The distribution of inhaled mineral fibers in the lung determines the site and severity of disease

Exploring the links between asbestos exposure and Mesothelioma is an ongoing practice

. One interesting study is called, "Persistence of long, thin chrysotile asbestos fibers in the lungs of rats." By P G Coin, V L Roggli, and A R Brody - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 - Environ Health Perspect. 1994 October; 102(Suppl 5): 197199. Here is an excerpt: "Abstract - The distribution of inhaled mineral fibers in the lung determines the site and severity of disease caused by the fibers. Some of our recent work has described the fate of inhaled asbestos fibers in rodents. After a brief inhalation exposure, asbestos fibers are deposited primarily at the first alveolar duct bifurcations, and fibrotic lesions are initiated. These sites of deposition occur as close to the visceral pleura as 220 micron. Several studies have suggested that short fibers are cleared from the lung more efficiently than long ones, and our data support this view. Our laboratory has shown that aerosolized chrysotile fibers longer than 16 microns can be deposited in the peripheral lung parenchyma of rats, and the measured clearance rate of these fibers is not significantly different from zero. Chrysotile, but no amphibole, fibers split longitudinally, so that the number of retained chrysotile fibers > or = 16 microns in length increases over time. We have not observed significant changes in chemical composition of chrysotile fibers up to 30 days post-deposition in the rat. Nor have we observed translocation of chrysotile fibers from the "central" regions of the lung toward the subpleural regions. However, 1 month after a single 3-hr exposure to chrysotile asbestos, the longest, most pathogenic fibers persist throughout the lung parenchyma. These retained fibers have the potential to cause disease in both parenchyma and pleura."

Another interesting study is called, "The Importance of Fiber Biopersistence and Lung Dose in Determining the Chronic Inhalation Effects of X607, RCF1, and Chrysotile Asbestos in Rats" by T. W. Hesterberga, 1, G. A. Harta, J. Chevalierb, W. C. Miillera, R. D. Hamiltona, J. Bauera and P. Thevenazc - Received 31 December 1997; Here is an excerpt: "Abstract - The chronic inhalation effects in rats of X607 (a rapidly dissolving synthetic vitreous fiber) were compared with those previously reported for RCF1 (a refractory ceramic synthetic vitreous fiber) and chrysotile asbestos. Of primary concern was the importance of biopersistence as a mechanism of fiber toxicity. Fischer rats were exposed to fiber aerosol by nose-only inhalation for 6 h/day, 5 days/week for 2 years. X607 and RCF1 aerosols were similar in concentration (200 fibers/cc) and average dimensions (approximately 20 1 m). Chrysotile aerosol was higher in concentration (10,600 fibers/cc) and an order of magnitude smaller in average dimensions. Lung fiber deposition after 6 h inhalation was greater for X607 than for RCF1. However, at later time points, fibers/lung (especially long fibers) were much lower for X607 than for RCF1, suggesting less biopersistence for X607. X607 was neither fibrogenic nor tumorigenic and induced only minimal lung cellularity that reversed after exposure was terminated. In contrast, RCF1 and chrysotile asbestos induced pulmonary fibrosis and thoracic neoplasms (chrysotile induced 32% more pulmonary neoplasms than RCF1). Lung deposition and fiber lengths did not explain the toxicologic differences between the three fibers. Fiber biodurability, including chemical and physical parameters, appears to be a major toxicologic determinant here. Chemical analysis of lung fibers revealed rapid leaching of X607 compared to RCF1. Inin vitrodissolution tests, X607 underwent rapid dissolution (kdis= 990 ng/cm2/h) and transverse fragmentation, RCF1 dissolved slowly (kdis= 6 ng/cm2/h) and did not fragment, and chrysotile dissolution was negligible (

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