THE PULMONARY MACROPHAGE POPULATION OF HUMAN SMOKERS

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Abstract
The lungs of human smokers contain many more pulmonary macrophages than the lungs of non-smokers, probably owing to both enhanced recruitment and diminished efflux; smokers' macrophages exhibit altered morphologic and functional characteristics. Phagocytosis, particularly of relatively indigestible paniculate matter, leads to enzyme release. The potential of cathepsins, particularly elastase and collagenase, to promote local lung damage in smokers is discussed. The enzyme aryl hydrocarbon hydroxylase may yet be of relevance to the epidemiology of human bronchial cancer and PAM levels of this enzyme are raised in smokers. Altered surfactant flux occurs in smokers and PAM play a part in this turnover. Although the analogy is strong, the relevance of pulmonary macrophages to the occupational lung diseases is as yet poorly understood, as is their role in any exacerbation of these dust diseases in tobacco smokers.