Succinonitrile

log Kow = -0.99

-0.99

-0.99

1.023 at 113 °F (NTP, 1992) - Denser than water; will sink

0.9867 g/cu cm @ 60 °C

1.02 g/cm³

0.99

50 to 100 mg/mL at 70 °F (NTP, 1992)

Soluble in acetone, chloroform, dioxane; slightly soluble in ethanol, benzene, ether, carbon sulfide

In water, 126.9 g/L @ 20 °C

Solubility in water, g/100ml at 20 °C: 13

13%

270 °F (NTP, 1992)

132 °C

270 °F (132 °C) (closed cup)

132 °C

270 °F

509 to 513 °F at 760 mmHg (NTP, 1992)

266 °C

Boiling point: 185 °C @ 60 mm Hg; 158-160 @ 20 mm Hg

265 °C

509 °F

After vacuum distillation of several tons of the nitrile at 150 C, lack of a receiver necessitated hot storage of the product at 80 C for 46 hours, and the drainage line blocked with solid. Though the bulk of the material was still liquid, heating to 195 C did not clear the line, and shortly afterwards decomposition occurred. It was subsequently found that the distillation residue had also decomposed at 175 C, 2 hours after distillation ended. Differntial thermal analysis showed that the nitrile is unusual in that no heat is evolved during the induction period of around 33 hours/200 C, or 1.5 hours/280 C, and the rapid onset and narrow peak width suggested a self-accelerating decomposition process, with Q = 700 J/g. No stabilising additives period for the nitrile to 20 percent of its value, while 1 percent of potassium cyanide reduced it to 2 percent.

May be heated to 200 °C for 72 hr without decomposition.

135 to 136 °F (NTP, 1992)

54.5 °C

54 °C

134 °F

Danger

H302 (95%): Harmful if swallowed [Warning Acute toxicity, oral]

P261, P262, P264, P264+P265, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P316, P319, P321, P330, P332+P317, P337+P317, P361+P364, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 80 reports by companies from 12 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: Butanedinitrile

Status: Active Update: 25-11-2021 https://echa.europa.eu/registration-dossier/-/registered-dossier/21898

Succinodinitrile: Does not have an individual approval but may be used under an appropriate group standard

This compound is combustible. (NTP, 1992)

Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

SUCCINONITRILE is incompatible with acids and oxidizing agents (such as peroxides and epoxides). Can react violently with strong oxidizing acids. Is hydrolyzed exothermically in both aqueous acid and base to give carboxylic acids (or salts of carboxylic acids). Can react vigorously with reducing agents.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Succinonitrile is produced, as an intermediate or a final product, by process units covered under this subpart.

Decomposes on burning. Decomposes on contact with acids. This produces toxic and corrosive fumes including nitrogen oxides and cyanides. Reacts with strong bases. This produces ammonia. Reacts with strong oxidants and strong reducing agents.

Fires involving this compound can be controlled with dry chemical, carbon dioxide or Halon extinguishers. (NTP, 1992)

Use water spray, powder, alcohol-resistant foam, carbon dioxide.

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give a slurry of activated charcoal in water to drink. Do NOT induce vomiting. Refer for medical attention .

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.

(General first aid procedures)

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminate 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.

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.

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.

Adequate precautions should be taken against skin or eye contact.

The worker should immediately wash the skin when it becomes contaminated.

For more Preventive Measures (Complete) data for SUCCINONITRILE (6 total), please visit the HSDB record page.

Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L97)

Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 28(SRC), determined from a structure estimation method(2), indicates that succinonitrile is expected to have very high mobility in soil(SRC). Volatilization of succinonitrile from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.5X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 0.00778 mm Hg(3), and water solubility, 126.9 g/L(4). Succinonitrile is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 0.00778 mm Hg(3). In studies with activated sludge, biodegradation of 1.5-3.8% was observed after 6-24 hours(5). These studies suggest that succinonitrile may have been toxic to the microorganisms, since a high concentration of succinonitrile was used(5).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 28(SRC), determined from a structure estimation method(2), indicates that succinonitrile 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 6.5X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 0.00778 mm Hg(4) and water solubility, 126.9 g/L(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow of -0.99(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions(9). In studies with activated sludge, biodegradation of 1.5-3.8% was observed after 6-24 hours(10). These studies suggest that succinonitrile may have been toxic to the microorganisms, since a high concentration of succinonitrile was used(10).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), succinonitrile, which has a vapor pressure of 0.00778 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. The reaction of vapor-phase succinonitrile with photochemically-produced hydroxyl radicals is not expected to be an important environmental fate based on the estimated half-life for this reaction in air of 380 days, calculated from its rate constant of 4.3X10-14 cu cm/molecule-sec at 25 deg (SRC) that was derived using a structure estimation method(3). Succinonitrile is not expected to be susceptible to direct photolysis by sunlight, since it does not contain functional groups that are expected to absorb light with wavelengths >290 nm(SRC).

The substance can be absorbed into the body by ingestion and by inhalation.

inhalation, skin absorption, ingestion, skin and/or eye contact

Oral (L96) ; inhalation (L96) ; dermal (L96)

Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)

Cough. Sore throat. Dizziness. Headache. Nausea. Convulsions.

Redness. Pain.

Redness. Pain.

