Efficient Degradation of 4-Acetamidoantipyrin Using a Thermally Activated Persulfate System

The extensive use of pharmaceuticals and personal care products (PPCPs) causes high concentrations of pharmaceutical metabolites to exist in aquatic environments. Though the removal of parent PPCPs has raised concerns, the degradation of pharmaceutical metabolites was rarely investigated. In this study, the degradation of 4-acetylaminoantipyrine (4-AAA), a typical dipyrone metabolite frequently detected worldwide in surface water and wastewater, was initially studied using persulfate (PDS)-based advanced oxidation processes (AOPs). Compared with commonly used activation methods of alkali, ultrasonic, ultraviolet, and Fe2+, 4-AAA achieved its best degradation (98.9%) within 30 min in a thermally activated PDS system due to the promotion of both radical production and the reaction rate with the rise in temperature. The optimum degradation of 4-AAA could be achieved with the temperature of 80 degrees C regardless of initial pH values, indicating a wide suitable pH range. Moreover, over 80% of the degradation of 4-AAA could be achieved with the presence of Cl- (0-16 mM), HCO3- (0-8 mM), and humic acid (0-30 mg/L), further indicating the application potential of the system. Both sulfate radicals (SO4 center dot-) and hydroxyl radicals (center dot OH) contributed to 4-AAA degradation and the contribution of center dot OH increased with the pH rising from 3 to 11 due to the transformation from SO4 center dot- when reacting with OH-. Three hydroxylated and ring-opening intermediates were detected during the 4-AAA degradation. The ECOSAR prediction indicated that the acute toxicity of most intermediates decreased than 4-AAA while the chronic toxicity increased, which suggested the transformation of intermediates should be further focused on in SO4 center dot- and center dot OH based AOPs. This study would provide technical reference for the control of 4-AAA in wastewater treatment processes, raise concerns on the influence of PPCPs metabolites, and throw light on reducing the harm of PPCPs and their metabolites in aquatic environments.