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Wastewater ozonation forms various toxic byproducts, such as aldehydes, bromate, and organic bromine. However, there is currently no clear understanding of the overall toxicity changes in ozonated wastewater because pretreatment with solid phase extraction cannot retain inorganic bromate and volatile aldehydes, yet contributions of known ozonation byproducts to toxicity are unknown. Moreover, compared with bromate, organic bromine did not receive widespread attention. This study evaluated the toxicity of ozonated wastewater by taking aldehydes, bromate, and organic bromine into consideration. In the absence of bromide, formaldehyde contributed 96–97% cytotoxicity and 92–95% genotoxicity to HepG2 cells among the detected known byproducts, while acetaldehyde, propionaldehyde, and glyoxal had little toxicity. Both formaldehyde and dibromoacetonitrile drove toxicity among the known byproducts when bromide was present. Toxicity assays in HepG2 cells showed that when secondary effluents contained no bromide, the cytotoxicity of the nonvolatile organic fraction (NVOF) was reduced by 56–70%, and genotoxicity was completely removed after ozonation. However, the formed aldehydes (volatile organic fraction, VOF) led to increased overall toxicity. In the presence of bromide, compared with the secondary effluent, ozonation increased the cytotoxicity of the NVOFBr from 3.4–4.0 mg phenol/L to 10.3–13.9 mg phenol/L, possibly due to the formation of organic bromine. In addition, considering the toxicity of VOFBr (VOF in the presence of bromide, including aldehydes, tribromomethane, etc.), the overall cytotoxicity and genotoxicity became much higher than those of the secondary effluent. Although bromate had a limited impact on cytotoxicity and genotoxicity, it caused an increase in oxidative stress in HepG2 cells. Therefore, when taking full account of nonvolatile, volatile, and inorganic fractions, ozonation generally increases the toxicity of wastewater.

Ammonia (NH 4 + ) and hydrogen peroxide (H 2 O 2 ) have been widely used to inhibit bromate formation during ozonation. However, organic byproducts can also pose a risk under these conditions. During bromate inhibition, the influence of NH 4+ and H 2 O 2 on organic byproducts and their toxicity should be elucidated. Our study found that NH 4 + suppressed organic bromine, but might result in increased toxicity. Adding 0.5 mg/L of NH 4 + −N substantially increased both the formation of cytotoxicity and genotoxicity (DNA double-strand breaks) of organic byproducts from 0.6 to 1.6 mg-phenol/L, and from 0.3 to 0.8 μg-4-NQO/L (0.5 mg/L Br − , 5 mg/L O 3 ). NH 4 + decreased bromate, but increased the overall toxicity of the integrated byproducts (organic byproducts and bromate). Organic nitrogen measurements and 15 N isotope analysis showed enhanced incorporation of nitrogen into organic matter when NH 4 + and Br − coexisted during ozonation. NH 4 + decreased the formation of brominated acetonitriles, but enhanced the formation of brominated nitromethanes and brominated acetamides. These brominated nitrogenous byproducts were partially responsible for this increase in toxicity. Different from ammonia, H 2 O 2 could reduce both bromate and the toxicity of organic byproducts. In the presence of 0.5 mg/L Br − and 10 mg/L O 3 , adding H 2 O 2 (0.5 mM) substantially suppressed bromate, cytotoxicity formation and genotoxicity formation by 88%, 63% and 67%. This study highlights that focusing on bromate control with NH 4 + addition might result in higher toxicity. Efforts are needed to effectively control the toxicities of bromate and organic byproducts simultaneously.

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