High Concentrations of Amosite and Crocidolite Asbestos Fibers and Mesothelioma Disease
One interesting study is called, "Involvement of protein kinase C, phospholipase C, and protein tyrosine kinase pathways in oxygen radical generation by asbestos-stimulated alveolar macrophage." By Y Lim, S H Kim, K A Kim, M W Oh, and K H Lee - Environ Health Perspect. 1997 September; 105(Suppl 5): 1325–1327. Here is an excerpt: "Abstract - Although asbestos stimulates oxygen radical generation in alveolar macrophages, the exact mechanism is still not clear. The purpose of this study was to compare the ability of three asbestos fibers (amosite, chrysotile, and crocidolite) to generate oxygen radicals in macrophages and examine the mechanism of this action. All asbestos fibers were able to induce chemiluminescence but chrysotile induced maximal chemiluminescence at higher concentrations than amosite and crocidolite. Protein kinase C (PKC) inhibitors (sphingosine and staurosporine) suppressed the ability of asbestos to induce oxygen radical generation. Phospholipase C (PLC) inhibitors (U73122 and neomycin) and protein tyrosine kinase (PTK) inhibitors (erbstatin and genistein) decreased oxygen radical generation of asbestos-stimulated alveolar macrophages. Oxygen radical generation was not suppressed by an adenylate cyclase activator (forskolin), a protein kinase A inhibitor (H-8), and a protein serine-threonine phosphatase inhibitor (okadaic acid). PLC and PTK inhibitors suppressed the increment of phosphoinositide turnover by amosite. These results suggest that asbestos fibers induce the generation of oxygen radicals through PTK, PLC, and PKC pathways in a dose-response pattern."
Another interesting study is called, "Asbestos bodies in a general hospital/clinic population" by Modin, B.E. ; Greenberg, S.D. ; Buffler, P.A. ; Lockhart, J.A. ; Seitzman, L.H. ; Awe, R.J. - Acta Cytol.; (United States); Journal Volume: 26:6. Here is an excerpt: "The presence of asbestos bodies in the sputum of individuals with known occupational asbestos exposure has been well documented. However, their prevalence and clinical implications in sputum and bronchial washings from patients not clinically known to have asbestos exposure remains controversial. From 1974 to 1979, 31,353 sputum and bronchial washing specimens were processed in the course of evaluating various pulmonary complaints of approximately 11,000 patients from the outpatient clinics and hospitals of the Harris County Hospital District in Houston, Texas. Asbestos bodies were incidentally found in five patients, and, in retrospect, each of them was discovered to have had significant occupational exposure to asbestos dust. Asbestos lung disease was also subsequently proven in four of the five patients and was felt, retrospectively, to have contributed to their presenting complaints and clinical course. It is concluded that asbestos bodies in sputum and bronchial washing specimens are highly specific markers for past asbestos exposure and reflect the presence of a significant asbestos load within the lungs. Sputum cytology is both painless and inexpensive and is recommended as a supplemental procedure to document clinically significant asbestos exposure."
Another interesting study is called, "Role of Transcription Factor NF-?B in Asbestos-Induced TNFa Response from Macrophages" by Ningli Chenga, Xianglin Shib, Jianping Yeb, Vincent Castranovab, Fei Chenc, Stephen S. Leonardb, Val Vallyathanb and Yon Rojanasakula, - Experimental and Molecular Pathology - Volume 66, Issue 3, August 1999, Pages 201-210. Here is an excerpt: "Abstract - Asbestos exposure in humans is associated with inflammatory, fibrotic, and malignant diseases in the lung. Increasing evidence supports the hypothesis that the production of proinflammatory cytokines such as tumor necrosis factor-a (TNFa) is an important mediator of the pathologic responses of asbestosis. In this study, we examine the role of nuclear transcription factor-?B (NF-?B) and free oxygen radicals in asbestos-induced TNFa gene and protein expression in lung macrophages. Exposure of the cells to crocidolite asbestos caused a parallel increase in TNFa production and NF-?B activation, as analyzed by enzyme-linked immunosorbent assay and electrophoretic mobility shift assay. Inhibition of NF-?B by SN50, an inhibitor of NF-?B nuclear translocation, or by sequence-specific oligonucleotides directed against the NF-?B binding site of TNFa promoter attenuated the asbestos effect on TNFa production. Gene transfection assays using an expression plasmid containing a luciferase reporter gene and a TNFa-derived NF-?B gene promoter further indicated the dependence of NF-?B activation on asbestos-induced gene expression. The effects of asbestos on NF-?B and TNFa activation were inhibited by oxygen radical scavengers and were enhanced by antioxidant enzyme inhibitors. These results indicate that asbestos-induced TNFa gene expression is mediated through a process that involves NF-?B activation and free radical reactions."
