Search

Background: Smokers are more prone to develop chronic obstructive pulmonary disease (COPD) than non-smokers, but this finding comes from studies spanning 10 years or less. The aim of this study was to determine the 25 year absolute risk of developing COPD in men and women from the general population. Methods: As part of the Copenhagen City Heart Study, 8045 men and women aged 30–60 years with normal lung function at baseline were followed for 25 years. Lung function measurements were collected and mortality from COPD during the 25 year observation period was analysed. Results: The percentage of men with normal lung function ranged from 96% of never smokers to 59% of continuous smokers; for women the proportions were 91% and 69%, respectively. The 25 year incidence of moderate and severe COPD was 20.7% and 3.6%, respectively, with no apparent difference between men and women. Smoking cessation, especially early in the follow up period, decreased the risk of developing COPD substantially compared with continuous smoking. During the follow up period there were 2912 deaths, 109 of which were from COPD. 92% of the COPD deaths occurred in subjects who were current smokers at the beginning of the follow up period. Conclusion: The absolute risk of developing COPD among continuous smokers is at least 25%, which is larger than was previously estimated. [ABSTRACT FROM AUTHOR]

During the last decade several long term studies of interventions in patients with COPD have been published. This review analyses the potential of these interventions to alter the progression of the condition. The only treatment that has unequivocally been shown to reduce the rate of decline in FEV(1) is smoking cessation. Active psychological intervention in combination with pharmacotherapy is required. Other treatments may have an effect on the rate of decline in FEV(1) but this appears to be very small, at most. Several treatments affect the exacerbation rate and therefore might affect the progression of the disease. Further studies are warranted to examine this effect. [ABSTRACT FROM AUTHOR]

Background: Little is known about the effects of changes in smoking habits on the subsequent risk of chronic obstructive pulmonary disease (COPD). The aim of this study was to investigate the relationship between smoking cessation and reduction and admission to hospital for COPD in a general population sample.Methods: A total of 19,709 participants from three prospective population studies in Copenhagen were followed with record linkage for date of first hospital admission for COPD until 1998 (mean follow up 14 years). Heavy smokers (>/=15 cigarettes/day) who reduced their tobacco consumption by at least 50% between the two initial examinations without quitting and smokers who stopped smoking during this time were compared with continuous heavy smokers using a Cox proportional hazards model.Results: During the follow up period 1,260 subjects (741 men and 519 women) were admitted to hospital for COPD. After multivariate adjustment, quitting smoking was associated with a significant reduction in the risk of hospital admission. The relative hazard (HR) was 0.57 (95% confidence interval (CI) 0.33 to 0.99). Those who reduced smoking did not show a significantly lower risk of hospitalisation than continuing heavy smokers (HR 0.93 (95% CI 0.73 to 1.18)). Exclusion of events during the first 5 study years, detailed adjustment for lung function, or restriction of analyses to participants with impaired pulmonary function did not reverse the observed trend.Conclusions: Self-reported smoking cessation is associated with a reduction in the risk of COPD morbidity of approximately 40%; the benefit of smoking reduction is questionable. [ABSTRACT FROM AUTHOR]

Background: Smoking and airway lability which is expressed by histamine airway hyperresponsiveness, are known risk factors for development of respiratory symptoms. Smoking is also associated with increased mortality risks. We studied whether airway hyperresponsiveness is associated with increased mortality and whether this risk was independent of smoking and reduced lung function. Methods: We followed up 2008 inhabitants of the communities of Vlagtwedde, Vlaardingen, and Meppel (Netherlands), who had histamine challenge test data from 1964-72 for 30 years. Follow-up was 99% successful (29 patients lost to follow-up) with 1453 participants alive and 526 deaths (246 died from cardiovascular disease, 54 from lung cancer, and 21 from chronic obstructive pulmonary disease (COPD)). Findings: Mortality from COPD increased with more severe hyper-responsiveness relative risks of 3.83 (95% Cl 0.97-15.1), 4.40 (1.16-16.7), 4.78 1.27-18.0), 6.69 (1.71-26.1), and 15.8 (3.72-67.1) were associated with histamine thresholds of 32 g/l, 16 g/l, 8 g/l, 4 g/I, and 1 g/l, respectively compared with no hyperresponsiveness. These risks were adjusted for sex, age, smoking, lung function, body mass index, positive skin tests, eosinophilia, asthma, and city of residence. Interpretation: Increased histamine airway hyper-responsiveness predicts modality from COPD. Although this trend was more pronounced in smokers, an increasing proportion of COPD deaths with increasing hyper-responsiveness was also present among individuals who had never smoked. [ABSTRACT FROM AUTHOR]

The epidemiology of chronic obstructive pulmonary disease (COPD) has been dominated by one hypothesis stating that cigarette smoking and chronic bronchitis were the key to pathogenesis and another that asthma, chronic bronchitis, and even emphysema are related to different expressions of a primary airway abnormality. The first hypothesis was rejected in the late 1960s based on a longitudinal study of working men where only a fraction of smokers developed COPD and where development of COPD was independent of the absence or presence of chronic bronchitis. Chronic bronchitis in more advanced COPD was subsequently associated with a more rapid decline in lung function and more frequent exacerbations. The second hypothesis is more difficult to test but longitudinal studies have shown that the presence of bronchial hyperresponsiveness may predict the subjects who go on to develop COPD. This brief review attempts to reconcile these findings with the pathology found in the lung. [ABSTRACT FROM AUTHOR]