Abstract We have known, since the 1980 eruption of Mount St. Helens, USA, that certain volcanic eruptions can generate crystalline silica, with some ash containing up to 25 wt.% cristobalite. Consequently, populations can be exposed to respirable volcanic crystalline silica (VCS) during volcanic crises. Over the last 45 yr, multidisciplinary efforts have sought to determine whether VCS is pathogenic, without definitive conclusions. Few clinical or epidemiological studies exist; they are constrained by difficulties in following dynamic cohorts longitudinally, variable eruption durations and exposures, and limited political will (and medical expertise), particularly given more pressing public health challenges in volcanically active lower-middle-income countries. In vitro toxicology studies generally find VCS-rich ash to be non-haemolytic and of low cytotoxicity at doses equivalent to crystalline silica standard dusts. Limited pro-inflammatory responses have been observed but do not necessarily correlate with VCS content. However, ash activates the NLRP3 inflammasome, suggesting a possible pathway for VCS reactivity. In vivo studies have shown lymph node granuloma formation but, similarly, it is unclear if VCS is causal. Physicochemical analyses identify limited VCS-related surface reactivity and show that all volcanic cristobalite contains elemental substitutions (Al, Na) and adhered minerals, both dampening toxicity. Evidence for VCS pathogenicity is therefore varied and insufficient to guide hazard management. In the absence of stronger evidence, a precautionary approach with public health interventions is warranted. This presentation will review the evidence and call for discussion on next steps to clarify the VCS hazard.
Horwell et al. (Thu,) studied this question.