Andreas M Neophytou1, Marquitta J White2, Sam S Oh2, Neeta Thakur2, Joshua M Galanter2,3, Katherine K Nishimura2, Maria Pino-Yanes2,4, Dara G Torgerson2, Christopher R Gignoux3, Celeste Eng2, Elizabeth A Nguyen2, Donglei Hu2, Angel C Mak2, Rajesh Kumar5, Max A Seibold6, Adam Davis7, Harold J Farber8, Kelley Meade7, Pedro C Avila9, Denise Serebrisky10, Michael A Lenoir11, Emerita Brigino-Buenaventura12, William Rodriguez-Cintron13, Kirsten Bibbins-Domingo14, Shannon M Thyne15, L Keoki Williams16,17, Saunak Sen18, Frank D Gilliland19, W James Gauderman19, Jose R Rodriguez-Santana20, Fred Lurmann21, John R Balmes1,22, Ellen A Eisen1, Esteban G Burchard2,3. 1. 1 Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, California. 2. 2 Department of Medicine. 3. 3 Department of Bioengineering and Therapeutic Sciences. 4. 4 Centro de Investigación Biomédica en Red de Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain. 5. 5 Children's Memorial Hospital and the Feinberg School of Medicine, Northwestern University, Chicago, Illinois. 6. 6 Integrated Center for Genes, Environment, and Health, National Jewish Health, Denver, Colorado. 7. 7 Children's Hospital and Research Center Oakland, Oakland, California. 8. 8 Department of Pediatrics, Section of Pulmonology, Baylor College of Medicine and Texas Children's Hospital, Houston, Texas. 9. 9 Department of Medicine, Northwestern University, Chicago, Illinois. 10. 10 Pediatric Pulmonary Division, Jacobi Medical Center, Bronx, New York. 11. 11 Bay Area Pediatrics, Oakland, California. 12. 12 Department of Allergy and Immunology, Kaiser Permanente-Vallejo Medical Center, Vallejo, California. 13. 13 Veterans Caribbean Health Care System, San Juan, Puerto Rico. 14. 14 Division of General Internal Medicine, Department of Medicine. 15. 15 Department of Pediatrics, University of California, San Francisco, San Francisco General Hospital, San Francisco, California. 16. 16 Center for Health Policy and Health Services Research and. 17. 17 Department of Internal Medicine, Henry Ford Health System, Detroit, Michigan. 18. 18 Department of Epidemiology and Biostatistics, and. 19. 19 Department of Preventative Medicine, University of Southern California, Los Angeles, California. 20. 20 Centro de Neumología Pediatrica, San Juan, Puerto Rico; and. 21. 21 Sonoma Technology, Inc., Petaluma, California. 22. 22 Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, San Francisco, California.
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.
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.
Entities:
Keywords:
air pollution; ancestry; children; lung function; minority
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