To determine the effect of smoking cessation on the number and type of inflammatory cells in the walls of the small airways, we examined the lungs of 13 lifetime nonsmokers, 25 patients who had stopped smoking for at least 6 months, and 49 current smokers. We found that, compared to nonsmokers, both ex-smokers and current smokers had significantly increased numbers of total inflammatory cells and polymorphonuclear leukocytes in the walls of the membranous, but not the respiratory bronchioles. These differences were found even when there was no emphysema present in the gross lung specimen, and current and ex-smokers were matched with the nonsmokers for age. The current and ex-smokers had similar numbers and types of inflammatory cells in the airway wall, and in both current and ex-smokers there was no difference in inflammatory cell number or type when the groups were subdivided based on emphysema score less than or greater than 5. Analysis of peribronchiolar alveolar attachments showed an increase in percentage of alveoli destroyed associated with an increased interalveolar distance in both the current and ex-smokers, which did not change with the presence of emphysema. Pulmonary function was similar in the current and ex-smokers, and the group with emphysema showed greater functional abnormalities compared to the group with little or no emphysema. We conclude that the cigarette smoking habit induces a stereotypical inflammatory response in the small airways. This inflammatory response does not abate after smoking cessation, and in this cross-sectional study, appears to be independent of the presence or absence of emphysema, but related to destruction of the peribronchiolar alveolar attachments.

We have previously shown that intratracheally instilled silica (quartz) produces both morphologic evidence of emphysema and small-airway changes, and functional evidence of airflow obstruction. To further define the nature of the airflow-associated lesions induced by silica, we compared silica-exposed rats to rats given intratracheal elastase, a standard model of emphysema. Both silica and elastase produced increases in RV and FRC along with upward shifts in the pressure-volume curves. Flows were decreased in both groups, but the changes were more severe in the silica-treated animals. Morphologically, the two treatments produced about the same degree of airspace enlargement, present in both alveoli and alveolar ducts, as well as decreased alveolar and alveolar duct surface area/unit lung volume. Elastic fiber length per unit volume was also decreased in both groups. However, small-airway walls were markedly thickened in the silica-treated compared to the elastase-treated group. We conclude that, in the parenchyma, both these agents produce morphologically similar airspace dilatation, and both induce destruction of elastic fibers. These lesions appear to correlate with abnormalities in the pressure-volume curve. Flow reductions seem to be primarily correlated with changes in small-airway wall structure.

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