Halogenated aliphatic and phenolic disinfection byproducts in chlorinated and chloraminated dairy wastewater: Occurrence and ecological risk evaluation.

The increasing demand for dairy products has led to the production of a large amount of wastewater in dairy plants, and disinfection is an essential treatment process before wastewater discharge. Disinfection byproducts (DBPs) in disinfected dairy wastewater may negatively influence the aquatic organisms in receiving water. During chlorine and chloramine disinfection of dairy wastewater, the concentrations of aliphatic DBPs increased from below the detection limits to 485.1 µg/L and 26.6 µg/L, respectively. Brominated and iodinated phenolic DBPs produced during chlor(am)ination could further react with chlorine/chloramine to be transformed. High level of bromide in dairy wastewater (12.9 mg/L) could be oxidized to active bromine species by chlorine/chloramine, promoting the formation of highly toxic brominated DBPs (Br-DBPs), and they accounted for 80.3% and 71.1% of the total content of DBPs in chlorinated and chloraminated dairy wastewater, respectively. Moreover, Br-DBPs contributed 49.9-75.9% and 34.2-96.4% to the cumulative risk quotient of DBPs in chlorinated and chloraminated wastewater, respectively. The cumulative risk quotient of DBPs on green algae, daphnid, and fish in chlorinated wastewater was 2.8-11.4 times higher than that in chloraminated wastewater. Shortening disinfection time or adopting chloramine disinfection can reduce the ecological risks of DBPs.

High efficiency removal of organic and inorganic iodine with ferrate[Fe(VI)] through oxidation and adsorption.

I- is a halogen species existing in natural waters, and the transformation of organic and inorganic iodine in natural and artificial processes would impact the quality of drinking water. Herein, it was found that Fe(VI) could oxidize organic and inorganic iodine to IO3-and simultaneously remove the resulted IO3- through Fe(III) particles. For the river water, wastewater treatment plant (WWTP) effluent, and shale gas wastewater treated by 5 mg/L of Fe(VI) (as Fe), around 63 %, 55 % and 71 % of total iodine (total-I) had been removed within 10 min, respectively. Fe(VI) was superior to coagulants in removing organic and inorganic iodine from the source water. Adsorption kinetic analysis suggested that the equilibrium adsorption amount of I- and IO3- were 11 and 10.1 µg/mg, respectively, and the maximum adsorption capacity of IO3- by Fe(VI) resulted Fe(III) particles was as high as 514.7 µg/mg. The heterogeneous transformation of Fe(VI) into Fe(III) effectively improved the interaction probability of IO3- with iron species. Density functional theory (DFT) calculation suggested that the IO3- was mainly adsorbed in the cavity (between the γ-FeOOH shell and γ-Fe2O3 core) of Fe(III) particles through electrostatic adsorption, van der Waals force and hydrogen bond. Fe(VI) treatment is effective for inhibiting the formation of iodinated disinfection by-products in chlor(am)inated source water.

Potential and mechanism of disinfection by-products removal in drinking water by bubbling corona discharge.

