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1.369 at 68 °F (NTP, 1992) - Denser than water; will sink

1.369 g/cu cm at 20 °C

10 to 50 mg/mL at 70.7 °F (NTP, 1992)

Soluble in methanol

Soluble in ethanol

greater than 212 °F (NTP, 1992)

Flash Point > 100 °C

234 to 235 °F at 760 mmHg (decomposes) (NTP, 1992)

112.5 °C

Dichloroacetonitrile is a clear liquid.

Clear liquid; [CAMEO] Colorless liquid; [MSDSonline]

Danger

H226 (100%): Flammable liquid and vapor [Warning Flammable liquids]

P210, P233, P240, P241, P242, P243, P260, P264, P270, P280, P301+P317, P301+P330+P331, P302+P361+P354, P303+P361+P353, P304+P340, P305+P354+P338, P316, P321, P330, P363, P370+P378, P403+P235, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 48 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

DICHLOROACETONITRILE is a halogenated nitrile. Nitriles may polymerize in the presence of metals and some metal compounds. They are incompatible with acids; mixing nitriles with strong oxidizing acids can lead to extremely violent reactions. Nitriles are generally incompatible with other oxidizing agents such as peroxides and epoxides. The combination of bases and nitriles can produce hydrogen cyanide. Nitriles are hydrolyzed in both aqueous acid and base to give carboxylic acids (or salts of carboxylic acids). These reactions generate heat. Peroxides convert nitriles to amides. Nitriles can react vigorously with reducing agents.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

FIREFIGHTING. Protective Equipment: Wear self-contained breathing apparatus and protective clothing to prevent contact with skin and eyes.

EXTINGUISHING MEDIA. For small (incipient) fires, use media such as "alcohol" foam, dry chemical, or carbon dioxide. For large fires, apply water from as far as possible. Use very large quantities (flooding) of water applied as a mist or spray; solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water.

SMALL SPILLS AND LEAKAGE: If you should spill this chemical, use absorbent paper to pick up all liquid spill material. Seal the absorbent paper, as well as any of your clothing which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Wash any surfaces you may have contaminated with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Contact a licensed professional waste disposal service to dispose of this material. ...Observe all federal, state, and local environmental regulations.

Do not breathe vapor. Do not get in eyes, on skin, on clothing. Avoid prolonged or repeated exposure.

SRP: When working with strong solutions of acids or bases or other caustic or corrosive materials, always wear a full face mask. When working with caustic or corrosive gases or vapors, a full face mask will not protect the eyes or prevent inhaling the material. A full face respirator is required.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Wear self-contained breathing apparatus, rubber boots, and heavy rubber gloves. In case of leak or spill, evacuate area; shut off all sources of ignition; use nonsparking tools.

For more Preventive Measures (Complete) data for DICHLOROACETONITRILE (7 total), please visit the HSDB record page.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

ENGINEERING CONTROLS. Safety shower and eye bath. Use nonsparking tools. Use only in a chemical fume hood.

PERSONAL PROTECTIVE EQUIPMENT. Respiratory: Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multi-purpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator.

Hand: Compatible chemical-resistant gloves. Eye: Chemical safety goggles. Other: Faceshield (8-inch minimum).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 13(SRC), determined from a structure estimation method(2), indicates that dichloroacetonitrile is expected to have very high mobility in soil(SRC). Volatilization of dichloroacetonitrile from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.8X10-6 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Dichloroacetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.8 mm Hg(SRC), determined from a fragment constant method(4). Dichloroacetonitrile is a by-product of water chlorination and hydrolyzes quickly; therefore, biodegradation is not expected to be an important fate in the environment(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 13(SRC), determined from a structure estimation method(2), indicates that dichloroacetonitrile is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 3.8X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 10 and 78 days, respectively(SRC). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of 0.29(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Dichloroacetonitrile hydrolyzes by a base-catalyzed reaction and its hydrolysis is catalyzed by chlorine(8-9). Dichloroacetonitrile is stable in water for several days, but in the presence of chlorine it disappears rapidly(8). The half-life of dichloroacetonitrile at pH 10 is about 35 min, but at pH 4 and 7 there is no noticeable change in concn in 2 hrs(8). In the presence of chlorine, such as may be a residual from water chlorination, the half-life of dichloroacetonitrile is 60, 25, and 15 min at pH 4, 7, and 10, respectively(8). The concn of dichloroacetonitrile in buffered water declined over the course of 10 days with roughly 90%, 69%, and 41% remaining at pH 6, 7, and 8, respectively(9). Dichloroacetonitrile has a hydrolysis rate constant of 5.6X10-6/sec at pH of 8.7(10), corresponding to a half-life of 1.4 days(SRC). Dichloroacetonitrile is a by-product of water chlorination and hydrolyzes quickly; therefore, biodegradation is not expected to be an important fate in the environment(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dichloroacetonitrile, which has an estimated vapor pressure of 2.8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase dichloroacetonitrile is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 300 days(SRC), calculated from its rate constant of 5.3X10-14 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3).

