Project Research Results
Main Center: R834509
Grantee Research Project Results
The Role of Endocrine Disruptors in Neurodevelopmental DisordersEPA Grant Number: R834509C002
Subproject: this is subproject number 002 , established and managed by the Center Director under grant R834509
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: The Columbia Center for Children’s Environmental Health
Center Director: Perera, Frederica P.
Title: The Role of Endocrine Disruptors in Neurodevelopmental Disorders
Investigators: Perera, Frederica P.
Current Investigators: Perera, Frederica P. , Rauh, Virginia
Institution: Columbia University in the City of New York
EPA Project Officer: Callan, Richard
Project Period: September 24, 2009 through September 23, 2014 (Extended to September 23, 2015)
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2009)
Research Category: Children's Health
17% of U.S. children have been diagnosed with a learning or behavior disorder. We are proposing policy relevant research on the contribution of prenatal exposures to the common endocrine disruptors, polycyclic aromatic hydrocarbons (PAH) and bisphenol A (BPA), to neurodevelopmental disorders in early adolescence, and epigenetic mechanisms as mediators of these effects. The project takes advantage of our ongoing cohort study of children residing in low-income, minority neighborhoods of New York City who have been followed by the Columbia Center for Children's Environmental Health (CCCEH) since 1998 and of our new study of younger siblings (Sibling/Hermanos cohort). Our cohorts provide a unique opportunity to evaluate the longer-term consequences of prenatal exposure to PAH and, for the first time, to assess the effect of prenatal BPA exposure through the peri-pubertal years, elucidating the role of epigenetic mechanisms in their neurobehavieral impacts.Expected Results:
Aim l: Determine whether prenatal exposures to the endocrine disruptors PAH and BPA are associated with adverse neurobehavieral outcomes in peri-pubertal children, as measured by diagnostic assessment of child psychopathology and cognitive functioning. Aim 2: Determine whether prenatal exposure to PAH or BPA is associated with epigenetic changes in umbilical cord white blood cells (DNA methylation validated by gene expression) in candidate genes/pathways associated with endocrine disruption and immune dysregulation known to be critical in fetal brain development, and whether altered methylation and gene expression is associated with the neurobehavieral outcomes described in Aim 1. Aim 3: Using GIS, determine the extent to which neighborhood-level conditions contribute to neurobehavieral outcomes and/or moderate the individual level associations between exposure to PAH or BPA and child neurodevelopment (as seen in Aims 1 and 2). Understanding of the multi-factorial etiology and mechanisms of developmental disorders that affect children's academic performance will open new avenues for prevention.Publications and Presentations:
Ambient air, human health, toxic, public policy, community-based, ethnic groups, susceptibility, epidemiology, Northeast,, RFA, Health, Scientific Discipline, INTERNATIONAL COOPERATION, ENVIRONMENTAL MANAGEMENT, POLLUTANTS/TOXICS, Chemicals, Biochemistry, Children's Health, Environmental Policy, Biology, Risk Assessment, air toxics, developmental neurotoxicity, air pollution, endocrine disruptors, childhood obesity, children's vulnerablity, assessment of exposure, children's environmental health, growth & development
Progress and Final Reports:
2012 Progress Report
Main Center Abstract and Reports:
R834509 The Columbia Center for Children’s Environmental Health
Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
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