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 neurobehavioral impacts.
Aim1 : 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.
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 neurobehavioral outcomes described in Aim 1.
Aim 3 : 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 (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.
These studies will ascertain how environmental exposures may be responsible for the neurodevelopmental and neurobehavioral disorders that are seen in the U.S. overall and in our target population. An understanding of how epigenetic mechanisms may be responsible for mediating the effects of prenatal exposures on these adverse health outcomes will allow targeted interventions to prevent long-term effects on children's health.
|Jedrychowski, Wies?aw A; Perera, Frederica P; Camann, David et al. (2015) Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children. Environ Sci Pollut Res Int 22:3631-9|
|Yan, Zhonghai; Zhang, Hanjie; Maher, Christina et al. (2014) Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) ? methylation in offspring, grand-offspring mice. PLoS One 9:e110706|
|Perera, Frederica; Weiland, Katherine; Neidell, Matthew et al. (2014) Prenatal exposure to airborne polycyclic aromatic hydrocarbons and IQ: estimated benefit of pollution reduction. J Public Health Policy 35:327-36|
|Lovinsky-Desir, Stephanie; Folch, Candace; Jung, Kyung Hwa et al. (2014) Urban adolescents readily comply with a complicated asthma research protocol. Clin Med Insights Circ Respir Pulm Med 8:5-9|
|Rosa, Maria José; Perzanowski, Matthew S; Divjan, Adnan et al. (2014) Association of recent exposure to ambient metals on fractional exhaled nitric oxide in 9-11 year old inner-city children. Nitric Oxide 40:60-6|
|Cai, Jing; Yan, Beizhan; Ross, James et al. (2014) Validation of MicroAeth® as a Black Carbon Monitor for Fixed-Site Measurement and Optimization for Personal Exposure Characterization. Aerosol Air Qual Res 14:1-9|
|Jung, Kyung Hwa; Liu, Bian; Lovinsky-Desir, Stephanie et al. (2014) Time trends of polycyclic aromatic hydrocarbon exposure in New York City from 2001 to 2012: assessed by repeat air and urine samples. Environ Res 131:95-103|
|Choi, Hyunok; Spengler, John (2014) Source attribution of personal exposure to airborne polycyclic aromatic hydrocarbon mixture using concurrent personal, indoor, and outdoor measurements. Environ Int 63:173-81|
|Iyer, Shoba; Perera, Frederica; Zhang, Bingzhi et al. (2014) 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 35:69-75|
|Jung, Kyung Hwa; Perzanowski, Matthew; Rundle, Andrew et al. (2014) Polycyclic aromatic hydrocarbon exposure, obesity and childhood asthma in an urban cohort. Environ Res 128:35-41|
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