Oxygen vacancies induced by Fe doping rewire MnO2 reactivity to sustain cephalosporin degradation at neutral and alkaline pH

Cephalosporins are widely used β -lactam antibiotics frequently detected in aquatic environments, posing risks to ecosystem health and contribute to the dissemination of antibiotic resistance. Manganese dioxide (MnO 2 ) has attracted considerable attention as a low-cost oxidant for cephalosporin degradation. However, its performance is severely limited under neutral and alkaline conditions. Here, we demonstrate that defect-rich ε -MnO 2 achieved over 60% removal of eight representative cephalosporins at pH 7.0 through the combined contributions of Mn redox reactions and oxygen-vacancy-mediated reactive oxygen species (ROS) pathways. Fe doping further increased surface oxygen-vacancy density and catalytic activity, producing Fe- ε -MnO 2 with boosted degradation performance across a broad pH range (3.0–11.0). Using ceftriaxone as a model compound, mechanistic investigations revealed that singlet oxygen ( 1 O 2 ) dominated under neutral conditions, whereas hydroxyl radicals (•OH) became increasingly important under alkaline conditions, compensating for reduced lattice-mediated oxidation and partially suppressed 1 O 2 production. To facilitate catalyst recovery and practical application, Fe- ε -MnO 2 was immobilized in situ onto a commercial melamine sponge, forming a stable composite with effective performance in diverse real water matrices. Toxicity assays confirmed substantial detoxification of ceftriaxone after treatment. Overall, this study demonstrates that defect-rich MnO 2 combined with Fe doping provides an effective strategy for enhancing antibiotic degradation and expanding catalytic activity across a wide pH range.