Epidemiology of chronic obstructive pulmonary disease

Abstract

Epidemiology of chronic obstructive pulmonary disease. J.M. Antó, P. Vermeire, J. Vestbo, J. Sunyer. #ERS Journals Ltd 2001. ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a leading cause of world-wide mortality and disability. On average y5-15% 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 y50% 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 a-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. Eur Respir J 2001; 17: 982-994.

Evaluation and Comparison of Respiratory Symptoms and Lung Capacities in Tile and Ceramic Factory Workers of Yazd

“…In all studies, a statistically significant relationship between cumulative respirable dust, loss of lung function, and bronchitis symptoms was found in both smokers and non-smokers (10). Reduced lung function has also been reported with exposure to low levels of concrete dust containing silica (1). A synergistic effect of smoking and silica dust exposure on COPD mortality was shown in South African gold miners (11).…”

“…Chronic obstructive pulmonary disease (COPD) is a major cause of chronic morbidity and mortality throughout the world, and further increase in the prevalence and mortality of the diseasecan be expected in the coming decades (1). Although cigarettesmoking is clearly the major risk factor for COPD, there is an increasing recognition that occupational exposure associated with coal mining, hard rock mining, tunnel mining and construction, concrete manufacturing (2), metal foundries, construction industry, glass or ceramics production, and granite or stone industries increase the likelihood of COPD (3).…”

Prevalence of Self-Reported Respiratory Symptoms, Asthma and Chronic Bronchitis in Slum Area of a Rapidly Developing Indian City

“…The epidemiology of asthma and COPD has consistently identified low socioeconomic status to be an important surrogate marker of the disease in world communities [1][2][3][4][5].…”

Dietary factors and lung function in the general population: wine and resveratrol intake

“…Furthermore, we calculated total resveratrol intake and assessed its association with the level and longitudinal decline of lung function that, if abnormally accelerated, can result in the development of COPD [18]. Additionally, we studied the role of SIRT1 genetic variations and their interaction with smoking in relation to lung function in two distinct, prospective cohorts, i.e.…”