4.7 Article

Personal and ambient air pollution exposures and lung function decrements in children with asthma

期刊

ENVIRONMENTAL HEALTH PERSPECTIVES
卷 116, 期 4, 页码 550-558

出版社

US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/ehp.10911

关键词

asthma; epidemiology; forced expiratory flow rates; longitudinal data analysis; nitrogen dioxide; panel study; particulate air pollution

资金

  1. NCRR NIH HHS [M01 RR000827, MO1-RR00827] Funding Source: Medline
  2. NICHD NIH HHS [HD048721, P01 HD048721] Funding Source: Medline
  3. NIEHS NIH HHS [ES11615, R01 ES011615] Funding Source: Medline
  4. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD048721] Funding Source: NIH RePORTER
  5. NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000827] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES011615] Funding Source: NIH RePORTER

向作者/读者索取更多资源

BACKGROUND: Epidemiologic studies have shown associations between asthma outcomes and outdoor air pollutants such as nitrogen dioxide and particulate matter mass < 2.5 mu m in diameter (PM2.5). Independent effects of specific pollutants have been difficult to detect because most studies have relied on highly correlated central-site measurements. OBJECTIVES: This study was designed to evaluate the relationship of daily changes in percent-predicted forced expiratory volume in 1 see (FEV1) with personal and ambient air pollutant exposures. METHODS: For 10 days each, we followed 53 subjects with asthma who were 9-18 years of age and living in the Los Angeles, California, air basin. Subjects self-administered home spirometry in the morning, afternoon, and evening. We measured personal hourly PM2.5 mass, 24-hr PM2.5 elemental and organic carbon (EC-OC), and 24-hr NO2, and the same 24-hr average outdoor central-site (ambient) exposures. We analyzed data with transitional mixed models controlling for personal temperature and humidity, and as-needed beta(2)-agonist inhaler use. RESULTS: FEV1 decrements were significantly associated with increasing hourly peak and daily average personal PM2.5, but not ambient PM2.5. Personal NO2 was also inversely associated with FEV1. Ambient NO2 was more weakly associated. We found stronger associations among 37 subjects not taking controller bronchodilators as follows: Personal EC-OC was inversely associated with morning FEV1; for an interquartile increase of 71 mu g/m(3) 1-hr maximum personal PM2.5, overall percent-predicted FEV1 decreased by 1.32% [95% confidence interval (CI), -2.00 to -0.65%]; and for an interquartile increase of 16.8 ppb 2-day average personal NO2, overall percent-predicted FLV1 decreased by 2.45% (95% CI, -3.57 to -1.33%). Associations of both personal PM2.5 and NO2 with FEV1 remained when co-regressed, and both confounded ambient NO2. CONCLUSIONS: Independent pollutant associations with lung function might be missed using ambient data alone. Different sets of causal components are suggested by independence of FEV1 associations with personal PM2.5 mass from associations with personal NO2.

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