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Exposure to High Levels of Asbestos Can be a Death Sentence

Mesothelioma is a consequence of exposure to asbestos fibers from a wide range of

products such as brake linings and clutch facings among auto mechanics. One interesting study is called, "Mitochondrial-derived free radicals mediate asbestos-induced alveolar epithelial cell apoptosis" by Vijayalakshmi Panduri,Sigmund A. Weitzman, Navdeep S. Chandel, and David W. Kamp Am J Physiol Lung Cell Mol Physiol 286: L1220-L1227, 2004. Here is an excerpt: "Asbestos causes pulmonary toxicity by mechanisms that in part involve reactive oxygen species (ROS). However, the precise source of ROS is unclear. We showed that asbestos induces alveolar epithelial cell (AEC) apoptosis by a mitochondrial-regulated death pathway. To determine whether mitochondrial-derived ROS are necessary for causing asbestos-induced AEC apoptosis, we utilized A549-o cells that lack mitochondrial DNA and a functional electron transport. As expected, antimycin, which induces an oxidative stress by blocking mitochondrial electron transport at complex III, increased dichlorofluoroscein (DCF) fluorescence in A549 cells but not in A549-o cells. Compared with A549 cells, o cells have less asbestos-induced ROS production, as assessed by DCF fluorescence, and reductions in total glutathione levels as well as less caspase-9 activation and apoptosis, as assessed by TdT-mediated dUTP nick end labeling staining and DNA fragmentation. A mitochondrial anion channel inhibitor that prevents ROS release from the mitochondria to the cytoplasm also blocked asbestos-induced A549 cell caspase-9 activation and apoptosis. Finally, a role for nonmitochondrial-derived ROS with exposure to high levels of asbestos (50 g/cm2) was suggested by our findings that an iron chelator (phytic acid or deferoxamine) or a free radical scavenger (sodium benzoate) provided additional protection against asbestos-induced caspase-9 activation and DNA fragmentation in o cells. We conclude that asbestos fibers affect mitochondrial DNA and functional electron transport, resulting in mitochondrial-derived ROS production that in turn mediates AEC apoptosis. Nonmitochondrial-associated ROS may also contribute to AEC apoptosis, particularly with high levels of asbestos exposure."

Another interesting study is called, "Malignant Mesothelioma and Asbestos Exposure among Auto Mechanics: Appraisal of Scientific Evidence" by Otto Wong - Applied Health Sciences, Inc. P.O. Box 2078, San Mateo, California, 94401 - Department of Epidemiology, Tulane University, New Orleans, Louisiana - Department of Community and Family Medicine, Chinese University of Hong Kong, Hong Kong - Regulatory Toxicology and Pharmacology Volume 34, Issue 2, October 2001, Pages 170-177. Here is an excerpt: "Abstract - In 1986 the U.S. Environmental Protection Agency (EPA) issued an official guideline on the prevention of asbestos disease among auto mechanics. In the EPA guideline, malignant mesothelioma was listed as a consequence of exposure to asbestos fibers from brake linings and clutch facings among auto mechanics. EPA formulated its 1986 opinion by relying solely on a few outdated case reports and not on epidemiologic studies. A review of the literature indicates that there are six epidemiologic studies providing relevant information on malignant mesothelioma among auto mechanics. Three of the six studies had already been published by 1986, the year in which EPA issued its guideline. The results of the six studies were remarkably consistent in that all six studies reported no increased risk of malignant mesothelioma among auto mechanics. The relative risks reported in the six studies ranged from 0.62 to 1.00. Based on a meta-analysis of the combined data of all six studies consisting of approximately 1500 malignant mesothelioma cases, the mesothelioma relative risk for auto mechanics is 0.90 (95% confidence interval 0.661.23). An application of Hill's causation criteria to epidemiologic data of malignant mesothelioma among auto mechanics clearly demonstrates that auto mechanics do not have an increased risk of malignant mesothelioma as a result of exposure to asbestos fibers from brake linings and clutch facings. However, in spite of the scientific evidence, EPA has not modified or revised its 1986 guideline. Occupational regulatory policies and guidelines, when based on proper scientific evidence, are invaluable and can prevent avoidable diseases in workers or other exposed individuals in the general public. On the other hand, it is the regulators' responsibility to develop, modify, and revise policies and guidelines in accordance with the most relevant and the latest scientific data. In this instance EPA as a regulator has not fulfilled its responsibility of providing the most accurate and up-to-date information to the workers or the general public."

Another interesting study is called, "Asbestos-related bilateral diffuse pleural thickening: natural history of radiographic and lung function abnormalities" by DH Yates, K Browne, PN Stidolph and E Neville - Am. J. Respir. Crit. Care Med., Vol 153, No. 1, Jan 1996, 301-306. Here is an excerpt: "Sixty-four subjects with asbestos-related diffuse pleural thickening attending the London Medical Boarding Centre for Respiratory Diseases (formerly, the Central Pneumoconiosis Panel) were studied to investigate symptomatology, lung function, and radiographic change over an average period of 8 to 9 yr. Chest pain was a common symptom, occurring in over half of the subjects. Approximately one-third of the subjects had a history of pleurisy or pleural effusion. Full long function, available in all cases, showed a highly significant decrement (p < 0.001) compared with predicted values in all variables except gas transfer coefficient (Kco) at initial presentation, consistent with a restrictive ventilatory defect. Longitudinal lung function, available over a mean period of 8.9 yr in 36 subjects, showed a significant decrement above that predicted in FEV1 and FVC only (p < 0.05). Decreases in other parameters were observed, although statistical significance was not achieved. Radiographic score increased with time but there was no correlation between change in lung function and increasing radiographic score, probably reflecting the initial severity of the disease in subjects studied. These observations confirm an initial decrement in lung function in diffuse pleural thickening which is followed by comparatively little change over time."

We all owe a debt of gratitude to these researchers. If you found any of these excerpts interesting, please read the studies in their entirety.

Exposure to High Levels of Asbestos Can be a Death Sentence

By: Montwrobleski77
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