Asbestos Induced Pulmonary Disease And The Mesothelioma Plague

Asbestos is a naturally occurring mineral that has been widely used throughout the industrial world. It only becomes dangerous when it is broken into tiny particles or fibers and inhaled or swallowed. One interesting study exploring the link between exposure and lung disease is called, Asbestos stimulates IL-8 production from human lung epithelial cells by GJ Rosenthal, DR Germolec, ME Blazka, E Corsini, P Simeonova, P Pollock, LY Kong, J Kwon and MI Luster - Environmental Immunology and Neurobiology Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 - The Journal of Immunology, Vol 153, Issue 7 3237-3244. Here is an excerpt: Studies have indicated that soluble products, including chemotactic factors, released by activated lung macrophages and fibroblasts are critical mediators in the pathogenesis of asbestos-induced pulmonary fibrosis. We provide evidence that mediators produced by lung epithelial cells in response to asbestos may also contribute to lung disease. In the present study, the carcinogenic and fibrogenic fibers, chrysotile and crocidolite asbestos, were shown to directly stimulate the human pulmonary type-II epithelial cell line, A549, and to a lesser degree primary human bronchial epithelial cells, to elicit the chemotactic cytokine IL-8 in the absence of endogenous stimuli such as IL-1 and TNF.

That the membrane signaling events responsible for asbestos-induced IL-8 production are distinct from those responsible for IL-8 induction by cytokines was confirmed by using membrane- stabilizing agents and protein synthesis inhibitors. Stimulation was not observed with nonfibrogenic fibers, wollastonite and titanium dioxide, and was the direct result of asbestos-induced initiation of transcription. Asbestos failed to stimulate the release of TNF, IL-1 beta, or monocyte chemoattractant protein-1 in A549 or primary bronchial epithelial cells, indicating that cytokine secretion by asbestos is highly selective. However, a slight release of IL-1 alpha, probably preformed, was released in human bronchial epithelial cells. These data suggest that epithelial cells may, in addition to macrophages and fibroblasts, be an important effector cell in the immunopathogenesis of asbestos-associated diseases and in particular, in the neutrophilic infiltration that is commonly observed after asbestos exposure.

Another interesting study is called, Asbestos fibers mediate transformation of monkey cells by exogenous plasmid DNA by J D Appel, T M Fasy, D S Kohtz, J D Kohtz, and E M Johnson - PNAS October 1, 1988 vol. 85 no. 20 7670-7674. Here is an excerpt: Abstract - We have tested the ability of chrysotile asbestos fibers to introduce plasmid DNA into monkey COS-7 cells and the ability of this DNA to function in both replication and gene expression. Chrysotile fibers are at least as effective as calcium phosphate in standard transfection assays at optimal ratios of asbestos to DNA. After transfection with chrysotile, a minor percentage of introduced plasmid DNA bearing a simian virus 40 origin of replication replicates after 24 hr. Fragmentation of entering DNA is more prominent with asbestos than with calcium phosphate, and after 72 hr most DNA introduced by asbestos is associated with chromosomal DNA. Cells transfected with plasmid p11-4, bearing the p53 protooncogene, express this gene. Cells transfected with pSV2-neo express a gene conferring resistance of antibiotic G418, allowing isolation of colonies of transformed cells after 18 days. The introduction of exogenous DNA into eukaryotic cells could cause mutations in several ways and thus contribute to asbestos-induced oncogenesis.

A third study is called, Concentrations and dimensions of coated and uncoated asbestos fibres in the human lung. By A Morgan, A Holmes - Br J Ind Med 1980; 37:25-32. Here is an excerpt: Abstract - Concentrations and length distributions of uncoated and coated amphibole-type fibres in samples of human lung taken at necropsy were measured by optical microscopy using the membrane filter technique that enables fibres with diameters down to about 0.2 micron to be detected. The subjects included 10 who died with mesothelial tumours, three with lung cancer, and eight of other causes. Measurements of fibre concentrations are compared with those of other workers. It can be deduced from the length distributions that fibres less than 5 microns long are cleared from the lung more efficiently than longer ones. The clearance of short fibres appears to be inhibited in subjects with asbestosis, however. The length distributions of uncoated and coated fibres were dissimilar. In general, few fibres less than 10 microns in length were coated and few greater than 40 microns in length were uncoated. The probability of a fibre of given length, however, becoming coated varied considerably from subject to subject. Possible reasons for this are discussed.

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

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