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Eur Respir J 2001; 17:982-994
Copyright ©ERS Journals Ltd 2001

Epidemiology of chronic obstructive pulmonary disease

J.M. Antó1,2, P. Vermeire3, J. Vestbo4 and J. Sunyer1

1 Respiratory and Environmental Health Research Unit, Institut Municipal d'Investigació Mèdica (IMIM), Barcelona, Spain, 2 Dept of Experimental and Health Sciences, Universitat Pompeu Fabra (UPF), Barcelona, Spain, 3 Dept of Pulmonary Medicine, University of Antwerp (UIA), Antwerp-Wilrijk, Belgium and 4 Dept of Respiratory Medicine, Hvidovre University Hospital, Denmark

CORRESPONDENCE: J.M. Antó, Respiratory and Environmental Health Research Unit, Institut Municipal d'Investigació Mèdica (IMIM), Carrer del Doctor Aiguader, 80, E-08003-Barcelona, Spain. Fax: 34 932213237

Keywords: {alpha}-1-antitrypsin deficiency, chronic obstructive pulmonary disease, epidemiology, passive smoking, smoking

Received: February 8, 2001
Accepted February 22, 2001

Abstract

Chronic obstructive pulmonary disease (COPD) is a leading cause of world-wide mortality and disability. On average ~5–15% of adults in industrialized countries have COPD defined by spirometry. In 1990, COPD was considered to be at the twelfth position world-wide as a cause of combined mortality and disability but is expected to become the fifth cause by the year 2020.

COPD has a chronic long-lasting course characterized by irreversible decline of forced expiratory volume in one second (FEV1), increasing presence of dyspnoea and other respiratory symptoms, and progressive deterioration of health status. After diagnosis the 10-yr survival rate is ~50% with more than one-third of patients dying due to respiratory insufficiency.

Several environmental exposures such as air pollution increase the risk of death in COPD patients. The aetiology of COPD is overwhelmingly dominated by smoking although many other factors could play a role. Particular genetic variants are likely to increase the susceptibility to environmental factors although little is known about which are the relevant genes. There is clear evidence about the role of the {alpha}-1-antitrypsin but the fraction of COPD attributable to the relevant variants is only 1%. Phenotypic traits that are considered to play a role in the development of COPD include sex, with females being at a higher risk, bronchial responsiveness and atopy. There is strong causal evidence regarding the relationship between smoking and COPD with decline in FEV1 levelling off after smoking cessation. Passive smoking has been found to be associated with a small though statistically significant decline in FEV1. Other risk factors that are likely to be relevant in the development of COPD are occupation, low socioeconomic status, diet and possibly some environmental exposures in early life.

Although there is accumulating evidence that oxygen therapy, pharmacological treatment and rehabilitation may improve the course of chronic obstructive pulmonary disease, preventing smoking continues to be the most relevant measure, not only to prevent chronic obstructive pulmonary disease, but also to arrest its development.




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