Mesothelioma is a form of lung cancer that affects the outer lining of the lungs. This deadly disease has only one known cause: exposure to the fibrous material asbestos. Asbestos was used extensively in the past for building materials, insulation and other applications. When inhaled, it can lodge in the lungs and lead to mesothelioma. But it takes years, even decades, for the disease to progress and show itself. Today, even though asbestos is a known risk that workers are protected against, many are suffering from mesothelioma. The exposures that occurred in the past are only recently manifesting into fully-fledged cancers.

One result of this has been legal action. Those who were exposed to hazardous asbestos are now calling for those who may have caused the exposure through negligence or carelessness to account for allowing workers to inhale the dangerous material. To aid them, several attorneys and law firms have veered toward specializing in mesothelioma cancer legal cases.

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The development of mesothelioma disease has been linked to asbestos exposure.  One interesting study examining this relationship is called, "The Hygiene Standard for Chrysotile Asbestos" - The Lancet, Volume 311, Issue 8062, Pages 484-489.  Here is an excerpt: "Abstract - Previous studies, including the analysis on which the current 2 fibres/cm3 hygiene standard is based, may have underestimated the risk of morbidity or mortality following exposure to low levels of asbestos dust. Accurate dose-response data at levels below 2 fibres/cm3 are unlikely to be available for the foreseeable future, and the biologically plausible assumption that excess cancer mortality is approximately proportional to dust level should be provisionally accepted. It may be reasonable, however, to postulate a safe threshold for mortality from asbestosis. If excess mortality from asbestos-related disease is proportional to dust level for each cause, approximately 10% of male asbestos workers might, under certain assumptions, eventually die of asbestos-induced disease after 50 years' exposure at 2 fibres/cm3. Peritoneal mesothelioma is usually due to crocidolite (blue asbestos) or other amphiboles, but exposure to chrysotile (white asbestos) alone may lead to a substantial risk of pleural mesothelioma. These predictions are based on rather small numbers in a single factory, and further studies in other working environments are required. Fibre counts based on optical microscopy are likely to be less relevant than total counts by electron microscopy, and excess mortality is virtually confined to men first exposed more than 20 years ago, when little or no accurate data on dust levels were collected."

Another interesting study is called, "Behavior of Crocidolite Asbestos during Mitosis in Living Vertebrate Lung Epithelial Cells" by Jeffrey G. Ault, Richard W. Cole, Cynthia G. Jensen, Lawrence C. W. Jensen, Lori A. Bachert, and Conly L. Rieder - Cancer Res February 15, 1995 55; 792.  Here is an excerpt: "Abstract - Asbestos has been described as a physical carcinogen in that long thin fibers are generally more carcinogenic than shorter thicker ones. It has been hypothesized that long thin fibers disrupt chromosome behavior during mitosis, causing chromosome abnormalities which lead to cell transformation and neoplastic progression. Using high-resolution time lapse video-enhanced light microscopy and the uniquely suited lung epithelial cells of the newt Taricha granulosa, we have characterized for the first time the behavior of crocidolite asbestos fibers, and their interactions with chromosomes, during mitosis in living cells. We found that the keratin cage surrounding the mitotic spindle inhibited fiber migration, resulting in spindles with few fibers. As in interphase, fibers displayed microtubule-mediated saltatory movements. Fiber position was only slightly affected by the ejection forces of the spindle asters. Physical interactions between crocidolite fibers and chromosomes occurred randomly within the spindle and along its edge. Crocidolite fibers showed no affinity toward chromatin and most encounters ended with the fiber passively yielding to the chromosome. In a few encounters along the spindle edge the chromosome yielded to the fiber, which remained stationary as if anchored to the keratin cage. We suggest that fibers thin enough to be caught in the keratin cage and long enough to protrude into the spindle are those fibers with the ability to snag or block moving chromosomes."

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The development of asbestos induced disease can vary depending on several critical factors.  One interesting study that examines this issue is called, "Asbestos-induced phosphorylation of epidermal growth factor receptor is linked to c-fos and apoptosis" by Christine L. Zanella, Cynthia R. Timblin, Andrew Cummins, Michael Jung, Jonathan Goldberg, Rachel Raabe, Thomas R. Tritton, and Brooke T. Mossman - Am J Physiol Lung Cell Mol Physiol 277 - Vol. 277, Issue 4, L684-L693, October 1999.  Here is an excerpt: "We examined the mechanisms of interaction of crocidolite asbestos fibers with the epidermal growth factor (EGF) receptor (EGFR) and the role of the EGFR-extracellular signal-regulated kinase (ERK) signaling pathway in early-response protooncogene (c-fos/c-jun) expression and apoptosis induced by asbestos in rat pleural mesothelial (RPM) cells. Asbestos fibers, but not the nonfibrous analog riebeckite, abolished binding of EGF to the EGFR. This was not due to a direct interaction of fibers with ligand, inasmuch as binding studies using fibers and EGF in the absence of membranes showed that EGF did not adsorb to the surface of asbestos fibers. Exposure of RPM cells to asbestos caused a greater than twofold increase in steady-state message and protein levels of EGFR (P < 0.05).

The tyrphostin AG-1478, which inhibits the tyrosine kinase activity of the EGFR, but not the tyrphostin A-10, which does not affect EGFR activity, significantly ameliorated asbestos-induced increases in mRNA levels of c-fos but not of c-jun. Pretreatment of RPM cells with AG-1478 significantly reduced apoptosis in cells exposed to asbestos. Our findings suggest that asbestos-induced binding to EGFR initiates signaling pathways responsible for increased expression of the protooncogene c-fos and the development of apoptosis. The ability to block asbestos-induced elevations in c-fos mRNA levels and apoptosis by small-molecule inhibitors of EGFR phosphorylation may have therapeutic implications in asbestos-related diseases."

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