Concentrations Of Dichloroacetonitrile Research Articles

Sorption Characteristics of Halogenated Acetonitriles (HANs) in Surface Water onto Activated Carbon Prepared from Walnut Shell

Sorption efficiencies of activated carbon prepared from walnut shell for the removal of Halogenated Acetonitriles (HANs) from surface water was investigated in this study, as an ethically sound-way of utilizing this unexploited abundant natural resource, and was also compared with burgoyne commercial activated carbon (BCAC). Major HANs created during the disinfection process consist of dichloroacetonitrile (DCAN) and bromoacetonitrile, (BCAN). Physicochemical properties of both raw and chlorinated water were determined using standard methods, and concentration of DCAN were determined from water treatment plant at different stages of treatment using High Performance liquid Chromatography (HPLC). Recovery experiments were carried out to validate experimental procedure. Batch adsorption experiments were carried out and different parameters such as adsorbent dosage (0.2, 0.4, 0.8 g), contact time (30, 60, 90 minutes), pH (5, 7, 9), and concentration (0.006 mg/L, 0.009 mg/L and 0.012 mg/L) were optimized for removal of DCAN using walnut shell activated carbon (WSAC). Experimental sorption data from different initial concentrations of DCAN were used to test conformity with Freundlich and Langmuir adsorption isotherms. Percentage recovery from experimental procedure is 86.01±0.62 to 100.0±0.00 for DCAN. Mean percentage adsorption efficiencies for simulation experiment is 16.670±0.467 to 41.67±1.103 for DCAN. Optimum conditions for DCAN were 0.8g adsorbent dosage, 60 minutes contact time, pH 9 and 0.012 mg/L initial concentration. Optimum values of theses parameters used for adsorption of DCAN in raw and chlorinated water serving the treatment plant gave an adsorption efficiency of 69.00±1.43% and 79.00±0.03 respectively. Adsorption efficiency of BCAC gave 94.4±0.42 and 98.00±1.41 for raw and chlorinated water respectively, with a total decrease in all physicochemical parameters examined after adsorption experiment. Adsorption isotherm studies indicated that Langmuir model was more suitable for the experimental data than Freundlich isotherm model. Conclusively, the effective adsorbent properties displayed by WSAC in the removal of DCAN indicate its potentials in treatment of water contaminations.

Identification of important precursors and theoretical toxicity evaluation of byproducts driving cytotoxicity and genotoxicity in chlorination

Chlorination, the most widely used disinfection process for water treatment, is unfortunately always accompanied with the formation of hazardous disinfection byproducts (DBPs). Various organic matter species, like natural organic matter (NOM) and amino acids, can serve as precursors of DBPs during chlorination but it is not clear what types of organic matter have higher potential risks. Although regulation of DBPs such as trihalomethanes has received much attention, further investigation of the DBPs driving toxicity is required. This study aimed to identify the important precursors of chlorination by measuring DBP formation from NOM and amino acids, and to determine the main DBPs driving toxicity using a theoretical toxicity evaluation of contributions to the cytotoxicity index (CTI) and genotoxicity index (GTI). The results showed that NOM mainly formed carbonaceous DBPs (C-DBPs), such as trichloromethane, while amino acids mainly formed nitrogenous DBPs (N-DBPs), such as dichloroacetonitrile (DCAN). Among the DBPs, DCAN had the largest contribution to the toxicity index and might be the main driver of toxicity. Among the precursors, aspartic acid and asparagine gave the highest DCAN concentration (200 g/L) and the highest CTI and GTI. Therefore, aspartic acid and asparagine are important precursors for toxicity and their concentrations should be reduced as much as possible before chlorination to minimize the formation of DBPs. During chlorination of NOM, tryptophan, and asparagine solutions with different chlorine doses and reaction times, changes in the CTI and GTI were consistent with changes in the DCAN concentration.

