The proposed project is an R24 infrastructure support grant responsive to RFA-ES-16-004, ?Maintain and Enrich Resource Infrastructure for Existing Environmental Epidemiology Cohorts.? We propose to maintain and enrich resource infrastructure for the Rhode Island Children's Health Study (RICHS), a cohort developed to examine the impact of the environment on newborn and early childhood health outcomes with a novel focus on the mechanistic role of placenta molecular function. RICHS is a highly productive cohort resource?data collection and analyses to date have resulted in over 40 peer-reviewed publications, and 3 research project grants since 2008 (R01MH094609, R01ES022223, R01ES025145); RICHS has also served as a resource for the training and independent research development of 21 pre- and postdoctoral students and junior faculty. Data and results from the cohort have contributed to the understanding of the fundamental molecular biology of the placenta, the impact of environmental exposures on placental epigenetic regulation, links between placental epigenetic variation in newborn growth and neurobehavioral outcomes, as well as novel methods development. The RICHS cohort is comprised of 840 mother-offspring pairs from the Rhode Island and Southeastern Massachusetts region enrolled from a single, population-representative medical center. RICHS offspring were studied in infancy, but maintenance funds are needed for longitudinal follow-up. The proposed infrastructure support would facilitate future prospective, longitudinal assessments within this extensively characterized prenatal cohort, including novel child health and disease outcomes, postnatal environmental exposures, as well as novel and repeated measures of molecular mediators and biomarkers during the critical window of susceptibility of childhood and early adolescence. The proposed infrastructure support will also allow extensive resource-sharing of RICHS data with the larger scientific community. The specific goals of this R24 are to: (1) recontact and reconsent all RICHS mother-child pairs to allow for continued and expanded follow-up, (2) develop an innovative website for cohort maintenance and cohort community building, (3) develop a web-based data collection system for ongoing data collection using REDCap, (4) provide ongoing incentives for maintaining participant investment in RICHS, (5) collect medical record, neurodevelopmental measures and biospecimens for future research studies, and (6) develop systems for broad sharing of cohort data with the larger research community. Our study fits with NIEHS goals to identify fundamental shared mechanisms, to consider the totality of human exposures, biological pathways, and disease pathogenesis, to foster collaboration, and to inspire new cadre of environmental health scientists. Ultimately, the proposed RICHS infrastructure support will maximize NIEHS investment in a unique cohort resource to allow for further seminal work from our highly productive research group and broad sharing of data and resources with the scientific community.

Public Health Relevance

The Rhode Island Child Health Study (RICHS) cohort provides a unique and innovative birth cohort resource focused on the fundamental role of the placenta in the programming of children's health and disease risk. Infrastructure support for the cohort will allow for further longitudinal assessments that will enable multiple high- impact research projects aimed at early risk assessment and intervention. Infrastructure support will also facilitate broad data sharing of this resource with the scientific community and public.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Resource-Related Research Projects (R24)
Project #
1R24ES028507-01
Application #
9385106
Study Section
Special Emphasis Panel (ZES1)
Program Officer
Gray, Kimberly A
Project Start
2017-09-30
Project End
2022-06-30
Budget Start
2017-09-30
Budget End
2018-06-30
Support Year
1
Fiscal Year
2017
Total Cost
Indirect Cost
Name
Emory University
Department
Public Health & Prev Medicine
Type
Schools of Public Health
DUNS #
066469933
City
Atlanta
State
GA
Country
United States
Zip Code
30322
Everson, Todd M; Punshon, Tracy; Jackson, Brian P et al. (2018) Cadmium-Associated Differential Methylation throughout the Placental Genome: Epigenome-Wide Association Study of Two U.S. Birth Cohorts. Environ Health Perspect 126:017010
Herceg, Zdenko; Ghantous, Akram; Wild, Christopher P et al. (2018) Roadmap for investigating epigenome deregulation and environmental origins of cancer. Int J Cancer 142:874-882
Felix, Janine F; Joubert, Bonnie R; Baccarelli, Andrea A et al. (2018) Cohort Profile: Pregnancy And Childhood Epigenetics (PACE) Consortium. Int J Epidemiol 47:22-23u
Everson, Todd M; Marsit, Carmen J (2018) Integrating -Omics Approaches into Human Population-Based Studies of Prenatal and Early-Life Exposures. Curr Environ Health Rep 5:328-337
Lester, Barry M; Marsit, Carmen J (2018) Epigenetic mechanisms in the placenta related to infant neurodevelopment. Epigenomics 10:321-333
Litzky, Julia F; Boulet, Sheree L; Esfandiari, Navid et al. (2018) Effect of frozen/thawed embryo transfer on birthweight, macrosomia, and low birthweight rates in US singleton infants. Am J Obstet Gynecol 218:433.e1-433.e10
Litzky, Julia F; Deyssenroth, Maya A; Everson, Todd M et al. (2018) Prenatal exposure to maternal depression and anxiety on imprinted gene expression in placenta and infant neurodevelopment and growth. Pediatr Res 83:1075-1083
Deyssenroth, Maya A; Gennings, Chris; Liu, Shelley H et al. (2018) Intrauterine multi-metal exposure is associated with reduced fetal growth through modulation of the placental gene network. Environ Int 120:373-381
Everson, Todd M; Kappil, Maya; Hao, Ke et al. (2017) Maternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes. Environ Res 158:233-244
Kingsley, Samantha L; Deyssenroth, Maya A; Kelsey, Karl T et al. (2017) Maternal residential air pollution and placental imprinted gene expression. Environ Int 108:204-211

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