Intrapulmonary distribution of inhaled chrysotile and crocidolite asbestos: ultrastructural features.
Although all commercial types of asbestos can cause pulmonary fibrosis, little is known about ultrastructural differences in the evolution of pulmonary lesions induced by amphiboles and serpentines. The present study was designed to compare the histological and ultrastructural effects produced by chronic inhalation of either crocidolite (amphibole) or chrysotile (serpentine) asbestos in the rat. Animals, exposed by intermittent inhalation for 3 months, were killed after 2 to 16 months. When inhaled, both types of asbestos caused thickened alveolar duct bifurcations associated with macrophage aggregates. Crocidolite inhalation also produced subpleural collections of alveolar macrophages and lymphocytes. Electron microscopy revealed some similarities, but also distinct differences, in the pulmonary distribution of inhaled chrysotile and crocidolite. Whereas both asbestos varieties were identified within the pulmonary interstitium, only crocidolite was detected inside alveolar macrophages. Chrysotile fibres were seen infrequently within the vascular compartment. Microcalcifications were noted after chrysotile inhalation, but were never observed following crocidolite exposure. Both asbestos types induced slight pulmonary fibrosis. These findings indicate that crocidolite and chrysotile produce different pathogenetic features, although both are fibrogenic.
D000818:Animals; D001194:Asbestos / Q000032:analysis / Q000633:toxicity*; D017638:Asbestos, Crocidolite; D017632:Asbestos, Serpentine; D008168:Lung / Q000032:analysis / Q000648:ultrastructure*; D008264:Macrophages / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D011650:Pulmonary Alveoli / Q000648:ultrastructure; D011658:Pulmonary Fibrosis / Q000209:etiology / Q000473:pathology; D051381:Rats; D011916:Rats, Inbred F344
D017632:Asbestos, Serpentine; D017638:Asbestos, Crocidolite; D001194:Asbestos