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=3018-12-0][Available from: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=3018-12-0]

Using a structure estimation method based on molecular connectivity indices(1), the Koc of dichloroacetonitrile can be estimated to be 13(SRC). According to a classification scheme(2), this estimated Koc value suggests that dichloroacetonitrile is expected to have very high mobility in soil.

/SIGNS AND SYMPTOMS/ Skin Contact: Causes burns. Skin Absorption: May be harmful if absorbed through the skin. Eye Contact: Causes burns. Inhalation: May be harmful if inhaled. Material is extremely destructive to the tissue of the mucous membranes and upper respiratory tract. Ingestion: May be harmful if swallowed.

/SIGNS AND SYMPTOMS/ Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea, and vomiting. Material is extremely destructive to tissue of the mucous membranes and upper respiratory tract, eyes, and skin. Inhalation may result in spasm, inflammation and edema of the larynx and bronchi, chemical pneumonitis, and pulmonary edema.

/GENOTOXICITY/ ... The ability of halogenated acetonitriles (HAN) to induce single-strand breaks on the DNA of HeLa S3 cells was investigated using the single-cell gel electrophoresis (SCGE) assay, which could be a good tool with which to evaluate the genotoxicity of chlorinated water. The results were compared to those obtained in the Ames fluctuation test using the Salmonella typhimurium TA100 strain without activation. With the Ames fluctuation test, a mutagenic effect was observed for chloroacetonitrile (MCAN), dichloroacetonitrile (DCAN), and trichloroacetonitrile (TCAN). No mutagenic effect was found with bromoacetonitrile (MBAN) or dibromoacetonitrile (DBAN). In the SCGE assay, all five HANs induced DNA damage in HeLa S3 cells, increasing the mean tail moment significantly. For each compound, a dose-effect relation was observed. ... Brominated acetonitriles were more genotoxic than chlorinated acetonitriles in the SCGE assay, and the genotoxicity increased with the number of halogenated atoms of the compound. This behavior had already been found with other genotoxicity tests.

/GENOTOXICITY/ The haloacetonitriles produced DNA strand breaks in cultured human lymphoblastic (CCRF-CEM) cells. Trichloroacetonitrile (TCAN) was the most potent DNA strand breaker, and bromochloroacetonitrile (BCAN) greater than dibromoacetonitrile (DBAN) greater than dichloroacetonitrile (DCAN) greater than chloroacetonitrile (CAN), which was only marginally active.

/GENOTOXICITY/ Chlorinated and brominated haloacetonitriles (HAN) ... produced DNA strand breaks in cultured human lymphoblastic (CCRF-CEM) cells. /Information pertaining to dose and duration of exposure not specified/. /Chlorinated & brominated haloacetonitriles/

Dichloroacetonitrile formation as a by-product of the chlorination of humic substances, algae and amino acids contained in drinking water(1-3) and pulp bleaching processes(4) will result in its release to the environment through various waste streams(SRC).

Dichloroacetonitrile is a by-product of the chlorination of humic substances, algae and amino acids(2,5,6). When humic and fulvic acids from three natural waters were chlorinated with sodium hypochlorite at pH 7, the mean concn of dichloroacetonitrile formed was 1.48 and 0.64 ug/mg of organic carbon, respectively(3). The respective yields of dichloroacetonitrile were 0.38 and 0.22% of total organic halogen formed(3). The yield correlated with the nitrogen to carbon ratio of the humic substances. Reactivity is reduced at high pHs. When the chlorination was performed at pH 12, dichloroacetonitrile was below the detection limit. Dichloroacetonitrile is formed during the chlorination of drinking water and waste water and its formation is believed to be due to the presence of humic substances in the water(3,4). When raw water from ten U.S. cities was chlorinated at pH 7 and 20 °C and held in the dark for 72 hr, the concn of dichloroacetonitrile in the water ranged from 3.0 to 12.0 ug/L and the yield ranged from 0.26 to 0.63% of organic halogen(3). The concns are higher at lower pHs and increase in time at low pH (5) and remain low or decrease in time at higher pH (7 and 9.4)(1).

