Prednisolone (PDNN) as an emergent micropollutant directly influences the regional ecological security. In this study, the degradation of PDNN by ultraviolet activated chlorine (UV/chlorine) oxidation process was comprehensively evaluated. The quenching experiment suggested that the PDNN degradation in UV/chlorine process was involved in the participation of hydroxyl radical (OH) and reactive chlorine species (RCS). Influence factors including chlorine dosage, pH, common anion and cation, fulvic acid (FA) on PDNN degradation via UV/chlorine process were investigated. A low chlorine (≤7.1 mg L−1) promoted the PDNN degradation, while a high chlorine dosage (>7.1 mg L−1) was adverse. The pH (4.0–10.0) showed negligible effect, while the investigated anions (Cl−, Br−, HCO3− and SO42−), NH4+ and FA exerted negative impact on PDNN degradation. An efficient process to minimize pharmaceutical micropollutants was the disposal of human urine containing a high concentration of pharmaceutical and potential toxic metabolites. An inhibitory effect was observed in the synthetic urine (fresh urine and hydrolyzed urine). The intermediates/products were identified and the mechanism of PDNN degradation was proposed. PDNN gone through three degradation routes, involving the direct addition of α, β-unsaturated ketone at C1 or C5, the photolysis of C17 and H-abstraction of C11. The main reactive sites were further determined by comparison of the frontier orbitals calculation and the proposed mechanism. Based on the toxicological tests for PDNN degradation, TP396 (TP396-C1Cl and TP396-C5Cl) and TP414-2-1 (TP414-C1ClC5OH) exhibited much higher toxicity than PDNN, and prolonging reaction time was necessary to achieve PDNN detoxification.
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