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 center dot). 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 (Fe-tet(3+)) substitutes Si tetrahedra in chrysotile, Fe-tet needs to redox cycle to ferrous Fe-tet (Fe-tet(2+)) to facilitate fiber-mediated reductions of H2O2 to HO center dot. This redox cycling has never been experimentally investigated. Here we demonstrate, by consecutive ascorbate and O-2 treatments, that structural Fe-tet in exposed Si sheets of chrysotile fibers can redox cycle between Fe-tet(3+) and Fe-tet(2+). Reduction, back-oxidation, and rereduction of Fe-tet(3+) 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 Fe-tet(3+) surface site concentration and associated Fenton reactivity once Fe-tet(3+)-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 Fe-tet(2+) surface sites, which, as the ultimate Fenton reactive iron species on chrysotile, contribute to the fibers' adverse chemical reactivity.

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ACS Earth and Space Chemistry

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American Chemical Society