Dibromoacetonitrile

198.845

198.84

221-843-2

VGJ91H57XU

3276

DTXSID3024940

Liquid

2926909090

23.8

0.47 (est)

Dibromoacetonitrile is a clear amber oily liquid. (NTP, 1992)

2.296 g/cm³ @ Temp: 25 °C

67-69 °C @ Press: 24 Torr

greater than 200° F (NTP, 1992)

1.538-1.543

In water, 9.6X10+3 mg/L at deg C (est)

Keep tightly closed.

3.01X10-1 mm Hg at 25 deg C (est)

Henry's Law constant = 4.06X10-7 atm-cu m/mol at 25 °C (est)

Conversion factor: mg/cu m = 8.13 X ppm|Hydroxyl radical reaction rate constant = 2.89X10-14 atm-cu m/mol at 25 °C (est)

This chemical may be sensitive to prolonged exposure to air and light. Slightly soluble in water.

Halogenated Organic Compounds

DIBROMOACETONITRILE is incompatible with strong acids, strong bases, strong oxidizing agents and strong reducing agents. (NTP, 1992). 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. Acetonitrile and propionitrile are soluble in water, but nitriles higher than propionitrile have low aqueous solubility. They are also insoluble in aqueous acids.

III

3

3275

3

R20/21/22

S36/37-S26

AL8450000

Xn: Harmful;T: Toxic;

Missing Phrase - N15.00950417-P280-P305 + P351 + P338

H301-H319-H351-H410

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.

Department of Health & Human Services/National Institute of Environmental Health Sciences, National Toxicology Program; Dibromoacetonitrile: Short-Term Reproductive and Developmental Toxicity Study when Administered to Sprague-Dawley Rats in the Drinking Water (CAS No: 3252-43-5), NTP Study No. RDGT94014 available at http://ntp.niehs.nih.gov/index.cfm?objectid=0847F1C4-974C-8718-313E67A0974E5986 as of August 1, 2008

Literature sources indicate that this compound is nonflammable. (NTP, 1992)

|Danger|H301 (69.91%): Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P261, P264, P270, P271, P273, P280, P281, P301+P310, P301+P312, P302+P352, P304+P312, P304+P340, P305+P351+P338, P308+P313, P312, P321, P322, P330, P332+P313, P337+P313, P362, P363, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 113 companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Excerpt from ERG Guide 151 [Substances - Toxic (Non-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: See ERG Table 1 - Initial Isolation and Protective Action Distances on the UN/NA 3276 datasheet. 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 spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing 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 protect this chemical from exposure to light. Keep the container tightly closed under an inert atmosphere, and store under refrigerated temperatures. (NTP, 1992)

RECOMMENDED RESPIRATOR: When working with this chemical, wear a NIOSH-approved full face chemical cartridge respirator equipped with the appropriate organic vapor cartridges. If that is not available, a half face respirator similarly equipped plus airtight goggles can be substituted. However, please note that half face respirators provide a substantially lower level of protection than do full face respirators. (NTP, 1992)|ENGINEERING CONTROLS. Use only in a chemical fume hood. Safety shower and eye bath.|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.

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.

Emits toxic fumes under fire conditions. Combustible liquid.

Absorb on sand or vermiculite and place in closed containers for disposal. Ventilate area and wash spill site after material pickup is complete.

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.|Do not breathe vapor. Avoid contact with eyes, skin, and clothing. Avoid prolonged or repeated exposure.|Wear self-contained breathing apparatus, rubber boots, and heavy rubber gloves. In case of leak or spill, evacuate area.|Wash thoroughly after handling.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.

May cause skin irritation. Causes eye irritation.

Dibromoacetonitrile was measured at 0.1 and 0.2 ug/L at the inlet to two of three wetland areas and was detected at 0.2 ug/L in one of three outlets in the Tres Rios Wetlands outside Phoenix, AZ(1).

