Tianze Liu,Xiaobin Liao,Xinna Lin,Jing Yu,Huan Qi,Zhibin Jiang,Jing Zou,Qingsong Li
This study was to evaluate the feasibility of controlling carcinogenic nitrosodiethylamine (NDEA) formation from greenhouse gas adsorbent 3-diethylaminopropylamine (DEAPA) by pre-O 3 in subsequent chlorination/chloramination processes. The result indicated that the NDEA yields (0.4 %) during chlorination was 1.3 times of that during chloramination (0.3 %); pre-oxidation with 4 mg/L O 3 significantly cut down its formation; the reduction rates were up to 67.5 and 48.5 %, respectively. OH scavenger greatly augmented the final NDEA amount from 1.86 to 5.05 μg/L during ozonation , while its roles on subsequent processes differed with disinfection methods as well as O 3 (g) dosages. Most of co-existed substances inhibited NDEA generation, except NO 2 − , CO 3 2− and SO 4 2− , which slightly promoted during ozonation. Basing on Gaussian calculation, GC/MS and UPLC-Q-TOF-MS analysis, the influencing mechanisms of pre-O 3 on NDEA formation in subsequent disinfection processes were proposed. In addition, the calculated toxicity analysis as well as the whole toxicity was applied to evaluate the possibility of pre-O 3 on risk control.
Huayu Zhang,Yueyun He,Xiaobin Liao,Xueping Tang,Qingsong Li,Jing Zou,Zhibing Jiang,Mazhan Zhuang,Zhimin Yang
N-nitrosodiethylamine (NDEA), which is the most toxic nitrosamine among the 9 detected species, has been widely detected in drinking water . Amines containing diethylamine (DEA) groups in the structure would generate NDEA during the disinfection processes. The aim of this study was to evaluate the feasibility of reducing NDEA formation from a commonly used dithiocarbamate pesticide sodium diethyldithiocarbamate (DEDTC) in subsequent chlorination and chloramination by pre-ozonation. The results demonstrated that NDEA could be generated directly during ozonation , its amounts increased from 0 to 14.34 μg/L with increasing ozone dosages (0–4 mg/L), which was higher than that chlorination (2.68 μg/L) and chloramination (4.91 μg/L) when the initial concentration of DEDTC was 20 μM. Pre-ozonation significantly raised NDEA formation from 2.68 to15.32 μg/L in subsequent chlorination; and that from 4.91 to 9.54 μg/L during subsequent chloramination processes. The addition of •OH scavenger tert-butanol (tBA) increased the production of NDEA from 8.14 to 20.80 μg/L during ozonation , and that from 6.76 to17.98 μg/L in O 3 /HClO process, 8.74 to 17.33 μg/L in O 3 /NH 2 Cl process. Except for NO 3 − and CO 3 2− , most of the co-existing substances promoted NDEA generation from DEDTC under disinfection conditions. Based on the results of Gaussian theory calculations, GC/MS and UPLC-Q-TOFMS analysis, the influencing mechanisms of pre-ozonation on NDEA generation in the subsequent disinfection process were proposed. In addition, not only acute/chronic toxicity calculation but also luminescent bacteria test was performed to assess the possibility of pre-ozonation on the risk control of DEDTC. The research results fill a gap in the control of NDEA pollution and help to develop a safer ozone oxidation technology .
N-Nitrosodiethylamine (NDEA), a carcinogen in some foods and medications, is linked to liver damage similar to non-alcoholic fatty liver disease (NAFLD). This study explores how NDEA disrupts liver lipid metabolism. Sprague-Dawley rats were given two doses of NDEA (100 mg/kg) orally, 24 h apart. Liver response was assessed through tissue staining, blood tests, and biochemical markers, including fatty acids, lipid peroxidation, and serum very-low density lipoprotein (VLDL) levels. Additionally, lipidomic analysis of liver tissues and serum was performed. The results indicated significant hepatic steatosis (fat accumulation in the liver) following NDEA exposure. Blood analysis showed signs of inflammation and liver damage. Biochemical tests revealed decreased liver protein synthesis and specific enzyme alterations, suggesting liver cell injury but maintaining mitochondrial function. Increased fatty acid levels without a rise in lipid peroxidation were observed, indicating fat accumulation. Lipidomic analysis showed increased polyunsaturated triglycerides in the liver and decreased serum VLDL, implicating impaired VLDL transport in liver dysfunction. In conclusion, NDEA exposure disrupts liver lipid metabolism, primarily through the accumulation of polyunsaturated triglycerides and impaired fat transport. These findings provide insight into the mechanisms of NDEA-induced liver injury and its progression to hepatic steatosis.
危险品化学品经营许可证（带存储）