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      Female smokers beyond the perimenopausal period are at increased risk of chronic obstructive pulmonary disease: a systematic review and meta-analysis

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          Abstract

          Background

          Recent reports indicate that over the next decade rates of chronic obstructive pulmonary disease (COPD) in women will exceed those in men in the western world, though in most jurisdictions, women continue to smoke less compared with men. Whether female adult smokers are biologically more susceptible to COPD is unknown. This study reviewed the available evidence to determine whether female adult smokers have a faster decline in forced expiratory volume in one second (FEV 1) compared with male adult smokers and whether age modifies the relationship between cigarette smoke and lung function decline.

          Methods

          A systematic review and a meta-analysis was performed of population-based cohort studies that had a follow-up period of at least 3 years, measured FEV 1 on at least two different time points, and presented FEV 1 data stratified by gender and smoking status in adults.

          Results

          Of the 646 potentially relevant articles, 11 studies met these criteria and were included in the analyses (N = 55 709 participants). There was heterogeneity in gender-related results across the studies. However, on average current smokers had a faster annual decline rate in FEV 1% predicted compared with never and former smokers. Female current smokers had with increasing age a significantly faster annual decline in FEV 1% predicted than male current smokers (linear regression analysis, R 2 = 0.56; p = 0.008). Age did not materially affect the rate of decline in FEV 1% predicted in male and female former and never smokers (p = 0.775 and p = 0.326, respectively).

          Conclusion

          As female smokers age, they appear to experience an accelerated decline in FEV 1% predicted compared with male smokers. Future research powered specifically on gender-related changes in lung function is needed to confirm these early findings.

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          Most cited references36

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          Alternative projections of mortality and disability by cause 1990–2020: Global Burden of Disease Study

          The Lancet, 349(9064), 1498-1504
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            The natural history of chronic airflow obstruction.

            A prospective epidemiological study of the early stages of the development of chronic obstructive pulmonary disease was performed on London working men. The findings showed that forced expiratory volume in one second (FEV1) falls gradually over a lifetime, but in most non-smokers and many smokers clinically significant airflow obstruction never develops. In susceptible people, however, smoking causes irreversible obstructive changes. If a susceptible smoker stops smoking he will not recover his lung function, but the average further rates of loss of FEV1 will revert to normal. Therefore, severe or fatal obstructive lung disease could be prevented by screening smokers' lung function in early middle age if those with reduced function could be induced to stop smoking. Infective processes and chronic mucus hypersecretion do not cause chronic airflow obstruction to progress more rapidly. There are thus two largely unrelated disease processes, chronic airflow obstruction and the hypersecretory disorder (including infective processes).
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              Chronic obstructive pulmonary disease: molecular and cellular mechanisms.

              Chronic obstructive pulmonary disease is a leading cause of death and disability, but has only recently been extensively explored from a cellular and molecular perspective. There is a chronic inflammation that leads to fixed narrowing of small airways and alveolar wall destruction (emphysema). This is characterised by increased numbers of alveolar macrophages, neutrophils and cytotoxic T-lymphocytes, and the release of multiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). A high level of oxidative stress may amplify this inflammation. There is also increased elastolysis and evidence for involvement of several elastolytic enzymes, including serine proteases, cathepsins and matrix metalloproteinases. The inflammation and proteolysis in chronic obstructive pulmonary disease is an amplification of the normal inflammatory response to cigarette smoke. This inflammation, in marked contrast to asthma, appears to be resistant to corticosteroids, prompting a search for novel anti-inflammatory therapies that may prevent the relentless progression of the disease.
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                Author and article information

                Journal
                Respir Res
                Respiratory Research
                BioMed Central
                1465-9921
                1465-993X
                2006
                29 March 2006
                : 7
                : 1
                : 52
                Affiliations
                [1 ]James Hogg iCAPTURE Center for Cardiovascular and Respiratory Research, University of British Columbia, Vancouver, B.C., Canada
                [2 ]Department of Medicine (Pulmonary Division), University of British Columbia, Vancouver, B.C., Canada
                [3 ]Department of Pulmonology, University Hospital, University of Groningen, Groningen, The Netherlands
                Article
                1465-9921-7-52
                10.1186/1465-9921-7-52
                1435894
                16571126
                06067315-d5d8-4ed9-8575-a34ec82c297e
                Copyright © 2006 Gan et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 January 2006
                : 29 March 2006
                Categories
                Research

                Respiratory medicine
                Respiratory medicine

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