... In a dose-response study, mice were administered a single oral dose of dibromoacetonitrile (DBAN) (30, 60 and 120 mg/kg) and were sacrificed after 1 hr. DBAN significantly reduced glutathione (GSH) content that was somehow dose-related, and inhibited glutathione-S-transferase (GST) activity in gastric tissues. The highest dose of DBAN (120 mg/kg) lowered GSH by 74% and induced a significant elevation of lipid peroxidation products, determined as thiobarbituric acid reactive substances (TBARS) by 69%. The same dose inhibited the gastric activities of GST, superoxide dismutase (SOD) and catalase (CAT) by 70, 57 and 23%, respectively. In a time-course study, mice were administered DBAN (60 mg/kg po) and sacrificed 0.5, 1, 3, 6, 12 and 24 hr after treatment. GSH was dramatically depleted at 0.5, 1, 3 and 6 hr (45, 38, 39 and 49% of control, respectively) and remained significantly low at 12 and 24 hr. Also, DBAN caused an accumulation of TBARS in gastric tissues starting from 3 hr and was maximum at 6 hr (133% of the control). The enzymatic activities of GST and SOD were maximally inhibited by DBAN treatment at 0.5 hr (32% for GST and 37% for SOD of the respective control). The activities of both enzymes returned to control values at 24 h. CAT activity was not affected by DBAN administration at all. Pretreatment of another group of mice with melatonin (10 mg/kg per day po 12 days) before administration of DBAN (60 mg/kg po) completely mitigated the aforementioned parameters. ...|... The ability of dibromoacetonitrile (DBAN) to induce oxidative stress in mouse testis and possible protective effect of an antioxidant tertiary butylhydroquinone (TBHQ) were addressed. Male albino mice were injected with a single dose of DBAN (50 mg/kg i.p.), and killed after 3 hr of treatment. Control animals received 10 mL/kg body weight ip of the vehicle DMSO. In both experiments, cauda epididymis were dissected and sperm count and motility were investigated. Also, testicular activity of lactic dehydrogenase-x (LDH-x) isozyme and histopathological changes were examined. Furthermore, testicular content of malonyldialdehyde (MDA) and reduced glutathione (GSH) were determined. A single ip dose of DBAN caused decrease in sperm count and motility to approximately 88 and 84%, respectively, compared with control animals. A 46% decrease in testicular activity of LDH-x, compared with control animals, was observed. A significant accumulation of MDA in DBAN-treated animals was increased to 99% while testicular content of GSH was decreased by 56% compared to control animals. Compared to DBAN-treated animals, treatment with TBHQ (100 mg/kg po) prior exposure to DBAN showed a remarkable degree of protection as indicated by enhancement of sperm count and motility, testicular activity of LDH-x, and GSH. Accumulation of testicular content of MDA significantly decreased following TBHQ treatment compared to DBAN-treated animals. In conclusion, results presented here indicate that DBAN is capable to induce oxidative stress in mouse testis. TBHQ may play a protective role against DBAN-induced testicular cellular damage.

LD50 Mouse (male) oral 289 mg/kg|LD50 Mouse (female) oral 303 mg/kg|LD50 Rat (male) oral 245 mg/kg|LD50 Rat (female) oral 361 mg/kg|LD50 Mouse iv 56 mg/kg