... Haloacetonitriles are by products of water chlorination. ... /Haloacetonitriles/

The occurrence of volatile halogenated compounds in spent liquors from kraft softwood and hard wood pulp bleaching processes was studied. The identity of the low molecular mass constituents was verified by capillary gas chromatography-mass spectrometry using an NBS/Wiley reference database and mass spectra of reference compounds. Identity was confirmed for fourteen components, of which two, dichloroacetonitrile and trichloromethanesulfonyl chloride, have not been previously identified in, eg, beach kraft effluents. ...

Dichloroacetonitrile

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 52: (1991) Chlorinated Drinking-water; Chlorination By-products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds

1999

1998

An estimated BCF of 3 was calculated in fish for dichloroacetonitrile(SRC), using an estimated log Kow of 0.29(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for dichloroacetonitrile is estimated as 3.8X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that dichloroacetonitrile is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 10 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 78 days(SRC). Dichloroacetonitrile's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Dichloroacetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.8 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Acute Exposure/ ... The acute oral LD50 values (mg/kg) in mice and rats are: ... mice: 270 (M), 279 (F); DCAN, rats: 339 (M), 330 (F). Death was preceded by slowed respiration, depressed activity, prostration, and coma. There were no apparent compound-related gross pathological effects.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Dichloroacetonitrile (DCAN) (in corn oil) was administered by gavage to male and female CD rats for 14 or 90 days at levels of 12, 23, 45, and 90 mg/kg/day or 8, 33, and 65 mg/kg/day, respectively. There were no deaths during the 14-day study. Compound-related mortality was 50% (M) and 25% (F) at 65 mg/kg, 10% (M) and 5% (F) at 33 mg/kg, and 5% (M) and 0% (F) at 8 mg/kg during the 90-day study. Body weights were significantly lower at 90 and 65 mg/kg/day; weight and ratios of spleen and gonads and cholesterol levels were significantly lower at 90 mg/kg/day. No consistent, significant adverse compound-related effects on any of the parameters evaluated were evident. The NOAEL for 14 days was 45 mg/kg/day and for 90 days was 8 mg/kg/day.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Dichloroacetonitrile did not induce gamma-glutamyltranspeptidase-positive foci in rat liver. An oral dose by gavage of 65 mg/kg bw/day for 90 days to male and female CD rats reduced body weights, spleen and gonad weights and serum cholesterol levels; other blood chemistry and hematological parameters were generally unchanged. Liver weights relative to body or brain weight were increased in female rats.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a screening assay based on the enhanced induction of lung tumors, groups of 40 female strain A/J mice, 10 weeks old, were given 10 mg/kg body weight ... dichloroacetonitrile, ... in 10% Emulfor by oral gavage three times per week for eight weeks. A group of 40 animals given 10% Emulfor only served as controls. Survival at the end of the study ( at nine months of age) was: control, 31/40; ... dichloroacetonitrile-treated, 30/40 ... . The numbers of animals with lung tumors and the average number of tumors per animal were: control, 3/31 and 0.1; ... dichloroacetonitrile-treated, 7/30 and 0.23.

For more Non-Human Toxicity Excerpts (Complete) data for DICHLOROACETONITRILE (19 total), please visit the HSDB record page.

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(2)O(2), (-)OH and O(2). Therefore, the effect of various concentrations of DCAN (100-400 uM) on the activity of 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-alpha was assessed since macrophages are known to secrete TNF-alpha 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 uM and 400 uM), 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-alpha (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 uM or 200 uM DCAN incites apoptotic cell death. At higher concentrations (400 uM), 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.

When administered orally to rats, the haloacetonitriles (HAN) were metabolized to cyanide and excreted in the urine as thiocyanate. The extent of thiocyanate excretion was chloroacetonitrile (CAN) greater than bromochloroacetonitrile (BCAN) greater than dichloroacetonitrile (DCAN) greater than dibromoacetonitrile (DBAN) much greater than trichloroacetonitrile (TCAN).