Disinfection by-products (DBPs) with significant teratogenic and carcinogenic properties have become a growing concern among the public. As an efficient and environmentally friendly technology, non-thermal plasma offers potential for removing emerging micro-pollutants. In this study, the degradation performance of bubbling corona discharge was evaluated on 24 halogenated alicyclic and aliphatic DBPs present in drinking water at concentrations ranging from ng/L to µg/L. The degradation of DBPs followed pseudo-first-order kinetics with rate constants (kobs) in the descending order of halonitromethanes (HNMs), halogenated benzoquinones (HBQs), haloacetonitriles, trihalomethanes (THMs), haloketones, halogenated aldehydes, and haloacetic acids (HAAs). THMs, HNMs, and HBQs were effectively removed within 5 min under a discharge power of 28 W. Degradation rates achieved by plasma treatment surpass those of other conventional treatment technologies. The required energy consumption was in the range of 5-30 kW·h/m3/order. Furthermore, the study investigated the effects of discharge power, initial concentration, and economic analysis on the degradation of four selected DBPs as representatives of mono-, di- and multi-carbon-containing DBPs, namely chloroform (TCM) and bromoform (TBM), tribromoacetic acid (TBAA), and 2,3,5,6-tetrachloro-1,4-benzoquinone (TetraC-BQ). Reactive radicals in the plasma system were investigated using electron paramagnetic resonance, optical emission spectroscopy, fluorimetry, and radical scavengers. Hydrated electrons and hydroxyl radicals played an important role in the removal of DBPs. The intermediates generated during the degradation of TCM, TBM, TBAA, and TetraC-BQ were identified, and the possible degradation pathways for mono- and binary C-DBPs and HBQs were deduced. The breakdown of HBQs did not produce secondary contamination with aliphatic DBPs. The carbon in DBPs was primarily converted to formic acid, acetic acid, and oxalic acid, and the halogens were mainly converted to halogen ions. Additionally, luminescent bacteria toxicity testing confirmed that plasma treatment could reduce the acute toxicity of water samples. These findings demonstrate the potential of plasma treatment as a post-treatment device at the household level.

Interpreting the degradation mechanism of triclosan in microbial fuel cell by combining analysis microbiome community and degradation pathway.

Microbes play a dominant role for the transformation of organic contaminants in the environment, while a significant gap exists in understanding the degradation mechanism and the function of different species. Herein, the possible bio-degradation of triclosan in microbial fuel cell was explored, with the investigation of degradation kinetics, microbial community, and possible degradation products. 5 mg/L of triclosan could be degraded within 3 days, and an intermediate degradation product (2,4-dichlorophen) could be further degraded in system. 32 kinds of dominant bacteria (relative intensity >0.5%) were identified in the biofilm, and 10 possible degradation products were identified. By analyzing the possible involved bioreactions (including decarboxylation, dehalogenation, dioxygenation, hydrolysis, hydroxylation, and ring-cleavage) of the dominant bacteria and possible degradation pathway of triclosan based on the identified products, biodegradation mechanism and function of the bacteria involved in the degradation of triclosan was clarified simultaneously. This study provides useful information for further interpreting the degradation mechanism of organic pollutants in mixed flora by combining analysis microbiome community and degradation pathway.

rFGF4 alleviates lipopolysaccharide-induced acute lung injury by inhibiting the TLR4/NF-κB signaling pathway.

Acute lung injury (ALI) is a serious and common clinical disease. Despite significant progress in ALI treatment, the morbidity and mortality rates remain high. However, no effective drug has been discovered for ALI. FGF4, a member of the FGF family, plays an important role in the regulation of various physiological and pathological processes. Therefore, in the present study, we aimed to study the protective effects of FGF4 against LPS-induced lung injury in vivo and in vitro. We found that rFGF4 treatment improved the lung W/D weight ratio, the survival rate, immune cell infiltration and protein concentrations in mice with LPS-induced ALI. Histological analysis revealed that rFGF4 significantly attenuated lung tissue injury and cell apoptosis. Furthermore, rFGF4 inhibited the activation of the TLR4/NF-κB signaling pathway and the production of pro-inflammatory mediators in LPS-injured lung tissues, murine alveolar macrophages (MH-S) and murine pulmonary epithelial (MLE-12) cells. The results of cell experiments further verified that rFGF4 inhibited the production of inflammatory mediators in MH-S cells and MLE-12 cells by regulating the TLR4/NF-κB signaling pathway. These results revealed that rFGF4 protected lung tissues and inhibited inflammatory mediators in mice with LPS-induced ALI by inhibiting the TLR4/NF-κB signaling pathway in MH-S and MLE-12 cells.

Anthracite Releases Aromatic Carbons and Reacts with Chlorine to Form Disinfection Byproducts in Drinking Water Production.

