Inflammation asbestos

Confronted with a chemical substance or group of compounds the reader has to consider the four potential categories of risk - inflammability, instability, toxicity and dangerous reactions resulting from contact with other substances and materiais. But procedure does not only relate to chemical substances. It concerns other materials (eg asbestos), and modes of operation and introduces most often a manipuiator . These processes occur in an environment which also can have significant role. 

Rola-Pleszczynski, M., Gouin, S. and Begin, R. (1984). Asbestos-induced lung inflammation. Inflammation 8, 53-62. 

Donaldson, K. et al. (2010) Asbestos, carbon nanotubes and the pleural mesothelium a review of the hypothesis regarding the role of long fibre retention in the parietal pleura, inflammation and mesothelioma. Particle and Fibre Toxicology, 7, 5. Hirsch, A. (2010) The era of carbon allotropes. Nat. Mater., 9 (11), 868-871. Tasis, D. et al. (2006) Chemistry of carbon nanotubes. Chemical Reviews, 106 (3), 1105-36. 

Pleural effusions, fluid occurring between the parietal pleura and the visceral pleura, which is often transient and quickly absorbed, may or may not be induced by exposure to asbestos they are therefore also not strictly a part of asbestosis but can be associated as a symptom. Other symptoms include pleurisy (inflammation of the pleura), pain, and breathlessness. 

Chemicals, which cause repeated inflammation (e.g., asbestos), could lead to increased numbers of mutations. Indeed, DNA in inflamed tissue has been shown to have more 8-oxo-dG (Fig. 6.41) than normal tissue. 

Other Cell-Mediated Mechanisms. In addition to the release of active oxygen species, alveolar macrophages and other cells, including pleural mesothelial and lung cells, release a number of cellular factors in response to asbestos exposure. These factors are mediators of a number of cellular reactions including inflammation, macrophage recruitment and cell proliferation (for reviews, see Driscoll et al. 

The vast majority of experimental studies of asbestos have been performed in rodent model systems. Results from inhalation studies indicate that rats are suitable qualitative models for asbestos-induced pulmonary diseases, demonstrating chronic inflammation, pulmonary fibrosis (see Section 3.2.1.2), lung cancer (see Section 3.2.1.8), and mesothelioma (see Section 3.2.1.8) following chronic asbestos exposure. Hamsters seem to be more sensitive than rats to mesothelioma development, but less sensitive to the development of pulmonary tumors (Warheit and Hartsky 1994). 

Animal experiments could be designed to determine whether there are age-related differences in pulmonary responses to inhaled asbestos fibers (e g., fibrosis, cell proliferation, gene expression, macrophage production of reactive chemicals). For example, adult rats have been shown to display, within 20 days, a range of dose-related changes in pulmonary inflammation indices, increases in pulmonary cell proliferation. 

Corsini E, Luster MI, Mahler J, et al. 1994. A protective role for T lymphocytes in asbestos-induced pulmonary inflammation and collagen deposition. Am J Respir Cell Mol Biol 11 531-539. 

Donaldson K, Brown GM, Brown DM, et al. 1989. Inflammation generating potential of long and short fibre amosite asbestos samples. Br J Ind Med 46 271-276. 

Ishihara Y, Kohyama N, Kagawa J. 1998. Contribution of human pulmonary macrophage-derived cytokines to asbestos-induced lung inflammation and fibrosis. Inhal Toxicol 10 205-225. 

Kamp DW, Israbian VA, Yeldandi AV, et al. 1995b. Phytic acid, an iron chelator, attenuates pulmonary inflammation and fibrosis in rats after intratracheal instillation of asbestos. Toxicol Pathol 23 689-695. 

Quinlan TR, Berube KA, Marsh JP, et al. 1995. Patterns of inflammation, cell proliferation, and related gene expression in lung after inhalation of chrysotile asbestos. Am J Pathol 147 728-739. 

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