Redox cycling of tetrahedral iron drives the Fenton-reactivity of chrysotile asbestos
Description
Chrysotile asbestos is a carcinogenic fibrous mineral. Its pathogenicity is partly governed by the ability of Fe on the fiber surface to catalyze the Fenton reduction of H2O2 (which is produced during inflammatory processes) to the highly toxic hydroxyl radical (HO•). Recently, tetrahedrally coordinated Fe (Fetet) in the fibers’ Si layers was identified as the principal Fe species to catalyze this process. However, as only ferric Fetet (Fe3+tet) substitutes Si tetrahedra in chrysotile, Fetet needs to redox cycle to ferrous Fetet (Fe2+tet) to facilitate fiber-mediated reductions of H2O2 to HO•. This redox cycling has never been experimentally investigated. Here we demonstrate, by consecutive ascorbate and O2 treatments, that structural Fetet in exposed Si layers of chrysotile fibers can redox cycle between Fe3+tet and Fe2+tet. Reduction, back-oxidation and re-reduction of Fe3+tet did not labilize the exposed Si layer and, consequently, did not promote fiber dissolution. However, in the presence of H2O2, prolonged redox cycling of Fetet increased fiber dissolution, presumably by accelerating Fetet dissolution and subsequent labilization of the exposed Si layer. The concentration of Fetet sites undergoing redox cycling on chrysotile surfaces generally decreased as a consequence of fiber dissolution. However, a rebound in Fe3+tet surface site concentration and associated Fenton-reactivity were observed when Fe3+tet-depleted layers were dissolved off the chrysotile fiber surfaces. Our results demonstrate that redox cycling of Fetet on chrysotile surfaces produces Fe2+tet surface sites, which – as the ultimate Fenton reactive iron species on chrysotile – contribute to the fibers’ adverse chemical reactivity.