Anthracite is globally used as a filter material for water purification. Herein, it was found that up to 15 disinfection byproducts (DBPs) were formed in the chlorination of anthracite-filtered pure water, while the levels of DBPs were below the detection limit in the chlorination of zeolite-, quartz sand-, and porcelain sandstone-filtered pure water. In new-anthracite-filtered water, the levels of dissolved organic carbon (DOC), dissolved organic nitrogen (DON), and ammonia nitrogen (NH3-N) ranged from 266.3 to 305.4 µg/L, 37 to 61 µg/L, and 8.6 to 17.1 µg/L, respectively. In aged anthracite (collected from a filter at a DWTP after one year of operation) filtered water, the levels of the above substances ranged from 475.1 to 597.5 µg/L, 62.1 to 125.6 µg/L, and 14 to 28.9 µg/L, respectively. Anthracite would release dissolved substances into filtered water, and aged anthracite releases more substances than new anthracite. The released organics were partly (around 5%) composed by the µg/L level of toxic and carcinogenic aromatic carbons including pyridine, paraxylene, benzene, naphthalene, and phenanthrene, while over 95% of the released organics could not be identified. Organic carbon may be torn off from the carbon skeleton structure of anthracite due to hydrodynamic force in the water filtration process.

Occurrence of Iodophenols in Aquatic Environments and the Deiodination of Organic Iodine with Ferrate(VI).

Toxic and odorous iodophenols are commonly identified as disinfection by-products (DBPs) in drinking water. Herein, ng/L levels of iodophenols were identified in river water, wastewater treatment plant effluent, and medical wastewater, with the simultaneous identification of µg/L to mg/L levels of iodide (I-) and total organic iodine (TOI). Oxidation experiment suggested that the I-, TOI, and iodophenols could be oxidized by ferrate [Fe(VI)], and more than 97% of TOI had been transformed into stable and nontoxic IO3-. Fe(VI) initially cleaved the C-I bond of iodophenols and led to the deiodination of iodophenols. The resulted I- was swiftly oxidized into HOI and IO3-, with the intermediate phenolic products be further oxidized into lower molecular weight products. The Gibbs free energy change (ΔG) of the overall reaction was negative, indicating that the deiodination of iodophenols by Fe(VI) was spontaneous. In the disinfection of iodine-containing river water, ng/L levels of iodophenols and chloro-iodophenols formed in the reaction with NaClO/NH2Cl, while Fe(VI) preoxidation was effective for inhibiting the formation of iodinated DBPs. Fe(VI) exhibited multiple functions for oxidizing organic iodine, abating their acute toxicity/cytotoxicity and controlling the formation of iodinated DBPs for the treatment of iodide/organic iodine-containing waters.

Reduced Graphene Oxide Triggers Peracetic Acid Activation for Robust Removal of Micropollutants: The Role of Electron Transfer.

Peracetic acid (PAA) serves as a potent and low-toxic oxidant for contaminant removal. Radical-mediated catalytic PAA oxidation processes are typically non-selective, rendering weakened oxidation efficacy under complex water matrices. Herein, we explored the usage of reduced graphene oxide (rGO) for PAA activation via a non-radical pathway. Outperforming the most catalytic PAA oxidation systems, the rGO-PAA system exhibits near-complete removal of typical micropollutants (MPs) within a short time (<2 min). Non-radical direct electron transfer (DET) from MPs to PAA plays a decisive role in the MP degradation, where accelerated DET is achieved by a higher potential of the rGO-PAA reactive surface complexes. Benefitting from DET, the rGO-PAA system shows robust removal of multiple MPs under complex water matrices and with low toxicity. Notably, in the DET regime, the electrostatic attraction of rGO to both PAA and target MP is a critical prerequisite for achieving efficient oxidation, depending on the conditions of solution pH and MP pKa. A heatmap model building on such an electrostatic interaction is further established as guidance for regulating the performance of the DET-mediated PAA oxidation systems. Overall, our work unveils the imperative role of DET for rGO-activated PAA oxidation, expanding the knowledge of PAA-based water treatment strategies.

Pseudoginsenoside-F11 promotes functional recovery after transient cerebral ischemia by regulating the microglia/macrophage polarization in rats.

