Air Pollution and Lung Function in Minority Youth with Asthma in the GALA II (Genes-Environments and Admixture in Latino Americans) and SAGE II (Study of African Americans, Asthma, Genes, and Environments) Studies

Abstract

Rationale: Adverse effects of exposures to ambient air pollution on lung function are well documented, but evidence in racial/ethnic minority children is lacking.

Objectives: To assess the relationship between air pollution and lung function in minority children with asthma and possible modification by global genetic ancestry.

Methods: The study population consisted of 1,449 Latino and 519 African American children with asthma from five different geographical regions in the mainland United States and Puerto Rico. We examined five pollutants (particulate matter ≤10 μm and ≤2.5 μm in diameter, ozone, nitrogen dioxide, and sulfur dioxide), derived from participant residential history and ambient air monitoring data, and assessed over several time windows. We fit generalized additive models for associations between pollutant exposures and lung function parameters and tested for interaction terms between exposures and genetic ancestry.

Measurements and main results: A 5 μg/m(3) increase in average lifetime particulate matter less than or equal to 2.5 μm in diameter exposure was associated with a 7.7% decrease in FEV1 (95% confidence interval = -11.8 to -3.5%) in the overall study population. Global genetic ancestry did not appear to significantly modify these associations, but percent African ancestry was a significant predictor of lung function.

Conclusions: Early-life particulate exposures were associated with reduced lung function in Latino and African American children with asthma. This is the first study to report an association between exposure to particulates and reduced lung function in minority children in which racial/ethnic status was measured by ancestry-informative markers.

Keywords: air pollution; ancestry; children; lung function; minority.

Figure 1.

Box plots of average lifetime pollutant concentrations stratified by recruitment region. CHI = Chicago; HOU = Houston; NY = New York; O₃ = ozone; PM_2.5 = particulate matter with aerodynamic diameter ≤2.5 μm; PM₁₀ = particulate matter with aerodynamic diameter ≤10 μm; PR = Puerto Rico; SF = San Francisco.

Figure 2.

Forest plots for percent change in FEV₁ associated with each 5 unit (μg/m³/ppb; results for SO₂ presented for 1 ppb increases) increase in pollutant concentrations averaged over the lifetime. Sample sizes (N) for each association varied depending on availability of data by pollutant and exposure window in question. CI = confidence interval; GALA II = Genes–Environments and Admixture in Latino Americans study; O₃ = ozone; PM_2.5 = particulate matter with aerodynamic diameter ≤2.5 μm; PM₁₀ = particulate matter with aerodynamic diameter ≤10 μm; SAGE II = Study of African Americans, Asthma, Genes, and Environments; SF = San Francisco.

Figure 3.

Forest plots for percent change in FEV₁ associated with each 5 unit (μg/m³/ppb; results for SO₂ presented for 1 ppb increases) increase in first year of life average pollutant concentrations. Sample sizes (N) for each association varied depending on availability of data by pollutant and exposure window in question. CI = confidence interval; GALA II = Genes–Environments and Admixture in Latino Americans study; O₃ = ozone; PM_2.5 = particulate matter with aerodynamic diameter ≤2.5 μm; PM₁₀ = particulate matter with aerodynamic diameter ≤10 μm; SAGE II = Study of African Americans, Asthma, Genes, and Environments; SF = San Francisco.