An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease

• Published in: American journal of respiratory and critical care medicine 2010-09, Vol.182 (5), p.693-718
• Main Authors: Eisner, Mark D, Anthonisen, Nicholas, Coultas, David, Kuenzli, Nino, Perez-Padilla, Rogelio, Postma, Dirkje, Romieu, Isabelle, Silverman, Edwin K, Balmes, John R
• Format: Article
• Language: English
• Subjects: Air Pollutants - adverse effects; Air pollution; Airway management; Asthma; Asthma - complications; Biomass; Bronchitis; Causality; Chronic obstructive pulmonary disease; Cigarettes; Committees; Diet; Diet - adverse effects; Environmental Exposure - adverse effects; Epidemiology; Genetic Predisposition to Disease; Health Policy; Humans; Indoor air quality; Mortality; Natural history; Outdoor air quality; Prevention; Public health; Pulmonary Disease, Chronic Obstructive - epidemiology; Pulmonary Disease, Chronic Obstructive - etiology; Pulmonary Disease, Chronic Obstructive - prevention & control; Risk Factors; Smoking; Smoking - adverse effects; Societies, Medical; Tobacco smoke; Tobacco Smoke Pollution - adverse effects; Tuberculosis; Tuberculosis, Pulmonary - complications; United States - epidemiology
• ISSN: 1073-449X; 1535-4970
• DOI: 10.1164/rccm.200811-1757st

Although cigarette smoking is the most important cause of chronic obstructive pulmonary disease (COPD), a substantial proportion of COPD cases cannot be explained by smoking alone. To evaluate the risk factors for COPD besides personal cigarette smoking. We constituted an ad hoc subcommittee of the American Thoracic Society Environmental and Occupational Health Assembly. An international group of members was invited, based on their scientific expertise in a specific risk factor for COPD. For each risk factor area, the committee reviewed the literature, summarized the evidence, and developed conclusions about the likelihood of it causing COPD. All conclusions were based on unanimous consensus. The population-attributable fraction for smoking as a cause of COPD ranged from 9.7 to 97.9%, but was less than 80% in most studies, indicating a substantial burden of disease attributable to nonsmoking risk factors. On the basis of our review, we concluded that specific genetic syndromes and occupational exposures were causally related to the development of COPD. Traffic and other outdoor pollution, secondhand smoke, biomass smoke, and dietary factors are associated with COPD, but sufficient criteria for causation were not met. Chronic asthma and tuberculosis are associated with irreversible loss of lung function, but there remains uncertainty about whether there are important phenotypic differences compared with COPD as it is typically encountered in clinical settings. In public health terms, a substantive burden of COPD is attributable to risk factors other than smoking. To prevent COPD-related disability and mortality, efforts must focus on prevention and cessation of exposure to smoking and these other, less well-recognized risk factors.