Although you cannot estimate with complete certainty the affect asbestos exposure will have on the human body, you can say with a reasonable degree of certainty that past exposure to asbestos is a significant factor in the development of lung cancer and mesothelioma. There is a large body of work that has studies this subject matter very closely. On study is called, “Deposition and clearance of chrysotile asbestos.” By Churg A. - Ann Occup Hyg. 1994 Aug;38(4):625-33, 424-5. Below is an excerpt:
“Studies of human lungs indicate that, for virtually all types of exposure, the relative proportion of amphibole asbestos retained in the lung far exceeds the proportion in the original dust and, conversely, the relative proportion of chrysotile is far less than that in the original dust. Although amphiboles appear to accumulate in lung in proportion to exposure and chrysotile does not, failure of chrysotile deposition is probably not the reason for the disproportionate retention of amphibole fibres. The available data suggest that chrysotile is deposited in the parenchyma but is cleared extremely rapidly, with the vast bulk of fibres removed from human lungs within weeks to months after inhalation; by comparison, amphibole clearance half-lives are of the order of years to decades. The mechanisms of preferential chrysotile clearance remain uncertain, but fragmentation of chrysotile into short fibres, possibly accompanied by extremely rapid dissolution of such fibres, appears to be important in this process. Chrysotile fibres do penetrate to the periphery of the lung, so that differences in mesothelial pathogenicity of chrysotile and amphiboles in regard to mesothelioma are not caused by failure of chrysotile to reach the pleura. The theory that the tremolite contaminant rather than the chrysotile itself is the cause of 'chrysotile-induced' disease (especially mesothelioma) is consistent with the available human data, but the contrary ideas that disease is caused either by the total transient burden of inhaled chrysotile fibres or by a small, sequestered, long-retained fraction of chrysotile fibres still need to be excluded.”
Another interesting study is called, “Interaction of crocidolite asbestos with hamster respiratory mucosa in organ culture” by Mossman BT, Kessler JB, Ley BW, and Craighead JE. - Lab Invest. 1977 Feb;36(2):131-9. Here is an excerpt:
“Organ cultures of hamster trachea were used to study the effects of crocidolite asbestos on the respiratroy epithelium and the uptake of asbestos by cells of the mucosa. International Union Against Cancer (U.I.C.C.) crocidolite was suspended in medium over a range of concentrations and precipitated on the epithelial surface for 1 hour. At intervals during the ensuing 4 weeks, morphologic changes were documented by light, scanning electron, and transmission electron microscopy. Cytotoxic alterations in differentiated mucosal cells appeared to relate to the amount of crocidolite added to the cultures. Necrosis and desquamation of surface cells were accompanied by basal cell hyperplasia. These proliferating cells phagocytosed the dust and incorporated it into lysosomes. Crocidolite was also found interposed between cells of the hyperplastic basal cell layer. Transport of asbestos particles to the submucosa and uptake by mesenchymal cells was apparent after 1 week.”
“Studies of human lungs indicate that, for virtually all types of exposure, the relative proportion of amphibole asbestos retained in the lung far exceeds the proportion in the original dust and, conversely, the relative proportion of chrysotile is far less than that in the original dust. Although amphiboles appear to accumulate in lung in proportion to exposure and chrysotile does not, failure of chrysotile deposition is probably not the reason for the disproportionate retention of amphibole fibres. The available data suggest that chrysotile is deposited in the parenchyma but is cleared extremely rapidly, with the vast bulk of fibres removed from human lungs within weeks to months after inhalation; by comparison, amphibole clearance half-lives are of the order of years to decades. The mechanisms of preferential chrysotile clearance remain uncertain, but fragmentation of chrysotile into short fibres, possibly accompanied by extremely rapid dissolution of such fibres, appears to be important in this process. Chrysotile fibres do penetrate to the periphery of the lung, so that differences in mesothelial pathogenicity of chrysotile and amphiboles in regard to mesothelioma are not caused by failure of chrysotile to reach the pleura. The theory that the tremolite contaminant rather than the chrysotile itself is the cause of 'chrysotile-induced' disease (especially mesothelioma) is consistent with the available human data, but the contrary ideas that disease is caused either by the total transient burden of inhaled chrysotile fibres or by a small, sequestered, long-retained fraction of chrysotile fibres still need to be excluded.”
Another interesting study is called, “Interaction of crocidolite asbestos with hamster respiratory mucosa in organ culture” by Mossman BT, Kessler JB, Ley BW, and Craighead JE. - Lab Invest. 1977 Feb;36(2):131-9. Here is an excerpt:
“Organ cultures of hamster trachea were used to study the effects of crocidolite asbestos on the respiratroy epithelium and the uptake of asbestos by cells of the mucosa. International Union Against Cancer (U.I.C.C.) crocidolite was suspended in medium over a range of concentrations and precipitated on the epithelial surface for 1 hour. At intervals during the ensuing 4 weeks, morphologic changes were documented by light, scanning electron, and transmission electron microscopy. Cytotoxic alterations in differentiated mucosal cells appeared to relate to the amount of crocidolite added to the cultures. Necrosis and desquamation of surface cells were accompanied by basal cell hyperplasia. These proliferating cells phagocytosed the dust and incorporated it into lysosomes. Crocidolite was also found interposed between cells of the hyperplastic basal cell layer. Transport of asbestos particles to the submucosa and uptake by mesenchymal cells was apparent after 1 week.”
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