Impact of biochar amendment on antibiotic removal and ARGs accumulation in constructed wetlands for low C/N wastewater treatment

Constructed wetlands (CWs) amended with biochar to stimulate antibiotic and antibiotic resistance genes (ARGs) removal from carbon restricts wastewater holds particular application prospect due to high efficiency and good stability. In this study, we conducted biochar amended constructed wetland (BCW) and non-biochar amended constructed wetland (NCW) to explore the feasibility and mechanisms for sulfamethoxazole (SMX) and ARGs removal from low C/N wastewater. Results showed that biochar-amended considerably stimulated the biological oxidation and reduction process in CW, as evidenced by higher chemical oxygen demand (COD), nitrogen, and SMX removal performance (7.1 +/- 2.6 %, 19.8 +/- 3.6 %, 36.8 +/- 6.2 %) than that in NCW. The accumulation of ARGs was negatively associated with SMX removal efficiency, where the int and sul genes performed lower concentration in BCW due to the higher SMX removal efficiency. The biochar's dissolved organic carbon release in CWs indicated that water and alkaline media portray the optimum conditions for SMX and ARGs removal. Microbial community analysis exposed that more functional consortia capable of SMX metabolism (e.g., Arthrobacter, Ramlibacter, Flavobacterium, and norank_f_JG30-KF-CM45) were enriched in BCW. This study demonstrated the feasibility and mechanism of biochar-amended CWs for regulated SMX removal and ARGs accumulation, which provides new insights for enhancing the depuration ability of CWs.

Automated summary

This study explored the feasibility and mechanism of biochar-amended constructed wetlands for regulating the removal of sulfamethoxazole and accumulation of antibiotic resistance genes in low C/N wastewater. Results showed that biochar amendment significantly enhanced the oxidation and reduction reactions in the wetlands, leading to improved removal of COD, nitrogen, and sulfamethoxazole, as well as reduced accumulation of antibiotic resistance genes.