Suppression of photoreactivation of E. coli by excimer far-UV light (222 nm) via damage to multiple targets.

Low-pressure mercury lamps emitting at 254 nm (UV254) are used widely for disinfection. However, subsequent exposure to visible light results in photoreactivation of treated bacteria. This study employed a krypton chloride excimer lamp emitting at 222 nm (UV222) to inactivate E. coli. UV222 and UV254 treatment had similar E. coli-inactivation kinetics. Upon subsequent irradiation with visible light, E. coli inactivated by UV254 was reactivated from 2.71-log to 4.75-log, whereas E. coli inactivated by UV222 showed negligible photoreactivation. UV222 treatment irreversibly broke DNA strands in the bacterium, whereas UV254 treatment primarily formed nucleobase dimers. Additionally, UV222 treatment caused cell membrane damage, resulting in wizened, pitted cells and permeability changes. The damage to the cell membrane was mainly due to the photolysis of proteins and lipids by UV222. Furthermore, the photolysis of proteins by UV222 destroyed enzymes, which blocked photoreactivation and dark repair. The multiple damages can be further evidenced by 4.0-61.1 times higher quantum yield in the photolysis of nucleobases and amino acids for UV222 than UV254. This study demonstrates that UV222 treatment damages multiple sites in bacteria, leading to their inactivation. Employing UV222 treatment as an alternative to UV254 could be viable for inhibiting microorganism photoreactivation in water and wastewater.

Roles of radical species in vacuum-UV/UV/peroxydisulfate advanced oxidation processes and contributions of the species to contaminant degradation at different water depths.

Vacuum-UV (VUV) (wavelength 185 nm)/ UV (wavelength 254 nm) are applied to improve performances of UV-based advanced oxidation processes. However, the improvements were strongly affected by water depth because of poor VUV transmittance in water. In this study, VUV/UV and peroxydisulfate (PDS) were used to degrade carbamazepine. More SO4•- oxidation occurred in VUV/UV/PDS than VUV/UV with similar •OH oxidation occurring. The additional SO4•- oxidation could be caused by VUV/PDS in superficial water or UV/PDS in deeper water. The synergistic factor for VUV/UV/PDS processes relative to VUV/UV and UV/PDS processes was 1.32. VUV/UV/PDS performances were affected by competition for photon absorption by dissolved organic matter (32-58 % inhibition), radical quenching by CO32-/HCO3- and NO3-, and conversion of •OH and SO4•- into reactive chlorine species by Cl-. Radical probe experiments and steady-state kinetic modeling simulations indicated that 34 %, 25 %, and 40 % of carbamazepine degradation occurring in 2-cm-deep bulk solution was due to •OH oxidation through VUV/H2O, SO4•- oxidation through VUV/PDS, and SO4•- oxidation through UV/PDS, respectively. Contribution of VUV-driven processes decreased with increasing water depth and became equivalent to contribution of 3.5-cm-deep UV-driven processes, which indicated the importance of optimizing water depth in VUV/UV-advanced oxidation process reactors.

Chlorination of isothiazolinone biocides: kinetics, reactive species, pathway, and toxicity evolution.

Due to the Covid-19 pandemic, the worldwide biocides application has been increased, which will eventually result in enhanced residuals in treated wastewater. At the same time, chlorine disinfection of secondary effluents and hospital wastewaters has been intensified. With respect to predicted elevated exposure in wastewater, the chlorination kinetics, transformation pathways and toxicity evolution were investigated in this study for two typical isothiazolinone biocides, methyl-isothiazolinone (MIT) and chloro-methyl-isothiazolinone (CMIT). Second-order rate constants of 0.13 M-1·s-1, 1.95 × 105 M-1·s-1 and 5.14 × 105 M-1·s-1 were determined for the reaction of MIT with HOCl, Cl2O and Cl2, respectively, while reactivity of CMIT was around 1-2 orders of magnitude lower. While chlorination of isothiazolinone biocides at pH 7.1 was dominated by Cl2O-oxidation, acidic pH and elevated Cl- concentration favored free active chlorine (FAC) speciation into Cl2 and increased overall isothiazolinone removal. Regardless of the dominant FAC species, the elimination of MIT and CMIT resulted in an immediate loss of acute toxicity under all experimental conditions, which was attributed to a preferential attack at the S-atom resulting in subsequent formation of sulfoxides and sulfones and eventually an S-elimination. However, chlorination of isothiazolinone biocides in secondary effluent only achieved <10% elimination at typical disinfection chlorine exposure 200 mg·L-1·min, but was predicted to be remarkably increased by acidizing solution to pH 5.5. Alternative measures might be needed to minimize the discharge of these toxic chemicals into the aquatic environment.