Stage-wise far-UVC/chlorine process curbs antimicrobial resistance in hospital wastewater: Short-burst inactivation and sustained suppression of recovery and resistance transfer.

Conventional UV254/chlorine can leave incomplete genetic damage and create a low-dose window that promotes horizontal gene transfer (HGT), limiting reliable antimicrobial-resistance (AMR) control. Here, UV222/chlorine (1 mg/L free chlorine) was evaluated in 0.22-μm-filtered hospital wastewater inoculated with E. coli DH5α-RP4 and compared with UV222, UV254, and UV254/chlorine. During UV222/chlorine treatment in hospital wastewater, free available chlorine (FAC) declined rapidly and approached the detection limit at approximately 35 mJ/cm2, whereas UV254/chlorine retained measurable FAC at 100 mJ/cm2. Chloride promoted conversion of Cl· to selective Cl2·-, whereas tert-butanol quenching indicated a smaller contribution from ·OH. Accordingly, the process comprised an initial chlorine-enhanced phase (0-35 mJ/cm2), which delivered ∼2.5-log greater ARB inactivation than UV222 alone, followed by a UV222-dominated phase after FAC depletion. Membrane permeabilization largely saturated during Stage 1, supporting an acute rather than dose-proportional envelope attack. At 100 mJ/cm2, UV222/chlorine prevented regrowth, reduced intracellular antibiotic resistance genes (ARGs) by 76.6-88.3%, and drove RP4 conjugation toward zero. In contrast, UV254/chlorine transiently increased conjugation to ∼150% of the control at low doses. Transcriptomics showed concurrent suppression of envelope maintenance, DNA repair, protein homeostasis, and metabolism. Thus, UV222/chlorine combines a short RCS shock with sustained multi-target damage to control ARB, ARG persistence, and plasmid-mediated HGT in complex wastewater.