Inhalation of chrysotile asbestos induces rapid cellular proliferation in small pulmonary vessels of mice and rats.

Asbestos inhalation in mice and rats causes a rapid proliferative response in epithelial and interstitial cells, followed by the development of an interstitial lesion at the first alveolar duct bifurcations where fiber deposition and alveolar macrophage accumulation occur. Here we report that endothelial and smooth muscle cells of arterioles and venules near the bifurcations incorporated significantly increased levels of 3H-TdR 19 to 72 hours after chrysotile exposure. As many as 28% of the vessels had labeled cells 31 hours after exposure. No labeled cells were observed in vessels from sham-exposed or iron-exposed controls. This proliferative response resulted in a doubling of both the number of smooth muscle cells and the thickness of the smooth muscle cell layer, determined by ultrastructural morphometry 1 month after exposure. The fact that a variety of cell types incorporates 3H-TdR so rapidly after asbestos inhalation leads us to speculate that the response involves the release of diffusible growth factors.