Electrochemical degradation of atrazine by BDD anode: Evidence from compound-specific stable isotope analysis and DFT simulations

Direct charge transfer (DCT) and center dot OH attack played important roles in contaminant degradation by BDD electrochemical oxidation. Their separate contributions and potential bond-cleavage processes were required but lacking. Here, we carried out promising compound-specific isotope fractionation analysis (CSIA) to explore C-13 and H-2 isotope fractionation of atrazine (ATZ), followed by assessing the reaction pathway by BDD anode. The correlation of H-2 and C-13 fractionation allows to remarkably differentiate DCT process and center dot OH attack, with L values of 18.99 and 53.60, respectively. Radical quenching identified that center dot OH accounted for 79.0%-88.5% in the whole reaction. While CSIA methods provided biased results, which suggested that ATZ degradation exhibited two stages with center dot OH contributions of 24.6% and 84.3% respectively, confirming CSIA was more sensitive and provided more possibilities to estimate degradation processes. Combined with Fukui index and intermediate products identification, we deduced that dechlorination-hydroxylation mainly occurred in the first 30 min by DCT reaction. While lateral chain oxidation with C-N broken was the governing route once center dot OH was largely generated, with the production of DEA (m/z 188), DIA (m/z 174), DEIA (m/z 146) and DEIHA (m/z 128). Our results demonstrated that isotope fractionation can offer isotopic footprints for identifying the rate-limiting steps and bond breakage process, and opens new avenues for degradation pathways of contaminants. (C) 2021 Elsevier Ltd. All rights reserved.

Automated summary

This study explored the reaction pathway of atrazine degradation by BDD electrode through compound-specific isotope fractionation analysis, revealing a significant correlation between H-2 and C-13 isotope fractionation. Radical quenching identified that ·OH radicals played a dominant role in the overall degradation reaction.