Enhanced venlafaxine degradation in amorphous FeS2 under redox-dynamic aqueous environments: Critical role of citrate in electron utilization for boosted hydroxyl radical generation.

Pharmaceuticals and organic acids ubiquitously coexist in urban riverine environments, yet the transformation mechanisms of antidepressants like venlafaxine (VNF) in iron sulfide-rich sediments under redox-dynamic conditions remain poorly resolved. This study comprehensively analyzed adsorption/desorption dynamics and reactive oxygen species (ROS)-mediated oxidative degradation of VNF in amorphous iron sulfide (FeS2(am)), emphasizing the role of citric acid (CA) in modifying these interactions. Our results revealed that VNF was stably adsorbed onto FeS2(am) under anoxic conditions with no observable degradation. Conversely, exposure to O2 triggered rapid desorption of VNF (93.58 %) and its partial degradation (16.96 %) mediated by hydroxyl radicals (•OH). Remarkably, CA amendment significantly promoted VNF degradation under oxic conditions, achieving 97.36 % degradation and increasing the observed rate constant (kobs) 17.4-fold (from 6.38 × 10-4 to 1.11 × 10-2 min-1). Mechanistically, CA optimized electron utilization efficiency in FeS2(am) through three synergistic pathways: (i) generation of carbon-centered radicals that amplified secondary •OH production via Fenton-like chain reactions; (ii) acceleration of Fe2+ regeneration through enhanced electron transfer from sulfur intermediates (e.g., S2-, S0) to Fe3+; and (iii) elevation of H2O2 into •OH conversion efficiency from 57.20 % to 83.20 %. Electrochemical analyses corroborated that CA enabled a more efficient four-electron O2 reduction pathway, thereby enhancing electron utilization for rapid •OH generation. Density functional theory calculations combined with LC-Orbitrap-HRMS analyses identified nine distinct VNF degradation pathways. Additionally, ECOSAR results indicated a significant reduction in ecotoxicity of the transformation products compared to the parent compound. Collectively, these findings pave the way for developing ligand-enhanced in situ remediation strategies for antidepressant contaminants in redox-dynamic sediments.