The potential toxicity of dibromoacetonitrile (DBAN) was evaluated using a short-term reproductive & developmental toxicity screen. This study design was selected to identify the process (development; female reproduction; male reproduction; various somatic organs/processes) that is the most sensitive to dibromoacetonitrile exposure. The dose-range finding study initially used concns of 250-2,000 ppm. This study was suspended after 4 days due to sharp reductions in fluid intake. The second dose-range finding study was conducted at concns of 0, 7, 20, 70, & 200 ppm of DBAN in the drinking water for 2 wks. Based on a slight dose-related decr in mean body weight & a decr in water consumption, concns of 0, 15, 50, & 150 ppm were selected for the main study, which utilized 1 group of male rats (10/dose level) & 2 groups of female rats designated as Group A (peri-conception exposure, 10/dose level) & Group B (gestational exposure, 13/dose level). Control animals received deionized water, the vehicle. During the treatment period, all animals survived to the scheduled necropsy & there were no clinical signs of general toxicity noted at any dose level. Over the course of the study, water consumption was decreased in the 50 ppm males & B females by 15-32% while water consumption was decreased by 28-49% at most of the intervals in all 150 ppm groups. The overall average calculated consumption of DBAN for Groups 2-4 was 1.7, 4.5, & 9.9 mg/kg/day, respectively. Male & female mean absolute body weights, clinical observations, & gross findings were comparable across dose groups, as were male organ weights, organ-to-body weight ratios, & clinical chemistry & hematology endpoints. Male feed consumption in the 150 ppm group was reduced by 11-18% at the first two measurement intervals only. There were no treatment-related reproductive effects in the males or females. Results of this study indicate that DBAN treatment reduced water consumption in the 50 & 150 ppm dose levels in males & females in the absence of reproductive toxicity. A max tolerated dose in both males & females was achieved at 50 ppm DBAN based on a >20% reduction in water consumption. From these data, DBAN may be a taste-aversive at 50 or 150 ppm in male & female rats, but is not a reproductive toxicant in males or females at dose levels up to 150 ppm DBAN.|2-WEEK STUDY IN RATS. Groups of five male and five female rats were exposed to drinking water containing 0, 12.5, 25, 50, 100, or 200 mg/L dibromoacetonitrile for 15 days (equivalent to average daily doses of approximately 2, 3, 7, 12, or 18 mg dibromoacetonitrile/kg body weight in males and 2, 4, 7, 12, or 19 mg/kg in females). All rats survived to the end of the study. The mean body weights of 200 mg/L males were significantly less than those of the control group. Water consumption was decreased in an exposure-related manner. Atrophy of the testicular germinal epithelium occurred in two males exposed to 200 mg/L. 2-WEEK STUDY IN MICE. Groups of five male and five female mice were exposed to drinking water containing 0, 12.5, 25, 50, 100, or 200 mg/L dibromoacetonitrile for 15 days (equivalent to average daily doses of approximately 2, 4, 8, 15, or 21 mg/kg in males and 2, 3, 10, 14, or 22 mg/kg in females). All mice survived to the end of the study. Mean body weights of all exposed groups were similar to those of the controls. Water consumption by mice exposed to 200 mg/L was less than that by the controls. The liver weights of females exposed to 50, 100, or 200 mg/L were significantly decreased. No lesions were attributed to exposure to dibromoacetonitrile.|3-MONTH STUDY IN RATS. Groups of 10 male and 10 female rats were exposed to drinking water containing 0, 12.5, 25, 50, 100, or 200 mg/L dibromoacetonitrile for 3 months (equivalent to average daily doses of approximately 1, 2, 3, 6, or 11 mg/kg in males and 1, 2, 4, 7, or 13 mg/kg in females). All rats survived to the end of the study. The mean body weights of 200 mg/L females were significantly less than those of the control group. Water consumption by 200 mg/L rats was less than that by the control groups. No histopathologic lesions were attributed to exposure to dibromoacetonitrile. 3-MONTH STUDY IN MICE. Groups of 10 male and 10 female mice were exposed to drinking water containing 0, 12.5, 25, 50, 100, or 200 mg/L dibromoacetonitrile for 3 months (equivalent to average daily doses of approximately 2, 3, 6, 11, or 18 mg/kg in males and females). All mice survived to the end of the study. The mean body weights of exposed groups were similar to those of the controls. Water consumption by 200 mg/L females was less than that by the controls. No histopathologic lesions were attributed to exposure to dibromoacetonitrile.|2-YEAR STUDY IN RATS. Groups of 50 male and 50 female rats were exposed to drinking water containing 0, 50, 100, or 200 mg/L dibromoacetonitrile for 105 to 106 weeks (equivalent to average daily doses of approximately 2, 4, or 7 mg/kg in males and 2, 4, or 8 mg/kg in females). Survival of all exposed groups of rats was similar to that of the controls. Mean body weights of 200 mg/L males were approximately 7% less than those of the controls during the second year of the study. Water consumption by the 100 and 200 mg/L groups was generally less than that by the controls throughout the study. The combined incidence of squamous cell papilloma or carcinoma of the oral mucosa or tongue was significantly increased in 200 mg/L males. The incidence of squamous cell papilloma in the oral mucosa or tongue was increased in 100 mg/L females, but not significantly. Oral cavity neoplasms are uncommon in untreated F344/N rats, occurring at a mean incidence of 1% or less in males and females. The incidence of squamous epithelial hyperplasia of the tongue was increased in 200 mg/L females. The latter lesion is considered to be part of the continuum of proliferative changes in oral cavity neoplasia. Glandular stomach adenomas were observed in two 200 mg/L males. This is a rare neoplasm that has not been seen in nearly 2,000 historical control male F344/N rats. The incidence of glandular ectasia of the glandular stomach in 200 mg/L females was significantly increased. The incidences of epithelial hyperkeratosis of the esophagus were significantly increased in 100 and 200 mg/L males and females. The incidences of squamous cell papilloma or keratoacanthoma (combined) and squamous cell papilloma, keratoacanthoma, basal cell adenoma, or basal cell carcinoma (combined) occurred with a positive trend in female rats. 2-YEAR STUDY IN MICE. Groups of 50 male and 50 female mice were exposed to drinking water containing 0, 50, 100, or 200 mg/L dibromoacetonitrile/L for 105 to 106 weeks (equivalent to average daily doses of approximately 4, 7, or 13 mg/kg to males and 3, 6, or 11 mg/kg to females). Survival of female mice exposed to 100 or 200 mg/L was significantly greater than that of the controls. Mean body weights of 200 mg/L males and females were less than those of the controls throughout most of the study. Water consumption by exposed groups was also less than that of controls throughout most of the study. The incidence of squamous cell papilloma or carcinoma (combined) of the forestomach was significantly increased in 200 mg/L males. The incidence of squamous cell papilloma of the forestomach was significantly increased in 200 mg/L females. Squamous cell neoplasms of the forestomach are uncommon in control male and female B6C3F1 mice, occurring at a mean incidence of about 1% to 2%. The incidences of epithelial hyperplasia of the forestomach were slightly increased in 50 and 200 mg/L males. The latter lesion is considered to be part of the continuum of proliferative changes in forestomach neoplasia. The incidence of hepatoblastoma was significantly increased in 50 mg/L males; the incidences of hepatocellular adenoma, hepatocellular carcinoma, or hepatoblastoma (combined) were significantly increased in 50 and 100 mg/L males.

