The components of volcanic ash are derived, in the truest sense, from the chemistry of the Earth, and the morphologies of ash particles are shaped by the most energetic force of nature.
Its mineral assemblage is source dependent, but can comprise any number of potentially toxic elements. For example, ash can contain the classically toxic crystalline silica (Baxter et al., 1999; Dollberg et al., 1986), including crystalline-silica nanofibres (Reich et al., 2009); a prominent morphology-of-interest in particle toxicology research. In addition to hazardous minerals, reactivity can be mediated by surface chemistry. For example, iron at the surface of particleshas been implicated in the pathogenic response to particulate matter (Fubini et al., 1995b). Freshly erupted ash differs from other hazardous particles in that the surfaces are un-weathered (and therefore not oxidised) or leached. As such, freshly erupted ash can serve as a carrier of adsorbed species, including fluorides, sulphates, chlorides, and various heavy
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metals. Similarly, there may be condensed acidic volatiles, polycyclic hydrocarbons, halogens and anthropogenic pollutants adsorbed to the surface (Horwell and Baxter, 2006).
With the available chemistry and temperatures in an eruptive column, even the formation of polychlorinated dibenzodioxins (PCDDs) on solid surfaces could be envisaged, as has been seen on fly ash (Lu et al., 2007). Therefore, it is difficult, from a toxicity perspective, to constrain the components responsible for the potential toxicity of ash as well as the contribution of each.
The toxicity of a particle is unlikely to be based upon a single overriding attribute which dictates toxicity, and it will likely be a combination of a variety of factors that come into play at different times during a particle’s journey from formation to exposure to internal effective dose to causation of a clinical disease (Boffetta, 1994). As noted, volcanic ash has the potential to cause harm through a variety of mechanisms. Two of the better established mineral-based pathways result from the presence of surface iron (Horwell et al., 2007;
Horwell et al., 2003a), with the corresponding generation of reactive oxygen species (ROS), especially the hydroxyl radical (•OH), and from the presence of crystalline silica, for which the pathogenic mechanisms of silica-induced inflammation and fibrosis are not well understood.
2.6.1 Oxidation-Reduction Chemistry
The transfer of electrons between a mineral and fluid drives a number of geochemical processes. Similarly, several lines of evidence support the notion that electron transfer processes at the surface of minerals are important in pathogenesis .Electron transfer has been attributed to the increased biological activity and heighted formation of free radicals associated with freshly fractured quartz compared to aged quartz (Fubini et al., 1987;
Vallyathan et al., 1991; Vallyathan et al., 1988). Further, Fubini et al. (1995b) reported that magnetite will break down hydrogen peroxide but hematite will not, suggesting ion (e.g., iron) coordination on the crystal face plays an important role in the formation of free radicals. Indeed, this has been confirmed for volcanic ash, and is considered in Chapter 6. In this way, minerals which provide a reaction surface to donate or accept electrons or protons can function in a similarly catalytic way to biological enzymes. At physiological temperatures, rates may be too low to effectively measure, but may be sufficiently high to provide a chronic source (or sink) of electrons for reduction (or oxidation) of fluid species to form free radicals.
The donor-acceptor characteristics of framework silicates are strongly influenced by the substitution of aluminium for silicon in the tetrahedral framework (Guthrie and Heaney, 1995). This substitution can be charge compensated in a number of ways, including the
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association of a proton with the under-bonded oxygen atoms around the aluminium, or by the presence of Na+ as was shown for volcanic cristobalite (e.g., Horwell et al., accepted). A number of different sites can exist on the surface of a mineral, and range from silanol groups (Si-O-OH) to the aluminium equivalent (Al-O-H) and protons associated with an aluminium exchange (e.g., Al-O(H)-Si). Surface sites (e.g., silanol groups) are thought to be responsible for silica toxicity because they function as hydrogen donors (Guthrie, 1997).
2.6.2 Crystalline Silica
The mechanism of silica-induced inflammation and fibrosis are still poorly understood (Mossman and Churg, 1998), although it is generally believed that no single characteristic is responsible for silica toxicity (Fubini, 1998). Exposure to crystalline silica results in the activation of both alveolar type II cells (Hefland et al., 2001; Hook and Viviano, 1996) and macrophages (Hamilton et al., 2008), amongst other cell types. Research into the mechanisms of silica-induced disease has focused on the physicochemical properties, particle retention and translocation, surface chemistry at silica-cell interfaces (e.g., Fubini et al., 1995a; Schins et al., 2002), and inflammatory response.
Historically, crystallinity has been considered a prerequisite for silica toxicity. Recent work, however, has shown completely amorphous vitreous silica to be cytotoxic and capable of generating free radicals, calling into question the role of crystallinity (Ghiazza et al., 2010).
Recently, global gene expression profiling was used to identify significantly affected gene expression following silica exposure in cultured type II epithelial cells and in the lungs of rats (Sellamuthu et al., 2011; Sellamuthu et al., 2012). The identified functions perturbed by silica exposure were involved in oxidative stress, inflammation, cancer, cellular proliferation and development, tissue remodelling and fibrosis; however, unresolved inflammation was the single most significant biological response to silica exposure. Further, excessive mucous production was identified as a potential novel mechanism for silica-induced pulmonary toxicity. Silica toxicity has also been linked to destabilisation of the phagosome, the vesicle formed around a particle engulfed by phagocytosis, following uptake (Hornung et al., 2008).
This process can result in apoptotic cell death and concomitant release of the ingested particle, which is available to be engulfed by another macrophage, initiating a cycle of sustained inflammation (Huaux, 2007).
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