Bromoacetonitrile

119.949

119.95

209-672-1

07K08J16VK

3276

DTXSID2021496

Pale yellow to light amber liquid

2926909090

23.8

0.20 (est)

Bromoacetonitrile is a pale yellow to light amber liquid. (NTP, 1992)

1.722

-36ºC

60-62 °C @ Press: 24 Torr

greater than 200° F (NTP, 1992)

1.469

In water, 50-100 mg/mL at 21.5 deg C

3.2 mm Hg at 25 deg C (est)

Henry's Law constant = 3.52X10-5 atm-cu m/mol at 25 °C (est)

May be sensitive to prolonged exposure to air and light; is incompatible with strong acids, strong bases, strong oxidizing agents and strong reducing agents|Hydroxyl radical reaction rate constant = 5X10-14 cu cm/molecule-sec at 25 °C (est)

May be sensitive to prolonged exposure to air and light. Water soluble.

Halogenated Organic Compounds

BROMOACETONITRILE may be sensitive to prolonged exposure to air and light. This chemical is incompatible with strong acids, strong bases, strong oxidizing agents and strong reducing agents. (NTP, 1992)

II

8

UN 3276 6.1/PG 3

3

R23/24/25;R36/37/38

S26-S36-S45-S24/25

AL7970000

T:Toxic;

P261-P280-P301 + P310-P305 + P351 + P338-P311

H301 + H311 + H331-H315-H319-H335

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity 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 and plant life; and conformance with environmental and public health regulations.

This chemical is probably combustible. (NTP, 1992)

|Danger|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|P260, P261, P264, P270, P271, P280, P284, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P311, P312, P320, P321, P322, P330, P332+P313, P337+P313, P361, P362, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 50 companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

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 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 protect this chemical from exposure to light. Keep the container tightly closed under an inert atmosphere, and store under refrigerated temperatures. (NTP, 1992)

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves. 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. RECOMMENDED GLOVE MATERIALS: If this chemical makes direct contact with your gloves, or if a tear, puncture or hole develops, replace them at once. Glove Type Model Number Thickness Bkthru Time Butyl rubber North B-174 0.64 mm 480 min PVA Edmont 25-545 0.25 mm 480 min Viton North F-091 0.23 mm 480 min (NTP, 1992)

The potential toxicity of bromoacetonitrile (BAN) was evaluated using a short-term reproductive and 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 bromoacetonitrile exposure. The dose-range finding study initially used concentrations of 625-5000 ppm. This study was suspended after 5 days due to significant reductions in body weight, and feed and water consumption. The second dose-range finding study was conducted at concentrations of 0, 30, 100, 200, and 500 ppm of BAN in the drinking water for two weeks. The 500 ppm animals were euthanized after 8 days as a result of sharp decreases in body weight, and feed and water consumption. Based on dose-related decreases in mean body weight and water consumption, concentrations of 0, 5, 30, and 100 ppm were selected for the main study, which utilized one group of male rats (10 per dose level) and two groups of female rats designated as Group A (peri-conception exposure, 10 per dose level) and Group B (gestational exposure, 13 per dose level). Control animals received deionized water, the vehicle. During the treatment period, all animals survived to the scheduled necropsy and there were no clinical signs of general toxicity noted at any dose level. The male body weights were comparable across dose groups, while both the 30 and 100 ppm Group A and B females body weights showed a slight (p greater than 0.05), but consistent decrease of 7-8% and 2-7% by SD 33 and GD 20, respectively, as compared to the controls. The 5 ppm Group A females body weight also showed a decrease (p greater than 0.05) of 5% by SD 33. Feed consumption in all treated groups was generally decreased by less than or equal to 23%. Over the course of the study and during treatment, water consumption was decreased in the 100 ppm animals by 30-52%, as compared to the controls. Although not always significant, water consumption was reduced in the 30 ppm animals by 12-34% and in the 5 ppm Group A females by 9-18%, as compared to the controls. The overall average calculated consumption of BAN for the 5, 30, and 100 ppm groups was 0.5, 2.4, and 6.0 mg/kg/day, respectively. There were no statistically significant changes in female reproductive parameters; however, there were several indications that female reproductive effects may have resulted from BAN. There was a small but consistent increase in post-implantation loss in both the Group A and B females: 38% and 33% increase in the 30 and 100 ppm Group A females, respectively, and 31%, 30%, and 57% increase in the 5, 30, and 100 ppm Group B females, respectively. In addition, the 100 ppm Group A females had an increase in pre-implantation loss of 147% and the 100 ppm Group B females had an increase in resorptions of 70%. These increases in pre- and post implantation losses and resorptions were largely the result of one or two dams in each group, although these females could not statistically be considered outliers. The blood urea nitrogen level of the 100 ppm males was increased by 19%, a small but biologically significant indicator of mild renal damage. However, this may be attributable to decreased fluid consumption, and therefore, the effects cannot be separated from dehydration. Male and female clinical observations, gross findings, organ weights, organ-to-body-weight ratios, and hematology endpoints were comparable across dose groups. Results of this study indicate that there was significant aversion to BAN in the water and suggest that BAN may be a possible mild renal toxicant at 100 ppm (approximately 7 mg/kg/d), as evidenced by an increase in BUN; and a potential reproductive toxicant at 100 ppm, as evidenced by increased (p greater than 0.05) post-implantation loss.

