Nanoscale silicate melt textures determine volcanic ash surface chemistry.

Explosive volcanic eruptions produce vast quantities of silicate ash, whose surfaces are subsequently altered during atmospheric transit. These altered surfaces mediate environmental interactions, including atmospheric ice nucleation, and toxic effects in biota. A lack of knowledge of the initial, pre-altered ash surface has required previous studies to assume that the ash surface composition created during magmatic fragmentation is equivalent to the bulk particle assemblage. Here we examine ash particles generated by controlled fragmentation of andesite and find that fragmentation generates ash particles with substantial differences in surface chemistry. We attribute this disparity to observations of nanoscale melt heterogeneities, in which Fe-rich nanophases in the magmatic melt deflect and blunt fractures, thereby focusing fracture propagation within aureoles of single-phase melt formed during diffusion-limited growth of crystals. In this manner, we argue that commonly observed pre-eruptive microtextures caused by disequilibrium crystallisation and/or melt unmixing can modify fracture propagation and generate primary discrepancies in ash surface chemistry, an essential consideration for understanding the cascading consequences of reactive ash surfaces in various environments.

Assessment of the potential for in-plume sulphur dioxide gas-ash interactions to influence the respiratory toxicity of volcanic ash.

BACKGROUND: Volcanic plumes are complex environments composed of gases and ash particles, where chemical and physical processes occur at different temperature and compositional regimes. Commonly, soluble sulphate- and chloride-bearing salts are formed on ash as gases interact with ash surfaces. Exposure to respirable volcanic ash following an eruption is potentially a significant health concern. The impact of such gas-ash interactions on ash toxicity is wholly un-investigated. Here, we study, for the first time, whether the interaction of volcanic particles with sulphur dioxide (SO2) gas, and the resulting presence of sulphate salt deposits on particle surfaces, influences toxicity to the respiratory system, using an advanced in vitro approach. METHODS: To emplace surface sulphate salts on particles, via replication of the physicochemical reactions that occur between pristine ash surfaces and volcanic gas, analogue substrates (powdered synthetic volcanic glass and natural pumice) were exposed to SO2 at 500 °C, in a novel Advanced Gas-Ash Reactor, resulting in salt-laden particles. The solubility of surface salt deposits was then assessed by leaching in water and geochemical modelling. A human multicellular lung model was exposed to aerosolised salt-laden and pristine (salt-free) particles, and incubated for 24 h. Cell cultures were subsequently assessed for biological endpoints, including cytotoxicity (lactate dehydrogenase release), oxidative stress (oxidative stress-related gene expression; heme oxygenase 1 and NAD(P)H dehydrogenase [quinone] 1) and its (pro-)inflammatory response (tumour necrosis factor α, interleukin 8 and interleukin 1ß at gene and protein levels). RESULTS: In the lung cell model no significant effects were observed between the pristine and SO2-exposed particles, indicating that the surface salt deposits, and the underlying alterations to the substrate, do not cause acute adverse effects in vitro. Based on the leachate data, the majority of the sulphate salts from the ash surfaces are likely to dissolve in the lungs prior to cellular uptake. CONCLUSIONS: The findings of this study indicate that interaction of volcanic ash with SO2 during ash generation and transport does not significantly affect the respiratory toxicity of volcanic ash in vitro. Therefore, sulphate salts are unlikely a dominant factor controlling variability in in vitro toxicity assessments observed during previous eruption response efforts.

Ash aggregation enhanced by deposition and redistribution of salt on the surface of volcanic ash in eruption plumes.

Interactions with volcanic gases in eruption plumes produce soluble salt deposits on the surface of volcanic ash. While it has been postulated that saturation-driven precipitation of salts following the dissolution of ash surfaces by condensed acidic liquids is a primary mechanism of salt formation during an eruption, it is only recently that this mechanism has been subjected to detailed study. Here we spray water and HCl droplets into a suspension of salt-doped synthetic glass or volcanic ash particles, and produce aggregates. Deposition of acidic liquid droplets on ash particles promotes dissolution of existing salts and leaches cations from the underlying material surface. The flow of liquid, due to capillary forces, will be directed to particle-particle contact points where subsequent precipitation of salts will cement the aggregate. Our data suggest that volcanically-relevant loads of surface salts can be produced by acid condensation in eruptive settings. Several minor and trace elements mobilised by surface dissolution are biologically relevant; geographic areas with aggregation-mediated ash fallout could be "hotspots" for the post-deposition release of these elements. The role of liquids in re-distributing surface salts and cementing ash aggregates also offers further insight into the mechanisms which preserve well-structured aggregates in some ash deposits.