The deadly cancer known as mesothelioma and chronic exposure to asbestos
Mesothelioma is a deadly form of cancer that can attack the membranes surrounding the heart,the lungs and stomach. An interesting article that examines asbestos exposure in vitro is called "Human Alveolar Macrophage Cytokine Release in response to in vitro and in vivo exposure to asbestos "by Raymond C. Perkins,Ronald K. Scheule 1,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 the Environment and Occupational Pensions 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 lung fibrosis. Knowledge of the effects of prolonged exposure to asbestos lung macrophage cytokine release should better define the role of macrophages in fibrogenesis.
This study examines the effects of acute in vitro exposure to asbestos and chronic in vivo exposure to asbestos on human alveolar macrophage cytokine release. As indicators of asbestos-induced activation of macrophages,the cellular release of IL-1β,TNF-α,IL-6,GM-CSF,and PGE2 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-α were elevated in response to asbestos exposure. Alveolar macrophages from asbestos-exposed individuals were placed in one of two groups based on their exposure history. These two groups were matched for age,smoking history,and diagnosis,none of the criteria for asbestosis. Cells isolated from patients who had been exposed to asbestos more than 10 years separated elevated basal amounts of IL-10,TNF-α,IL-6 and PGE2,while those already exposed less than 10 years. The results indicate that during the asbestos minimal acute effects on cytokine production was by human alveolar macrophages,intense,chronic Exposure to asbestos leads to increased basal release of substantial amounts of several cytokines that the fibroblast activity,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. July 1995,28 (1):123-42. Here's an excerpt:"Abstract –In 1987-1992,the Finnish Institute of Occupational Health (FIOH) implemented a nationwide program aimed at preventing asbestos from asbestos-related risks in close cooperation with governments,business,unions,health care systems and,and the mass media. The goals were to minimize any exposure to asbestos,to identify people exposed at work and improving the diagnosis of asbestos-related diseases,particularly cancer. This program involved a number of concrete actions and extensive dissemination of information and training,services,and scientific research. As proposed by the State Asbestos Committee,new use of asbestos was banned products and strict rules were applied to the inspection and refurbishment of old buildings. The screening study of 18,943 asbestos-induced diseases current and retired employees of the housing,shipyard and asbestos industry. Pleural and parenchymal changes were found in 4133 persons (22%) who were referred to further clinical trials as suspected cases of occupational disease. It was estimated that past exposure to asbestos in the Finnish population of 5 million causes>150 mesothelioma and lung cancer each year,a total of>2000 asbestos-induced cancer deaths in 2010. Although a large number of control actions were taken or initiated during the program,most of the preventive work still lies ahead. "
A third interesting article called,"Dose-responsive increases in pulmonary fibrosis after inhalation of asbestos "Quinlan TR,Marsh JP,Janssen YM,Leslie KO,Hemenway D,Vacek P,and Mossman BT –Department of Pathology,University of Vermont,Burlington 05405. Hour. J. Respir. Crit. Care Med.,Vol 150,No. 1,July 1994,200-206. Here's an excerpt:"We have focused here on steady-state mRNA levels of genes involved in antioxidant defense,ie,manganese superoxide dismutase and copper-zinc superoxide dismutase,in cell proliferation,ie,ornithine decarboxylase,c-jun,and glyceraldehyde-3-phosphate dehydrogenase throughout the lung homogenates from Fischer 344 rats at 3 hours and 20 d after exposure to asbestos crocridolite. Changes in gene expression were correlated with histopathologic findings,total and differentiated cells in bronchoalveolar lavage,and the level of hydroxyproline in the lungs. Dose-dependent increase in mRNA levels of antioxidant enzymes and proliferation-related genes were observed. Differential cell counts showed a dose-related increases in infiltration of neutrophils which preceded gene expression. Neutrophil infiltration in the lungs and focal lesions of fibrosis and increased levels of hydroxyproline were observed only at high concentrations of asbestos. These results indicate that high concentrations of airborne asbestos molecular changes in the lungs that may be related to antioxidant defenses and cause the onset of cell proliferation,a feature of asbestosis and lung cancer. "
If you found any of these interesting excerpts,read the studies in their entirety. We all have a great debt to these fine researchers.