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      The Global Contribution of Outdoor Air Pollution to the Incidence, Prevalence, Mortality and Hospital Admission for Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis

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          Abstract

          Objective: This study aimed to investigate the quantitative effects of outdoor air pollution, represented by 10 µg/m 3 increment of PM 10, on chronic obstructive pulmonary disease in China, United States and European Union through systematic review and meta-analysis. Methods: Publications in English and Chinese from PubMed and EMBASE were selected. The Cochrane Review Handbook of Generic Inverse Variance was used to synthesize the pooled effects on incidence, prevalence, mortality and hospital admission. Results: Outdoor air pollution contributed to higher incidence and prevalence of COPD. Short-term exposure was associated with COPD mortality increased by 6%, 1% and 1% in the European Union, the United States and China, respectively ( p < 0.05). Chronic PM exposure produced a 10% increase in mortality. In a short-term exposure to 10 µg/m 3 PM 10 increment COPD mortality was elevated by 1% in China ( p < 0.05) and hospital admission enrollment was increased by 1% in China, 2% in United States and 1% in European Union ( p < 0.05). Conclusions: Outdoor air pollution contributes to the increasing burdens of COPD.10 µg/m 3 increase of PM 10 produced significant condition of COPD death and exacerbation in China, United States and European Union. Controlling air pollution will have substantial benefit to COPD morbidity and mortality.

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          Most cited references26

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          The Lancet, 380(9859), 2224-2260
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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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              COPD and chronic bronchitis risk of indoor air pollution from solid fuel: a systematic review and meta-analysis.

              Over half the world is exposed daily to the smoke from combustion of solid fuels. Chronic obstructive pulmonary disease (COPD) is one of the main contributors to the global burden of disease and can be caused by biomass smoke exposure. However, studies of biomass exposure and COPD show a wide range of effect sizes. The aim of this systematic review was to quantify the impact of biomass smoke on the development of COPD and define reasons for differences in the reported effect sizes. A systematic review was conducted of studies with sufficient statistical power to calculate the health risk of COPD from the use of solid fuel, which followed standardised criteria for the diagnosis of COPD and which dealt with confounding factors. The results were pooled by fuel type and country to produce summary estimates using a random effects model. Publication bias was also estimated. There were positive associations between the use of solid fuels and COPD (OR=2.80, 95% CI 1.85 to 4.0) and chronic bronchitis (OR=2.32, 95% CI 1.92 to 2.80). Pooled estimates for different types of fuel show that exposure to wood smoke while performing domestic work presents a greater risk of development of COPD and chronic bronchitis than other fuels. Despite heterogeneity across the selected studies, exposure to solid fuel smoke is consistently associated with COPD and chronic bronchitis. Efforts should be made to reduce exposure to solid fuel by using either cleaner fuel or relatively cleaner technology while performing domestic work.
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                Author and article information

                Contributors
                Role: External Editor
                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                14 November 2014
                November 2014
                : 11
                : 11
                : 11822-11832
                Affiliations
                [1 ]Beijing Key Laboratory of Cancer Therapeutic Vaccine, Capital Medical University Cancer Center, Beijing Shijitan Hospital, Tie Yi Road 10, Haidian District, Beijing 100038, China; E-Mail: songqingkun@ 123456gmail.com
                [2 ]Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA; E-Mail: dchris@ 123456hsph.harvard.edu
                [3 ]The Chinese University of Hong Kong, Hong Kong 999077, China; E-Mail: xrwang@ 123456cuhk.edu.hk
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: renjun9688@ 123456yahoo.com ; Tel./Fax: +86-10-6392-6317.
                Article
                ijerph-11-11822
                10.3390/ijerph111111822
                4245645
                25405599
                75ba642b-fa09-47cd-9565-918a89797acf
                © 2014 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 31 July 2014
                : 29 October 2014
                : 31 October 2014
                Categories
                Article

                Public health
                ambient air pollution,chronic obstructive pulmonary disease,environmental health,epidemiology,particulate matter

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