Dichloroacetonitrile

109.937

109.94

221-159-4

O0L64V63M9

60511

2810

DTXSID3021562

Liquid

2926909090

23.8

0.29 (est)

Dichloroacetonitrile is a clear liquid.

1.369 g/cm³ @ Temp: 20 °C

112.5 °C

greater than 212° F (NTP, 1992)

1.448

In water, 3.35X10+4 mg/L at 25 deg C (est)

Keep tightly closed. Keep away from heat, sparks, and open flame.

2.82 mm Hg at 25 deg C (est)

Henry's Law constant = 3.79X10-6 atm-cu m/mol at 25 °C (est)

Conversion factor: mg/cu m = 4.50 X ppm|When heated to decomposition it emits toxic fumes of /Hydrogen Chloride/, /Cyanide/, and /Nitrogen oxides/.|Hydroxyl radical reaction rate constant = 5.32X10-14 cu cm/molec-sec at 25 °C (est)

Burns slowly, emitting a thick black smoke, but will not flash (NTP, 1992). Water soluble.

Halogenated Organic Compounds

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.

Corrosive

II

3

UN 2920 8/PG 2

3

R10;R22;R34

S26-S36/37/39-S45-S25-S16

AL8465000

C:Corrosive;

Stable. Combustible. Incompatible with strong oxidizing agents.

P280-P305 + P351 + P338-P310

H226-H302-H314

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.

This chemical is probably combustible. (NTP, 1992)

|Danger|H226 (100%): Flammable liquid and vapor [Warning Flammable liquids]|P210, P233, P240, P241, P242, P243, P260, P264, P270, P280, P301+P312, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P310, P321, P330, P363, P370+P378, P403+P235, P405, and P501|Aggregated GHS information provided by 47 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

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. STORAGE PRECAUTIONS: You should store this material under ambient temperatures. (NTP, 1992)

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).

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.

Flammable liquid. Emits toxic fumes under fire conditions.

Cover with dry-lime, sand, or soda ash. Place in covered containers using non-sparking tools and transport outdoors. Ventilate area and wash spill site after material pickup is complete.

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.

Symptoms of exposure may include burning sensation... .

Dichloroacetonitrile was measured at 2.6, 3.4, and 3.0 ug/L at the inlet to three wetland areas and was not detected in the outlets in the Tres Rios Wetlands outside Phoenix, AZ(1).

LD50 Mouse (male) oral 270 mg/kg|LD50 Mouse (female) oral 279 mg/kg|LD50 Rat (male) oral 339 mg/kg|LD50 Rat (female) oral 330 mg/kg

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. ...

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 rate constant for the vapor-phase reaction of dichloroacetonitrile with photochemically-produced hydroxyl radicals has been estimated as 5.3X10-14 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 300 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Dichloroacetonitrile hydrolyzes by a base-catalyzed reaction and its hydrolysis is catalyzed by chlorine(2-3). Dichloroacetonitrile is stable in water for several days, but in the presence of chlorine it disappears rapidly(2). 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 hr(2). 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(2). 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(3). In samples buffered at pH 7.2 and held for a week at room temperature, 20% of the dihaloacetonitriles were lost(4). Little or no loss occurred when the samples were maintained at 5 °C(4). Dichloroacetonitrile has a hydrolysis rate constant of 5.6X10-6/sec at pH of 8.7(5).

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).

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.

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).