Bromoacetonitrile's production and use as an intermediate in organic synthesis(1) may result in its release to the environment through various waste streams(SRC). Bromoacetonitrile is a water disinfection byproduct of chlorination treatments(2-5).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 9(SRC), determined from a structure estimation method(2), indicates that bromoacetonitrile is expected to have very high mobility in soil(SRC). Volatilization of bromoacetonitrile from moist soil surfaces is expected to occur(SRC) given an estimated Henry's Law constant of 3.52X10-6 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Bromoacetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.2 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). The aqueous hydrolysis rate constant for bromoacetonitrile at 20 °C and pH 8.7 was experimentally determined to be 2.7X10-6/sec(5) which corresponds to a half-life of 2.9 days(SRC); hydrolysis rates at neutral or acidic conditions is much slower(5) by approximately one to two orders of magnitude based on observed hydrolysis rates of the nine haloacetonitriles used in the study(SRC). Therefore, hydrolysis may be an important fate process, especially in moist alkaline soils(SRC). Biodegradation data in soil were not available(SRC, 2012).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 9(SRC), determined from a structure estimation method(2), indicates that bromoacetonitrile is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected to occur(3) based upon an estimated Henry's Law constant of 3.52X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 12 and 87 days, respectively(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from an estimated log Kow of 0.20(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available. The aqueous hydrolysis rate constant for bromoacetonitrile at 20 °C and pH 8.7 was experimentally determined to be 2.7X10-6/sec(5) which corresponds to a half-life of 2.9 days(SRC); hydrolysis rates at neutral or acidic conditions is much slower(5) by approximately one to two orders of magnitude based on observed hydrolysis rates of the nine haloacetonitriles used in the study(SRC). Biodegradation data in water were not available(SRC, 2012).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bromoacetonitrile, which has an estimated vapor pressure of 3.2 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 bromoacetonitrile 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 323 days(SRC), calculated from its rate constant of 5X10-14 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Bromoacetonitrile may be sensitive to prolonged exposure to light(3); therefore, bromoacetonitrile may be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of bromoacetonitrile with photochemically-produced hydroxyl radicals has been estimated as 5X10-14 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 323 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The aqueous hydrolysis rate constant for bromoacetonitrile at 20 °C and pH 8.7 was experimentally determined to be 2.7X10-6/sec(2) which corresponds to a half-life of 2.9 days(SRC). Hydrolysis rates at neutral or acidic conditions is much slower(2) by approximately one to two orders of magnitude based on observed hydrolysis rates of the nine haloacetonitriles used in the study(SRC). Under basic conditions, aqueous hydrolysis of bromoacetonitrile yields the corresponding acetamide, which in basic media can be further hydrolyzed to the corresponding acid(2). Bromoacetonitrile may be sensitive to prolonged exposure to light(3); therefore, bromoacetonitrile may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for bromoacetonitrile(SRC), using an estimated log Kow of 0.20(1) and a regression-derived equation(1). According to a classification scheme(1), 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 bromoacetonitrile can be estimated to be 9(SRC). According to a classification scheme(2), this estimated Koc value suggests that bromoacetonitrile is expected to have very high mobility in soil.