Role of ammonia on haloacetonitriles and halonitromethanes formation during Ultraviolet irradiation followed by chlorination/chloramination

Combination of ultraviolet (UV) disinfection and chlorination became a common multi-barrier approach taken by water utilities against microbial pathogens in drinking water disinfection. Halogenated disinfection byproducts (DBPs) have been monitored and regulated in drinking water under various jurisdictions around the world for decades. More recently, several nitrogenous DBPs (N-DBPs), like haloacetonitriles (HANs) and halonitromethanes (HNMs), have been identified in chlorinated drinking waters, whose precursors are N-containing organic compounds of various origins and structures. Rising concerns over the N-DBPs formation due to their more potent genotoxic and cytotoxic activity than the regulated carbonaceous-DBPs have prompted extensive research on drinking water disinfection processes. To examine the effect of ammonia nitrogen (NH3-N) on N-DBPs formation during UV disinfection of drinking water followed by chlorination/chloramination, as a first attempt, synthetic waters prepared by humic acid with different NH3-N concentrations were exposed to UV dose up to 300 mJ/cm2 from either low pressure (LP) or medium pressure (MP) lamps, followed by chlorination/chloramination. To investigate trends, the study employed synthetic waters with elevated precursor concentrations and disinfectant exposures to generate significant byproduct formation possible. LP UV treatment had no obvious effect on N-DBP formation, whereas MP UV irradiation produced more dichloroacetonitrile (DCAN). The existence of ammonia (≤1 mg/L-N) increased DCAN concentration in high organics synthetic waters under varying MP UV doses, respectively. In high organics synthetic water samples exposed to a MP UV dose of 300 mJ/cm2 DCAN reached a maximum yield of 13.7 μg/L in the presence of 0.5 mg/L NH3-N, whereas lower yields were observed at NH3-N ≥ 2 mg/L, i.e. 2.9 μg /L and 1.8 μg/L at 2 and 10 mg/L NH3-N, respectively.

Health risk assessment of haloacetonitriles in drinking water based on internal dose.

To estimate the health risk of haloacetonitriles in different kinds of drinking water, the concentrations of haloacetonitriles in tap water, boiled water and direct drinking water were detected. The physiologically based pharmacokinetic (PBPK) model was used to calculate internal dose in the human body for haloacetonitriles through ingestion, and the probability distributions of the non-carcinogenic risk of haloacetonitriles for human via drinking water were assessed. This study found that the mean concentrations of dichloroacetonitrile (DCAN) in tap water, boiled water and direct drinking water were 0.955μg/L, 0.207μg/L and 0.127μg/L, and those of dibromoacetonitrile (DBAN) were 0.221μg/L, 0.104μg/L, 0.089μg/L, respectively. In China, direct drinking water is used most frequently, so the concentrations of haloacetonitriles in direct drinking water were used to obtain data on the internal dose of haloacetonitriles. In addition, the simulation results for the PBPK model showed that the highest and lowest concentrations of DCAN occurred in the liver and venous blood, respectively. The peak concentrations of DBAN in each tissue were in the decreasing order liver>rapidly perfused tissue>kidney>slowly perfused tissues>fat>arterial blood (venous blood). In addition, the highest 95th percentile hazard quotients (HQ) value of haloacetonitriles via drinking water for humans was 8.89×10-3, much lower than 1. The 95th percentile hazard index (HI) was 0.046, which was also lower than 1, suggesting that there was no obvious non-carcinogenic risk.

Acute toxicity of dichloroacetonitrile (DCAN), a typical nitrogenous disinfection by-product (N-DBP), on zebrafish (Danio rerio)

Dichloroacetonitrile (DCAN) is a typical nitrogenous disinfection by-product (N-DBP) and its toxicity on aquatic animals is investigated for the first time. The present study was designed to investigate the potential adverse effects of DCAN on zebrafish. DCAN could induce developmental toxicity to zebrafish embryos. A significant decrease in hatchability and an increase in malformation and mortality occurred when DCAN concentration was above 100µg/L. Heart function alteration and neuronal function disturbance occurred at concentration higher than 500 and 100µg/L, respectively. Further, DCAN was easily accumulated in adult zebrafish. The rank order of declining bioconcentration factor (BCF) was liver (1240–1670)> gill (1210–1430)> muscle (644–877). DCAN caused acute metabolism damage to adult zebrafish especially at 8 days exposure, at which time the “Integrated Biomarker Response” (IBR) index value reached 798 at 1mg/L DCAN dose. Acute DNA damage was induced to adult zebrafish by DCAN even at 10µg/L dose.