The polarization of microglia/macrophages after cerebral ischemia is critical for post-stroke damage/recovery. Previously, we found that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, has neuroprotective effects on permanent and transient cerebral ischemia in rats. This study aimed to investigate the effects and potential mechanisms of PF11 on microglia/macrophage polarization following transient cerebral ischemia in rats. In vivo data showed that oral administration of PF11 (12 mg/kg) significantly attenuated cognitive deficits and sensorimotor dysfunction, infarct volume and brain edema in transient middle cerebral artery occlusion (tMCAO)-treated rats, as well as reduced the loss of neurons and the over-activation of microglia in penumbra of ipsilateral striatum and cortex. Notably, the proportion of M2 microglia/macrophages in the total activated microglia/macrophages peaked on day 14 after tMCAO in rats, while PF11 promoted its peak advancing to day 3 post-tMCAO, which allowing the damaged brain to enter the repair period more quickly. Furthermore, PF11 increased the expression of anti-inflammatory markers and decreased the expression of pro-inflammatory markers in ipsilateral striatum and cortex. In addition, in vitro data showed that PF11 inhibited the induction of M1 microglia by oxygen glucose deprivation/re-oxygenation (OGD/R)-induced neurons, and promoted the polarization of microglia to M2 phenotype in a Jumonji domain-containing protein 3 (Jmjd3)-dependent manner. Moreover, PF11 promoted the protection of M2 microglia and attenuated the exacerbation of M1 microglia on OGD/R-induced neuronal damage. Taken together, these results indicate that PF11 protects ischemic neurons by promoting M2 microglia/macrophage polarization in a Jmjd3-dependent manner, ultimately facilitating the functional recovery following transient cerebral ischemia.

Chlorination decreases acute toxicity of iodophenols through the formation of iodate and chlorinated aliphatic disinfection byproducts.

Highly toxic iodinated phenolic by-products were frequently detected in the oxidative treatment and disinfection of iodine-containing water. Herein, it was found that three model iodinated phenolic disinfection byproducts (DBPs), 2-iodophenol, 4-iodophenol and 2,4,6-triiodophenol, were reactive with HOCl, and the reaction rate constants (at pH 7.0 and 25℃) were 1.86 ×102, 1.62 ×102 and 7.5 ×101 M-1s-1, respectively. When HOCl was in excess (HOCl/iodophenol = 40/1, [iodophenol]0 = 20 µM), acute toxicity of water sample containing iodophenols could be largely eliminated (> 85%), with the conversion of iodophenols into stable and non-toxic iodate (IO3-) and iodinated and chlorinated aliphatic DBPs. Besides IO3-, seven kinds of aromatic intermediate products including iodophenols, chloroiodophenols, iodoquinones, chloroiodoquinones, chloroquinones, chlorophenols, and coupling products were detected. C-I bond of iodophenols was cleaved in the reaction and the resulted aromatic products were further transformed into chlorinated aliphatic DBPs [trichloromethane (TCM), trichloroacetic acid (TCAA), dichloroacetic acid (DCAA), and chloral hydrate (CH)] (mg/L level) and iodinated trihalomethanes (µg/L level). HOCl was effective for converting iodophenols into IO3- and less toxic chlorinated aliphatic DBPs. Considering that chlorine was widely used as disinfectant, transformation and toxicity alteration of emerging DBPs during chlorination/booster chlorination warrant further investigations.

Correction: Neuroinflammatory inhibitors from Gardneria nutans Siebold & Zuccarini.

[This corrects the article DOI: 10.1039/D1RA05204G.].

Neuroinflammatory inhibitors from Gardneria nutans Siebold & Zuccarini.

