EFFECTS OF CIGARETTE-SMOKE AND ASBESTOS ON AIRWAY, VASCULAR AND MESOTHELIAL CELL-PROLIFERATION

In order to determine whether exposure to both cigarette smoke and asb estos leads to enhanced cell proliferation, and whether pleura cell pr oliferation reflects the presence of fibres at or near the pleura, rat s were exposed to air (control), daily cigarette smoke, a single intra tracheal instillation of amosite asbestos, or a combination of smoke a nd asbestos. Dividing cells were labelled with bromodeoxyuridine (BrdU ) and animals were sacrificed at 1, 2, 7 or 14 days. Both cigarette sm oke and asbestos produced increases in the labelling index of small ai rway wail, epithelial cells and pulmonary artery cells. In the smalt a irways there was a brief marked positive synergistic interaction betwe en these two agents, but synergism was not seen in the vessels. Cigare tte smoke did not increase the labelling of mesothelial or submesothel ial cells, whereas asbestos caused a persisting increase in mesothelia l cell labelling. There was no correlation between the number of BrdU labelled mesothelial or submesothelial cells and the number of fibres touching the pleura, or located within 180 mu m of the pleura. We conc lude that the combination of cigarette smoke and asbestos exposure pro duces a complex set of interactions and has the potential to markedly increase cell proliferation in the parenchyma, an effect that may be i mportant in both fibrogenesis and carcinogenesis. In contrast to the d iminishing effects over time of a single dose of asbestos on cell prol iferation in the small airways and vessels, the same dose of asbestos leads to sustained mesothelial cell proliferation. However, the latter process does not correlate with local accumulation of asbestos fibres .