Formation Of Dichloroacetic Acid Research Articles

Oxidative abatement of saccharin by ozone and its influence on DBPs formation during postchlorination

As one of artificial sweeteners, saccharin (SAC) is widely used in food, personal care products and animal feed industry. SAC cannot be effectively metabolized by organisms and most of them are discharged into the water environment through multiple channels, leading to general detection in water source. In this study, the fate of SAC in the advanced ozone treatment of drinking water and subsequent chlorination disinfection was investigated. The results showed ozone could effectively degrade SAC and >99 % of 20 mg/L SAC could be removed under 7.10 mg/min ozone flow within 60 min. While, the mineralization was comparably low by 80 %, which indicated that ozone converted SAC into organic intermediate products. Therefore, SAC characterized with anti-chlorination property was changed to disinfection by-product precursor. Disinfection by-products including trichloromethane (TCM), dichloroacetic acid (DCAA), trichloroacetic acid (TCAA) and dichloroacetonitrile (DCAN) were found during subsequent chlorination. The yields of TCM, DCAA, TCAA and DCAN were found to be 8.1, 0.4, 1.2 and 0.1 μg/mg SAC, respectively, 3, 39, 41 and 178 times of those produced by direct chlorination. In addition, the increase of ozone flux promoted the formation of disinfection by-products. Meta-alkalescence was conducive to the formation of DCAA, TCAA and DCAN in pH range of 6 to 8. The presence of anions including Cl−, NO3− and CO32− reduced the formation of TCM, DCAA and DCAN.

Formation of dichloroacetic acid and dichloroacetamide from phenicol antibiotic abatement during ozonation and post-chlor(am)ination

This study investigated the formation of dichloroacetamide (DCAM) and dichloroacetic acid (DCAA) from the abatement of three phenicol antibiotics (PABs, chloramphenicol, thiamphenicol, and florfenicol) during ozonation and post-chlor(am)ination. Results show that the three PABs have a low ozone reactivity (kO3 = 0.11‒0.12 M−1 s−1), and therefore are mainly abated through the hydrogen abstraction mechanism by hydroxyl radicals (•OH) during ozonation. During PAB degradation, the carboxamide moiety in the parent molecules can be cleaved off by •OH attack and thus gives rise to DCAM. The formed DCAM can then be further oxidized by O3 and/or •OH to DCAA as a more stable transformation product (TP). When the three PABs were adequately abated (abatement efficiency of ∼82 %‒95 %), the molar yields of DCAM and DCAA were determined to be 2.79 %‒4.71 % and 32.9 %‒37.2 %, respectively. Furthermore, post-chloramination of the ozonation effluents increased the yields of DCAM and DCAA slightly to 4.20 %‒6.45 % and 39.0 %‒41.1 %, respectively. In comparison, post-chlorination eliminated DCAM in the solutions, but significantly increased DCAA yields to ∼100 % due to the further conversion of DCAM and other ozonation TPs to DCAA by chlorine oxidation. The results of this study indicate that high yields of DCAM and DCAA can be generated from PAB degradation during ozonation, and post-chlorination and post-chloramination will result in very different fates of DCAM and DCAA in the disinfected effluent. The formation and transformation of DCAM and DCAA during PAB degradation need to be taken into account when selecting multi-barrier treatment processes for the treatment of PAB-containing water.

Treatment of NOM fractions of reservoir sediments: Effect of UV and chlorination on formation of DBPs