Two new monoterpene indole alkaloid glycosides nutanoside A-B (1-2), two new phenolic glycoside esters nutanester A-B (6-7), together with five known compounds (3-5, 8-9) were isolated from the ethanol extract of Gardneria nutans Siebold & Zuccarini. Their structures were established on the basis of extensive spectroscopic analysis and TDDFT/ECD calculations. Compounds 1 and 2 are two rare monoterpene indole alkaloids with the glucosyl moiety located at C-12 and represent the first two examples of enantiomer of ajmaline type monoterpene indole alkaloids. Compounds 3, 4 and 6 displayed significant inhibitory effects on NO production in over-activated BV2 microglial cells, with the IC50 values of 2.29, 6.36, and 8.78 µM, respectively. Compounds 1, 5, 7 could significantly inhibit the mRNA expression of inflammatory factors TNF-α and IL-6 induced by LPS in BV2 microglial cells at the effective concentration. Moreover, compound 3 exhibited stronger cytotoxicities against U87 and HCT116 cell lines than taxol with IC50 values of 10.58 and 14.60 µM, respectively.

Pseudoginsenoside-F11 ameliorates ischemic neuron injury by regulating the polarization of neutrophils and macrophages in vitro.

Pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, has neuroprotective effects on permanent and transient cerebral ischemia in rats by alleviating autophagic/lysosomal defects and repressing calcium overload, respectively. Ischemic stroke triggers peripheral innate immune cells, mainly neutrophils and macrophages, to infiltrate the damaged brain. The polarization of neutrophils and macrophages after cerebral ischemia is essential for post-stroke damage/recovery. However, it remains elusive whether PF11 ameliorates ischemic neuron injury by regulating the polarization of neutrophils and macrophages. The present study demonstrated for the first time that conditioned media from ischemic neurons induced neutrophils and macrophages to polarize into N1 and M1 phenotypes, respectively. Furthermore, PF11 (30, 100 µM) inhibited the induction of N1 neutrophils by conditioned media from oxygen glucosedeprivation/re-oxygenation (OGD/R)-induced ischemic neurons and promoted the polarization of neutrophils to N2 phenotypes. In addition, PF11 (100 µM) attenuated the exacerbation of N1 neutrophils and facilitated the protection of N2 neutrophils on OGD/R-induced neuronal damage. Similarly, PF11 (100 µM) inhibited the induction of M1 macrophages by conditioned media from ischemic neurons and facilitated the polarization of macrophages to M2 phenotypes. What's more, PF11 (100 µM) attenuated the aggravation of M1 macrophages and promoted the protection of M2 macrophages on OGD/R-induced primary neuron injury. In summary, the present study indicates that PF11 ameliorates ischemic neuron damage by regulating neutrophils and macrophages polarization, suggesting that neutrophils and macrophages may be promising targets for the treatment of cerebral ischemia.

Ferrate Oxidation of Phenolic Compounds in Iodine-Containing Water: Control of Iodinated Aromatic Products.

Highly toxic iodinated products would form in oxidation and disinfection of iodine-containing water. Variation of iodinated aromatic products in ferrate [Fe(VI)] oxidation of phenolic compounds (phenol, bisphenol A (BPA), and p-hydroxybenzoic acid (p-HBA)) in iodine-containing water was investigated. At pH 5.0, oxidation of phenolic compounds was inhibited by competitive reaction of ferrate with I-, and no formation of iodinated aromatic products was detected. Almost all I- was converted into nontoxic IO3-. At pH 7.0, 8.0, and 9.0, HOI formed in ferrate oxidation of I- and further reacted with phenols, with the formation of iodinated aromatic products. Mass spectrometry analysis showed that both kinds and contents of iodinated aromatic products were raised with the increase in solution pH and the content of I-, and these iodinated aromatic products were further oxidized by ferrate. Ferrate deprived iodine from iodinated aromatic products and transferred highly toxic organic iodine into nontoxic IO3-. An electron-donating substituent (alkyl) increased the reactivity of phenol with ferrate and HOI and facilitated ferrate oxidation of iodinated phenols. An electron-drawing substituent (carboxyl) decreased the reactivity of phenol with ferrate and HOI and hindered the further oxidation of iodinated aromatic products. A kinetic model about the variation of phenol, BPA, and p-HBA in reaction with ferrate in iodine-containing water was developed, and the oxidation profile of phenolic compounds could be satisfactorily predicted at various iodide concentrations.

