see no associations between DESR trajectory group membership and intake of total calories, calories of protein, calories of carbohydrates, calories of fat, and ratios of protein, carbohydrates, and fat to total calories. We also see no associations between DESR trajectory group and intake of sweets and fruits and vegetables.
Project 3: An MRI Study of the Effects of Prenatal and Early Childhood PAH Exposure on Brain Maturation and Its Mediating Influences on Adverse Adolescent Outcomes
This project has assessed the effects of prenatal and early childhood exposure to PAH and PM2.5 on the structure, function, and metabolism of self-regulatory systems (frontal, parietal, and mesial temporal cortices, and subcortical nuclei) in the brains of 350 cohort children who have undergone MRI scanning at 9-12 years of age. Both exposures (PAH and PM2.5) produced a similar overall spatial pattern of association with anatomical MRI measures. They are both associated with functional and metabolic alterations in brain regions that support executive functioning. PM2.5 and PAH exposures were both associated with altered DTI (diffusion tensor imaging) measures of white matter organization fractional anisotropy (FA) values primarily in subcortical gray matter nuclei (caudate, lenticular nuclei, and thalamus) and altered NAA (N-acetyl aspartate, a metabolic index of neuronal viability) and choline concentrations regions that support executive functioning. PAH was associated with regional cerebral blood flow (rCBF) alterations to these same regions. Sex of the participant significantly moderated these associations of exposure levels with brain measures.
We have a very advanced draft of a manuscript reporting the above findings for the age 9-12 MRI findings for all 4 modalities (anatomical, DTI, spectroscopy, and perfusion) shown above (Aims 1 & 2). We are finalizing details of the statistical analyses and maps of exposure effects and then will submit to a high-ranking journal.
We have begun statistical analyses as described in the grant application for newly acquired MRI data (Specific Aim 3) and will be writing that manuscript as soon as those analyses are complete.
We are planning several papers reporting associations of brain measures with neurocognitive test performance. Those associations are very strong in this dataset and will help to define the neural systems that support cognitive processes.
Administrative Core
Throughout our NCE period, the Administrative Core (AC) has continued to carry out the aims of the Core by providing oversight and coordination of the Projects and Cores, managing the involvement of the External Advisory Committee, facilitating career development of the Career Development Investigator and future public health professionals, and coordinating with the COTC and Pediatric Health Specialists to facilitate the translation of scientific findings and dissemination to key stakeholders.
Community Outreach and Translation Core (COTC): Engaging community on mobile environmental applications, air pollution policy impacts, and dissemination of Center findings
Bus Fleet: We sought to develop and validate indicators of intensity of exposure to bus fleet changes occurring as part of the Clean Fuel Bus program in New York City from 2009 to 2014. These indicators were examined as predictors of change in nitrous oxide exposure estimates and related metrics (NO2 and black carbon) from the New York City Community Air Survey (NYCCAS). We obtained data on bus service frequency by route and bus fleet composition by depot to quantify changes in the fleet and map where these changes would have the greatest benefit. Other covariates of interest included truck routes and total traffic volume estimates. Additionally, a geographic indicator variable was created to adjust for the higher density of buses in the city core versus the outer boroughs. Christian Treat and Gina Lovasi presented this work under the umbrella of other presentations about monitoring and acting on air pollution at the 14th International Conference on Urban Health in Coimbra, Portugal. The talk was presented in the context of creating tools, metrics, and measurements for healthy urban planning and research. We are currently finalizing for submission of a manuscript on this analysis, which shows a dose-response relationship between the shift toward clean buses (operationalized as above the median, at or below the median, or no bus service) and declining ambient nitric oxide (NO) exposure between 2009 and 2014. For example, considering only compressed natural gas or hybrid electric buses as “clean,” those areas of the city with an above average increase in the proportion of clean bus service had a significantly greater decline in ambient NO than other areas, detectable as statistically significant (p<0.001) even against a backdrop of declining NO citywide and adjustment for covariates. The significant difference persisted in models using NO2 or black carbon, as well as those using a more inclusive definition of clean busses (adding ultra low sulfur diesel and newer vintage busses).
NYC Taxi Fleet: We have estimated the distribution of benefits from the shift away from No. 6 and No. 4 heating oil to cleaner fuels. Our preliminary analysis showed that neighborhoods in Northern Manhattan were slower to shift to cleaner fuel sources; and a higher concentration of buildings burning No. 4 heating oil remained in Northern Manhattan. We have consulted with several contacts at NYC organizations including Iyad Kheirbek, Executive Director of the Air Quality Program at New York Department of Health and Human Services and John Lee, Deputy Director for Green Buildings and Energy Efficiency at the Mayor’s Office of Long Term Planning and Sustainability. We received a benchmarking data set for energy usage from the Mayor’s Office that we are using in this analysis.
Journal Articles: 9 Displayed | Download in RIS Format
Other center views: | All 12 publications | 9 publications in selected types | All 9 journal articles |
---|
Type | Citation | ||
---|---|---|---|
|
Conrad L, Rauh V, Hopener L, Acosta L, Perera F, Rundle A, Arteaga-Solis E, Miller R, Perzanowski M. Report of prenatal maternal demoralization and material hardship and infant rhinorrhea and watery eyes. Annals of Allergy Asthma & Immunology 2020;125(4):399. |
R836154 (2019) R832144 (Final) |
Exit |
|
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. |
R836154 (Final) R827027 (2002) R832141 (Final) R834509 (Final) |
Exit Exit |
|
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. |
R836154 (2017) R834509 (Final) |
|
|
Hopson MB, Margolis A, Rauh V, Herbstman JB. Impact of the home environment on the relationship between prenatal exposure to environmental tobacco smoke and child behavior. International Journal of Child Health and Human Development 2016;9(4):453-464. |
R836154 (2017) |
|
|
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. |
R836154 (2017) R834509 (2013) R834509C001 (Final) |
|
|
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. |
R836154 (2017) R834509 (Final) |
Exit Exit |
|
Perera FP, Wheelock K, Wang Y, Tang D, Margolis AE, Badia G, Cowell W, Miller RL, Rauh V, Wang S, Herbstman JB. Combined effects of prenatal exposure to polycyclic aromatic hydrocarbons and material hardship on child ADHD behavior problems. Environmental Research 2018;160:506-513. |
R836154 (2017) R836154 (2018) |
Exit Exit Exit |
|
Perera F, Nolte ELR, Wang Y, Margolis AE, Calafat AM, Wang S, Garcia W, Hoepner LA, Peterson BS, Rauh V, Herbstman J. Bisphenol A exposure and symptoms of anxiety and depression among inner city children at 10-12 years of age. Environmental Research 2016;151:195-202. |
R836154 (2017) |
Exit Exit Exit |
|
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. |
R836154 (2017) R834509C001 (Final) |
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).
R836154C001 The Impact of PAH Exposure on Adolescent Neurodevelopment: Disruption of Self-Regulatory Processes
R836154C002 The Impact of PAH Exposure on Childhood Growth Trajectories and Visceral Adipose Tissue
R836154C003 An MRI Study of the Effects of Prenatal and Early Childhood PAH Exposure on Brain Maturation and Its Mediating Influences on Adverse Adolescent Outcomes
The perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.
Project Research Results
- 2019 Progress Report
- 2018 Progress Report
- 2017 Progress Report
- 2016 Progress Report
- Original Abstract
9 journal articles for this center