... Haloacetonitriles are by products of water chlorination. ... /Haloacetonitriles/|Dibromoacetonitrile's formation as a result of the chlorination of water(1,2) will result in its release to the environment(SRC). During chlorination, bromide present in the water is oxidized to bromine and chlorination and bromination become competitive reactions(2). Dibromoacetonitrile was only found in water treated with chlorine(1,3) and chlorine with bromide(3).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 13(SRC), determined from a structure estimation method(2), indicates that dibromoacetonitrile is expected to have very high mobility in soil(SRC). Volatilization of dibromoacetonitrile from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.1X10-7 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Dibromoacetonitrile is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.3 mm Hg(SRC), determined from a fragment constant method(4). Dibromoacetonitrile 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 dibromoacetonitrile is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 4.1X10-7 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of 0.47(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Dibromoacetonitrile hydrolyzes by a base-catalyzed reaction and is catalyzed by chlorine(8). The concn of dibromoacetonitrile in buffered water declined over the course of 10 days with roughly 95%, 89%, and 81% remaining at pH 6, 7, and 8, respectively(8). Dibromoacetonitrile has a hydrolysis rate constant of 4.0X10-6/sec at pH of 8.7(9), corresponding to a half-life of 2 days(SRC). Dibromoacetonitrile 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), dibromoacetonitrile, which has an estimated vapor pressure of 0.3 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 dibromoacetonitrile 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 560 days(SRC), calculated from its rate constant of 2.9X10-14 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 dibromoacetonitrile with photochemically-produced hydroxyl radicals has been estimated as 2.9X10-14 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 560 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Dibromoacetonitrile hydrolyzes by a base-catalyzed reaction and is catalyzed by chlorine(2). The concn of dibromoacetonitrile in buffered water declined over the course of 10 days with roughly 95%, 89%, and 81% remaining at pH 6, 7, and 8, respectively(2). The concn in of dibromoacetonitrile in tap water was generally 20-50% of that at the treatment plants indicating that hydrolysis occurred during transport(3). Dibromoacetonitrile has a hydrolysis rate constant of 4.0X10-6/sec at pH of 8.7(4), corresponding to half-life of approximately 2 days(SRC).

An estimated BCF of 3 was calculated in fish for dibromoacetonitrile(SRC), using an estimated log Kow of 0.47(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 dibromoacetonitrile can be estimated to be 13(SRC). According to a classification scheme(2), this estimated Koc value suggests that dibromoacetonitrile is expected to have very high mobility in soil.

The Henry's Law constant for dibromoacetonitrile is estimated as 4.1X10-7 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that dibromoacetonitrile is expected to be essentially nonvolatile from water surfaces(2). Dibromoacetonitrile is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.3 mm Hg(SRC), determined from a fragment constant method(3).