N2 neutrophils may participate in spontaneous recovery after transient cerebral ischemia by inhibiting ischemic neuron injury in rats.

Neutrophils have been traditionally considered as the major mediators of harmful inflammatory responses in ischemic stroke, whereas accumulating evidence indicates that neutrophils can be polarized into an N2 phenotype. Similar to M2 microglia, N2 neutrophils contribute to resolution of inflammation and may participate in neuroprotection. However, it remains unclear whether N2 neutrophils protect ischemic neurons and whether they are associated with long-term outcomes after transient cerebral ischemia in rats. The present study proved that N2 neutrophils protected against oxygen glucosedeprivation/re-oxygenation (OGD/R)-induced primary cortical neuron injury via brain-derived neurotrophic factor/tropomyosin-related kinase B (BDNF/TrkB) signaling. In addition, in vivo studies revealed that transient middle cerebral artery occlusion (tMCAO)-induced injury exhibited spontaneous recovery over time in rats. Moreover, neutrophils could infiltrate the ipsilateral brain parenchyma from the periphery after transient cerebral ischemia. Pearson's correlation analysis indicated that the proportion of N2 neutrophils in ipsilateral brain parenchyma was negatively correlated with the number of degenerating neurons, modified Neurological Severity Score (mNSS), brain water content and infarct volume, and positively correlated with the number of surviving neurons and grip strength. In summary, the present study shows that N2 neutrophils likely participate in spontaneous recovery after transient cerebral ischemia by inhibiting ischemic neuron damage in rats, which indicates that N2 neutrophils may represent promising therapeutic target for promoting recovery after ischemic stroke.

Enhanced Permanganate Oxidation of Sulfamethoxazole and Removal of Dissolved Organics with Biochar: Formation of Highly Oxidative Manganese Intermediate Species and in Situ Activation of Biochar.

Sulfamethoxazole (SMX) is a broad-spectrum antibiotic and was largely used in breeding industry. The reaction rate of SMX with KMnO4 is slow, and the adsorption efficiency of biochar for SMX was inferior (less than 11% in 30 min). By adding biochar powder into SMX solution with the addition of permanganate, the oxidation ratio of SMX surged to 97% in 30 min, and over 58% of the total organic carbon (TOC) was simultaneously removed. KMnO4 interacted with biochar and resulted in the formation of highly oxidative intermediate manganese species, which transformed SMX into hydrolysis products, oxygen-transfer products, and self-coupling products. Brunauer-Emmett-Teller (BET) analysis showed that surface area, total pore volume, and micropore volume of biochar increased by 32.1%, 36.4%, and 80.6%, respectively, after reaction process. This in situ activation of biochar with KMnO4 enhanced its adsorption capacity and led to great improvement of TOC removal. Besides KMnO4 oxidation, biochar also enhanced TOC removal in Mn(III) oxidation (KMnO4+ bisulfite) and ozonization of SMX. Considering that KMnO4 could react with biochar and result in the formation of intermediate manganese species, while biochar can be simultaneously activated and exhibit high capacity for organic adsorption, the combination of biochar with the chemical/advanced oxidation could be a promising process for the removal of environmental pollutants.

Comparative study on ferrate oxidation of BPS and BPAF: Kinetics, reaction mechanism, and the improvement on their biodegradability.

Bisphenol S (BPS) and bisphenol AF (BPAF) were increasingly consumed and these compounds are resistant to environmental degradation. Herein, ferrate oxidation of BPS and BPAF was investigated, and biodegradability of the oxidation products was examined. The second-order reaction rate constants of ferrate with BPS and BPAF were 1.3 × 103 M-1s-1 and 3 × 102 M-1s-1, respectively, at pH 7.0, 25 °C. In the oxidation process, some BPS molecules dimerized, while other BPS molecules were oxidized through oxygen-transfer process, leading to the formation of hydroxylation products and benzene-ring cleavage products. The dominant reaction of BPAF with ferrate was oxygen-transfer process, and BPAF was degraded into lower molecular weight products. The variation of assimilable organic carbon (AOC) suggested that the biodegradability of BPAF and BPS was largely improved after ferrate oxidation. Compared with the BPS oxidation products, the BPAF oxidation products were easier to be bio-consumed. Pure culture test showed that BPAF inhibited the growth of Escherichia coli, while ferrate oxidation completely eliminated this toxic effect. Co-existing humic acid (HA, 1 mg C/L to 5 mg C/L) decreased the removal of BPS and BPAF with ferrate. Compared with BPAF, more oxidation intermediates formed in the ferrate oxidation of BPS may be reduced by HA to the parent molecular. Thus, the inhibition effect of HA on the ferrate oxidation of BPS was more obvious than that on BPAF.