The Henry's Law constant for bromoacetonitrile is estimated as 3.52X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that bromoacetonitrile is expected to volatilize slowly 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 12 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 87 days(SRC). Bromoacetonitrile's Henry's Law constant(1) indicates that volatilization from moist soil surfaces may occur(SRC). Bromoacetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.2 mm Hg at 25 °C(SRC), determined from a fragment constant method(1).

DRINKING WATER: Bromoacetonitrile was selected as a priority disinfection by-product to be included in a US nantionwide occurrence study(1,2). Based on a study of 35 water utilities across the US by the EPA and State of California Department of Health Services, the quarterly median concentrations of haloacetoniriles were 2.8, 2.5, 3.5 and 4.0 ug/L from the spring of 1988 through the winter of 1989(3). Specific concentrations of bromoacetonitrile were not reported, but may have been detected(3). Bromoacetonitrile was qualitatively detected in drinking water collected in Israel that had undergone disinfection treatment via chlorination and chlorine dioxide(3); the source waters were high in bromide content(4).

Occupational exposure to bromoacetonitrile may occur through inhalation and dermal contact with this compound at workplaces where bromoacetonitrile is produced or used(SRC). Bromoacetonitrile is reported to be a disinfectant by-product of drinking water chlorination via chlorine, chloramine or chlorine dioxide treatment(1-4); therefore, the general population may be exposed to bromoacetonitrile through tap water containing this by-product(SRC).

Haloacetonitriles, which are water chlorination by-products, are mutagens, carcinogens and teratogens. In vitro, the reaction of the haloacetonitriles bromoacetonitrile (BAN), chloroacetonitrile (CAN), dichloroacetonitrile (DCAN) and trichloroacetonitrile (TCAN) with calf thymus DNA produced fluorescent DNA derivatives. The reactivity of haloacetonitriles towards DNA was in the order of BAN > CAN > DCAN > TCAN. ... The DNA interaction was dependent on haloacetonitrile concentration. Higher affinity of haloacetonitriles towards single-stranded DNA (SS-CT-DNA) than towards double-stranded DNA (DS-CT-DNA) was observed. ... A major fluorescent peak was detected in the enzymatic hydrolysate that was not present in unreacted DNA. In the acid hydrolysate, one fluorescent peak was detected that was not present in unreacted DNA. Authentic 7-(cyanomethyl)guanine was synthesized by the reaction of CAN with 2'-deoxyguanosine and the product was purified and characterized spectroscopically. The product, 7-(cyanomethyl)guanine, was found to be chromatographically and spectroscopically identical to the fluorescence product that was obtained following haloacetonitrile-DNA interaction. This study shows that haloacetonitriles, in vitro, are capable of alkylating DNA at the guanine moiety to form a 7-(cyanomethyl)guanine adduct.|Acetonitrile (AN) and seven of its halogenated derivatives known to be water disinfectant by-products were evaluated for their action on hepatic cytosolic glutathione S-transferase (GST) activity using 1-chloro-2,4-dinitrobenzene (CDNB) as substrate. Increasing concentrations of acetonitrile, monofluoroacetonitrile (MFAN), monochloroacetonitrile (MCAN), and monobromoacetonitrile (MBAN) up to 10 mM failed to produced 50% inhibition of the activity of GST enzyme. ...|... In vitro, the reaction of the haloacetonitriles bromoacetonitrile (BAN), chloroacetonitrile (CAN), dichloroacetonitrile (DCAN) and trichloroacetonitrile (TCAN) with calf thymus DNA produced fluorescent DNA derivatives. The reactivity of haloacetonitriles towards DNA was in the order of BAN > CAN > DCAN > TCAN. The emission fluorescence spectra of the reaction product(s) of various haloacetonitriles with DNA has a peak at 404 nm at fixed excitation wavelength (300 nm). The fluorescence intensity of the reaction product(s) was pH dependent with an optimum intensity at pH 7.4. The DNA interaction was dependent on haloacetonitrile concentration. Higher affinity of haloacetonitriles towards single-stranded DNA (SS-CT-DNA) than towards double-stranded DNA (DS-CT-DNA) was observed. To characterize the type of fluorescent product(s) formed, samples of the reaction product of SS-CT-DNA with BAN were hydrolyzed (a) enzymatically by micrococcal nuclease and spleen phosphodiesterase to nucleotides and nucleotide derivative(s) or (b) chemically by formic acid to nucleobases and nucleobase adducts. The hydrolysates were analyzed by reversed phase HPLC. A major fluorescent peak was detected in the enzymatic hydrolysate that was not present in unreacted DNA. In the acid hydrolysate, one fluorescent peak was detected that was not present in unreacted DNA. Authentic 7-(cyanomethyl)guanine was synthesized by the reaction of CAN with 2'-deoxyguanosine and the product was purified and characterized spectroscopically. The product, 7-(cyanomethyl)guanine, was found to be chromatographically and spectroscopically identical to the fluorescence product that was obtained following haloacetonitrile-DNA interaction. This study shows that haloacetonitriles, in vitro, are capable of alkylating DNA at the guanine moiety to form a 7-(cyanomethyl)guanine adduct. /haloacetonitriles/

