ABSTRACT
Pulmonary emphysema was first described by Laennec in 1834 from observations of the cut surface of postmortem human lungs that had been air dried in inflation (1). The lesions were attributed to the compression of capillaries by overinflation of the lung, interference with blood flow, and atrophy of the tissue. This hypothesis persisted in major textbooks of pathology as late as 1940 (2), but it fell into disfavor as reports implicating infection and inflammation in the pathogenesis of emphysema began to appear. The concept that inflammation of the alveoli was an important cause of emphysema was advanced by McLean in Australia (3). Leopold and Gough (4) in the United Kingdom, and Andersen and Foraker in North America (5) in the 1950s and 1960s, but the theory was resisted, because the terminal bronchopneumonia complicated the histological picture in these postmortem studies. The fact that a cigarette smoke-induced inflammatory process is present in all smokers was established by subsequent studies based on careful postmortem examination of sudden deaths (6), examination of surgically resected lungs (7), and bronchoalveolar lavage (8). The current hypothesis is that a proteolytic imbalance within this inflammatory process
is responsible for the lung destruction in emphysema (9), but there is no clear agreement as to which cells are involved (10-12) and even less agreement as to which proteolytic enzyme is responsible for the lung destruction (10,13,14). The fact that all smokers develop lung inflammation (6-8) and only a fraction develop emphysema (15-17) is similarly unexplained.
