Electro-activating of peroxymonosulfate via boron and sulfur co-doped macroporous carbon nanofibers cathode for high-efficient degradation of levofloxacin

化学 硫黄 阴极 降级(电信) 兴奋剂 碳纤维 纳米纤维 无机化学 化学工程 纳米技术 材料科学 有机化学 物理化学 复合材料 工程类 复合数 电信 光电子学 计算机科学
作者
Xian Li,Yongyou Hu,Changyong Zhang,Chun Xiao,Jianhua Cheng,Yuancai Chen
出处
期刊:Journal of Hazardous Materials [Elsevier]
卷期号:442: 130016-130016 被引量:70
标识
DOI:10.1016/j.jhazmat.2022.130016
摘要

To address the difficulty of precisely regulating the two-electron oxygen reduction reaction (2e-ORR) and investigate the synergistic effect of hydrogen peroxide (H2O2) and peroxymonosulfate (PMS), a heterogeneous electro-catalyst was synthesized via carbonation of boron (B) and sulfur (S) co-doping electrospun nanofibers containing iron and cobalt (B, S-Fe/Co@C-NCNFs-900), and used to degrade levofloxacin (Levo) in the electro-activating PMS with self-made cathode material (E-cathode-PMS) system. The morphological, structural, and electrochemical characteristics have been investigated. The results showed that B and S co-doping could remarkably enhance electron transfer and manage two-electron oxygen reduction, which was more favorable for H2O2 generation. Levo degradation efficiency could reach 99.63% with a reaction rate of 0.3056 min−1 in 20 min under the appropriate conditions (pH = 4, current = 20 mA, and [PMS] = 8.0 mM). The steady-state concentration of singlet oxygen (1O2) was calculated to be 669.17 × 10−14 M, which was 15.42, 29.74, and 45.00 times respectively than that of HO2·/O2·- (43.40 × 10−14 M), ·OH (22.25 × 10−14 M) and SO4-·(14.87 × 10−14 M), signifying that 1O2 was the predominant reactive oxygen species (ROS) involved in Levo removal. The high TOC removal (74.19%), low energy consumption (0.14 kWh m−3 order−1), few intermediates toxicity, and excellent Levo degradation efficiency for complex wastewater with various anions and matrixes showed the prospective practical applications of the E-cathode-PMS system. Overall, this study provides a useful strategy to regulate and control the 2e-ORR pathway.
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