Antó J M, Vermeire P, Vestbo J, Sunyer J
Respiratory and Environmental Health Research Unit, Institut Municipal d'Investigació Mèdica, Barcelona, Spain.
Eur Respir J. 2001 May;17(5):982-94. doi: 10.1183/09031936.01.17509820.
Chronic obstructive pulmonary disease (COPD) is a leading cause of world-wide mortality and disability. On average approximately 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 approximately 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 FEVI 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.
慢性阻塞性肺疾病（COPD）是全球范围内导致死亡和残疾的主要原因。在工业化国家，平均约5%-15%的成年人通过肺功能测定被诊断患有COPD。1990年，COPD在全球综合死亡率和残疾原因中位列第十二位，但预计到2020年将升至第五位。COPD病程呈慢性且持久，其特征为一秒用力呼气容积（FEV1）不可逆下降、呼吸困难及其他呼吸道症状日益加重，以及健康状况逐渐恶化。诊断后10年生存率约为50%，超过三分之一的患者死于呼吸功能不全。空气污染等多种环境暴露会增加COPD患者的死亡风险。COPD的病因绝大多数由吸烟主导，尽管许多其他因素也可能起作用。特定的基因变异可能会增加对环境因素的易感性，不过对于哪些是相关基因却知之甚少。虽然有明确证据表明α-1抗胰蛋白酶起作用，但由相关变异导致的COPD比例仅为1%。被认为在COPD发病中起作用的表型特征包括性别（女性风险更高）、支气管反应性和特应性。吸烟与COPD之间的关系有确凿的因果证据，戒烟后FEV1下降趋于平稳。已发现被动吸烟与FEV1虽有小幅但具有统计学意义的下降有关。其他可能与COPD发病相关的危险因素包括职业、社会经济地位低、饮食以及可能早期生活中的一些环境暴露。尽管越来越多的证据表明氧疗、药物治疗和康复可能改善慢性阻塞性肺疾病的病程，但预防吸烟仍然是最关键的措施，不仅可预防慢性阻塞性肺疾病，还能阻止其发展。