The excretion and tissue distribution of (1-14C)dichloroacetonitrile and (2-14C)dichloroacetonitrile were studied in male Fischer 344 rats and male B6C3F1 mice. ...The differences in the route of excretion of (1-14C)DCAN compared to (2-14C)DCAN indicated that the molecule was being cleaved in the body and metabolized by different mechanisms.

The excretion and tissue distribution of (1-14C)dichloroacetonitrile and (2-14C)dichloroacetonitrile were studied in male Fischer 344 rats and male B6C3F1 mice. Three dose levels of dichloroacetonitrile (DCAN) (0.2, 2, or 15 mg/kg) were administered to rats and two dose levels of DCAN (2 or 15 mg/kg) to mice. Daily excreta including exhaled volatiles and radiolabeled carbon dioxide (14CO2) were analyzed for radiolabeled carbon (14C) until greater than 70% of the radioactivity was excreted. At that time the animals were sacrificed and tissues were collected. Tissues and excreta were analyzed for 14C by combustion and liquid scintillation counting. Rats administered (1-14C)DCAN excreted 62 to 73% of the 14C in 6 days, with 42 to 45% in urine, 14 to 20% in feces, and 3 to 8% as CO2. Rats administered (2-14C)DCAN excreted 82 to 86% of the 14C in 48 hr, with 35 to 40% in urine, 33 to 34% as CO2, and 10 to 13% in feces. Mice administered (1-14C)DCAN excreted 83 to 85% of the 14C in 24 hr, with 64 to 70% in urine, 9 to 13% in feces, and 5 to 6% as CO2. Mice administered (2-14C)DCAN excreted 84 to 88% of the 14C in 24 hr with 42 to 43% in urine, 8 to 11% in feces, and 31 to 37% as CO2. Liver tissues retained the most 14C in all studies except the study of (1-14C)DCAN in rats, where blood contained the most 14C. These results indicate that DCAN was absorbed rapidly after oral administration in water. The differences in the route of excretion of (1-14C)DCAN compared to (2-14C)DCAN indicated that the molecule was being cleaved in the body and metabolized by different mechanisms.

After oral administration of 0.02 mmol/kg body weight (2.0 mg/kg body weight) or 0.14 mmol/kg body weight (15 mg/kg body weight) (14)C-dichloroacetonitrile to mice by gavage in water, 85 and 83%, respectively, of the dose was eliminated in the urine, feces and expired air (as (14)C-carbon dioxide) by 24 hours. The urine contained 64-70% of the dose, the feces contained 9-13% and about 5% was eliminated as carbon dioxide; 11-12% was retained in the tissues. The largest amount of radiolabel was found in the liver about 4% of dose, muscle and skin (about 2%) and blood and fat (about 1%). When mice were given 0.02 mmol/kg body weight (2.0 mg/kg) or 0.14 mmol/kg body weight (15 mg/kg) 2-(14)C-dichloroacetonitrile by gavage in water, 84-88% of the dose was eliminated in the urine, feces and expired air (as (14)C-carbon dioxide) within 24 hours; the urine (42-43% of dose) and expired air 31-37%) contained the most radiolabel. Nine percent of the administered radiolabel was retained in the tissues after 24 hours; most was found in the liver (about 5% of dose), and 0.5-1% of the dose was present in muscle, kidney and skin.

Studies with [1-14C]dichloroacetonitrile in rats and mice and [2-14C]dichloroacetonitrile in rats indicated that the substance is rapidly absorbed after oral administration in water. Excretion of radioactivity following dosing with [1-14C]dichloroacetonitrile is more rapid in mice than in rats. In mice, approximately 84% of the dose was excreted in 24 hr (67% in urine, 11% in feces, 5% as CO2), compared with 67% in rats in six days (44% in urine, 17% in feces, 6% as CO2). Excretion of [2-14C]dichloroacetonitrile radioactivity in rats accounted for about 84% of the dose within 48 hr (38% in urine, 12% in feces, 34% as CO2). The quantitative differences in the route of excretion of the two labels in rats indicate that dichloroacetonitrile is being cleaved in vivo. The 1-14Clabelled compound behaved like cyanide

A by-product of water chlorination; [ChemIDplus]

Sewer and Wastewater Treatment [Category: Industry]

The reaction of cyanoethanoic acid with chlorine in aqueous medium at ... pH 4 and 7 produced dichloroacetonitrile. ... At pH 10, dichloroacetonitrile /was also produced/.

Haloacetonitriles ... are chemical by-products of chlorine disinfection of drinking water. /Halogenated acetonitriles/