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• W2016494437 abstract "To the never-ending annoyance of physicians trying to convince their patients to quit smoking, nearly everyone knows of someone who “smoked cigarettes all their life” and never had any smoking-related health problems. In the past, the fact that not everyone who smoked cigarettes predictably acquired cigarette-related diseases undoubtedly helped perpetuate the notion that smoking had not been “proven” to cause cardiovascular or respiratory disease. Although there is a clear relationship to total life-time cigarette consumption, in the case of COPD, cross-sectional and longitudinal studies of regular cigarette smokers show only approximately 20% acquire significant airflow limitation.1Fletcher C Peto R The natural history of chronic airflow obstruction.BMJ. 1977; 1: 1645-1648Crossref PubMed Scopus (1773) Google Scholar2Jaen Diaz JI de Castro Mesa C Gontan G et al.Prevalence of chronic obstructive pulmonary disease and risk factors in smokers and ex-smokers.Arch Bronconeumol. 2003; 39: 554-558Crossref PubMed Google Scholar Potential explanations for why some cigarette smokers acquire chronic airways disease but not others include genetic differences in inflammatory and repair processes and/or modulation of these responses by infections or other environmental insults at prenatal, early childhood, or adult stages.3Calverley PMA Walker P Chronic obstructive pulmonary disease.Lancet. 2003; 362: 1053-1061Abstract Full Text Full Text PDF PubMed Scopus (228) Google Scholar In this issue of CHEST (see page 1706), Schulz et al report that compared to smokers without COPD, the bronchial epithelial cells from smokers with COPD respond to an inflammatory stimulus (tumor necrosis factor-α) with substantially greater expression and release of the neutrophil chemoattractants interleukin-8 and growth-related oncogene-α. These findings certainly fit with the hypothesis that airflow limitation develops in individuals primed to having a greater inflammatory response to the irritants in cigarette smoke. Whether this greater inflammatory phenotype is genetically determined or acquired due to other occupational or infectious exposures remains to be determined. There is no doubt that the scientific questions addressed by Schulz et al give us potentially valuable insights into the pathogenesis of cigarette-induced airways disease. However, what is the end product from these studies? As having cigarette-induced pulmonary disease is usually not sufficient to convince patients to stop smoking, being able to accurately predict smokers at high risk for airways disease is unlikely to be an effective deterrent. Such a test is therefore only likely to be used to justify continued smoking in patients with a low-risk phenotype, hardly a desirable outcome given its many other harmful effects. Even worse would be a pharmacologic agent that slowed or prevented the development of airways disease in smokers, almost certainly leading to even greater consumption of cigarettes. Where then may these insights into the causes of smoking-induced airways disease be useful? After cessation of smoking in patients with mild COPD, the rate of decline in FEV1 gradually falls back to the nonsmoking rate over several years.1Fletcher C Peto R The natural history of chronic airflow obstruction.BMJ. 1977; 1: 1645-1648Crossref PubMed Scopus (1773) Google Scholar4Burchfiel CM Marcus EB Curb JB et al.Effects of smoking and smoking cessation on longitudinal decline in pulmonary function.Am J Respir Crit Care Med. 1995; 151: 1778-1785Crossref PubMed Scopus (150) Google Scholar An intervention that maximized the benefits of stopping cigarette smoking by returning the rate of decline in FEV1 to normal more rapidly would certainly be of interest, especially in patients who already have symptomatic disease. It is also possible that such an intervention may have a role in other forms of inhalation lung injury. In patients who continue to smoke, there is evidence that episodes of infection accelerate the decline in FEV1.5Kanner RE Anthonisen NR Connett JE Lower respiratory illnesses promote FEV1decline in current smokers but not ex-smokers with mild chronic obstructive pulmonary disease: results from the Lung Health Study.Am J Respir Crit Care Med. 2001; 164: 358-364Crossref PubMed Scopus (514) Google Scholar If this more rapid decline is due to inflammatory mechanisms such as those demonstrated by Schulz et al, then again there is some potential for therapeutic agents at the time of an acute exacerbation of COPD to lessen the subsequent decline in lung function. In summary, continued research into the mechanisms of cigarette-induced airways disease has some merit and potential applications. However, we should not lose sight of the fact that the primary problem is the cigarette smoking habit itself, and that our primary efforts should be directed to stopping patients smoking, hopefully one day making the interesting work of Schulz et al no longer relevant." @default.
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• W2016494437 title "Do We Really Want To Know Why Only Some Smokers Get COPD?" @default.
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• W2016494437 doi "https://doi.org/10.1378/chest.125.5.1599" @default.
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