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题名: 饮用水源水化合物的氯化复合致毒机制与控制
作者: 常洋洋1
学位类别: 博士
答辩日期: 2017-05
授予单位: 中国科学院生态环境研究中心
授予地点: 北京
导师: 曲久辉 ; 柏耀辉
关键词: 复合污染,遗传毒性,消毒副产物,高锰酸钾预氧化,生物锰氧化 ; Combined pollution, Genotoxicity, Desinfection by-products, KMnO4 preoxidation, Biological manganese oxidation
其他题名: Mechanism and control of the combined genetoxicity produced from chlorinated compounds in source drinking water
学位专业: 环境工程
中文摘要: 氯是饮用水中最常用的消毒剂之一。在氯化过程中,它能与天然有机物、人工合成物和无机盐离子等反应,生成具有遗传毒性效应、致突变和致癌活性的消毒副产物(disinfection by products,DBPs)。尽管水中大多数 DBPs的浓度很低(〜1至 100 μg/L),但由于持续暴露和/或联合效应的存在,它们对人体的健康构成了危害。目前大多数研究者仅关注了单个消毒副产物的毒性或者单个前驱体消毒后生成 DBPs的毒性。这些研究都忽略了 DBPs之间联合作用而造成的毒性放大和缩小效应,导致低估或高估了复合体系的生态环境风险。因此,研究多个前驱体混合氯化后复合毒性的发生机理及相应的控制技术是非常必要的。 为研究氯化复合致毒机制,我们采用 SOS/umu方法考察了两种前驱物(酪氨酸和二苯甲酮(BP-4))混合氯化后遗传毒性与单独氯化后毒性加合的差异关系,试验结果证实了这种差异并发现 pH是导致差异的关键因子。在 pH 5.0–6.1范围内,混合氯化后毒性大于单独氯化后毒性的加和;而在 pH 6.3–8.0的范围内,与之相反。研究进一步发现含氮消毒副产物的产量和联合作用(协同作用和拮抗作用)共同决定了毒性差异的大小。非线性回归分析发现有机氮( total organic nitrogen,TON)比值(TON混合氯化产物/TON单独氯化产物之和)可以估算这种毒性差异。 在复合毒性控制上,研究首先考察了常规工艺中 KMnO4预氧化对酪氨酸和BP-4混合与单独氯化后毒性的去除作用。结果表明尽管 KMnO4不能氧化 BP-4,但能通过氧化 BP-4的氯化产物,降低其毒性。而在 KMnO4和酪氨酸初始摩尔比为 1:1时,对其氯化产物毒性的降低作用最为显著。研究证明,KMnO4和生成的MnO2(KMnO4的还原产物)对酪氨酸的氧化作用,以及 MnO2对其氯化产物的氧化作用,都能降低产物毒性。值得关注的是,预氧化生成的 Mn与酪氨酸竞2+争氯,使得与酪氨酸反应的氯量减少,从而升高产物的毒性。此外,由于酪氨酸和 BP-4的预氧化-氯化产物之间存在联合作用,所以随着 KMnO4投加量的升高,混合预氧化-氯化产物的毒性由高于转变为低于单独预氧化 -氯化产物的毒性加和。 适量 KMnO4预氧化虽能降低 DBPs的毒性,但同时带来了余锰的问题。已有研究证明 Mn2+对余锰及消毒副产物前驱物的去除。研究利用具有锰氧化能力的假单胞菌 QJX-1作为模式菌种来考察它对酪氨酸、BP-4和Mn2+的去除效果。结果发现,QJX-1能够利用酪氨酸作为唯一的C/N源进行生长,并将 Mn2+具有遗传毒性效应。因此,我们探讨了后续工艺(如生物滤池)氧化为生物氧化锰(biological manganese oxide,BMO)。而生成的 BMO通过吸附氧化作用能够去除水体中的微量污染物 BP-4。同时,BP-4的存在刺激了 QJX-1的生长,并促进了锰氧化的发生。研究利用 RNA-seq技术和蛋白组学技术在分子水平上探究产生这种现象的原因。发现 BP-4主要刺激了酪氨酸代谢过程中的丙酮酸和糖异生代谢通路,加快了 QJX-1的生长。而蛋白组学和超氧自由基检测结果表明,锰离子的氧化主要和由于饥饿效应产生的超氧自由基相关。BP-4的加入导致了超氧自由基的提前产生,从而促进了锰氧化的发生。
英文摘要: hlorine is one of the most commonly used disinfectants in drinking water. It can react with natural organic materials, anthropogenic chemicals and salts, and produces a wide variety of disinfection by-products (DBPs) with genotoxic, mutagenic and carcinogenic activities during chlorination. Although the concentrations of most DBPs in water are at low levels (~1 to 100 μg/L), they pose a human health hazard as a result of persistent exposure and/or their combined effects. Many previous studies have focused on the toxicity of a single DBP or a single chlorinated compound. However,these studies ignore the combied effects of different DBPs, thus leading to an unreasonable estimation of their ecological risks. Therefore, it is essential to study the mechanism and control of combined toxicity of DBPs produced from multiple precursors. Here we examined the genotoxicity using the SOS/umu test when two precursors (tyrosine (Tyr) and benzophenone-4 (BP-4)) were chlorinated together and separately.We sought to examine whether the genotoxicity of the mixture (GCM) could be estimated from the sum of the genotoxicities of the individual precursors (GCI), which were chlorinated separately. The results revealed that GCM was not identical to GCI. pH was an important factor in determining the difference in genotoxicity