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      Epidemiological study of PM 2.5 and risk of COPD-related hospital visits in association with particle constituents in Chuncheon, Korea

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          Abstract

          Background and objective

          Aside from smoking, which is already recognized as a strong risk factor for COPD, interest in the impact of particulate matter (PM) on COPD is increasing. This study aimed to investigate the effect of PM, especially with an aerodynamic diameter ≤2.5 µm (PM 2.5), and its chemical constituents on the exacerbation of COPD.

          Methods

          Data on hospital visits including admission and outpatient clinic visits for exacerbation of COPD in Chuncheon, Korea, between 2006 and 2012 were extracted from the National Health Insurance Service database. PM 2.5 and its chemical constituents were measured on the roof of the four-story Kangwon National University Natural Sciences building once every 3 days. Meteorological data were provided by the Korean Meteorological Administration.

          Results

          During the study period, the mean level of PM 2.5 was 35.0±25.2 µg/m 3, and the number of daily hospital visits were 6.42±4.28 and 2.07±1.93 for males and females, respectively. The number of COPD-related hospital visits increased with increasing PM 2.5 after adjusting for meteorological covariates and females tended to be more affected sooner than males. Among the PM 2.5 constituents, Al, Si, and elemental carbon were associated with increased hospital visits and there was a difference according to sex. In males, some constituents of PM 2.5 were related to an increased risk of a hospital visit, mainly on the first and second days of measurement (Lag1 and Lag2). In contrast, there was no significant increase in the risk of hospital visits due to any of the PM 2.5 constituents in females.

          Conclusion

          Concentrations of PM 2.5 mass and some of the PM 2.5 constituents were associated with increased COPD-related hospital visits in Chuncheon.

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          Most cited references 34

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          Chronic obstructive pulmonary disease in non-smokers.

          Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Tobacco smoking is established as a major risk factor, but emerging evidence suggests that other risk factors are important, especially in developing countries. An estimated 25-45% of patients with COPD have never smoked; the burden of non-smoking COPD is therefore much higher than previously believed. About 3 billion people, half the worldwide population, are exposed to smoke from biomass fuel compared with 1.01 billion people who smoke tobacco, which suggests that exposure to biomass smoke might be the biggest risk factor for COPD globally. We review the evidence for the association of COPD with biomass fuel, occupational exposure to dusts and gases, history of pulmonary tuberculosis, chronic asthma, respiratory-tract infections during childhood, outdoor air pollution, and poor socioeconomic status.
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            Elemental Carbon-Based Method for Monitoring Occupational Exposures to Particulate Diesel Exhaust

             M. E. Birch,  R. Cary (1996)
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              An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease.

              Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. To evaluate the risk factors for COPD besides personal cigarette smoking. We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2018
                12 January 2018
                : 13
                : 299-307
                Affiliations
                [1 ]Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kyung Hee University Medical Center, Seoul
                [2 ]Data Analysis Center
                [3 ]Department of Environmental Science, Kangwon National University
                [4 ]Department of Internal Medicine and Environmental Health Center, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Gangwon-do, Korea
                Author notes
                Correspondence: Woo Jin Kim, Department of Internal Medicine and Environmental Health Center, Kangwon National University Hospital, Kangwon National University School of Medicine, 1 Kangwondaehak-gil, Chuncheon, Gangwon-do, 24341, Korea, Tel +82 32 258 9364, Fax +82 32 258 2404, Email pulmo2@ 123456kangwon.ac.kr
                Article
                copd-13-299
                10.2147/COPD.S149469
                5769598
                © 2018 Jo et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Respiratory medicine

                hospital visit, constituents, pm2.5, copd

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