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Uptake of Long Asbestos Fibers by the Metaplastic Squamous Mucosa
Disease development among people exposed to hazardous asbestos has been carefully studied over the years. One interesting study is called, “Squamous metaplasia of the respiratory tract. Possible pathogenic role in asbestos-associated bronchogenic carcinoma.” By Woodworth CD, Mossman BT, Craighead JE – Lab Invest. 1983 May;48(5):578-84. Here is an excerpt: “Abstract – Asbestos workers who smoke have a substantially greater risk of developing bronchogenic carcinoma than nonsmokers. Squamous metaplasia often replaces the mucociliary epithelium in the respiratory tract of chronic users of cigarettes. As a result, clearance mechanisms are altered. Using both scanning and transmission electron microscopy, we examined the interaction of chrysotile and crocidolite asbestos with the metaplastic mucosa found in the bronchi of cigarette smokers and produced in cultures of hamster trachea by enriched, serum-free medium. After deposition on the squamous epithelium, both “long” and “short” fibers were either phagocytosed by, or moved between, the cells of the mucosa. The interaction of asbestos with the mucociliary epithelium differed. Most long fibers were cleared, whereas short fibers were taken up by the mucosa. The apparent increase in uptake of long asbestos fibers by the metaplastic squamous mucosa could contribute to the synergism between this unique mineral and cigarette smoke in the causation of bronchogenic neoplasms.”
A second study is called, “Asbestos and cancer: human natural killer cell activity is suppressed by asbestos fibers but can be restored by recombinant interleukin-2.” By
Robinson BW – Am Rev Respir Dis. 1989 Apr;139(4):897-901. Here is an excerpt: “Abstract – Inhalation of asbestos fibers is associated with a marked increase in the risk of developing pulmonary malignancy, particularly bronchogenic carcinoma. As natural killer (NK) cells are specialized lymphocytes that are considered to have an important in vivo role in the recognition and destruction of malignant cells, we examined the capacity of asbestos fibers (chrysotile, amosite, and crocidolite) to interfere with the NK activity of nylon wool-nonadherent, human blood lymphocytes (51Cr-release assay, K562 target cells, 14 h effector-to-target ratio = 50:1). Final asbestos concentrations used were 1 to 1,000 micrograms/ml. None of the fibers altered spontaneous target cell lysis or lymphocyte viability. All types of asbestos suppressed NK activity in a dose-dependent fashion. This effect was most marked with chrysotile, which exerted a profound inhibitory effect on blood NK cell activity; at 100 micrograms/ml, NK activity was inhibited 84 +/- 2% (p less than 0.001). The suppressive effects of asbestos were exerted directly on the NK cells (large granular lymphocytes, 91 +/- 2% inhibition at 100 micrograms/ml; p less than 0.001). Exposure of lymphocytes to recombinant interleukin-2 (IL-2, 150 units/ml) for 24 h prior to exposure to asbestos restored the level of activity to 99 +/- 6% of the original value (p less than 0.001), and lung lymphocytes that were exposed to IL-2 in vivo (active sarcoidosis) were resistant to suppression by asbestos. Similar results were observed in a group of patients with asbestosis. This suppression of NK activity may contribute to the increased susceptibility of asbestos-exposed persons to the development of pulmonary malignancy.”
A third study is called, “An epidemiological survey of immunological abnormalities in asbestos workers: II. Serum immunoglobulin levels” by A. Langea – Environmental Research – Volume 22, Issue 1, June 1980, Pages 176-183. Here is an excerpt: “Abstract – A significant elevation of serum IgA and IgG was found in female asbestos workers below age 36. Higher values of serum IgA, IgG, and IgM were found in male asbestos workers over age 35, when compared to matched controls. Female asbestos workers, over age 35, statistically differ from their controls only with respect to IgG levels. Patients, with asbestosis and with an impairment of blood oxygen saturation, contribute greatly to the elevation of serum immunoglobulin levels in asbestos workers. The asbestosis process, but not chronic bronchitis, is responsible for high serum IgA and IgG levels.”
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.
About the Author
Monty Wrobleski is the author of this article, for more information please visit the following links
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