DRINKING WATER: Based on a study of 35 water utilities across the U.S. by the EPA and State of California Department of Health Services, the quarterly median concns of dichloroacetonitrile from the spring of 1988 through the winter of 1989 were 1.2, 1.1, 1.1, and 1.2 ug/L(1). The quarterly dichloroacetonitrile concns in the facility with the highest bromide level ranged from 0.24 to 0.34 ug/L(1). Dichloroacetonitrile was detected, but not quantified in Philadelphia drinking water between 1977 and 1979(2) and Cincinnati drinking water(3). The concn of dichloroacetonitrile in two water treatment plants using chlorine treatment was 2.0 and 4.5 ug/L(4). The concns of dichloroacetonitrile in the same plants using a combination of chlorination and ozonation were 0.72 and 3.3 ug/L(4). Tap water samples taken in Phoenix, AZ contained 4.0 ug/L of dichloroacetonitrile(5). Dichloroacetonitrile was not detected when using chlorine dioxide, chlorine dioxide with bromide, chlorine, chlorine with bromide, ozone, or ozone with bromide treatments, however dichloroacetonitrile was detected when using chloramination at 2.67 ug/L and chloramination with bromide at 2.35 ug/L(6). Experiments performed on the concn of dichloroacetonitrile over time in raw and finished water at various pHs, found that in raw water at pH 5, the concn of dichloroacetonitrile increased from 5.5 ug/L at 4 hr post treatment to 13.5 ug/L at 144 hr(7). The water at pH 7 decreased from 6 to 2 ug/L over the same time period. The water at pH 9.4 was consistently <1 ug/L(7). The concns of dichloroacetonitrile in finished water were lower but the trends were the same(7).|DRINKING WATER: The concn of dichloroacetonitrile in 6 Dutch treatment plants that chlorinated their water and in distributed water from these plants was 0.04-0.34 ug/L and <0.04-0.24 ug/L, respectively, while it was absent in three plants that did not use chlorine(1). Water supplies of 10 southern Ontario cities contained 0.3-7.6 ppb of dichloroacetonitrile at the treatment plant and 0.5-8.1 ppb in the distribution system, 1 mi from the plant(2). The source of the water was surface water(2). Dichloroacetonitrile was found in treated water in 7 of 10 Great Lakes treatment plants at a mean concn of 0.3 ug/L, but not in raw water(3). Dichloroacetonitrile was not detected in raw water and at the granulated carbon filter stage at a water treatment plant in Barcelona, Spain, but was found in pre-chlorinated, sand filters, ozone and post-chlorinated stages at 0.6-1.6, 1-2, 0.9-16 and 0.2-1.0 ug/L, respectively(4). Dichloroacetonitrile, studied in 5 locations in each of 3 treatment plants for a one year period from Jan to Dec 1994, contained concns of <0.1-3.0 ug/L in a plant with source water from the Ottawa River using chlorine/chloramine treatment, 0.4-5.2 ug/L in another plant with source water from the Ottawa River but using chlorine/chlorine treatment and 0.4-4.8 ug/L in a plant with source water from LaLievre River using ozone/chlorine treatment(5). Dichloroacetonitrile was found in 97% of samples taken from 53 water treatment facilities throughout Canada, concns ranged from <0.1-16.3 ug/L in winter and <0.1-11.2 ug/L in summer(6). In a survey of 14 treated drinking water supplies of varied sources in England, dichloroacetonitrile was detected in 11 supplies, all but one of which was derived from surface sources(7).|SURFACE WATER: Dichloroacetonitrile was detected in the Salt River at the 91st Ave location at 0.6 ug/L and at 115th Ave location at 0.3 ug/L but not detected at the Bullard Ave location in Phoenix, AZ(1). Dichloroacetonitrile was not detected in Gila River, Phoenix, AZ(1).

Monitoring data indicate that the general population may be exposed to dichloroacetonitrile via ingestion of and dermal contact with drinking water. (SRC)|The workplace air of a softwood and hardwood kraft pulp mill, utilizing chlorine-containing bleaching agents, was monitored for 40 organohalogen compounds(1). No dichloroacetonitrile was detected.

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

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 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.

ACUTE/CHRONIC HAZARDS: When heated to decomposition this chemical emits toxic fumes of chlorine, cyanides and nitrogen oxides. (NTP, 1992)

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. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

/SRP:/ Immediate first aid: Remove patient from contact with the material. Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Cyanide and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Administer amyl nitrite ampules as per protocol and physician order ... . Monitor for shock and treat if necessary ... . Monitor for pulmonary edema and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . /Cyanide and related compounds/|/SRP:/ Advanced treatment: Consider Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Administer cyanide antidote kit (sodium nitrite, amyl nitrite, sodium thiosulfate) as per protocol and physician order ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Cyanide and related compounds/|Emergency and supportive measures. Treat all cyanide exposures as potentially lethal. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat coma, hypotension, and seizures if they occur. Start an intravenous line and monitor the patient's vital signs and ECG closely. /Cyanide/|For more Antidote and Emergency Treatment (Complete) data for DICHLOROACETONITRILE (6 total), please visit the HSDB record page.

/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

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/

Method: EPA-OGWDW/TSC 551.1; Procedure: gas chromatography with electron capture detector; Analyte: dichloroacetonitrile; Matrix: finished drinking water, drinking water during intermediate stages of treatment, and raw source water; Detection Limit: 0.001 ug/L.