다이브로모아세토나이트릴

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.

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

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 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.

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.

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.

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.

... 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.

LC50; Species: Pimephales promelas (Fathead minnow, standard length 20.5 mm, weight 150 mg); Conditions: freshwater, static, 16.6-17.0 °C, pH 7.8-8.3, hardness 98-113 mg/L CaCO3, alkalinity 75-87 mg/L CaCO3, dissolved oxygen 8.7-9.6 mg/L; Concentration: 710 ug/L for 24 hr (95% confidence interval: 650-780 ug/L) /96% purity/

LC50; Species: Pimephales promelas (Fathead minnow, standard length 20.5 mm, weight 150 mg); Conditions: freshwater, static, 16.6-17.0 °C, pH 7.8-8.3, hardness 98-113 mg/L CaCO3, alkalinity 75-87 mg/L CaCO3, dissolved oxygen 8.7-9.6 mg/L; Concentration: 670 ug/L for 48 hr (95% confidence interval: 620-740 ug/L) /96% purity/

LC50; Species: Pimephales promelas (Fathead minnow, standard length 20.5 mm, weight 150 mg); Conditions: freshwater, static, 16.6-17.0 °C, pH 7.8-8.3, hardness 98-113 mg/L CaCO3, alkalinity 75-87 mg/L CaCO3, dissolved oxygen 8.7-9.6 mg/L; Concentration: 600 ug/L for 72 hr (95% confidence interval: 540-690 ug/L) /96% purity/

LC50; Species: Pimephales promelas (Fathead minnow, standard length 20.5 mm, weight 150 mg); Conditions: freshwater, static, 16.6-17.0 °C, pH 7.8-8.3, hardness 98-113 mg/L CaCO3, alkalinity 75-87 mg/L CaCO3, dissolved oxygen 8.7-9.6 mg/L; Concentration: 550 ug/L for 96 hr (95% confidence interval: 490-620 ug/L) /96% purity/

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 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=3252-43-5]

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.

/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/

... 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).

Dibromoacetonitrile

Group 2B: Possibly carcinogenic to humans

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

2013

2011

Dibromoacetonitrile

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).