Enhanced norfloxacin oxidation with an Fe(VI)/peroxydisulfate-quinone process: iron species-driven multi-oxidation, quinone-based regulation, and density functional theory analysis

Abstract

The individual Fe(VI) as FeO4 2- or peroxydisulfate (PDS) oxidation process faces challenges of limited oxidation efficiency, excessive dosage consumption, and a narrow pH range. Fe is an important component in both Fe(VI) oxidation and PDS activation. We propose linking Fe in the combined Fe(VI)/PDS process to address the challenges of their individual processes. The contribution of Fe species to reactive oxygen species (ROS) production in the Fe(VI)/PDS process and the regulatory effects of quinones on Fe species in the Fe(VI)/PDS-benzoquinone (BQ) process were investigated. The reactive oxidation species generated by the Fe(VI)/PDS process included high-valency iron species such as Fe(VI), Fe(V), and Fe(IV); hydroxy radicals (∙OH), singlet oxygen (1O2), and SO4˙ˉ contributed differently at varying pH levels. PDS accelerated the conversion of Fe(VI) to Fe(V) and Fe(IV), which are more reactive, and facilitated their regeneration from Fe(III) and Fe(II). The Fe(II) concentration in the Fe(VI)/PDS process increased by 35.0 % after BQ addition, which enhanced PDS activation and shifted the dominant oxidizer from high-valency iron to ROS. In the Fe(VI)/PDS-BQ process, norfloxacin underwent oxidative degradation via piperazinyl ring degradation, defluorination, and quinolone group degradation, as evidenced by degradation byproducts and further supported by density functional theory calculations. The Fe(VI)/PDS-BQ process significantly reduced the toxicity of norfloxacin. A novel Fe(VI)/PDS-BQ process was developed with the potential to eliminate antibiotics from water and to identify the Fe-involved oxidation mechanism regulated by BQ addition and pH.