Sodium Acetate-Modulated Fe(III)/O3 Homogeneous Catalytic Ozonation for Sulfamethoxazole Removal: Performance, Oxidation Pathways, and Toxicity Assessment
Sulfamethoxazole (SMX), a persistent sulfonamide antibiotic widespread in aquatic environments, resists conventional water treatment degradation. This work developed a NaOAc/Fe3+/O3 homogeneous ozonation system for SMX abatement. Four comparative reaction groups confirmed significant synergism between trace Fe3+ and sodium acetate. Under optimized near-neutral conditions, 96.19% SMX was removed within 30 min with kobs = 0.107 min−1, outperforming sole O3, O3/NaOAc and O3/Fe3+ by 11.0%, 31.0% and 21.9% respectively. Single-factor tests revealed excess Fe3+ or acetate suppressed catalytic activity, while alkaline conditions accelerated degradation yet aggravated iron precipitation. Radical quenching and p-CBA probing indicated that acetate coordination did not increase bulk ·OH exposure, while the stronger TEMP-derived TEMPO response after acetate addition was consistent with enhanced 1O2-associated oxidation, suggesting that acetate altered the relative contributions of ozone-derived oxidation pathways. Post acetate background deduction, the ternary system achieved higher TOC/COD elimination. Twelve SMX intermediates were identified via LC-MS, with three ring-opening degradation pathways proposed. QSAR toxicity evaluation indicated that most intermediates possessed lower bioconcentration and developmental risks than raw SMX. Overall, the results indicate that weak acetate ligands can alter iron-mediated ozone oxidation pathways, providing a low-dose and economical strategy for antibiotic wastewater treatment.
Authors
- He Guo
- Fan Yang
- Jingsi Liu
Institutions
- Nanjing Forestry University (CN)
- Beijing Municipal Ecological and Environmental Monitoring Center (CN)
Publication Details
- Journal
- Catalysts
- Published
- 2026-08-26
- DOI
- https://doi.org/10.3390/catal16090769
- Primary Topic
- Advanced oxidation water treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00