Chronic obstructive pulmonary disease: NHLBI Workshop on the Primary Prevention of Chronic Lung Diseases

Abstract

Chronic obstructive pulmonary disease (COPD) is a complex set of conditions with multiple risk factors, disease mechanisms, and clinical manifestations. These characteristics make primary prevention of COPD challenging. Semantic issues related to prevalent and incident disease (e.g., the use of specific cut points on a continuous range) should not derail development of primary prevention initiatives. Potential targets for COPD prevention occur along the spectrum of disease development. Understanding risk factors early in life, whether specific to COPD or not, allows for study of interventions to optimize lung function at birth and to prolong the lung function plateau, potentially reducing the development of COPD. It is necessary to identify noninvasive ways to screen for early COPD in those at risk before progression to clinically significant disease. Identification of specific COPD subgroups, such as individuals with chronic bronchitis, those with α1-antitrypsin deficiency, or early radiographic changes with normal spirometry, may offer specific opportunities for primary prevention. A better understanding of why COPD progresses despite smoking cessation is needed. Future research initiatives should also focus on identifying the underlying mechanisms and relevant interventions for nonsmokers with COPD, a currently poorly studied group. Ultimately, preventing the development of COPD will serve to reduce the tremendous burden of this chronic disease worldwide.

Figure 1.

Lung development and growth and chronic obstructive pulmonary disease (COPD) risk. Intrauterine events can compromise lung growth (dashed line). Events in childhood and adolescence can compromise lung growth (dotted line). Both of these can alter maximally attained lung function. The relationships between intrauterine development and growth and lung growth in childhood and adolescence are unknown, but could interact to further compromise maximally attained lung function. In most individuals, lung function generally remains at the maximally attained function achieved in young adulthood for 10 years or so, then gradually declines. Whether this is “normal” or represents the consequence of pathological processes is unknown. Shortened duration of the plateau of lung function will result in lower lung function with aging (solid lines). These lines are drawn starting from the same level to emphasize the effect of the shortened plateau. If a shortened plateau were related to alterations in maximally attained lung function, the risk for reduced lung function would be greater. FEV₁ = forced expiratory volume in 1 second.

Figure 2.

The progression of chronic obstructive pulmonary disease (COPD) is incompletely understood. COPD, characterized by reduced lung function, may develop through several natural histories. Theoretically, some individuals may lose lung function at an accelerated rate throughout life (curve A), some may progress like “normal” for some time, then enter a period of very accelerated loss of function (curve B), and some may have acute exacerbations that eventually compromise lung function (curve C) (33). These natural histories are not easily distinguishable when the disease is clinically apparent in the 50s or 60s. It is now recognized that some individuals with COPD may improve, at least modestly, but consistently, over several years (dashed line, curve D) (34). Graphic modified from Burrows (33), which was modified from Fletcher and Peto (35). FEV₁ = forced expiratory volume in 1 second.