Formation and control of nitrogenous DBPs from Western Australian source waters: Investigating the impacts of high nitrogen and bromide concentrations

We studied the formation of four nitrogenous DBPs（N-DBPs） classes（haloacetonitriles,halonitromethanes, haloacetamides, and N-nitrosamines）, as well as trihalomethanes and total organic halogen（TOX）, after chlorination or chloramination of source waters. We also evaluated the relative and additive toxicity of N-DBPs and water treatment options for minimisation of N-DBPs. The formation of halonitromethanes, haloacetamides, and N-nitrosamines was higher after chloramination and positively correlated with dissolved organic nitrogen or total nitrogen. N-DBPs were major contributors to the toxicity of both chlorinated and chloraminated waters. The strong correlation between bromide concentration and the overall calculated DBP additive toxicity for both chlorinated and chloraminated source waters demonstrated that formation of brominated haloacetonitriles was the main contributor to toxicity. Ozone–biological activated carbon treatment was not effective in removing N-DBP precursors. The occurrence and formation of N-DBPs should be investigated on a case-by-case basis, especially where advanced water treatment processes are being considered to minimise their formation in drinking waters, and where chloramination is used for final disinfection.

Chloramination of wastewater effluent: Toxicity and formation of disinfection byproducts

The reclamation and disinfection of waters impacted by human activities（e.g., wastewater effluent discharges） are of growing interest for various applications but has been associated with the formation of toxic nitrogenous disinfection byproducts（N-DBPs）. Monochloramine used as an alternative disinfectant to chlorine can be an additional source of nitrogen in the formation of N-DBPs. Individual toxicity assays have been performed on many DBPs, but few studies have been conducted with complex mixtures such as wastewater effluents. In this work, we compared the cytotoxicity and genotoxicity of wastewater effluent organic matter（Ef OM） before and after chloramination. The toxicity of chloraminated Ef OM was significantly higher than the toxicity of raw Ef OM, and the more hydrophobic fraction（HPO）isolated on XAD-8 resin was more toxic than the fraction isolated on XAD-4 resin.More DBPs were also isolated on the XAD-8 resin. N-DBPs（i.e., haloacetonitriles or haloacetamides） were responsible for the majority of the cytotoxicity estimated from DBP concentrations measured in the XAD-8 and XAD-4 fractions（99.4% and 78.5%, respectively）.Measured DBPs accounted for minor proportions of total brominated and chlorinated products, which means that many unknown halogenated compounds were formed and can be responsible for a significant part of the toxicity. Other non-halogenated byproducts（e.g.,nitrosamines） may contribute to the toxicity of chloraminated effluents as well.

Monohalogenated acetamide-induced cellular stress and genotoxicity are related to electrophilic softness and thiol/thiolate reactivity

Haloacetamides（HAMs） are cytotoxic, genotoxic, and mutagenic byproducts of drinking water disinfection. They are soft electrophilic compounds that form covalent bonds with the free thiol/thiolate in cysteine residues through an S_N2 reaction mechanism.Toxicity of the monohalogenated HAMs（iodoacetamide, IAM; bromoacetamide, BAM;or chloroacetamide, CAM） varied depending on the halogen substituent. The aim of this research was to investigate how the halogen atom affects the reactivity and toxicological properties of HAMs, measured as induction of oxidative/electrophilic stress response and genotoxicity. Additionally, we wanted to determine how well in silico estimates of electrophilic softness matched thiol/thiolate reactivity and in vitro toxicological endpoints.Each of the HAMs significantly induced nuclear Rad51 accumulation and ARE signaling activity compared to a negative control. The rank order of effect was IAM 〉 BAM 〉 CAM for Rad51, and BAM ≈ IAM 〉 CAM for ARE. In general, electrophilic softness and in chemico thiol/thiolate reactivity provided a qualitative indicator of toxicity, as the softer electrophiles IAM and BAM were more thiol/thiolate reactive and were more toxic than CAM.