Immunotoxicity of asbestos

Abstract The study of asbestos immunotoxicity is generally applied toward understanding the mechanisms that lead to its infamous outcomes, mesothelioma and asbestosis, rather than as an outcome itself. However, emerging evidence suggests that asbestos exposure has critical inflammatory and autoimmune effects. Although crystalline silica is broadly accepted as an exposure trigger for systemic autoimmune diseases (SAID), the literature supporting asbestos as another SAID trigger is limited. Challenges for establishing causality between asbestos exposure and autoimmunity include small, often occupationally-exposed cohorts, a tendency to focus on carcinogenicity or lung pathology, and poor characterization of fiber type in a given exposure scenario. However, a growing set of studies strongly supports inclusion of amphibole asbestos (AA) as an environmental trigger for autoimmunity. Both human and animal studies have revealed that AA, but not the common commercial asbestos (chrysotile), drives autoantibody production, alters cytokine profiles, and is associated with autoimmune disease. The potential public health impact of these findings are highlighted in the growing awareness of “naturally occurring asbestos” in geographic locations where it was not previously predicted to occur, leading to environmental exposures in wide areas of the world as a component of dust. As climate change brings warmer and dryer conditions to the more arid parts of the world, wind-blown mineral dusts containing asbestos may become more common. It is essential that epidemiologists, clinicians and regulatory agencies become aware of this emerging risk to health by an environmental immunotoxicant.