Abstract Humic acid (HA), fulvic acid (FA) and hydrophilic fraction of fulvic acid (FAHPI) were isolated from bottom sediments of a drinking water reservoir in North China. The effects of ultraviolet (UV) irradiation on the structure of the sedimentary natural organic matter (NOM) and subsequent disinfection by-products (DBPs) formation were investigated, with the comparison of commercial humic substances. HA sample mainly consisted of aromatic, methyl and guaiacyl lignin groups, which were reactive with chlorine to form trichloromethane (TCM). FA and FAHPI samples mainly contained ester, phenolic hydroxyl and aromatic ketone groups, among them, phenolic hydroxyl groups were highly reactive toward chlorine and primarily formed dichloroacetic acid (DCAA) during chlorination. UV irradiation decreased the hydrophobicity and increased the hydrophilicity of NOM. UV irradiation eliminated the aromatic, methyl and guaiacyl lignin groups of the HA sample, decreasing the formation of TCM, but increased the phenolic hydroxyl groups of FA and FAHPI samples, enhancing the formation of DCAA. In addition, UV irradiation promoted the trichloroacetic acid (TCAA) formation of the NOM samples from subsequent chlorination. Medium pressure (MP) UV irradiation had greater impacts on NOM fractions and DBPs formation during subsequent chlorination.

Pharmacokinetic analysis of trichloroethylene metabolism in male B6C3F1 mice: Formation and disposition of trichloroacetic acid, dichloroacetic acid, S-(1,2-dichlorovinyl)glutathione and S-(1,2-dichlorovinyl)- l-cysteine

Trichloroethylene (TCE) is a well-known carcinogen in rodents and concerns exist regarding its potential carcinogenicity in humans. Oxidative metabolites of TCE, such as dichloroacetic acid (DCA) and trichloroacetic acid (TCA), are thought to be hepatotoxic and carcinogenic in mice. The reactive products of glutathione conjugation, such as S-(1,2-dichlorovinyl)- l-cysteine (DCVC), and S-(1,2-dichlorovinyl) glutathione (DCVG), are associated with renal toxicity in rats. Recently, we developed a new analytical method for simultaneous assessment of these TCE metabolites in small-volume biological samples. Since important gaps remain in our understanding of the pharmacokinetics of TCE and its metabolites, we studied a time-course of DCA, TCA, DCVG and DCVG formation and elimination after a single oral dose of 2100 mg/kg TCE in male B6C3F1 mice. Based on systemic concentration-time data, we constructed multi-compartment models to explore the kinetic properties of the formation and disposition of TCE metabolites, as well as the source of DCA formation. We conclude that TCE-oxide is the most likely source of DCA. According to the best-fit model, bioavailability of oral TCE was ∼ 74%, and the half-life and clearance of each metabolite in the mouse were as follows: DCA: 0.6 h, 0.081 ml/h; TCA: 12 h, 3.80 ml/h; DCVG: 1.4 h, 16.8 ml/h; DCVC: 1.2 h, 176 ml/h. In B6C3F1 mice, oxidative metabolites are formed in much greater quantities (∼ 3600 fold difference) than glutathione-conjugative metabolites. In addition, DCA is produced to a very limited extent relative to TCA, while most of DCVG is converted into DCVC. These pharmacokinetic studies provide insight into the kinetic properties of four key biomarkers of TCE toxicity in the mouse, representing novel information that can be used in risk assessment.

Effect of thermal treatment on the photocatalytic degradation of ethylene, trichloroethylene, and chloroform

The thermal treatment of TiO2 pellets prepared by the sol–gel method decreased the photocatalytic activity. The activity divided by the specific surface area of the pellets for the complete mineralization of ethylene or chloroform was maximized at the firing temperature of 400°C. For the photocatalytic degradation of trichloroethylene (TCE), most of them were converted to chlorinated by-products, such as dichloroacetic acid, chloroform, and phosgene, and the stoichiometric ratio of [CO2]formed/[TCE]degraded showed a maximal value at 400°C. The electron spin resonance (ESR) spin-trapping with 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) in the flow injection system indicated that firing at 400°C gave the highest signal intensity of DMPO–OH adducts. These findings indicated that the OH radical was produced most effectively on the TiO2 fired at 400°C, which would be related to the content of anatase and rutile. Concerning the formation of chlorinated by-products from TCE, more dichloroacetic acid (DCAA) were detected and less CHCl3 and COCl2 were formed at lower firing temperatures, suggesting that the branching ratio of chloroethoxy radicals to the formation of DCAA or CHCl3 and COCl2 by C–C bond scission depended on the firing temperature.

