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The effects of inhaled silica and chrysotile on the elastic properties of rat lungs; physiological, physical and biochemical studies of lung surfactant.

TLDR
Both the surface tension and biochemical estimations on a control group of rats suggest that there is an increase in the amount of surfactant in the lungs up to about 12 months of age.
Abstract
When rats breathed air containing approximately 70 mg m-3 of respirable crystalline silica 7 h daily for 10 days (2000 mg m-3 h) the surface tension forces of the alveolar lining film were reduced This was shown both by surface tension measurements on lung extracts and by pressure-volume studies with air and saline filling of excised lungs Larger quantities of inhaled silica produced similar effects Chrysotile inhalation caused an even more marked decrease in the surface tension forces In the chrysotile studies these findings were supported by biochemical estimations of the quantity of surfactant in the lungs, which was increased 10-fold by an inhalation of 6500 mg m-3 h Electron microscopy showed an increased number of the type II alveolar cells which produce surfactant and of free phospholipid lattices in the air spaces of the lungs of rats exposed to chrysotile and silica Both the surface tension and biochemical estimations on a control group of rats suggest that there is an increase in the amount of surfactant in the lungs up to about 12 months of age

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Journal Article

Fiber localization and its relationship to lung reaction in rats after chronic inhalation of chrysotile asbestos.

TL;DR: Findings show that during exposure to asbestos fibers, macrophages and alveolar epithelial cells contain statistically significant amounts of asbestos and are associated with histologic changes indicating marked epithelial injury, and increased amounts of fibers are also localized in the lung interstitium with continued exposure, which is associated with a progressive interstitial fibrotic reaction.
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Pulmonary toxicology of silica, coal and asbestos.

TL;DR: Pulmonary fibrosis required a direct in vitro approach in which the products of the macrophage-particle interaction were utilized to provoke collagen formation by fibroblasts in a two-phase system, and application of the technique to coal dusts appears promising.
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Biochemical and cellular mechanisms of dust-induced lung fibrosis.

TL;DR: Final consideration is given to the step from fibrogenesis to fibrosis and it is suggested that this step may involve other tissue proteins apart from collagen and that the irreversible nature of fibrosis can be explained by the formation of strong intermolecular crosslinks between different proteins.
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Toxicology of Inhaled Materials

TL;DR: Monooxygenase activities in human lung and liver micro somes (values are means from 3-9 individual cases)
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Risk of occupational exposure to asbestos, silicon and arsenic on pulmonary disorders: Understanding the genetic-epigenetic interplay and future prospects

TL;DR: The role of molecular pathogenesis of occupational lung diseases based on the genetic variability and epigenetic alterations is addressed and the promising aspect of dietary interventions to counter toxic outcomes upon occupational exposure to asbestos, silicon or arsenic is highlighted.
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