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The Lancet Regional Health – Southeast Asia.This article has an online supplement, which is accessible from this issue's table of contents at Author disclosures are available with the text of this article at The Lancet Gastroenterology & Hepatology All authors contributed to the critical revision of the manuscript and approved of the final submitted version. M.B.R was responsible for designing the study and supervised all aspects of the project including data collection, analysis, and interpretation and writing of the manuscript. guided personal and community-level exposure assessment, calibration of the monitors, and interpretation of the exposure data.
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provided expertise in statistical methodology and development of the analytical plan. performed data collection, analysis, and interpretation and wrote the initial draft of the manuscript. Furthermore, USEPA does not endorse the purchase of any commercial products or services mentioned in the publication.Īuthor Contributions: L.N. This work’s contents are solely the responsibility of the grantee and do not necessarily represent the official views of the USEPA. Environmental Protection Agency (USEPA) grant RD-835872. Supported by National Institute of Environmental Health Sciences grants K23ES026204, R01ES031252, and P30ES000002 and the U.S. Future research is needed to verify if eosinophil level is a biomarker for susceptibility to air pollution in COPD. Personal and community-level exposure to particulate matter ⩽2.5 μm in aerodynamic diameter and community-level NO 2 were negatively associated with FEV 1 among the 55.2% of participants with the higher eosinophil level ( P interaction < 0.05).Ĭonclusions: Our study highlights the need to address air pollution exposure among patients with COPD. Each interquartile range (5.1 parts per billion )–higher previous-day personal exposure to NO 2 was associated with an 11.3 ml (95% confidence interval, −18.7 to −4.0) lower forced expiratory volume in 1 second (FEV 1) and an 18.0 ml (95% CI, −32.0 to −4.2) lower forced vital capacity. Results: A total of 3,314 observations with exposure and lung function data were collected. We constructed multilevel linear mixed-effects models with random intercepts for person and observation month, adjusted for temperature, humidity, age, sex, race, height, weight, income, and season, to assess associations of previous-day pollutant exposure with lung function and effect modification by eosinophil count (<150/μl vs.
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Previous-day exposure to pollutants (particulate matter ⩽2.5 μm in aerodynamic diameter, nitrogen dioxide, and ozone) were measured by portable and community monitors. Participants measured morning lung function and carried a portable air quality monitor daily. Methods: We recruited 30 former smokers with moderate to severe COPD living in the Boston area and followed them for up to 4 nonconsecutive months in different seasons. Objectives: To evaluate if daily pollutant exposures are associated with lung function and if associations are modified by eosinophil level in COPD. Blood eosinophil level may be a biomarker of airway inflammation and pollution susceptibility. Rationale: Few studies have assessed personal exposure to pollutants and lung function among adults with chronic obstructive pulmonary disease (COPD).
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