Redox Cycling of Tetrahedral Iron Drives the Fenton Reactivity of Chrysotile Asbestos

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 form the highly toxic hydroxyl radical (HO^•). Recently, tetrahedrally coordinated Fe (Fe_tet) in the fibers’ Si sheets was identified as the principal Fe species to catalyze this process. However, as only ferric Fe_tet (Fe³⁺_tet) substitutes Si tetrahedra in chrysotile, Fe_tet needs to redox cycle to ferrous Fe_tet (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 Fe_tet in exposed Si sheets of chrysotile fibers can redox cycle between Fe³⁺_tet and Fe²⁺_tet. Reduction, back-oxidation, and rereduction of Fe³⁺_tet did not labilize the exposed Si sheet and, consequently, did not promote fiber dissolution. However, in the presence of H₂O₂, prolonged redox cycling of Fe_tet increased fiber dissolution, presumably by accelerating Fe_tet dissolution and subsequent labilization of the exposed Si sheet. Chrysotile fibers for which the concentration of Fe_tet surface sites undergoing redox cycling was lowered through selective Fe removal showed a rebound in Fe³⁺_tet surface site concentration and associated Fenton reactivity once Fe³⁺_tet-depleted Si sheets were dissolved off from the fiber surfaces. To conclude, our results demonstrate that redox cycling of Fe_tet 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.