Antibiotic-Induced Decoupling of CO ₂ , CH ₄ , and N ₂ O Emissions in Biofilters

In biofilters, antibiotics alter microbial community structure and function, thereby regulating emissions of carbon dioxide (CO 2 ), methane (CH 4 ), and nitrous oxide (N 2 O). However, these gases may respond differently due to distinct production pathways, resulting in decoupled emission dynamics that remain poorly understood. This study quantified CO 2, CH 4, and N 2 O emissions in biofilters exposed to sulfamethoxazole (SMX), assessed their integrated greenhouse impact using CO 2 -equivalent (CO 2 -eq), and explored the underlying microbial mechanisms. The results indicated that CO 2 and CH 4 emissions increased initially and then stabilized at higher SMX concentrations, while N 2 O emission rose at low concentrations but declined at higher levels, indicating decoupled responses. SMX served as a labile carbon source stimulating microbial metabolism and CO 2 and CH 4 production at low concentrations but inhibiting microbial activity at higher levels, reflecting a concentration-dependent shift. Although SMX inhibited nitrogen-transforming microorganisms, its impact on the nos Z gene involved in N 2 O consumption was more pronounced than on arch - amo A and nir S genes for N 2 O production, driving the initial N 2 O surge followed by decline. These gas-specific responses produced a nonlinear total CO 2 -eq pattern, with net climate forcing first increasing and then decreasing as SMX concentrations rose, accompanied by a diminishing marginal response per unit antibiotic exposure.