Origin of a public health concern: Cristobalite in ash from the May 18, 1980 Mt St Helens eruption

Abundant cristobalite, a toxic form of crystalline silica, in respirable volcanic ash was an unforeseen hazard prior to the 1980 eruption of Mt St Helens. Its discovery prompted widespread concern of the effects of ash exposure on human health owing to the known hazard of respirable crystalline silica in occupational settings. Its presence continues to be of concern during eruptions that produce ashfall in populated areas, with cristobalite quantification being a key step in rapid screening strategies to assess potential health hazards.

Our understanding of the cristobalite hazard has increased immensely since 1980. It is a secondary mineral in altered edifices, lavas and volcanic domes, where its metastable formation is facilitated by structural substitution of aluminum for silicon. Well-constrained samples from basaltic andesite to rhyolite dome-forming eruptions reveal that cristobalite crystallization commences immediately, and abundance is associated with dome residence time. In the lead up to the May 18 eruption, cristobalite crystallized in the cryptodome through preferential devitrification of visually-distinguishable 'black' dacite compared to 'grey' dacite (11-13 wt.% vs. 3-6 wt.% cristobalite). This bimodality aligns with assertions that the grey dacite was sufficiently ductile to undergo secondary vesiculation upon depressurization, thereby also limiting sub-solidus cristobalite crystallization.

Medical studies following major eruptions since 1980 conclude that cristobalite-bearing ash is minimally reactive relative to pure-phase standards. This adheres to a well-established thesis of crystalline silica being variably pathogenic, whereby reactivity is governed by its origin and modification history. The diminished reactivity has been tied, in part, to the Al impurities (up to 4 wt.%), which can dampen crystalline silica reactivity. Therefore, lattice substitutions of Al appear to mediate both the existence and suppression of the volcanic cristobalite hazard, but are insufficient to abrogate reactivity completely. These constraints on the origin and reactivity of cristobalite in volcanic ash garnered in the wake of the 1980 eruption strengthen our capacity for health risk assessments and continue to bolster our communication of ash health hazards during volcanic crises.