5. How and/or why did the patient develop COPD?
In developed countries, the predominant risk factor for development of COPD is cigarette smoking. According to the National Health and Nutrition Examination Survey (NHANES), dust and fumes may also cause COPD. After smoking and other confounders are accounted for, a slightly increased incidence of COPD is seen in certain occupations, including construction, plastics manufacturing, and utility work.
Only about 5 percent of physician-diagnosed COPD occurs in non-smokers. COPD in non-smokers is more common in those with asthma and in older individuals.
A key question in the pathogenesis of COPD is why so many people with significant exposure to known causes are spared the disease. Studies clearly show an increase in macrophage-predominant inflammation in the alveolar spaces and terminal bronchioles of current smokers. However, only 20 percent or fewer of chronic smokers develop symptomatic COPD. The current theory is that environmental, developmental, and genetic risk factors combine to create susceptibility to enhanced lung inflammation and failure of defenses against lung destruction (Figure 1).
Normal lung function is maximal at eighteen to twenty years of age. Maximal lung function may be significantly decreased by environmental or genetic factors in some asymptomatic individuals. The normal, age-related decline in lung function may be accelerated by environmental toxins like cigarette smoke. Although smoking cessation alters the rate of decline, some former smokers and many older individuals will eventually experience a decline in lung function below that which defines obstructive lung disease. However, the risk of respiratory specific mortality remains low until significant loss of lung function occurs.
Variations in lung development, age-related decline in lung function, and exposure to noxious substances result in variable, age-dependent development of COPD. The nonmeasurability of genetic and environmental effects, along with an ability to estimate tobacco smoke exposure only roughly results in poor accuracy in predicting development of COPD in chronic smokers.
Individual differences in molecular pathogenic mechanisms of smoking-induced lung remodeling likely result in the variation of emphysematous versus airway predominant disease phenotype despite the same inciting cause.
Which individuals are at greatest risk of developing COPD?
Risk factors can be classified as environmental and genetic. The relative contribution of each in patients with COPD cannot be defined. Ideally, future studies will permit a directed therapeutic approach, based upon risk for disease progression.
Reposted with permission from Decision Support in Medicine, LLC.