Comprehensive assessment of toxicity and environmental risk associated with sulfamethoxazole biodegradation in sulfur-mediated biological wastewater treatment.

Incomplete mineralization of sulfamethoxazole (SMX) in wastewater treatment systems poses a threat to ecological health. The toxicity and environmental risk associated with SMX biodegradation in the sulfur-mediated biological process were examined for the first time through a long-term (180 days) bioreactor study and a series of bioassays. The results indicated that the sulfur-mediated biological system was highly resistant and tolerant to SMX toxicity, as evidenced by the enrichment of sulfate-reducing bacteria (SRB), the improved microbial metabolic activity, and the excellent performance on pollutants removal under long-term SMX exposure. SMX can be effectively biodegraded by the cleavage and rearrangement of the isoxazole ring, hydrogenation and hydroxylation reactions in sulfur-mediated biological wastewater system. These biodegradation pathways effectively reduced the acute toxicity, antibacterial activity, and ecotoxicities of SMX and its biotransformation products (TPs) in the effluent of the sulfur-mediated biological system. The TPs produced via hydrogenation (TP1), hydroxylation, and isoxazole ring cleavage (TP3, TP4, TP5, TP8, and TP9) exhibited lower toxicity than SMX. Under SMX stress, although the abundance of sulfonamide resistance genes increased, the total abundance of ARGs decreased due to the extrusion of some intracellular SMX by the efflux pump genes and the inactivation of some SMX through the biodegradation process. Efflux pump and inactivation, as the main resistance mechanisms of antibiotics in the sulfur-mediated biological system, play a crucial role in microbial self-defense. The findings of this study demonstrate the great potential of the sulfur-mediated biological system in SMX removal, detoxication, and ARGs environmental risk reduction.

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Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.