Pulmonary fibrogenesis after three consecutive inhalation exposures to chrysotile asbestos
| Autor: | Victor L. Roggli, Alvaro Osornio-Vargas, Arnold R. Brody, P G Coin |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Pulmonary and Respiratory Medicine
Male Pathology medicine.medical_specialty Asbestos Serpentine Pulmonary Fibrosis Critical Care and Intensive Care Medicine medicine.disease_cause Asbestos Rats Sprague-Dawley Fibrosis Pulmonary fibrosis Chrysotile Administration Inhalation Macrophages Alveolar medicine Animals Inhalation exposure Lung Inhalation Dose-Response Relationship Drug business.industry Respiratory disease DNA medicine.disease Rats medicine.anatomical_structure business |
| Zdroj: | American journal of respiratory and critical care medicine. 154(5) |
| ISSN: | 1073-449X |
| Popis: | Previously, this laboratory developed a model of asbestos-induced pulmonary fibrogenesis in rats and mice after a brief (1 to 3-h) inhalation exposure. However, typical human environmental exposures would be repeated, although at lower concentrations than those used in our animal model. Here we have extended this model to encompass repeated exposures and consequent long-term effects. Groups of rats were exposed to chrysotile aerosol (10 mg/m3) for 3- to 5-h periods over 3 consecutive days. Lung fiber burden and pathologic features were studied for as long as 6 mo after exposure. We found that many of the longest (> or = 8 microm) fibers were retained in the lung for at least 6 mo, whereas shorter fibers were cleared more rapidly. The three exposures to chrysotile caused a large increase in DNA synthesis in the epithelium of terminal bronchioles and more proximal airways. When compared with a single exposure, the triple exposure caused an enhanced inflammatory response as well as a prolonged period of increased DNA synthesis in the proximal alveolar region. Hyperplastic, fibrotic lesions subsequently developed in the same region and persisted for at least 6 mo after exposure. These findings will be valuable in directing future studies of the mechanisms of pulmonary fibrosis in this model. |
| Databáze: | OpenAIRE |
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