Electrochemical Treatment of the Antibiotic Sulfachloropyridazine: Kinetics, Reaction Pathways, and Toxicity Evolution

Abstract

The electro-Fenton treatment of sulfachloropyridazine (SCP), a model for sulfonamide antibiotics that are widespread in waters, was performed using cells with a carbon-felt cathode and Pt or boron-doped diamond (BDD) anode, aiming to present an integral assessment of the kinetics, electrodegradation byproducts, and toxicity evolution. H(2)O(2) electrogeneration in the presence of Fe(2+) yielded (•)OH in the solution bulk, which acted concomitantly with (•)OH adsorbed at the anode (BDD((•)OH)) to promote the oxidative degradation of SCP (k(abs,SCP) = (1.58 ± 0.02) × 10(9) M(-1) s(-1)) and its byproducts. A detailed scheme for the complete mineralization was elucidated. On the basis of the action of (•)OH onto four different SCP sites, the pathways leading to total decontamination includes fifteen cyclic byproducts identified by HPLC and GC-MS, five aliphatic carboxylic acids, and a mixture of Cl(-), SO(4)(2-), NH(4)(+), and NO(3)(-) that accounted for 90-100% of initial Cl, S, and N. The time course of byproducts was satisfactorily correlated with the toxicity profiles determined from inhibition of Vibrio fischeri luminescence. 3-Amino-6-chloropyridazine and p-benzoquinone were responsible for the increased toxicity during the first stages. Independent electrolyses revealed that their toxicity trends were close to those of SCP. The formation of the carboxylic acids involved a sharp toxicity decrease, thus ensuring overall detoxification.

Adsorption and reaction of sulfachloropyridazine sulfonamide antibiotic on a high silica mordenite: A structural and spectroscopic combined study

“…In the light of the GC-MS and NMR results the reaction product was undoubtedly identified as 4-amino-N-(6-hydroxyl-3-pyridazinyl)benzene sulfonamide (see structure in Table 1). The same structure has been proposed in a previous work on the basis of MS spectra of degradation products obtained by electrochemical destruction of sulfachloropyridazine [42].…”

Efficient degradation of sulfamethoxazole by the Fe(II)/HSO5− process enhanced by hydroxylamine: Efficiency and mechanism

“…P-189 could be further oxidized to lose sulfuric acid and finally yield aniline (P-94), which indicated the reactivity of sulfonated moiety with HO • (Gonçalves et al, 2012). For the pathway B, hydroxylamine derivative of SMX (P-269) with m/z of [M+16] + indicated the attack of HO • through abstracting the hydrogen of -NH2 to form hydroxylamine moiety (Dirany et al, 2012). The hydroxylamine moiety of P-269 could be further oxidized by HO • to yield nitroso-SMX (P-267) and nitro-SMX (P-283) (Kim C. et al, 2015).…”

UV photolysis kinetics of sulfonamides in aqueous solution based on optimized fluence quantification

“…The pollution sources of antibiotics are mainly discharges from sewage treatment plants, pharmaceutical industrial wastewater, and landfill leachate (Dirany et al, 2012). Sulfonamides (SAs) represent one important class of antibiotics commonly used in veterinary and human medical practices because of their broad antimicrobial spectrum, strong antibacterial activity, stable chemical property, and low price (Hess et al, 1999;Huang et al, 2012).…”

“…Sulfonamides (SAs) represent one important class of antibiotics commonly used in veterinary and human medical practices because of their broad antimicrobial spectrum, strong antibacterial activity, stable chemical property, and low price (Hess et al, 1999;Huang et al, 2012). SAs are amphoteric and water-soluble compounds with a high environmental mobility (Dirany et al, 2012), so their traces are ubiquitous in almost all waters (e.g., waste, surface, ground, and drinking waters) (Lanuza, 2010;Capdeville and Budzinski, 2011;Fatta-Kassinos et al, 2011). Even though no direct human health effects have been reported (Le et al, 2005), SAs tend to bio-accumulate and have potential adverse effects on aquatic and terrestrial ecosystems by interrupting the normal activities of some microorganisms as well as developing and spreading antibiotic resistance genes (Elmolla and Chaudhuri, 2010;Rivas et al, 2011;Yuan et al, 2011).…”