between GCM and GCI (GΔ). GCM was higher than GCI (GΔ > 0) at pH 5.0–6.1, and lower than GCI (GΔ < 0) at pH 6.3–8.0. We found that GΔ was determined by the nitrogen-containing DBPs and combined effects between DBPs produced from Tyr and BP-4. We propose that the total organic nitrogen (TON) ratio, TON(chlorinated mixture)/TON(the sum of chlorinated individuals), is useful to estimate GΔ. Based on the above, we investigated the effect of potassium permanganate (KMnO4)preoxidation on the decrease/removal in/of DBPs’genotoxicity from signle and mixture precursors. Results revealed that although KMnO4 could not oxidize BP-4, after chlorination KMnO4 could oxidize the chlorination byproducts of BP-4 and thus decrease the genotoxicity production. For Tyr, the optimal initial molar ratio of KMnO4 to Tyr was confirmed to be 1:1. It has been proved that both the oxidation of Tyr by KMnO4 and manganese dioxide (MnO2, the reduction product of KMnO4) and the oxidation of chlorination byproducts by MnO2 can decrease the genotoxicity production of chlorinated Tyr. Remarkably, during chlorination, the competition of Mn oxidation with Tyr oxidation can result in less chlorine reacting with Tyr, to induce an increase in genotoxicity. This is the main cause for the increase in genotoxicity of chlorinated Tyr after KMnO4 preoxidation. Additionally, the genotoxicity of the chlorinated mixture was shifted from being higher than the sum of individual genotoxicities of the chlorinated precursors to being lower than their sum with increasing KMnO4 dosage, due to the combined effects between the preoxidation-chlorination products from the two compounds. Although a proper dose of KMnO4 preoxidation could decrease the genetoxicity of DBPs, it resulted in the production of Mn2+ explore whether the subsequent conventional treatment (e.g., biolfilter) can remove the DBPs’ precursors and Mn2+ together. We adapted a Mn2+ -oxidizing Pseudomonas sp. QJX-1 as the model strain to investigate its effect on the removal of Tyr, BP-4, and . Results showed that QJX-1 could utilize Tyr as the sole carbon and nitrogen source, and catalyze the transformation of Mn2+ to biological manganese oxide (BMO). The formed BMO further adsorbed and oxidized BP-4. Concurrently, BP-4 promoted the growth and Mn2+ oxidation of QJX-1. RNA-seq data suggests that BP-4 stimulates with genetoxic activity. Thus, it is urgent to Mn2+ the up-regulation of the pyruvate and gluconeogenesis metabolic pathway of Tyr for QJX-1 growth. Further, protein identification and extracellular superoxide detection indicate that Mn2+ oxidation is largely driven by the formation of superoxide in response to starvation; the acceleration of superoxide production, due to BP-4 accelerating Tyr consumption, is responsible for the promotion effect of BP-4 on the Mn2+ oxidation of QJX-1.
内容类型: 学位论文
URI标识: http://ir.rcees.ac.cn/handle/311016/38604
Appears in Collections:环境水质学国家重点实验室_学位论文

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作者单位: 1.中国科学院生态环境研究中心

Recommended Citation:
常洋洋. 饮用水源水化合物的氯化复合致毒机制与控制[D]. 北京. 中国科学院生态环境研究中心. 2017.
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