Lu Wang,Deyang Kong,Yuefei Ji,Junhe Lu,Xiaoming Yin,Quansuo Zhou
Formation of halogenated disinfection by-products (DBPs) in sulfate radical-based advanced oxidation processes (SR-AOPs) have attracted considerable concerns recently. Previous studies have focused on the formation of chlorinated and brominated DBPs. This research examined the transformation of I − in heat activated PS oxidation process. Phenol was employed as a model compound to mimic the reactivity of dissolved natural organic matter (NOM) toward halogenation . It was found that I − was transformed to free iodine which attacked phenol subsequently leading to iodinated DBPs such as iodoform and iodoacetic acids . Iodophenols were detected as the intermediates during the formation of the iodoform and triiodoacetic acid (TIAA). However, diiodoacetic acid (DIAA) was formed almost concomitantly with iodophenols. In addition, the yield of DIAA was significantly higher than that of TIAA, which is distinct from conventional halogenation process. Both the facts suggest that different pathway might be involved during DIAA formation in SR-AOPs. Temperature and persulfate dose were the key factors governing the transformation process. The iodinated by-products can be further degraded by excessive SO 4 − and transformed to iodate . This study elucidated the transformation pathway of I − in SR-AOPs, which should be taken into consideration when persulfate was applied in environmental matrices containing iodine.
Zijun Dong,Feng Wang,Xiulan Song,Miao Zhang,Chengchun Jiang,Feiyun Sun,Mu Li
Iodoform (CHI 3 ) is one of the disinfection by-products (DBPs) that is formed in the pre-oxidation and disinfection processes of drinking water treatment. In this study, Fe(II)-activated persulfate oxidation (Fe 2+ /PS) was employed to degrade iodoform, the effects of initial reactants concentration, reaction parameters, kinetics model were investigated, and the underlying mechanisms of CHI 3 degradation in Fe 2+ /PS oxidation process was unveiled. The results showed that the mole ratio Fe 2+ /PS of 1:5, initial PS concentration of 15 μmmol/L, and pH of 3.0 were identified as the optimum operating parameters. In addition, a relatively higher temperature could enhance CHI 3 removal and deiodination. The kinetic model has two different reaction steps: a fast one during the first ten minutes of reaction; then followed by a much slower one. Suppression of the reaction by TBA and MeOH showed that the combined effects of SO 4 − · and ·OH contributed to the degradation of CHI 3 , but ·OH played a dominant role. The degradation pathways and the products of total liberated iodine species demonstrate that the applicability of the Fe 2+ /PS oxidation process for CHI 3 degradation. These results indicated that the Fe 2+ /PS oxidation process is an effective advanced oxidation process for CHI 3 removal in water treatment.
Disinfection by-products (DBPs) generated from water treatment have serious adverse effects on human health and natural ecosystems. However, research on the mutagenicity of DBPs with different chemical structures is still limited. In the present study, we compared the mutagenicity of 8 typical DBPs in human-hamster hybrid (A L ) cells and clarified the mechanisms involved. Our data displayed that the rank order for mutagenicity was as follows: iodoacetamide (IAcAm) > iodoacetonitrile (IAN) > iodoacetic acid (IAA) > bromoacetamide (BAcAm) ≈ bromoacetonitrile (BAN) > bromoacetic acid (BAA), which was confirmed by DNA double strand breaks and oxidative DNA damage. In contrast, bromoform (TBM) and iodoform (TIM) had minimal mutagenicity. The mutation spectrum analysis further revealed that IAN, IAcAm, and IAA could induce multilocus deletions in mammalian cells. Interestingly, nitrogenous DBPs (N-DBPs) and IAA were found to cause varying degrees of iron overload and lipid peroxidation, which was mediated by the activation of the Nrf2/HO-1 signaling pathway. Moreover, the presence of deferoxamine (DFO), an iron ion inhibitor, effectively reduced γ-H2AX and 8-OHdG induced by N-DBPs and IAA. These results indicated that the variations in genotoxicity among DBPs with different structures were associated with their ability to disrupt iron homeostasis. This study provided new insights into the mechanisms underlying the structure-dependent toxicity of DBPs and established a foundation for a more comprehensive understanding and intervention of the health risks associated with DBPs.
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