Effect of electrolytes on the simultaneous electrochemical oxidation of sulfamethoxazole, propranolol and carbamazepine: behaviors, by-products and acute toxicity.

Abstract

In this work, the effect of supporting electrolytes on the simultaneous electrochemical oxidation of the pharmaceuticals sulfamethoxazole (SMX), propranolol (PRO), and carbamazepine (CBZ) in aqueous solutions has been studied. Based on the identified by-products, the degradation mechanisms were proposed and the acute toxicity was evaluated for each electrolyte. Assays were carried out in batch mode in a 2L undivided reactor using a niobium coated with boron-doped diamond (Nb/BDD) mesh anode and Ti cathode at 2.5A in presence of different supporting electrolytes (Na2SO4, NaCl, or NaBr) at the same concentration of 7mM. The degradation rates were higher in the assays with NaCl and NaBr. Reaction by-products were identified by gas chromatography-mass spectrometry. Indirect oxidation by electrogenerated reactive halogen species (RHS) was the main mechanism when halide ions were used as electrolytes. Ten by-products were detected using Na2SO4 as electrolyte, while 19 (12 non-halogenated and 7 halogenated) and 20 (10 non-halogenated and 10 halogenated) using NaCl and NaBr respectively. The proposed degradation pathways involve transformation (hydroxylation, deamination, desulfonation, and halogenation) and bond rupture to produce less molecular weight compounds and their further transformation until total degradation. Chlorinated and brominated by-products confirm halogenation reactions. The electrogenerated RHS presented a significant inhibition effect on Vibrio fischeri; nevertheless, acute toxicity was not presented using Na2SO4 as electrolyte and a pharmaceutical concentration of 5μg/L. In this view, the role of the supporting electrolyte in electrochemical oxidation process is crucial since it strongly influence degradation rate, by-products, and acute toxicity.