Persistence of long, thin chrysotile asbestos fibers in the lungs of rats.

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 pm. 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 pm 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 not amphibole, fibers split longitudinally, so that the number of retained chrysotile fibers .16 pm 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. -Environ Health Perspect 102 (Suppl 5):197-199 (1994)

New Insight into Intrachromosomal Deletions Induced by Chrysotile in the gpt delta Transgenic Mutation Assay

“…It has been reported that fiber dimension, biopersistence, composition, surface reactivity, and physical durability are important criteria for the carcinogenicity of the fibers, indicating that carcinogenic mechanisms of asbestos are likely to be complex and involve multiple pathways (Bernstein et al 2003; Coin et al 1994). Various highly quantitative genotoxicity assays ranging from DNA strand breaks to gene mutations in rodent cells have been performed to estimate the carcinogenic potential of asbestos fibers (Lezon-Geyda et al 1996; Poser et al 2004).…”

In situ microscopic analysis of asbestos and synthetic vitreous fibers retained in hamster lungs following inhalation.

“…The health effects of exposure to airborne asbestos and synthetic fibers have been extensively studied, as reviewed by DeVuyst et al (1) and Hesterberg et al (2). The respiratory system's response to fibers depends greatly on fiber composition, fiber length, the sites of deposition, the tissue compartments through which fibers move, and the rates at which they are cleared (3,4). Such health effects also depend on the amount of fiber deposition in the respiratory system and the resulting fiber burden.…”

The toxicology of chrysotile-containing brake debris: implications for mesothelioma

“…The first step could be considered as being the longitudinal splitting of chrysotile fibers due to the breakage of weak bonds holding the chrysotile fibrils together. This leads to an initial increase in the long fiber number in the lung, a phenomenon that has been observed in several in vivo studies (Bellmann et al 1986;Roggli et al 1987;Coin et al 1992Coin et al , 1994. The second step is the rapid dissolution of magnesium from the chrysotile fibrils which derives from brucitic layer [Mg(OH) 2 ] which alternates between the silicate layers (Fubini 1997) within the fibers as shown in Figure 2.…”