EARLY EFFECTS OF SHORT-TIME CIGARETTE-SMOKING ON THE HUMAN LUNG - A STUDY OF BRONCHOALVEOLAR LAVAGE FLUIDS

We investigated the early effects of cigarette smoking in healthy subj ects by means of lung lavage, looking at markers of alveolar permeabil ity, the alveolar cell profile, the immunophenotyping of macrophages a nd lymphocytes, and the level and profile of surfactant phospholipids. Bronchoalveolar lavages (BAL) were performed in 33 healthy subjects [ 20 nonsmokers (nS), 13 moderate and short-time smokers (S)]. In the ac ellular supernatants we measured the markers of alveolar permeability (i.e., total proteins, albumin, albumin/urea), the alveolar epithelial lining fluid (AELF), the surfactant amounts and profile, and explored the blood lymphocytes by in vitro exposure. The cell pellet establish ed the alveolar formula and a membrane mapping of macrophages (LFA-1 a nd HLA-DRII expression) and lymphocytes (CD4, CD8, LFA-1, HLA-DRII exp ression). We found no significant increase of alveolar permeability in our smokers, but an increased alveolar cellularity (more than 3-fold vs nS, P < 0.05) evenly distributed between sub-populations except for an enhanced number of eosinophils in smokers (P < 0.05 vs nS). Smoker s' alveolar macrophages had an overloaded cytoplasm, a decreased perce ntage of antigen-handling cell expression (HLA DRII: P < 0.05 vs nS) a nd a low percentage of cell to cell adhesion molecule expression (LFA- 1: P < 0.05 vs nS). Smoking history and LFA-1 expression on alveolar m acrophages were interrelated. Smokers' alveolar lymphocyte subsets wer e more often T suppressor cells (CD8+) and had an increased percentage of antigen-presenting cell expression (HLA DRII: P < 0.05 vs nS). Smo kers' BAL fluid did not show the inhibitory control of phytohemaggluti nin-induced lymphocyte proliferation present in nonsmokers' fluids. Su rfactant phospholipid amounts were similar, hut phosohatidylethanolami ne was raised and the ratio of phosphatidylcholine to sphingomyelin de creased in smokers (P < 0.05 vs nS). We observed-specific cellular and biochemical alterations in the lung lavage of short-time smokers. Alv eolar macrophage and lymphocyte expression of LFA-1 and HLA-DRII molec ules was altered. Smokers' alveolar fluids lost the physiologic regula tory control of T mitogen-induced lymphocyte proliferation. Membrane p hospholipids released by cellular damage increased early in tobacco-ex posed lung fluids. This profile of alterations may be an early and sen sitive marker of smoking-induced lung damage.