The Lethal Cancer Known As Mesothelioma And Chronic Exposure To Asbestos

Mesothelioma is a lethal cancer that can attack the membranes surrounding the heart

, lung, and stomach. One interesting article that examines asbestos exposure in vitro is called, Human Alveolar Macrophage Cytokine Release in Response to in Vitro and in Vivo Asbestos Exposure by Raymond C. Perkins, Ronald K. Scheule1, Raymond Hamilton, Glen Gomes, Gary Freidman and Andrij Holian - Division of Pulmonary and Critical Care Medicine, Departments of Internal Medicine and Pharmacology, University of Texas Medical School at Houston and Environmental and Occupational Research Center, Houston, TX. Experimental Lung Research - 1993, Vol. 19, No. 1, Pages 55-65 - Here is an excerpt: The lung macrophage is proposed to be involved in the development of asbestos-induced pulmonary fibrosis. Knowledge of the effects of long-term asbestos exposure on lung macrophage cytokine release should better define the role of the macrophage in fibrogenesis.

This study examines the effects of acute in vitro asbestos exposure and chronic in vivo asbestos exposure on human alveolar macrophage cytokine release. As indicators of asbestos-induced macrophage activation, the cellular release of IL-1, TNF-, IL-6, GM-CSF, and PGE2 was mesaured during a 24-h in vitro culture. Alveolar macrophages from normal volunteers were cultured in vitro with chrysotile asbestos. Of the factors measured, only TNF- was elevated in response to asbestos exposure. Alveolar macrophages from asbestos-exposed individuals were placed into one of two groups based on their exposure history. These two groups were matched for age, smoking history, and diagnosis; none met the criteria for asbestosis. Cells isolated from subjects that had been exposed to asbestos for more than 10 years secreted enhanced basal amounts of IL-10, TNF-, IL-6, and PGE2, while those who had been exposed for less than 10 years did not. The results indicate that while asbestos had minimal acute effects on cytokine production by the human alveolar macrophage, intense, chronic exposure to asbestos leads to the enhanced basal release of significant amounts of several cytokines that have activity for the fibroblast, even in the absence of overt fibrosis.

Another interesting article by Huuskonen MS, Koskinen K, Tossavainen A, Karjalainen A, Rinne JP, Rantanen J. - Finnish Institute of Occupational Health Asbestos Program 1987-1992. Am J Ind Med. 1995 Jul;28(1):123-42. Here is an excerpt: Abstract - In 1987-1992, the Finnish Institute of Occupational Health (FIOH) implemented a nationwide asbestos program aimed at preventing asbestos-related risks in good cooperation with governmental authorities, industry, trade unions, the health care and insurance systems, and mass media. The goals were to minimize all exposure to asbestos, identify people exposed at work, and improve the diagnostics of asbestos diseases, especially cancers. The program entailed several concrete actions and extensive dissemination of information, training, services, and scientific research. As proposed by the State Asbestos Committee, new use of asbestos products was banned and strict regulations were applied to renovation and inspection of old buildings. The screening study of asbestos-induced diseases included 18,943 current and retired workers from house building, shipyard, and asbestos industries. Pleural and parenchymal changes were found in 4,133 persons (22%), who were referred to further clinical examinations as suspected cases of an occupational disease. It was estimated that past exposure of asbestos among the Finnish population of 5 million causes > 150 mesotheliomas and lung cancers annually, totalling > 2,000 asbestos-induced cancer deaths by the year 2010. Although several major control actions were made or started during the program, the bulk of the preventive work still lies ahead.

A third interesting article is called, Dose-responsive increases in pulmonary fibrosis after inhalation of asbestos by TR Quinlan, JP Marsh, YM Janssen, KO Leslie, D Hemenway, P Vacek and BT Mossman - Department of Pathology, University of Vermont, Burlington 05405. Am. J. Respir. Crit. Care Med., Vol 150, No. 1, 07 1994, 200-206. Here is an excerpt: We focused here on steady-state mRNA levels of genes involved in antioxidant defense, i.e., manganese superoxide dismutase and copper- zinc superoxide dismutase, and in cell proliferation, i.e., ornithine decarboxylase, c-jun, and glyceraldehyde-3-phosphate-dehydrogenase in whole-lung homogenates from Fischer 344 rats at 3 h to 20 d after exposure to crocridolite asbestos. Changes in gene expression were correlated with histopathologic findings, total and differential cell counts in bronchoalveolar lavage, and levels of hydroxyproline in lung. Dosage-dependent increases in mRNA levels of antioxidant enzymes and proliferation-related genes were observed. Differential cell counts revealed a dose-related infiltration of neutrophils that preceded elevations in gene expression. Neutrophil infiltration into lung and focal lesions of fibrosis as well as increased levels of hydroxyproline were observed only at high concentrations of asbestos. These results indicate that high airborne concentrations of asbestos cause molecular changes in lung that may be related to antioxidant defense and the triggering of cell proliferation, a feature of asbestosis and lung cancer.

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

by: Mont Wrobleski

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