Characteristics of Natural Organic Matter and Formation of Chlorinated Disinfection By-Products from Two Source Waters that Respond Differently to Ozonation

This study investigated the characteristics of natural organic matter (NOM) in two different raw surface water sources that respond differently to ozonation: one for which ozonation decreases the disinfection by-product (DBP) formation potentials (i.e., Capilano Reservoir, Vancouver, Canada), and one for which ozonation does not (i.e., South Thompson River, Kamloops, Canada); and evaluated the effect of ozonation on these characteristics and on the DBP formation potential of the different size and polar fractions of the NOM. Although the South Thompson River and the Capilano Reservoir waters had relatively similar total organic carbon concentrations, the characteristics of the NOM (e.g., size and polar distribution, specific UV absorption), in these water sources differed significantly. In general, no clear and consistent trend was observed with respect to the tendency of different size and polar fractions of NOM to generate DBPs. Nonetheless, the results from the present study suggest that hydrophobic NOM has a higher tendency to form DBPs. In addition, when considering individual size and polar fractions, specific UV absorption was a good overall indicator of the DBP formation potential for a given water source. The effect of ozonation on South Thompson River and Capilano Reservoir waters also differed significantly. For both source waters, ozonation appeared to have a greatest effect on the more hydrophilic fractions, generally increasing the DBP formation potential of the smaller more hydrophilic NOM, while generally decreasing that of the larger more hydrophilic NOM. The beneficial effect of ozonation on reducing haloacetic acid (HAA) formation potentials was due to a reduction in both the dichloroacetic acid (DCAA) and trichloroacetic acid (TCAA) formation potentials, while the negative effect of ozonation on increasing HAA formation potentials was due to an increase in the DCAA formation potentials. The results from the present study clearly indicate that the use of ozone as a primary disinfectant does not necessarily reduce the DBP formation potential of NOM in all water sources, further demonstrating the complex structure of NOM and the fact that NOM from different sources cannot be simply treated as one entity and compared with one another.

Modeling dichloroacetic acid formation from the reaction of monochloramine with natural organic matter

A kinetic model was developed to predict dichloroacetic acid (DCAA) formation in chloraminated systems. Equations describing DCAA formation were incorporated into an established comprehensive monochloramine–natural organic matter (NOM) reaction model. DCAA formation was theorized to be proportional to the amount of NOM oxidized by monochloramine and described by a single dimensionless DCAA formation coefficient, θ DCAA ( M DCAA / M DOC ox ) . The applicability of the model to describe DCAA formation in the presence of six different NOM sources was evaluated. DCAA formation could be described by considering a single NOM source-specific value for θ DCAA over a wide range of experimental conditions (i.e., pH, NOM, free ammonia, and monochloramine concentrations). DCAA formation appears to be directly proportional to the amount of active chlorine (monochloramine and free chlorine) that reacted with the NOM under these experimental conditions. Values of θ DCAA for all six NOM sources, determined by nonlinear regression analysis, varied from 6.51×10 −3 to 1.15×10 −2 and were linearly correlated with specific ultraviolet absorbance at 280 nm (SUVA 280). The ability to model monochloramine loss and DCAA formation in the presence of NOM provides insight into disinfection by-product (DBP) formation pathways under chloramination conditions. The subsequent model and correlations to SUVA has the potential to aid the water treatment industry as a tool in developing strategies that minimize DBP formation while maintaining the microbial integrity of the water distribution system.

