Lung Injury And Disease Resulting From Asbestos Exposure
Asbestos dust exposure can result in the development of disease
. This fact has been a strong impetus for research. One interesting study involving the disease development in the lungs of rats is called, Hydroxyl radicals are formed in the rat lung after asbestos instillation in vivo. By Schapira RM, Ghio AJ, Effros RM, Morrisey J, Dawson CA, Hacker AD - Division of Pulmonary and Critical Care Medicine, Medical College of Wisconsin, Milwaukee - Am J Respir Cell Mol Biol. 1994 May;10(5):573-9. Here is an excerpt: The hydroxyl radical (.OH) has been implicated as a cause of lung injury following asbestos exposure. However, despite in vitro evidence associating asbestos with .OH production, there has been no demonstration of such generation in vivo.We tested the hypothesis that .OH is formed in the lungs of rats exposed to asbestos in vivo by using salicylate as a free radical trap. Asbestos was instilled intratracheally, and control rats were sham-exposed. Six to seven days after exposure, the rats were given salicylate, the lungs were isolated, and salicylate hydroxylation products (2,3- and 2,5-dihydroxybenzoic acid), reflecting .OH production, were measured. There was significantly more 2,3-dihydroxybenzoic acid in asbestos-exposed lungs compared with control lungs (2.32 +/- 0.360 nmol/lung versus 0.292 +/- 0.125, respectively, P < 0.001) and 2,5-dihydroxybenzoic acid (9.69 +/- 1.65 nmol/lung versus 2.63 +/- 0.274, respectively, P < 0.001). To demonstrate that the dihydroxybenzoic acid was actually formed in the lungs, the lungs from asbestos-exposed and control rats were isolated and perfused with either salicylate or 2,3-dihydroxybenzoic acid. In the lungs perfused with salicylate, 2,3- and 2,5-dihydroxybenzoic acids were detectable only in asbestos-exposed lungs. In the isolated lungs perfused with 2,3-dihydroxybenzoic acid, there was no significant difference in 2,3-dihydroxybenzoic acid between asbestos-exposed and control lungs. We conclude that asbestos stimulates .OH production in lungs in vivo.
Another interesting article is called, The consequences of exposure to asbestos dust in a wartime gas-mask factory. By Jones JS, Smith PG, Pooley FD, Berry G, Sawle GW, Madeley RJ, Wignall BK, Aggarwal A - IARC Sci Publ. 1980;(30):637-53. Here is an excerpt: This further study of wartime gas-mask workers who were exposed to asbestos dust has shown that among those who worked with crocidolite there is a considerable excess of cases of mesothelioma, a more modest excess of bronchial carcinoma, but no excess of any other type of malignant disease. A dose-response relationship is established in the mesothelioma and bronchial carcinoma patients. It is not possible to base any conclusions on the limited data available for the small number of people exposed to chrysotile for a maximum period of five months. We believe that the identification and measurement of fibres in autoptic lung tissue from patients with accurately known occupational histories of asbestos dust exposure is useful, and a similar study on a population exclusively exposed to chrysotile would be of considerable interest.
A third article worth looking at is called, Predictions of mortality from mesothelial tumours in asbestos factory workers. By M L Newhouse, G Berry - Br J Ind Med 1976;33:147-151. Here is an excerpt: Abstract - Using the accumulated data on deaths from mesothelial tumours among cohorts of male and female factory workers at a London asbestos textile factory, the mortality from this cause up to the year 2000 AD has been predicted. The limitations of the methods used are pointed out, but it is estimated that for men the mortality due to mesothelial tumours will be between 7% and 11% of the total mortality and somewhat higher for women. The highest number of deaths from mesothelial tumours will occur during the 1980s, thereafter the numbers will decline because of the decreasing size of the cohort resulting from general mortality.
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