Rapid oxidation of iodide and hypoiodous acid with ferrate and no formation of iodoform and monoiodoacetic acid in the ferrate/I-/HA system.

Toxic and odorous iodinated disinfection byproducts (I-DBPs) could form in the chemical oxidation of iodine-containing water. A critical step for controlling the hazardous I-DBPs is to convert the iodine species into stable and harmless iodate (IO3-) while inhibiting the accumulation of highly reactive hypoiodous acid (HOI). Herein, the oxidation of I- and HOI with ferrate was investigated, and the formation profile of HOI was determined based on 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonate) (ABTS) coloring method through a stopped-flow spectrophotometer. The second-order rate constants (kapp) of ferrate with HOI decreased from 1.6 × 105 M-1s-1 to 8.3 × 102 M-1s-1 as the solution pH varied from 5.3 to 10.3, which were 7.5, 7.2 and 13.8 times higher than that of ferrate with I- at pH 6.0, 7.0 and 8.0, respectively. Compared with other oxidants such as ozone, hypochlorous acid, chloramine and potassium permanganate, ferrate would swiftly oxidize HOI formed in the I- oxidation process. For the ferrate oxidation of I-containing water, HOI was swiftly oxidized to IO3- from pH 5.0 to 9.0. Phosphate buffer promoted the oxidation of I- while inhibited the oxidation of HOI with ferrate. When 5 mgC/L of humic acids (HA) existed in the solution, no formation of iodoform and monoiodoacetic acid (MIAA) was observed in the oxidation of iodide (20 µM) with ferrate (from 10 µM to 80 µM). These results suggested that ferrate oxidation could be an effective method for the control of I-DBPs in iodine-containing water treatment.

Highly efficient removal of trace thallium from contaminated source waters with ferrate: Role of in situ formed ferric nanoparticle.

Thallium (Tl) is highly toxic to mammals and relevant pollution cases are increasing world-widely. Convenient and efficient method for the removal of trace Tl from contaminated source water is imperative. Here, the removal of trace Tl by K2FeO4 [Fe(VI)] was investigated for the first time, with the exploration of reaction mechanisms. Six different types of water treatment agents (powdered activated carbon, Al2(SO4)3, FeCl3, δ-MnO2, MnO2 nano-particles, and K2FeO4) were used for the removal of Tl in spiked river water, and K2FeO4 showed excellent removal performance. Over 92% of Tl (1 µg/L) was removed within 5 min by applying 2.5 mg/L of K2FeO4 (pH 7.0, 20 °C). XPS analysis revealed that in the reaction of Tl(I) with K2FeO4, Tl(I) was oxidized to Tl(III), and removed by the K2FeO4 reduced ferric particles. The removal of Tl by in situ formed and ex situ formed ferric particle was examined respectively, and the results revealed that the removal of trace Tl could be attributed to the combination of adsorption and coprecipitation processes. The hydrodynamic size of the reduced particle from K2FeO4 ranged from 10 nm to 100 nm, and its surface was negatively charged under neutral pH condition. These factors were conducive for the efficient removal of Tl by K2FeO4. The effects of solution pH, coexisting ions (Na+, Ca2+, and HCO3-), humic acid, solution temperature, and reductive environment on the removal and desorption of Tl were investigated, and the elimination of Tl in polluted river water and reservoir water was performed. These results suggest that K2FeO4 could be an efficient and convenient agent on trace Tl removal.