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Exposure to hazardous asbestos fibers has been linked to several deadly diseases such as lung cancer and mesothelioma.  One interesting study is called, “Fiber burden and patterns of asbestos-related disease in workers with heavy mixed amosite and chrysotile exposure” by A Churg and S Vedal – Department of Pathology, University of British Columbia, Vancouver, Canada. – Am. J. Respir. Crit. Care Med., Vol 150, No. 3, Sep 1994, 663-669.   Here is an excerpt: “To attempt to determine the mineralogic factors that relate to the appearance of specific types of asbestos-related disease in workers with heavy mixed exposure to amphiboles and chrysotile, we analyzed the pulmonary asbestos fiber burden in a series of 144 shipyard workers and insulators from the Pacific Northwest. Amosite was found in all lungs, and tremolite and chrysotile in most lungs, but the vast majority of fibers were amosite. Tremolite and chrysotile concentrations were significantly correlated, indicating that the tremolite originated from chrysotile products, but no correlation was found between tremolite or chrysotile concentration and amosite concentration. Time since last exposure was correlated with decreasing amosite concentration and the calculated clearance half time was about 20 yr. In a multiple regression analysis that accounted for the presence of more than one disease in many subjects, a high concentration of amosite fibers was correlated with the presence of airway fibrosis and asbestosis, whereas subjects with mesothelioma, lung cancer, pleural plaques, or no asbestos-related disease had about the same, much lower, amosite concentration. No relationship was found between the concentration of chrysotile or tremolite and any disease. Analysis of fiber size measures (length, width, aspect ratio, surface, mass) showed that pleural plaques were strongly associated with high aspect ratio amosite fibers and suggested that mesotheliomas were associated with low aspect ratio amosite fibers.”

Another interesting study is called, “Asbestos in Drinking Water and Cancer Incidence in the San Francisco Bay Area – by Marty S. Kanarek, Paul M. Conforti, Lorene A. Jackson, Robert C. Cooper, and Jack C. Murchio – American Journal of Epidemiology Vol. 112, No. 1: 54-72.  Here is an excerpt: “Age-adjusted, sex- and race-specific 1969–1971 cancer incidence ratios for the 722 census tracts of the San Francisco-Oakland Standard Metropolitan Statistical Area were compared with measured chrysotile asbestos counts in tract drinking waters. The water supplies serving the area have varying contact with naturally occurring serpentine. The t test for multiple regression coefficients and the t test for correlation coefficients showed significant (p << 0.01) relationships between chrysotile asbestos content of tract drinking water and white male lung, white female gall bladder and pancreas, and peritoneal cancers in both sexes. Of weaker significance (0.01 0.05) were female esophagus, pleura and kidney, as well as stomach cancers in both sexes. These associations appeared to be independent of income, education, asbestos occupation, marital status, country of origin and mobility.”

Another interesting study is called, “Asbestos-stimulated tumour necrosis factor release from alveolar macrophages depends on fibre length and opsonization” by Kenneth Donaldson, Xiao Yang Li, Shashi Dogra, Brian G. Miller, Geraldine M. Brown – The Journal of Pathology – Volume 168 Issue 2, Pages 243 – 248.  Here is an excerpt: “Abstract – Fibre length has been shown to be an important factor in the ability of respirable fibres to cause lung fibrosis and cancer. We have reported that a long sample of amosite asbestos is more carcinogenic and fibrogenic than a short sample of similar diameter. These amosite asbestos samples were studied with regard to their ability to stimulate the release of the pro-inflammatory cytokine tumour necrosis factor (TNF) from rat alveolar macrophages in vitro. The long fibre sample was found to stimulate substantially greater release of the cytokine than the short sample. Furthermore, on treatment of the fibres with rat immunoglobulin G (IgG), there was an increase in the ability of both the long and the short sample to stimulate TNF secretion, although the long sample retained by far the greatest activity. Coating of the fibres with a range of other proteins had no substantial effect on their ability to stimulate TNF secretion. Quartz and titanium dioxide (TiO2) were included as control particles and the TNF-stimulating activity of quartz was notably increased by opsonization with IgG. TiO2 showed a similar low activity to that of the short fibre sample of amosite but this again could be modestly increased by opsonization with IgG. The simulation of TNF release caused by treatment with immunoglobulin-opsonized long fibre amosite could be inhibited by treatment of the macrophages with the protein kinase C-inhibitor staurosporine. The study demonstrates a fibre length-related ability to stimulate cytokine secretion by alveolar macrophages, and its enhancement by opsonization with IgG. This is likely to be relevant to the relationship between fibre length and pathogenic potential to the lung.”

If you found any of these excerpts, please read them in their entirety.  We all owe a debt of gratitude to these researchers.

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