Role of co-existing anions in non-radical and radical processes of carbocatalyzed persulfate activation for acetaminophen degradation

We investigated the effect of co-existing anions of Cl-, SO42-, NO3-, CO32-, and HCO3- on potassium persulfate (PS) activation by multiwalled carbon nanotubes (MWCNTs) and N-doped MWCNTs (N-MWCNTs) for acetaminophen (ACP) degradation. The results of radical quenching studies and electron paramagnetic resonance (EPR) analyses affirmed that non-radical (O-1(2)) and radical (O-2(-), HO, and SO4-) species initiated the ACP degradation. Catalytic performance studies demonstrated that CO32- and HCO3- provided higher ACP degradation compared to Cl-, SO42-, and NO3-. The observed beneficial and adverse impacts of Cl-, SO42-, and NO3- depend on their concentration. EPR analysis confirms that the radical pathway was modified in the presence of CO32- or HCO3-, which proved that HO and SO4- were scavenged by CO32- and HCO3-. Non-radical TEMP-O-1(2) adduct signals were not changed by co-existing anions, inferring that the high selectivity O-1(2) species were resistant to the impact of co-existing anions. An ACP degradation mechanism via electron transfer, acetamide cleavage, mono- and dihydroxylation was proposed based on liquid chromatography-mass spectroscopy analysis. The co-existing anions did not noticeably affect the formation of degradation products via the electron transfer mediative pathway, however, Cl-, SO42- and CO32- notably limited the di-hydroxylation pathways.

Automated summary

We investigated the effect of co-existing anions on the activation of potassium persulfate by multiwalled carbon nanotubes and N-doped multiwalled carbon nanotubes for the degradation of acetaminophen. The results showed that CO32- and HCO3- had a higher catalytic performance compared to Cl-, SO42-, and NO3-. The presence of CO32- and HCO3- modified the radical pathway, while the non-radical pathway was not affected by co-existing anions. Co-existing anions did not significantly affect the formation of degradation products via the electron transfer mediative pathway, but limited the di-hydroxylation pathways.