© 2007 American Thoracic Society
Does Regular Physical Activity Reduce Lung Function Decline and COPD Risk among Smokers?From the Authors:We thank Dr. Singh for his letter commenting on our recent article (1). He argues that there is important variability in the inflammatory response to smoking among smokers, as well as in the level of disability among patients with chronic obstructive pulmonary disease (COPD), which could be explained by genetic polymorphisms. Although we agree, we do not think that these circumstances could reduce the validity of our findings. The presence of variability in the physical activity level or in the inflammatory response, irrespective of the origin of such variability, likely results in an underestimation of the associations under study, and thus in an observed effect of physical activity on COPD risk that is smaller than it really is (2). Dr. Singh adduces that an exaggerated inflammatory response is not the only mechanism implicated in COPD pathogenesis and that the lack of effect in former smokers puts the hypothesis into question. We were also surprised with the results for former smokers. A stratified analysis showed that the effect of physical activity in the subgroup of former smokers who had quit more recently was similar to the observed effects in current smokers (recent quitters with moderate to high physical activity improved lung function decline by gaining 4 ml/yr of FEV1 and 5 ml/yr of FVC, as compared with the low physical activity group), supporting the inflammation hypothesis. Unfortunately, sample size did not allow for a deeper analysis. Whether inflammation is the only or the main mechanism for the reported associations should be tested in further mechanistic studies. We agree with the current view of COPD as a multicausal disease, with the possibility of interaction among its several risk factors (3). There is evidence that smoking is the main risk factor for COPD, but other environmental exposures (air pollution, infections, or socioeconomic status) or host factors (genes, airway hyperresponsiveness, or lung growth) have been independently related to an increased risk of COPD. Manual workers fulfill several of these risk factors, and the high prevalence of chronic bronchitis in the Himalayas has been attributed to high domestic smoke exposure (4). The role of diet as a risk factor for COPD is not clear as yet, although its association with lung function decline is strongly suggested in several population-based studies (5). We feel that a residual confounding by diet, which could remove the association between physical activity and COPD risk, is very unlikely, given that adjustment for most known risk factors of COPD only slightly changed the magnitude of the estimates. Since we are also concerned with the role of diet in COPD, it will be explored, together with the role of other closely related factors, such as physical activity, in the ongoing Phenotype and Course of COPD (PAC-COPD) study (6). Our present findings allow the addition of physical activity to the list of risk factors of COPD, which is important given the possibility of individual modification of this risk factor.
Institut Municipal d'Investigació Mèdica, Barcelona, Spain
Bispebjerg University Hospital, Copenhagen, Denmark and Hvidovre University Hospital, Hvidovre, Denmark
Institut Municipal d'Investigació Mèdica, Barcelona, Spain
Bispebjerg University Hospital, Copenhagen, Denmark
Institut Municipal d'Investigació Mèdica and Universitat Pompeu Fabra, Barcelona, Spain FOOTNOTES Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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