We all owe a debt of gratitude to these fine researchers for their important work. If you found any of these excerpts helpful, please read the studies in their entirety.
Another interesting study is called, "Asbestos bodies in a general hospital/clinic population" by Modin, B.E. ; Greenberg, S.D. ; Buffler, P.A. ; Lockhart, J.A. ; Seitzman, L.H. ; Awe, R.J. - Acta Cytol.; (United States); Journal Volume: 26:6. Here is an excerpt: "The presence of asbestos bodies in the sputum of individuals with known occupational asbestos exposure has been well documented. However, their prevalence and clinical implications in sputum and bronchial washings from patients not clinically known to have asbestos exposure remains controversial. From 1974 to 1979, 31,353 sputum and bronchial washing specimens were processed in the course of evaluating various pulmonary complaints of approximately 11,000 patients from the outpatient clinics and hospitals of the Harris County Hospital District in Houston, Texas. Asbestos bodies were incidentally found in five patients, and, in retrospect, each of them was discovered to have had significant occupational exposure to asbestos dust. Asbestos lung disease was also subsequently proven in four of the five patients and was felt, retrospectively, to have contributed to their presenting complaints and clinical course. It is concluded that asbestos bodies in sputum and bronchial washing specimens are highly specific markers for past asbestos exposure and reflect the presence of a significant asbestos load within the lungs. Sputum cytology is both painless and inexpensive and is recommended as a supplemental procedure to document clinically significant asbestos exposure."
Another interesting study is called, "Role of Transcription Factor NF-?B in Asbestos-Induced TNFa Response from Macrophages" by Ningli Chenga, Xianglin Shib, Jianping Yeb, Vincent Castranovab, Fei Chenc, Stephen S. Leonardb, Val Vallyathanb and Yon Rojanasakula, - Experimental and Molecular Pathology - Volume 66, Issue 3, August 1999, Pages 201-210. Here is an excerpt: "Abstract - Asbestos exposure in humans is associated with inflammatory, fibrotic, and malignant diseases in the lung. Increasing evidence supports the hypothesis that the production of proinflammatory cytokines such as tumor necrosis factor-a (TNFa) is an important mediator of the pathologic responses of asbestosis. In this study, we examine the role of nuclear transcription factor-?B (NF-?B) and free oxygen radicals in asbestos-induced TNFa gene and protein expression in lung macrophages. Exposure of the cells to crocidolite asbestos caused a parallel increase in TNFa production and NF-?B activation, as analyzed by enzyme-linked immunosorbent assay and electrophoretic mobility shift assay. Inhibition of NF-?B by SN50, an inhibitor of NF-?B nuclear translocation, or by sequence-specific oligonucleotides directed against the NF-?B binding site of TNFa promoter attenuated the asbestos effect on TNFa production. Gene transfection assays using an expression plasmid containing a luciferase reporter gene and a TNFa-derived NF-?B gene promoter further indicated the dependence of NF-?B activation on asbestos-induced gene expression. The effects of asbestos on NF-?B and TNFa activation were inhibited by oxygen radical scavengers and were enhanced by antioxidant enzyme inhibitors. These results indicate that asbestos-induced TNFa gene expression is mediated through a process that involves NF-?B activation and free radical reactions."
We all owe a debt of gratitude to these fine researchers for their important work. If you found any of these excerpts helpful, please read the studies in their entirety.