It is important to raise awareness of some of the notable research done on asbestos and its links to mesothelioma. Over 20 million workers have been exposed to hazardous asbestos over the years with profound consequences.

One important study is called, "Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4." By Dubois CM, Bissonnette E, Rola-Pleszczynski M. Am Rev Respir Dis. 1989 May;139(5):1257-64. Department of Pediatrics, Faculty of Medicine, University of Sherbrooke, Québec, Canada. Here is an excerpt:

"Alveolar macrophages (AM) can play a crucial role in the pathogenesis of pulmonary disease via their ability to produce potent inflammatory and fibrogenic mediators. We found that rat AM cultured with 1 to 100 micrograms/ml of silica particles or asbestos fibers produced tumor necrosis factor (TNF) and leukotriene B4 (LTB4) in a concentration-dependent fashion, whereas latex beads, an inert phagocytic stimulus, failed to induce significant augmentation of either TNF or LTB4. In a time course study, AM stimulated for 2 h with silica or asbestos produced an increased amount of LTB4, which preceded the rise in TNF activity detected 7 and 24 h after culture initiation. The induction appears to involve the synthesis of new protein since actinomycin D and cycloheximide abrogate the majority of the stimulatory effect. We next examined the role of LTB4 in mineral-dust-induced TNF production. The lipoxygenase inhibitors nordihydroguaiaretic acid (NDGA) and AA861 used at 1 to 50 micrograms/ml reduced in a concentration-dependent fashion asbestos- or silica-stimulated TNF release. On the other hand, "reconstitutive" experiments in which we added exogenous LTB4 (10(-14) to 10(-8) M) to AM treated with lipoxygenase inhibitors showed partial restoration of TNF production induced by chrysotile or silica, with peak effect at 10(-10)M LTB4. The present study demonstrated that AM incubated in the presence of chrysotile A or silica can produce both LTB4 and TNF and that endogenous lipoxygenase metabolites as well as exogenous LTB4 can act to amplify TNF production. These observations suggest a common mechanism by which asbestos and silica may modulate the production of inflammatory and fibrogenic cytokines."

Another interesting study is called, "Pulmonary macrophage accumulation and asbestos-induced lesions at sites of fiber deposition." By Warheit DB, Chang LY, Hill LH, Hook GE, Crapo JD, Brody AR. Am Rev Respir Dis. 1984 Feb;129(2):301-10.

Here is an excerpt:

"Inhaled chrysotile asbestos fibers are deposited at alveolar duct bifurcations and subsequently are phagocytized there by pulmonary macrophages. The characteristics of the rapid macrophage response at alveolar duct bifurcations following asbestos inhalation has been further evaluated. Significant numbers of pulmonary macrophages accumulated at sites of asbestos deposition within 48 h after a 1-h exposure, whereas duct surfaces of sham-exposed animals were essentially devoid of macrophages. The influx of macrophages was associated with a significantly increased bifurcation tissue area (p less than 0.025), and this alteration persisted for at least 1 month. Two thirds of the accumulated macrophages from alveolar duct bifurcations could be removed by bronchoalveolar lavage. Macrophages recovered by lavage had significant changes (p less than 0.01) in their morphology and in their phagocytic and chemotactic capacities. These cellular alterations could play a role in the pathogenesis of asbestos-related lung disease."

If you found either of these excerpts interesting, please visit the studies in their entirety. With continued dedication and research, we may someday find a cure to mesothelioma.