CIFEEST eddorials Chronic Bronchitis

CHEST / 89 / 3 / MARCH, 1986 321 Oxidant Damage by Leukocytes T he pathogenesis of chronic bronchitis remains poorly understood. Particularly significant is our lack of understanding of why only a minority of patients with “simple” chronic bronchitis progress to the advanced form of the disease with chronic airflow obstruction. Much of our knowledge of this disease is derived from morphologic studies of cigarette smokers detailing the hypersecretory changes in the airway epithelium.’2 Similar changes, including an increased bronchial gland/wall ratio and increased numbers of secretory cells in the surface epithelium, have been produced in animals by exposure to tobacco smoke, NO2, ozone, and SO2.2A fundamental concept in each of these studies is that the hypersecretory changes occur directly in response to a noxious agent or stimulus. While this concept may explain the mucous hypersecretion, it may not explain why only a portion of chronic bronchitis patients develop chronic airflow obstruction. Significant obstructive disease occurs only when there has been extensive damage to the bronchiolar compartment of the lung.3’4 Although mucous hypersecretion with recurrent cycles of obstruction and infection has been the presumed mechanism for bronchiolar damage, it is likely that other factors are involved. Host inflammatory processes activated within the tracheobronchial tree may be one factor contributing to disease progression in chronic bronchitis patients. In this context, large airway inflammatory changes, including leukocytes in the bronchial walls5 and increases in serum immunoglobulin in bronchial secretions,6 have been noted in humans. Although unproven, it has been assumed that these inflammatory changes in smokers occur in response to chronic colonization and infection of the large airways by infectious agents. However, infection almost certainly does not explain the prominent inflammation, or “bronchiolitis,” that occurs in the small airways of young cigarette smokers. Niewoehner et a17 have shown that the initial morphologic lesion in smokers is a respiratory bronchiolitis that is characterized by a marked accumulation of pigmented alveolar macrophages. Consistent with this observation, bronchoalveolar lavage studies of young smokers have also VOLUME 89 / NUMBER 3 / MARCH, 1986