GROUND WATER: Dibromoacetonitrile was not detected in ground water from the Salt River alluvium in Phoenix, AZ(1).|DRINKING WATER: In 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 dibromoacetonitrile from the spring of 1988 through the winter of 1989 were 0.54, 0.48, 0.51, and 0.46 ug/L(1). The quarterly dibromoacetonitrile concns in the facility with the highest bromide level (2.8-3.0 ppm) from the summer of 1988 through the winter of 1989 were 5.9, 6.7, and 6.0 ug/L(1). Another facility with seasonal changes in bromide level, 0.41 to 0.79 ppm, had quarterly dibromoacetonitrile levels ranging from 4.6 to 11 ug/L(1). The concn of dibromoacetonitrile in two water treatment plants using chlorine treatment were 0.41 and 5.8 ug/L(2). The concns of dibromoacetonitrile in the same plants using a combination of chlorination and ozonation were 0.79 and 5.3 ug/L(2). Dibromoacetonitrile was detected in 1 of 2 distilled, low chlorinated seawater, tap water samples(3). Tap water samples taken in Phoenix, AZ contained 1.4 ug/L of dibromoacetonitrile(4). Dibromoacetonitrile was not detected when using chloramination, chloramination with bromide, chlorine dioxide, chlorine dioxide with bromide, ozone, or ozone with bromide treatments, however dibromoacetonitrile was detected when using chlorine at 0.07 ug/L and chlorine with bromide at 0.37 ug/L(5).|DRINKING WATER: The concn of dibromoacetonitrile in 6 Dutch treatment plants that chlorinated their water and distributed water from these plants was <0.04- 0.81 ug/L and <0.04-0.70 ug/L, respectively, while it was absent in three plants that did not use chlorine(1). The concn in tap water was generally 20-50% of that at the treatment plants indicating that hydrolysis occurred during transport(1). In a survey of 14 treated drinking water supplies of varied sources in England, dibromoacetonitrile was detected in 8 supplies(2). Dibromoacetonitrile 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 0.6-7.6, 4.6-8.7, 5.5-9.9 and 0.6-3.1 ug/L, respectively(3). Dibromoacetonitrile, 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 ug/L in a plant with source water from the Ottawa River using chlorine/chloramine treatment, in another plant with source water from the Ottawa River but using chlorine/chlorine treatment and in a plant with source water from LaLievre River using ozone/chlorine treatment(4). Dibromoacetonitrile was identified, not quantified in drinking water from the Sea of Galilee, Israel in May and Sept 1999 and July 2000(5). Dibromoacetonitrile was found in 57% of samples taken from 53 water treatment facilities throughout Canada, concns were <5(6).|SURFACE WATER: Dibromoacetonitrile was not detected in the Salt River at the 91st Ave, 115th Ave or Bullard Ave location in Phoenix, AZ(1). Dibromoacetonitrile was not detected in Gila River in Phoenix, AZ(1).|SEAWATER: Dibromoacetonitrile was not found in unchlorinated seawater from an off shore oil platform(1).

Monitoring data indicate that the general population may be exposed to dibromoacetonitrile via ingestion of and dermal contact with drinking water. (SRC)

Approximately 8% of a single oral dose of 149 mg/kg bw of dibromoacetonitrile to rats was excreted in urine within 24 hr as thiocyanate, the product of released cyanide metabolized by rhodanese.

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).|Approximately 8% of a single oral dose of 149 mg/kg bw of dibromoacetonitrile to rats was excreted in urine within 24 hr as thiocyanate, the product of released cyanide metabolized by rhodanese.

SYMPTOMS: Symptoms of exposure to this compound include irritation of the eyes, mucous membranes and upper respiratory tract, burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea and vomiting. It is a lachrymator. ACUTE/CHRONIC HAZARDS: This compound may be fatal by ingestion, inhalation or skin absorption. It is an irritant of the eyes, mucous membranes and upper respiratory tract. It is also a lachrymator. When heated to decomposition it emits highly toxic fumes of carbon monoxide, carbon dioxide, nitrogen oxides, bromine, hydrogen bromide gas and cyanides. (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 DIBROMOACETONITRILE (6 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ Skin Contact: May cause skin irritation. Skin Absorption: May be harmful if absorbed through the skin. Eye Contact: Causes eye irritation. Inhalation: May be harmful if inhaled. Material may be irritating to mucous membranes and upper respiratory tract. Ingestion: Harmful if swallowed.|/SIGNS AND SYMPTOMS/ Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea, and vomiting...|/GENOTOXICITY/ ...The ability of halogenated acetonitriles (HANs) to induce single-strand breaks on the DNA of HeLa S3 cells was investigated using the single-cell gel electrophoresis (SCGE) assay ... 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. ...|/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 /treated for 1 hr with up to 3.0 mM dibromoacetonitrile/. /Chlorinated & brominated haloacetonitriles/

dibromoacetonitrile

Acetonitrile, 2,2-dibromo-: ACTIVE|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: dibromooacetonitrile; Matrix: finished drinking water, drinking water during intermediate stages of treatment, and raw source water; Detection Limit: 0.006 ug/L.