Formation of disinfection by-products during chlorine dioxide pre-oxidation of chironomid larvae metabolites followed by chlorination

The objective of this research was to investigate the formation of disinfection by-products (DBPs) during chlorine dioxide pre-oxidation of chironomid larvae metabolites followed by chlorination. The mode of action of chlorine dioxide/chlorine combination was clarified, including the impact of different factors on DBP formation. The results indicated that pre-oxidation suppressed the production of most DBPs such as trihalomethanes, haloacetic acids, haloacetonitriles, and haloketones, compared to when chlorination was used alone. The concentrations of trichloromethane (TCM), dichloroacetic acid (DCAA), trichloroacetic acid (TCAA), dichloroacetonitrile (DCAN), and 1,1-dichloro-2-propanone (1,1-DCP) decreased with prolonged pre-oxidation times, with the highest yields observed for DCAA and TCAA. The solution pH had a distinct influence on DBP formation, with the concentrations of DCAA, TCAA, DCAN, 1,1-DCP, and 1,1,1-trichloro-2-propanone (1,1,1-TCP) initially increasing and then decreasing with increasing pH. The maximum concentrations of DCAA and TCAA were observed at pH 7–8, whereas the TCM content increased continuously on increasing the pH up to 8–9. Other DBPs reached their maxima at pH 6–7. Regarding thermal effects, the formation of 1,1,1-TCP enhanced at higher temperatures, while the concentrations of DCAN, 1,1,-DCP, and TCM first increased between 10 and 20°C and then decreased between 20 and 30°C. The concentrations of DCAA and TCAA decreased from 10 to 20°C and then increased between 20 and 30°C.

Impact of Water Heaters on the Formation of Disinfection By‐products

This study examined the effect of water heaters and home‐heating scenarios on the formation and decomposition of disinfection by‐products (DBPs). Residential concentrations of DBPs were investigated in cold and hot tap water samples from 18 houses equipped with conventional water heaters or on‐demand, tankless heaters. The houses were served by a western Massachusetts water system. On‐demand heating without long‐term storage of hot water resulted in little or no change in DBP formation. In contrast, the research indicated that long‐term storage could lead to an increase in trihalomethanes, haloacetic acid, and chloropicrin, whereas the concentrations of dichloroacetonitrile and trichloropropane resulted from competition and decomposition. In the bench‐scale study for this article, laboratory incubation and different heating scenarios (short‐term and long‐term) were tested to confirm the effect of stagnation and high temperature on DBP concentrations in different types of heaters.

Formation of halogenated C-, N-DBPs from chlor(am)ination and UV irradiation of tyrosine in drinking water

The formation of regulated and emerging halogenated carbonaceous (C-) and nitrogenous disinfection by-products (N-DBPs) from the chlor(am)ination and UV irradiation of tyrosine (Tyr) was investigated. Increased chlorine contact time and/or Cl 2/Tyr ratio increased the formation of most C-DBPs, with the exception of 4-chlorophenol, dichloroacetonitrile, and dichloroacetamideChloroform and dichloroacetic acid increased with increasing pH, dichloroacetonitrile first increased and then decreased, and other DBPs had maximum yields at pH 7 or 8. The addition of ammonia significantly reduced the formation of most C-DBPs but increased 4-chlorophenol, dichloroacetonitrile, dichloroacetamide, and trichloroacetonitrile yields for short prechlorination contact times before dosing ammonia. When UV irradiation and chlorination were performed simultaneously, the concentrations of the relatively stable C-DBPs increased, and the concentrations of dichloroacetonitrile, dichloroacetamide, and 4-chlorophenol decreased with increasing UV dose. This information was used to develop a mechanistic model for the formation of intermediate DBPs and end products from the interaction of disinfectants with tyrosine.

