Perspectives in Biology and Medicine

PULMONARY EMPHYSEMA: REDEFINITION AND PATHOGENESIS, A VIEW FROM THE EPIDEMIOLOGICAL ARMCHAIR CARLJ. MARIENFELD, M.D., M.P.H.* The results of a recent study of spontaneous pneumothorax among college students were consistent with the hypothesis that inhaled carbon soot particles containing adsorbed acids produce multiple small chemical cauterizations of the pulmonary alveolar walls [I]. Alveolar wall destruction has been shown by a number of investigators to lead variously to a localized emphysema, to the escape ofair into the lung parenchyma, and upon occasion to the development and subsequent rupture of subpleural blebs to produce spontaneous pneumothorax [2-4]. It should not then be surprising to expect that a lesser degree of localized emphysema would be found in a much larger number of individuals similarly exposed to the inhalation of such acid-laden soot [5, 6]. Relatively few of those who might develop such localized or generalized emphysema would thereafter be expected to develop an episode of spontaneous pneumothorax. Many more of those exposed would show a lesser degree of alveolar wall destruction and varying degrees of emphysema without the subsequent escape of air into the parenchyma. Few individuals would further be expected to develop the additional bronchiolar "flap valve" which has been considered to be necessary for the continuing buildup of air pressure and the formation and rupture of subpleural blebs [7]. It is therefore suggested that perhaps idiopathic spontaneous pneumothorax among the young and the most common types ofchronic pulmonary emphysema of the centriacinar, panacinar, and combined varieties in the older adult are dose-, time-, and host-related manifestations of the same underlying disease process and are caused by the same etiologic agent. A number ofepidemiologic similarities suggesting such an assumption have been described in both chronic obstructive lung disease and *Professor, Department of Community Health and Medical Practice and director of the Environmental Health Surveillance Center, University of Missouri, R.R. 4, Columbia, Missouri 65201. Perspectives in Biology and Medicine · Winter 1976 | 171 idiopathic spontaneous pneumothorax. Among these are the great preponderance of both conditions among males in comparison to the number in females [8, 9]. The incidence rates for both conditions are also higher in urban and smoke-polluted areas than in rural areas [1, 10]. Outdoor urban exposure, as well as strenuous labor or excessive activity in a smoke-polluted environment, appears also to predispose to both conditions [1, 11, 12]. The significance of cigarette smoking as a contributing cause for pulmonary emphysema has been amply documented [13, 14] and it has similarly been implicated in the causation of spontaneous pneumothorax [15]. Pathologically, the most commonly encountered form of pulmonary emphysema, that of the centrilobular or centriacinar type, and idiopathic spontaneous pneumothorax also share the unique property of involving predominantly the apices of the lung. Emphysema and emphysematous bullae are almost universally found at the time of surgical repair for spontaneous pneumothorax [16, 17]. As a corollary, subpleural blebs and pulmonary bullae, the usual precursors for spontaneous pneumothorax, are also often found when the pathologist examines the emphysematous lung [18]. An additional shared factor is the pathologic finding of amorphous carbon particulate matter in the earliest lesions of emphysema and in spontaneous pneumothorax at those points where the air has escaped to dissect through the pulmonary parenchyma [7, 19]. These epidemiologic and pathologic similarities lead to the suggestion that the usual etiology or the "sufficient" cause for both diseases is the inhalation of caustic particulate matter, primarily amorphous carbon soot produced by the incomplete combustion of fossil and other organic fuels. Such soot contains adsorbed and concentrated acids or other caustic compounds [20, 21]. These adsorbed caustic chemicals are thought to be subsequently released to initiate chemical "burns" beneath the point of impaction of the particulate upon the alveolar walls [22, 23]. The additional or the "necessary" cause in the pathogenesis of the two diseases involves repetitive or continuing pulmonary airway obstruction to the expiratory phase of respiration. The consequent hyperinflation serves to induce the pathognomonic tearing and disruption of the damaged acinar walls. A most important cause of such repetitive obstruction and intermittent hyperinflation is the cough. Epidemiologically the cough is most commonly due to the bronchial irritation caused by heavy cigarette smoking [24, 25...