Changwoo Han1, Youn-Hee Lim2,3, Kweon Jung4, Yun-Chul Hong1,2,3. 1. From the Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea. 2. Institute of Environmental Medicine, Seoul National University Medical Research Center, Seoul, Korea. 3. Environmental Health Center, Seoul National University College of Medicine, Seoul, Korea. 4. Seoul Metropolitan Institute of Public Health and Environment, Seoul, Korea.
Abstract
BACKGROUND: Spontaneous pneumothorax is hypothesized to be associated with air pollution exposure based on pathophysiological mechanisms involving airway inflammation. Therefore, we analyzed the association between daily concentrations of air pollutants [sulfur dioxide, nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), particulate matter (PM) less than 2.5 μm in diameter (PM2.5), PM less than 10 μm in diameter (PM10), and coarse PM (PM10-2.5)] and the number of spontaneous pneumothorax-related hospital visits. METHODS: We analyzed a subset of data from the National Health Insurance Service-National Sample Cohort, a nationally representative dynamic cohort based on health insurance claims data in Korea. Using time series analysis with the Poisson generalized additive model, we evaluated hospital visit data of over 100,000 male cohort members residing in Seoul from 2007 to 2010. RESULTS: We identified 516 hospital visits due to spontaneous pneumothorax. In a single-pollutant model, an interquartile range increase of PM and CO exposure at lag day 1 was associated with spontaneous pneumothorax hospital visits (relative risk, 95% confidence interval: PM2.5: 1.10 (1.01, 1.21); PM10: 1.09 (1.01, 1.18); PM10-2.5: 1.06 (1.00, 1.12); CO: 1.11 (1.01, 1.23)). For lag day 2, NO2 and PM exposure was associated with pneumothorax hospital visits (NO2: 1.15 (1.01, 1.32); PM10: 1.10 (1.02, 1.18); PM10-2.5: 1.07 (1.02, 1.13)). In a multipollutant model, the association was consistent for PM. CONCLUSION: The number of hospital visits due to spontaneous pneumothorax increased with air pollution exposure, especially with PM. Our finding suggests that air pollution is a possible predisposing factor for spontaneous pneumothorax.
BACKGROUND: Spontaneous pneumothorax is hypothesized to be associated with air pollution exposure based on pathophysiological mechanisms involving airway inflammation. Therefore, we analyzed the association between daily concentrations of air pollutants [sulfur dioxide, nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), particulate matter (PM) less than 2.5 μm in diameter (PM2.5), PM less than 10 μm in diameter (PM10), and coarse PM (PM10-2.5)] and the number of spontaneous pneumothorax-related hospital visits. METHODS: We analyzed a subset of data from the National Health Insurance Service-National Sample Cohort, a nationally representative dynamic cohort based on health insurance claims data in Korea. Using time series analysis with the Poisson generalized additive model, we evaluated hospital visit data of over 100,000 male cohort members residing in Seoul from 2007 to 2010. RESULTS: We identified 516 hospital visits due to spontaneous pneumothorax. In a single-pollutant model, an interquartile range increase of PM and CO exposure at lag day 1 was associated with spontaneous pneumothorax hospital visits (relative risk, 95% confidence interval: PM2.5: 1.10 (1.01, 1.21); PM10: 1.09 (1.01, 1.18); PM10-2.5: 1.06 (1.00, 1.12); CO: 1.11 (1.01, 1.23)). For lag day 2, NO2 and PM exposure was associated with pneumothorax hospital visits (NO2: 1.15 (1.01, 1.32); PM10: 1.10 (1.02, 1.18); PM10-2.5: 1.07 (1.02, 1.13)). In a multipollutant model, the association was consistent for PM. CONCLUSION: The number of hospital visits due to spontaneous pneumothorax increased with air pollution exposure, especially with PM. Our finding suggests that air pollution is a possible predisposing factor for spontaneous pneumothorax.