Analysis of dichloroacetic acid in rat blood and tissues by hydrophilic interaction liquid chromatography with tandem mass spectrometry

Dichloroacetic acid (DCA) is a compound found in chlorinated drinking water. In addition, the compound is a metabolite of several halogenated solvents, including trichloroethylene (TCE) and perchloroethylene (PCE). Exposure to DCA is of concern because high doses of the compound have been shown to cause cancer in laboratory animals. Dosages of TCE administered to animals in cancer studies are designed to elicit maximal DCA formation in vivo, whereas levels of DCA to which individuals are exposed in drinking water are very low. Analysis of DCA in biological samples has been quite challenging. Derivatizing reagents commonly used to convert DCA into a more volatile form for analysis by gas chromatography (GC) have been found to convert trichloroacetic acid (TCA), a major metabolite of TCE and PCE, into DCA. High-performance liquid chromatography (HPLC) analysis does not require derivatization of DCA and can thus avoid this problem. However, the most popular stationary phases in HPLC columns do not retain small, polar compounds such as DCA well. The liquid chromatography/tandem mass spectrometry (LC/MS/MS) method described in this paper uses hydrophilic interaction liquid chromatography (HILIC), a type of chromatography that is able to retain these small, polar compounds. Method validation was performed using the United States Food and Drug Administration (USFDA) and International Conference on Harmonziation (ICH) Guidance for Industry: Bioanalytical Method Validation as a guide. Levels of DCA found in rats dosed with 2 g/kg TCE were 17.2 ng/mL (liver), 262.4 ng/mL (kidney), 175.1 ng/mL (lung), and 39.5 ng/mL (blood).

Monochloramine loss in the presence of humic acid.

Free chlorine has been used extensively as a primary and secondary disinfectant for potable water. Where it is difficult to maintain a free chlorine residual or when disinfection by-products (DBPs) are of concern, monochloramine has been used to provide a stable disinfectant residual in distributions systems. Reactions of disinfectants, free chlorine or monochloramine, with natural organic matter (NOM) consequently result in the formation of DBPs such as trihalomethanes and haloacetic acids. However, few studies have focused on the fate and kinetics of monochloramine loss in the presence of reactive constituents such as NOM. Monochloramine is inherently unstable and decays even without reactive constituents present via a mechanism known as autodecomposition. Therefore, to predict monochloramine concentrations in the presence of NOM is clearly associated with the ability to adequately model autodecomposition. This study presents the results of a semi-mechanisiic model capable of predicting the loss of monochloramine in the presence of humic material in the pH range of 6.55-8.33. The model accounts for both fast and a slow monochloramine demand to explain the loss of monochloramine over the pH range of this study. The formation of dichloroacetic acid was also predicted due to the ability of the model to differentiate monochloramine reaction pathways in the presence NOM. The results shown here demonstrate the ability of a semi-mechanistic model to predict monochloramine residuals and DBP formation in the presence of humic material.

EFFECT OF ENTEROHEPATIC CIRCULATION ON THE PHARMACOKINETICS OF CHLORAL HYDRATE AND ITS METABOLITES IN F344 RATS

Chloral hydrate (CH) is a commonly found disinfection by-product in water purification, a metabolite of trichloroethylene, and a sedative/hypnotic drug. CH and two of its reported metabolites, trichloroacetic acid (TCA) and dichloroacetic acid (DCA), are hepatocarcinogenic in mice. Another metabolite of CH, trichloroethanol (TCE), is also metabolized into TCA, and the enterohepatic circulation (EHC) of TCE maintains a pool of metabolite for the eventual production of TCA. To gain insight on the effects of EHC on the kinetics of CH and on the formation of TCA and DCA, dual cannulated F344 rats were infused with 12, 48, or 192 mg/kg of CH and the blood, bile, urine, and feces were collected over a 48-h period. CH was cleared rapidly (>3000 ml/h/kg) and displayed biphasic elimination kinetics, with the first phase being elimination of the dose and the second phase exhibiting formation rate-limited kinetics relative to its TCE metabolite. The effects of EHC on metabolite kinetics were only significant at the highest dose, resulting in a 44% and 17% decease in the area under the curve (AUC) of TCA and TCE, respectively. The renal clearance of CH, free TCE (f-TCE), and TCA of 2, 2.7, and 38 ml/h/kg, respectively, indicates an efficient reabsorption mechanism for all of these small chlorinated compounds. DCA was detected at only trace levels (<2 muM) as a metabolite of CH, TCA, or TCE.