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. It can also cause corrosion. ACUTE/CHRONIC HAZARDS: This compound is harmful by ingestion, inhalation or skin absorption. It is an irritant of the eyes, mucous membranes and upper respiratory tract. It is corrosive. It is also a lachrymator. When heated to decomposition it emits toxic fumes of carbon monoxide, carbon dioxide, nitrogen oxides and hydrogen bromide gas. (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. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas. 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. Corrosive chemicals will destroy the membranes of the mouth, throat, and esophagus and, in addition, have a high risk of being aspirated into the victim's lungs during vomiting which increases the medical problems. 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. IMMEDIATELY transport the victim to a hospital. 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. Transport the victim IMMEDIATELY to a hospital. (NTP, 1992)

/SRP:/ Immediate first aid: 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 if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the 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. /Poisons A and B/|/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 needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock 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 ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: 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 ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/CASE REPORTS/ A 28-year-old chemist,with no history of skin disease,working in a pharmaceutical laboratory, presented with eczema on the hands,with scaling and fissuring of the fingers. She was occupationally exposed to numerous chemicals and generally wore protective gloves in her work. She was patch tested with the GEIDC standard series and with 26 different compounds that she was using at that moment in the laboratory. At D2 and D4, there were positive reactions (++) to ethyl bromoacetate (1% pet.) and bromoacetonitrile (1% pet.), but no reactions to any other substance. Patch tests in 25 controls were negative. After she was instructed to avoid further contact with ethyl bromoacetate and bromoacetonitrile, her eczema subsided within a few weeks. No recurrence was observed during 2-year follow-up.|/GENOTOXICITY/ HAN produced DNA strand breaks in cultured human lymphoblastic (CCRF-CEM) cells, bound to the nucleophilic trapping agent 4-(p-nitrobenzyl)pyridine and formed a covalent bond to polyadenylic acid in a cell-free reaction system. Thus, we have demonstrated that these chemicals are genotoxic, which would indicate a potential for carcinogenic activity and for human health hazard. /haloacetonitriles/|/ALTERNATIVE and IN VITRO TESTS/ The present studies were initiated to measure the permeation coefficients (K(p) ) for haloacetonitriles (HANs) and chloral hydrate (CH), important cytotoxic DBPs. The K(p) values measured using fully hydrated dermatomed torso skin at 37 °C for the HANs ranged from 0.099 to 0.17 cm h(-1) , and was 0.0039 cm h(-1) for CH. Of the HANs, dibromoacetonitrile had the highest permeability while chloroacetonitrile had the lowest permeability and a direct relationship was observed between their K(p) and their octanol/water partition coefficients (K(ow) ). The K(p) values of the HANs were also approximately 30 times that of CH. The monthly dermal and ingestion doses of HANs and CH of an average American population were estimated using Monte Carlo simulations. The dermal doses of HANs from showering and bathing ranged from 0.39 to 0.78 times their ingestion doses but only approximately 0.02 times their ingestion doses for CH, assuming that the K(p) values determined are applicable to shorter water contact times. However, that ratio can vary markedly with chlorinated swimming pool exposures, with a range of 0.30-2.3 for HANs and 0.19-0.25 for CH. Dermal exposure to HANs and CH seems to be a significant route of exposure and should be considered when evaluating their total exposure during the routine usage of water for bathing and swimming. /haloacetonitriles/

bromoacetonitrile

Water disinfection byproduct