This paper reports that the main component of respirable volcanic ash, allophane, induces lipid peroxidation (LP), the oxidative degradation of lipids in cell membranes, and cytotoxicity in murin monocyle/macrophage cells. Naturally-occurring allophane collected from New Zealand, japan, and Ecuador was studied. The quantification of LP was conducted using the Thiobarbituric Acid Reactive Substances (TBARS) assay. The cytotoxic effect was determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide calorimetric assay. Electron-Paramagnetic Resonance (EPR) determinations of naturally-occurring allophane confirmed the incorporation in the structure and clustering of structural Fe3+, and nucleation and growth of small-sized Fe (oxyhydr)oxide or gibb-site. LP induced by allophane varied with time, and solid concentration and composition, reaching 6.7 +/- 0.2 nmol TBARS mg prot(-1). LP was surface controlled but not restricted by structural or surfacebound Fe3+, because redox processes induced by soluble components other than perferryl iron. The reactivity of Fe3+ soluble species stemming from surface-bound Fe3+ or small-sized Fe3+ refractory minerals in allophane surpassed that of structural Fe3+ located in tetrahedral or octahedral sites of phyllosilicates or bulk iron oxides. Desferrioxamine B mesylate salt (DFOB) or ethylenediaminetetraacetic acid (EDTA) inhibited LP. EDTA acted as a more effective inhibitor, explained by multiple electron transfer pathways. Registered cell-viability values were as low as 68.5 +/- 6.7%. (C) 2014 Elsevier B.V. All rights reserved.