Adsorption characteristics of haloacetonitriles on functionalized silica-based porous materials in aqueous solution

The effect of the surface functional group on the removal and mechanism of dichloroacetonitrile (DCAN) adsorption over silica-based porous materials was evaluated in comparison with powdered activated carbon (PAC). Hexagonal mesoporous silicate (HMS) was synthesized and functionalized by three different types of organosilanes (3-aminopropyltriethoxysilane, 3-mercaptopropyltrimethoxysilane and n-octyldimethysilane). Adsorption kinetics and isotherm models were used to determine the adsorption mechanism. The selective adsorption of five haloacetonitriles (HANs) in the single and mixed solute systems was also studied. The experiments revealed that the surface functional groups of the adsorbents largely affected the DCAN adsorption capacities. 3-Mercaptopropyl-grafted HMS had a high DCAN adsorption capacity compared to PAC. The adsorption mechanism is believed to occur via an ion–dipole electrostatic interaction in which water interference is inevitable at low concentrations of DCAN. In addition, the adsorption of DCAN strongly depended on the pH of the solution as this related to the charge density of the adsorbents. The selective adsorption of the five HANs over PAC was not observed, while the molecular structure of different HANs obviously influenced the adsorption capacity and selectivity over 3-mercaptopropyl-grafted HMS.

Possible role of hydroxyl radicals in the oxidation of dichloroacetonitrile by Fenton-like reaction

Dichloroacetonitrile (DCAN), is a member of haloacetonitrile group and detected in drinking water supplies as a by-product of chlorination process. The mechanism of DCAN-induced carcinogenesis is believed to be mediated by oxidative bioactivation of DCAN molecules. The present study was designed to investigate if reactive oxygen species (ROS), similar to that generated in biological systems, are capable of oxidative activation of DCAN. A model ROS generation system (Fenton-like reaction; Fe 2+ and H 2O 2) that predominantly produces hydroxyl radical (OH ·) was used. DCAN oxidation was monitored by the extent of cyanide (CN −) release. The results indicate that DCAN was markedly oxidized by this system, and the rate of oxidation was dependent on DCAN concentration. Four-fold increase in H 2O 2 concentration (50–200 mM) resulted in a 35-fold increase in CN − release. The rates of DACN oxidation in presence of various transition metals were in the following order; iron>copper>titanium. DCAN oxidation was enhanced significantly by the addition of vitamin C and sulfhydryl compounds such as glutathione, N-acetyl- l- cysteine, and dithiothreitol (10 mM) to 140, 130, 145 and 136% of control, respectively. Addition of H 2O 2 scavenger; catalase or iron chelator; desferrioxamine (DFO) resulted in a significant decrease in CN − release 47 and 41% of control, respectively. Addition of various concentrations of the free radical scavengers, DMSO, or mannitol, to the incubation mixtures caused a significant decrease in DCAN oxidation, 32 and 50% of control, respectively. Michaelis–Menten kinetic analysis of the rates of this reaction, with or without inhibitors, indicated that ROS mediated oxidation of DCAN was inhibited by catalase ( K i=0.01 mM)>DFO (0.02 mM)>mannitol (0.09 mM)>DMSO (0.12 mM). In conclusion, our results indicate that DCAN is oxidized by a ROS-mediated mechanism. This mechanism may have an important role in DCAN bioactivation and DCAN-induced genotoxicity at target organs where multiple forms of ROS generating systems are abundant.

Formation and degradation of dichloroacetonitrile in drinking waters

Dichloroacetonitrile (DCAN) is an important example of a reactive disinfection by-product for which a large body of occurrence data exists. Although it is known to undergo base-catalysed hydrolysis, DCAN9s peculiar dependence on reaction time, chlorine dose and pH has never been fully reconciled with expectations based on its presumed precursor (i.e. amino acid residues). The purpose of this research was to improve existing models for DCAN degradation and to use this information for interpretation of DCAN concentration profiles. Laboratory studies were performed using buffered solutions of DCAN, natural organic matter (NOM) and treated drinking waters, both with and without free residual chlorine. DCAN concentrations were measured as a function of reaction time. Results indicate a decomposition scheme encompassing three pathways of hydrolysis: attack by hydroxide, hypochlorite and water. Any one of the three pathways may predominate in drinking water systems, depending on the pH and chlorine residual. The resulting chemical kinetic model was used to show that the DCAN formed (and subsequently decomposed) was often many times the actual measured DCAN concentration. DCAN formation was found to agree with expectations based on the underlying chemistry of chlorine attack on proteinaceous material.