A Human Physiologically Based Pharmacokinetic Model for Trichloroethylene and Its Metabolites, Trichloroacetic Acid and Free Trichloroethanol

Nine male and eight female healthy volunteers were exposed to 50 or 100 ppm trichloroethylene vapors for 4 h. Blood, urine, and exhaled breath samples were collected for development of a physiologically based pharmacokinetic (PBPK) model for trichloroethylene and its two major P450-mediated metabolites, trichloroacetic acid and free trichloroethanol. Blood and urine were analyzed for trichloroethylene, chloral hydrate, free trichloroethanol and trichloroethanol glucuronide, and trichloroacetic acid. Plasma was analyzed for dichloroacetic acid. Trichloroethylene was also measured in exhaled breath samples. Trichloroethylene, free trichloroethanol, and trichloroacetic acid were found in blood samples of all volunteers and only trace amounts of dichloroacetic acid (4–12 ppb) were found in plasma samples from a few volunteers. Trichloroethanol glucuronide and trichloroacetic acid were found in urine of all volunteers. No chloral hydrate was detected in the volunteers. Gender-specific PBPK models were developed with fitted urinary rate constant values for each individual trichloroethylene exposure to describe urinary excretion of trichloroethanol glucuronide and trichloroacetic acid. Individual urinary excretion rate constants were necessary to account for the variability in the measured cumulative amount of metabolites excreted in the urine. However, the average amount of trichloroacetic acid and trichloroethanol glucuronide excreted in urine for each gender was predicted using mean urinary excretion rate constant values for each sex. A four-compartment physiological flow model was used for the metabolites (lung, liver, kidney, and body) and a six-compartment physiological flow model was used for trichloroethylene (lung, liver, kidney, fat, and slowly and rapidly perfused tissues). Metabolic capacity (Vmaxc) for oxidation of trichloroethylene was estimated to be 4 mg/kg/h in males and 5 mg/kg/h in females. Metabolized trichloroethylene was assumed to be converted to either free trichloroethanol (90%) or trichloroacetic acid (10%). Free trichloroethanol was glucuronidated forming trichloroethanol glucuronide or converted to trichloroacetic acid via back conversion of trichloroethanol to chloral (trichloroacetaldehyde). Trichloroethanol glucuronide and trichloroacetic acid were then excreted in urine. Gender-related pharmacokinetic differences in the uptake and metabolism of trichloroethylene were minor, but apparent. In general, the PBPK models for the male and female volunteers provided adequate predictions of the uptake of trichloroethylene and distribution of trichloroethylene and its metabolites, trichloroacetic acid and free trichloroethanol. The PBPK models for males and females consistently overpredicted exhaled breath concentrations of trichloroethylene immediately following the TCE exposure for a 2- to 4-h period. Further research is needed to better understand the biological determinants responsible for the observed variability in urinary excretion of trichloroethanol glucuronide and trichloroacetic acid and the metabolic pathway resulting in formation of dichloroacetic acid.

Novel Metabolite of Trichloroethylene in a Methanotrophic Bacterium, Methylocystis sp. M, and Hypothetical Degradation Pathway.

Previously, a new type II methanotrophic bacterium, Methylocystis sp. M (strain M), was isolated in our laboratory [H. Uchiyama et al., Agric. Bioi. Chem., 53, 2903-2907 (1989)]. In this paper, metabolites resulting from the degradation of trichloroethylene (TCE) by strain M were studied with gas chromatography-mass spectrometry. Trichloroacetic acid, dichloroacetic acid, and a small amount of 2,2,2-trichloroethanol were detected in the water-soluble fraction of the reaction mixture. These results suggest that the conversion of TCE to trichloroacetaldehyde via a CI-shift reaction, followed by the formation of trichloroacetic acid and 2,2,2-trichloroethanol, as well as a spontaneous breakdown of TCE oxide, with subsequent formation of dichloroacetic acid, etc., is involved in the TCE degradation pathway of the methanotrophic bacterium.