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      Smoking cessation affects the natural history of COPD

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          Abstract

          Background

          Cigarette smoking is the most commonly encountered and readily identifiable risk factor for COPD. However, it is not clear which quantitative factors related to smoking influence the prognosis of COPD patients.

          Methods

          A total of 204 patients with a long-term history of smoking were enrolled into this study and followed up for 5 years. Patients were divided into “death” or “survival” groups based on follow-up results and “quitting-smoking” or “continuing-smoking” groups based on whether they gave up smoking.

          Results

          Patients in the death group had a longer smoking time, lower prevalence of quitting smoking, later onset of COPD symptoms, older age at quitting smoking, lower forced expiratory volume in one second (FEV 1) % predicted, and lower ratio of FEV 1/forced vital capacity. Age, age at quitting smoking, and FEV 1% predicted were independently associated with mortality from COPD. Compared to the continuing-smoking group, the quitting-smoking group had a lower mortality rate, longer course of COPD, earlier onset of COPD symptoms, and lower residual volume percent predicted. During the 5-year follow-up, 113 deaths were recorded (quitting-smoking group: n=92; 40 deaths; continuing-smoking group: n=112; 73 deaths). The mortality risk remained significantly higher in the continuing-smoking group than the quitting-smoking group (log-rank test, 13.59; P=0.0002).

          Conclusion

          Smoking time may be related to the mortality rate from COPD. Smoking cessation has the greatest capacity to influence the natural history of COPD.

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          Most cited references 18

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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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            The effects of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial.

            Randomized clinical trials have not yet demonstrated the mortality benefit of smoking cessation. To assess the long-term effect on mortality of a randomly applied smoking cessation program. The Lung Health Study was a randomized clinical trial of smoking cessation. Special intervention participants received the smoking intervention program and were compared with usual care participants. Vital status was followed up to 14.5 years. 10 clinical centers in the United States and Canada. 5887 middle-aged volunteers with asymptomatic airway obstruction. All-cause mortality and mortality due to cardiovascular disease, lung cancer, and other respiratory disease. The intervention was a 10-week smoking cessation program that included a strong physician message and 12 group sessions using behavior modification and nicotine gum, plus either ipratropium or a placebo inhaler. At 5 years, 21.7% of special intervention participants had stopped smoking since study entry compared with 5.4% of usual care participants. After up to 14.5 years of follow-up, 731 patients died: 33% of lung cancer, 22% of cardiovascular disease, 7.8% of respiratory disease other than cancer, and 2.3% of unknown causes. All-cause mortality was significantly lower in the special intervention group than in the usual care group (8.83 per 1000 person-years vs. 10.38 per 1000 person-years; P = 0.03). The hazard ratio for mortality in the usual care group compared with the special intervention group was 1.18 (95% CI, 1.02 to 1.37). Differences in death rates for both lung cancer and cardiovascular disease were greater when death rates were analyzed by smoking habit. Results apply only to individuals with airway obstruction. Smoking cessation intervention programs can have a substantial effect on subsequent mortality, even when successful in a minority of participants.
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              COPD: balancing oxidants and antioxidants

              Chronic obstructive pulmonary disease (COPD) is one of the most common chronic illnesses in the world. The disease encompasses emphysema, chronic bronchitis, and small airway obstruction and can be caused by environmental exposures, primarily cigarette smoking. Since only a small subset of smokers develop COPD, it is believed that host factors interact with the environment to increase the propensity to develop disease. The major pathogenic factors causing disease include infection and inflammation, protease and antiprotease imbalance, and oxidative stress overwhelming antioxidant defenses. In this review, we will discuss the major environmental and host sources for oxidative stress; discuss how oxidative stress regulates chronic bronchitis; review the latest information on genetic predisposition to COPD, specifically focusing on oxidant/antioxidant imbalance; and review future antioxidant therapeutic options for COPD. The complexity of COPD will necessitate a multi-target therapeutic approach. It is likely that antioxidant supplementation and dietary antioxidants will have a place in these future combination therapies.
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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
                2017
                16 November 2017
                : 12
                : 3323-3328
                Affiliations
                [1 ]Department of Respiratory and Critical Care Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai
                [2 ]Department of Respiratory Medicine, Second Peoples Hospital of Nantong, Nantong, Jiangsu Province
                [3 ]Department of Tuberculosis, Anhui Chest Hospital, Hefei, Anhui Province, People’s Republic of China
                Author notes
                Correspondence: Jin-Fu Xu, Department of Respiratory and Critical Care Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 507 Zhengmin Road, Shanghai, 200433, People’s Republic of China, Tel +86 21 6511 5006, Fax +86 21 5566 3299, Email jfxucn@ 123456gmail.com
                Article
                copd-12-3323
                10.2147/COPD.S150243
                5695262
                © 2017 Bai 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.

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                Original Research

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