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CHILDHOOD ASTHMA: DISEASE COURSE AND LUNG FUNCTION TRAJECTORIES AND AIR POLLUTION EXPOSURE

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Principal Investigator: Matsui, Elizabeth C.
Institute Receiving Award University Of Texas At Austin
Location Austin, TX
Grant Number R01ES035131
Funding Organization National Institute of Environmental Health Sciences
Award Funding Period 01 Feb 2024 to 30 Nov 2028
DESCRIPTION (provided by applicant): Project Summary Childhood asthma is a major risk factor for lung disease in adulthood, yet what causes some children, but not others, to have a worse disease course, characterized by persistence of disease and decrements in lung function growth, is unclear. Although some genetic factors have been linked to lung function trajectories, much of the variability in disease course remains unexplained, suggesting that environmental factors are likely important in shaping disease course. Several studies have demonstrated that exposure to higher concentrations of particulate matter (PM) leads to worse lung function growth, but the effects of specific PM sources and composition on disease course and lung function growth are largely unknown. Thus, our overarching hypothesis is that exposure to PM from certain sources and of specific compositions predict persistence of asthma severity and decrements in lung function growth. To test this hypothesis, we will conduct a prospective cohort study of 300 multi-ethnic children, the Texas Home Assessment of Asthma and Lung Exposures (TexHALE) study. We will repeatedly measure lung function, asthma severity, and PM exposure (sources, composition, and concentrations) and examine associations between: 1) lung function growth; 2) persistence of disease severity; and 3) biomarkers associated with airway remodeling and lung function decline with PM exposure (sources, composition, and concentrations).The proposed aims will greatly advance our current understanding of the natural history of asthma, which is critical for developing interventions that modify the trajectory of childhood asthma. The proposed work will identify PM sources that are implicated in worse disease course, providing evidence to extend current air pollution regulation to prioritize targeting certain sources. Moreover, the findings will lend insight into racial and ethnic disparities in disease course, the potential contribution of PM exposure to these disparities, and any disparate effects of PM exposure among racial and ethnic minority populations.
Science Code(s)/Area of Science(s) Primary: 69 - Respiratory
Secondary: 03 - Carcinogenesis/Cell Transformation
Publications No publications associated with this grant
Program Officer Ashlinn Quinn
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