Influence Mechanism of Anions on Iron Doping into Swine Bone Char: Promoting Non-Radical Oxidation of Acetaminophen in a Fenton-like System.

The application of iron-doped biochar in peroxymonosulfate (PMS) activation systems has gained increasing attention due to their effectiveness and environmental friendliness in addressing environmental issues. However, the behavioral mechanism of iron doping and the detailed O-1(2) generation mechanism in PMS activation systems remain ambiguous. Here, we investigated the effects of three anions (Cl-, NO(3)(-)and SO42-) on the process of iron doping into bone char, leading to the synthesis of three iron-doped bone char (Fe-ClBC, Fe-NBC and Fe -SBC). These iron-doped bone char were used to catalyze PMS to degrade acetaminophen (APAP) and exhibited the following activity order: Fe-ClBC > Fe-NBC > Fe-SBC. Characterization results indicated that iron doping primarily occurred through the substitution of calcium in hydroxyapatite within BC. In the course of the impregnation, the binding of SO42- and Ca2+ hindered the exchange of iron ions, resulting in lower catalytic activity of Fe-SBC. The primary reactive oxygen species in the Fe-ClBC/PMS and Fe-NBC/PMS systems were both O-1(2). O-1(2) is produced through O-2(center dot-) conversion and PMS self-dissociation, which involves the generation of metastable iron intermediates and electron transfer within iron species. The presence of oxygen vacancies and more carbon defects in the Fe-ClBC catalyst facilitates O-1(2) generation, thereby enhancing APAP degradation within the Fe-ClBC/PMS system. This study is dedicated to in-depth exploration of the mechanisms underlying iron doping and defect materials in promoting O-1(2) generation.