ABSTRACT
The cigarette smoking habit is the single most important risk factor for developing COPD. This habit produces lung inflammation in all smokers (1), and this inflammatory process underlies the pathogenesis of the chronic bronchitis (2), airways obstruction (3,4), emphysematous destruction (5), and the early vascular lesions associated with pulmonary hypertension in COPD (6-8). However, there is not a tight correlation between the total accumulated dose of smoking and disease, and large series of cases such as that shown in Figure 1 have established that smoking accounts for only a small percentage of the variance in the decline in lung function. This suggests that other factors must add to the risk of smoking, and epidemiological studies have identified age, gender, environmental pollution, occupation, socioeconomic status, birth weight, recurrent infections, allergy, and genetic constitution as factors that independently increase the risk of developing COPD (9). The purpose of this chapter is to review the pathology of the lung lesions that contribute to the natural history of COPD and the changes that occur during acute exacerbations that periodically complicate this condition.
