Oxidation of pyrazolone pharmaceuticals by peracetic acid: Kinetics, mechanism and genetic toxicity variations

Abstract

Peracetic acid (PAA) oxidation is an emerging technology in water disinfection and purification. This study evaluated the oxidation of three pyrazolone pharmaceuticals (i.e., Aminopyrine (AMP), Antipyrine (ANT), and Isopropylphenazone (PRP) by PAA. Experimental results showed that PAA exhibited structure selectivity to the above three pharmaceuticals and oxidized AMP with the highest reactivity. The degradation kinetics of AMP was investigated by calculating the apparent second-order rate constants (kapp) under different initial pH. Through kinetic simulation, the second-order rate constants of elementary reactions between AMP (i.e., neutral (AMP0) and protonated (AMP+) species) with PAA (i.e., neutral (PAA0) and anionic (PAA−) species) were obtained to be 0.34 ± 0.077 M−1 s−1(k”AMP+, PAA0), 0.89 ± 0.091 M−1 s−1(k”AMP0, PAA-) and 5.94 ± 0.142 M−1 s−1(k”AMP0, PAA0), respectively. The PAA could oxidize AMP via electrophilic attack, and the degradation site of AMP was confirmed to be the central nitrogen of –N(CH3)2 with the highest relative electrophilicity (sk-/sk+, 48.8614) by Density Functional Theory (DFT) calculation. The intermediates/products of AMP degradation were identified by high-performance liquid chromatography-mass spectrometry (LC-MS/MS), and the transformation pathways of AMP during PAA oxidation were inferred to be hydroxylation, demethylation, and CC cleavage. The genetic toxicity of AMP contaminated water could be reduced after PAA oxidation, which was evaluated by the micronucleus test of Vicia faba root tips.