Recruitment and Activation of Pleural Macrophages and Mesothelioma Disease

Recruitment and Activation of Pleural Macrophages and Mesothelioma Disease

One of the main problems with asbestos exposure is the fact that the mineral is so ubiquitous as it is used in thousands of ordinary products.  The relation between asbestos exposure and mesothelioma disease is well documented.  One interesting study is called, “Pleural macrophage recruitment and activation in asbestos-induced pleural injury.” By N Choe, S Tanaka, W Xia, D R Hemenway, V L Roggli, and E Kagan – Department of Pathology, Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Bethesda, MD 20814-4799, USA – Environ Health Perspect. 1997 September; 105(Suppl 5): 1257–1260.   Here is an excerpt: “Abstract – The pathogenesis of asbestos-induced pleural fibrosis is poorly understood. Moreover, there has been a long-standing controversy regarding the relative potential of different commercial types of asbestos to cause pleural disease. We postulated that inhaled asbestos fibers translocate to the pleural space where they stimulate the recruitment and activation of pleural macrophages. To test this hypothesis, and to determine whether there are differences between inhaled amphibole and serpentine asbestos, Fischer 344 rats were exposed by intermittent inhalation (6 hr/day for 5 days/week over 2 weeks) to either National Institute of Environmental Health Sciences (NIEHS) crocidolite (average concentration 7.55 mg/m3) or NIEHS chrysotile fibers (average concentration 8.51 mg/m3). Comparisons were made with sham-exposed rats. The rats were sacrificed at 1 and 6 weeks after the cessation of exposure. More pleural macrophages were recovered at 1 and 6 weeks after crocidolite and chrysotile exposure than after sham exposure. Small numbers of crocidolite fibers (approximately 1 per 4000 cells) were detected in the pleural cell pellet of one crocidolite-exposed rat by scanning electron microscopy. Pleural macrophage supernatants were assayed for production of nitric oxide (NO) (by the Griess reaction) and tumor necrosis factor alpha (TNF-alpha) (by an enzyme-linked immunosorbent assay method). Significantly greater amounts of NO as well as TNF-alpha were generated by pleural macrophages at 1 and 6 weeks after either crocidolite or chrysotile inhalation than after sham exposure. Conceivably, translocation of asbestos fibers to the pleural space may provide a stimulus for persistent pleural space inflammation, cytokine production, and the generation of toxic oxygen and nitrogen radicals. Enhanced cytokine secretion within the pleural space may in turn upregulate adhesion molecule expression and the synthesis of extracellular matrix constituents by pleural mesothelial cells. Thus, our findings may have significance for the development of asbestos-induced pleural injury.”

Another interesting study is called, “IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage.” By Scheule RK, Holian A. – Am J Respir Cell Mol Biol. 1989 Oct;1(4):313-8.  Here is an excerpt: “Abstract – The interaction of chrysotile asbestos with alveolar macrophages in vitro is known to stimulate cellular superoxide anion production. However, it is likely that particulates in the respiratory tract are present together with components of the pulmonary surfactant, and it is not known how these components may alter the bioactivity of the particulate. We now show that guinea pig immunoglobulin G, a surfactant protein, causes a significant, dose-dependent enhancement of superoxide anion production by nonadherent guinea pig alveolar macrophages in response to chrysotile asbestos. This enhancement could not be mimicked by other particulates or proteins, including IgG fragments, implying that the interaction between IgG, cell, and chrysotile is relatively specific. The enhancing effect of IgG in solution could be reproduced by pretreating the chrysotile asbestos with IgG. The fact that IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production, in turn, leads to a proposal for a molecular mechanism by which asbestos may stimulate the guinea pig macrophage, namely, by crosslinking cell-surface immunoglobulin Fc receptors. In view of the submicromolar concentrations at which IgG was effective in enhancing macrophage stimulation by chrysotile asbestos in vitro, these results also suggest that IgG adsorption may play a role in the progression of asbestos-induced pulmonary fibrosis.”

A third study is called, “Asbestos exposure in a Yale building : Analysis and resolution” by Robert N. Sawyer – Environmental Research – Volume 13, Issue 1, February 1977, Pages 146-169 – Preventive and Occupational Medicine, Yale Health Service, 17 Hillhouse Avenue, New Haven, Connecticut 06520, USA.  Here is an excerpt: “Abstract – The Yale University Art and Architecture building has 118,000 sq ft (10,000 m2) of floor space and houses the School of Art, the School of Architecture, and the schools’ library. Completed in 1963, the nine-level reinforced concrete structure is a major building on the campus and has been used by over 2000 persons each academic year. The ceiling material in the building, a spray-applied mixture of asbestos and fibrous glass, caused occupant exposure to asbestos fibers under all conditions of usual activity. The measured asbestos fiber concentrations in some situations exceeded Occupational Safety and Health Administration allowable limits for industrial exposure, and in all cases were above the ambient city levels. Many air samples indicated potentially carcinogenic asbestos exposures. To eliminate this health hazard, the asbestos was removed from the building. Building isolation, protective equipment, surfactant treated water, and decontamination procedures afforded contamination control for the workers and the surrounding community. Ninety-two tons of wet asbestos-contaminated material was removed during a 20-day operation. Over 500 air samples were obtained during surveillance, experimentation, and asbestos removal. This report presents data obtained from 200 samples examined to date and outlines procedures used in the operation.”

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

Monty Wrobleski is the author of this article, for more information please visit the following links

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