Unexpected mitigation of microplastic-induced nitrification inhibition by sulfamethoxazole: The pivotal roles of polymer aging and microbial metabolic shifts.

Microplastics (MPs) and antibiotics are ubiquitous emerging co-contaminants in wastewaters, yet how microplastic aging modulates their combined toxicity to biological nitrification remains poorly defined. This limits accurate risk assessment of MPs in biological treatment systems. Here, metagenomic sequencing was used to systematically compare the individual and combined effects of virgin and aged polyvinyl chloride (PVC) and polylactic acid (PLA) MPs, co-occurring with sulfamethoxazole (SMX), on nitrification in continuous-flow bioreactors. The results demonstrate that aging exerts polymer-specific contrasting effects: aging exacerbated PVC-induced nitrification inhibition, reducing nitrification rate decreased from 9.55 to 6.91 mg N/g-SS·h and increasing inhibition from 16.4% to 39.5%, while aging mitigated PLA-induced inhibition from 7.0% to 1.2%, driven by aging-altered surface properties and polymer-specific differences in dissolved organic carbon leaching. Unespectedly, co-exposure to 50 μg/L SMX alleviated microplastic-induced nitrification inhibition, reshaped microbial community structure by replacing dominant nitrifier Nitrospira with Nitrosomonas, and modulated the abundance of functional genes encoding ammonia monooxygenase to rewire nitrogen metabolism. These findings reveal that microplastic aging status and polymer identity are critical regulators of nitrification toxicity, and low-concentration antibiotic co-contamination can mitigate inhibition via microbial community and metabolic reprogramming, advancing mechanistic understanding of microplastic ecotoxicity in biological wastewater treatment.