David Damby
Claire J. Horwell
Paul M Ayris
Pierre Delmelle
Christopher J Ottley
Pablo Cubillas
Ana S Casas
Christoph Bisig
Alke Petri-Fink
Donald B. Dingwell
Martin J D Clift
Barbara Drasler
Barbara Rothen-Rutishauser
Ines Tomasek
2019
<div id="abssec0010"><h3 id="sectitle0015" class="u-h4 u-margin-m-top u-margin-xs-bottom">Background</h3><p id="abspara0010"><span>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 (SO</span><sub>2</sub><span>) gas, and the resulting presence of sulphate salt deposits on particle surfaces, influences toxicity to the respiratory system, using an advanced </span><i>in vitro</i><span> </span>approach.</p></div><div id="abssec0015"><h3 id="sectitle0020" class="u-h4 u-margin-m-top u-margin-xs-bottom">Methods</h3><p id="abspara0015">To emplace surface sulphate salts on particles,<span> </span><i>via</i><span> 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 SO</span><sub>2</sub><span> 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 1β at gene and protein levels).</span></p></div><div id="abssec0020"><h3 id="sectitle0025" class="u-h4 u-margin-m-top u-margin-xs-bottom">Results</h3><p id="abspara0020">In the lung cell model no significant effects were observed between the pristine and SO<sub>2</sub>-exposed particles, indicating that the surface salt deposits, and the underlying alterations to the substrate, do not cause acute adverse effects<span> </span><i>in vitro</i>. 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.</p></div><div id="abssec0025"><h3 id="sectitle0030" class="u-h4 u-margin-m-top u-margin-xs-bottom">Conclusions</h3><p id="abspara0025">The findings of this study indicate that interaction of volcanic ash with SO<sub>2</sub><span> </span>during ash generation and transport does not significantly affect the respiratory toxicity of volcanic ash<span> </span><i>in vitro</i>. Therefore, sulphate salts are unlikely a dominant factor controlling variability in<span> </span><i>in vitro</i><span> </span>toxicity assessments observed during previous eruption response efforts.</p></div>
application/pdf
10.1016/j.envres.2019.108798
en
Elsevier
Assessment of the potential for in-plume sulphur dioxide gas-ash interactions to influence the respiratory toxicity of volcanic ash
article