This proposal is submitted in response to the RFA-ES-06-001 DISCOVER initiative. The fetus and young child have physiologic, developmental, metabolic, and behavioral patterns that make them uniquely vulnerable to hazards in their environments. Ambient air pollution has been implicated as a major risk factor for asthma and asthma exacerbation, however epidemiological studies have been hampered by uncertainties in exposures and the nature of airway responses. The Columbia Center for Children's Environmental Health (CCCEH) Disease Investigation through Specialized Clinically-Oriented Ventures in Environmental Research (DISCOVER) seeks to understand when and how airborne polycyclic aromatic hydrocarbons (PAHs) and diesel exhaust particles (DEP) increase the risk for childhood asthma and airway inflammation, develop new biomarkers to identify children at risk and improve clinical treatment, evaluate the success of a public policy intervention, and implement physician education initiatives as a mode of intervention. This proposal includes four closely linked projects and Administrative and Data Management and Biostatistics Cores each ensuring the seamless coordination of the multiple research activities involved in this proposal. The cores play vital roles in the quality of research information and statistical analyses and the administrative/financial oversight and translational components of the four main DISCOVER research project initiatives. The four project aims are: 1) Take advantage of repeat PAH measurements pre- and post-natally to distinguish between the biological effects of prenatal PAH exposure versus postnatal exposure during early childhood and pre-adolescence;2) To advance the understanding of the influence of diesel exhaust exposures, which include PAHs, in acute asthma exacerbations by linking innovative exposure and outcome measures;3) To determine whether epigenetic changes related to PAH exposure are involved in the pathogenesis of childhood asthma;4) To ascertain if traffic related PAHs affect B2AR function in airway smooth muscle cells in vitro, alter B2AR function following in utero and early life exposures, affect B2AR expression and function in airway epithelial cells in vitro. The research is translational to asthma prevention, clinical treatment, physician education, and policy.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Specialized Center (P50)
Project #
5P50ES015905-05
Application #
8080996
Study Section
Special Emphasis Panel (ZES1-JAB-C (DI))
Program Officer
Gray, Kimberly A
Project Start
2007-09-29
Project End
2013-05-31
Budget Start
2011-06-01
Budget End
2013-05-31
Support Year
5
Fiscal Year
2011
Total Cost
$1,971,928
Indirect Cost
Name
Columbia University (N.Y.)
Department
Public Health & Prev Medicine
Type
Schools of Public Health
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
Jung, Kyung Hwa; Torrone, David; Lovinsky-Desir, Stephanie et al. (2017) Short-term exposure to PM2.5 and vanadium and changes in asthma gene DNA methylation and lung function decrements among urban children. Respir Res 18:63
Jung, Kyung Hwa; Lovinsky-Desir, Stephanie; Yan, Beizhan et al. (2017) Effect of personal exposure to black carbon on changes in allergic asthma gene methylation measured 5 days later in urban children: importance of allergic sensitization. Clin Epigenetics 9:61
Miller, Rachel L; Yan, Zhonghai; Maher, Christina et al. (2016) Impact of prenatal polycyclic aromatic hydrocarbon exposure on behavior, cortical gene expression and DNA methylation of the Bdnf gene. Neuroepigenetics 5:11-18
Lovinsky-Desir, Stephanie; Miller, Rachel L; Bautista, Joshua et al. (2016) Differences in Ambient Polycyclic Aromatic Hydrocarbon Concentrations between Streets and Alleys in New York City: Open Space vs. Semi-Closed Space. Int J Environ Res Public Health 13:
Jung, Kyung Hwa; Lovinsky-Desir, Stephanie; Perzanowski, Matthew et al. (2015) Repeatedly high polycyclic aromatic hydrocarbon exposure and cockroach sensitization among inner-city children. Environ Res 140:649-56
Peterson, Bradley S; Rauh, Virginia A; Bansal, Ravi et al. (2015) 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 72:531-40
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
de Planell-Saguer, Mariàngels; Lovinsky-Desir, Stephanie; Miller, Rachel L (2014) Epigenetic regulation: the interface between prenatal and early-life exposure and asthma susceptibility. Environ Mol Mutagen 55:231-43
Pitiranggon, Masha; Perzanowski, Matthew S; Kinney, Patrick L et al. (2014) Determining urea levels in exhaled breath condensate with minimal preparation steps and classic LC-MS. J Chromatogr Sci 52:1026-32
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

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