Decomposition of dihaloacetonitriles in water solutions and fortified drinking water samples

An investigation of the decomposition of dihaloacetonitriles (DHANs) in water solutions and fortified drinking water samples was conducted. The concentrations of dichloroacetonitrile (CHCl 2CN, DCAN), bromochloroacetonitrile (CHBrClCN, BCAN) and dibromoacetonitrile (CHBr 2CN, DBAN) were determined by a gas chromatography–mass spectrometry (GC–MS) method at regular time intervals and different temperatures. The effect of sodium thiosulfate (Na 2S 2O 3), which is used as a preservative in water samples, was also examined. The rates of decomposition were determined for each compound. The results show that the reactions are faster in fortified drinking water samples than in ultrapure water solutions. They are also favored at higher temperature, especially when sodium thiosulfate is present. The highest decomposition rate is shown by DCAN, followed by BCAN and DBAN, while at the presence of sodium thiosulfate the decomposition of DBAN is the fastest.

Induction of oxidative stress and TNF- α secretion by Dichloroacetonitrile, a water disinfectant by-product, as possible mediators of apoptosis or necrosis in a murine macrophage cell line (RAW)

The water disinfectant by-product dichloroacetonitrile (DCAN) is a direct-acting mutagen and induces DNA strand breaks in cultured human lymphoblastic cells. Cellular activation by environmental agents may exert detrimental effects to the cells. Activated macrophages produce reactive oxygen intermediates such as H 2O 2, −OH and O 2. Therefore, the effect of various concentrations of DCAN (100–400 μ m) on the activity macrophage cells (RAW 264.7) was studied. In these cells, DCAN-induced oxidative stress was characterized by the production of reactive oxygen intermediates (ROI). Also, the ratios of intracellular GSH/GSSG was assessed and used as a biomarker for oxidative stress. The secretion of TNF- α was assessed since macrophages are known to secrete TNF- α as a result of cellular oxidative stress. Electrophoretic detection of DNA degradation and light microscopy was utilized for the characterization of DCAN-induced apoptosis. Lactate dehydrogenase (LDH) leakage and trypan blue exclusion were used as markers of cellular necrosis. Following exposure to DCAN (200 μ m and 400 μ m), intracellular GSSG was increased (2.5-fold of control, P<0.05). DCAN activation of RAW cells was detected by elevated levels of intracellular ROI (1.9–2.5-fold than control, P<0.05) and increased secretion of TNF- α (4.5 fold–than control, P <0.05). Elecrophoresis of genomic DNA of treated cells indicated a dose-dependent increase in degradation of genomic DNA. Morphological studies also indicated that exposure of RAW cells to 100 μ m or 200 μ m DCAN incites apoptic cell death. At higher concentrations (400 μ m), however, significant ( P<0.05) increase in LDH leakage and decrease in cell viability (55% of control) indicative of cellular necrosis, were observed. These studies indicate that DCAN induces dose-dependent apoptosis or necrosis in RAW cells that could be due to the disturbance in intracellular redox status and initiation of ROI-mediated oxidative mechanisms of cellular damage.

Philadelphia drinking water

The formation of regulated and emerging halogenated carbonaceous (C-) and nitrogenous disinfection by-products (N-DBPs) from the chlor(am)ination and UV irradiation of tyrosine (Tyr) was investigated. Increased chlorine contact time and/or Cl2/Tyr ratio increased the formation of most C-DBPs, with the exception of 4-chlorophenol, dichloroacetonitrile, and dichloroacetamideChloroform and dichloroacetic acid increased with increasing pH, dichloroacetonitrile first increased and then decreased, and other DBPs had maximum yields at pH 7 or 8. The addition of ammonia significantly reduced the formation of most C-DBPs but increased 4-chlorophenol, dichloroacetonitrile, dichloroacetamide, and trichloroacetonitrile yields for short prechlorination contact times before dosing ammonia. When UV irradiation and chlorination were performed simultaneously, the concentrations of the relatively stable C-DBPs increased, and the concentrations of dichloroacetonitrile, dichloroacetamide, and 4-chlorophenol decreased with increasing UV dose. This information was used to develop a mechanistic model for the formation of intermediate DBPs and end products from the interaction of disinfectants with tyrosine.