Abdominal pain. Diarrhoea. Headache. Nausea. Vomiting. Convulsions.

irritation eyes, skin, respiratory system; headache, dizziness, lassitude (weakness, exhaustion), confusion, convulsions; blurred vision; dyspnea (breathing difficulty); abdominal pain, nausea, vomiting

Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (L96, L97)

Medical surveillance should include pre-employment and periodic examinations focused on skin disorders and the cardiovascular, pulmonary and central nervous systems. A history of fainting spells or convulsive disorders might present an added risk for nitrile workers. /Nitriles/

Using a structure estimation method based on molecular connectivity indices(1), the Koc for succinonitrile can be estimated to be 28(SRC). According to a classification scheme(2), this estimated Koc value suggests that succinonitrile is expected to have very high mobility in soil.

/SIGNS AND SYMPTOMS/ Exposure to toxic nitriles may rapidly cause death by asphyxiation similar to that resulting from exposure to hydrogen cyanide. Individuals who survived exposure to high concentrations of nitriles were said to have no evidence of residual physiological effects after the recovery from the acute episode; this has led to the opinion that the person either succumbs to the nitrile exposure or recovers completely. /Nitriles/

/SIGNS AND SYMPTOMS/ Potential symptoms of overexposure are irritation of eyes, skin, respiratory system; headache, dizziness, weakness, giddiness, confusion, convulsions; blurred vision; dyspnea; abdominal pain, nausea, vomiting.

/CASE REPORTS/ A 53 yr old male with polyarthritis and chronic bronchitis had been treated for 3 weeks with anti-catarrhal drugs, vitamins, and a daily intramuscular injection of 200 mg succinonitrile. Two hours after the last injection, the patient began vomiting and showed signs of psychomotor agitation and mental confusion accompanied by cold sweating. He was admitted to a hospital with convulsions and mental disorientation. The patient died 2 hours after he was hospitalized during a convulsion. Autopsy showed pronounced visceral congestion and cerebral and pulmonary edema. Histological examination showed a massive and vacuolar hepatic degeneration and a significant nephrosis of the tubules. Because of the odor of bitter almonds when the skull was opened, a chemical analysis for cyanide compounds was conducted. Cyanide concentrations of 0.265 to 1.500 mg/100 mL, reported as potassium-cyanide, were found in the liver, brain, kidney, lungs, and urine. No evidence of cyanide was found in the blood or gastric contents. An ampule of the pharmaceutical product containing the succinonitrile was analyzed. No trace of cyanide was found. .../It was concluded/ that death was due to cyanide poisoning, the cyanide having accumulated in the body as a result of a metabolic disorder when succinonitrile was administered.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Succinonitrile is produced, as an intermediate or a final product, by process units covered under this subpart.

/A study/... determined that rats and rabbits converted about 60% of the succinonitrile to cyanide.

...The release of cyanide from succinonitrile in rats and rabbits in vivo and in vitro /was investigated/. In the in vivo studies, male rabbits weighing 2-3 kg and male rats weighing 400-450 g were administered succinonitrile in iv doses of 25-40 mg/kg and 25-50 mg/kg, respectively. Levels of cyanide and thiocyanate were determined in samples of urine from rabbits and rats. The total number of rats that were studied was not mentioned. In the in vitro studies, levels of cyanide and thiocyanate were determined in liver slices and homogenates of rat or rabbit liver or with isolated mitochondrial, microsomal, and soluble fractions. Samples (0.1-2.0 mL) of filtered 24 hr urine output were collected form groups of two rats and from each rabbit pre- and post-administration with succinonitrile to determine thiocyanate concentrations. In another study, rats were pretreated with 2 mL/kg of carbon tetrachloride sc 48 hr prior to succinonitrile administration. Filtered urine samples were collected, and cyanide concentrations were determined colorimetrically. ...A sixfold increase in urinary thiocyanate following iv-injected doses of 25 mg/kg of succinonitrile /was found/ compared with the controls. Forty-eight to 120 hours postadministration of succinonitrile, thiocyanate levels approached control values. Pretreatment of rats by sc injection of 2 mL/kg carbon tetrachloride inhibited urinary thiocyanate excretion. Urinary excretion of cyanide increased over fivefold 48 hours posttreatment with succinonitrile. The values at 72-120 hours posttreatment approached normal values. ...Rat and rabbit liver slices catalyzed the release of cyanide from succinonitrile. However, 0.1-2.0 mg/g of Triton-X-100 strongly inhibited cyanide release from succinonitrile in rat liver slices. Liver slices of rats pretreated with carbon tetrachloride did not release detectable amounts of cyanide for succinonitrile. .../It was/ concluded that rabbits and rats converted about 60% of the administered succinonitrile to cyanide, which was excreted as thiocyanate. The release of cyanide was inhibited by carbon tetrachloride and Triton-X-100. The authors also postulated that disruption of the liver cells, as by centrifugation to separate their contents, depressed or eliminated their ability to liberate cyanide ions or to form thiocyanate. The authors proposed that cellular membranes contain enzymes or enzyme complexes that are responsible for the conversion of succinonitrile to cyanide, which is excreted as thiocyanate. However, following homogenization, these enzyme or enzyme complexes may be destroyed or damaged by homogenization.

/One study/ ...concluded that succinonitrile was either excreted unmetabolized or was metabolized to cyanide and excreted as thiocyanate in mice within 24 hours posttreatment. The authors postulated that the high percentage of metabolites excreted in 24 hr urine samples may be due to the presence of two reactive centres in the succinonitrile molecule, resulting in the formation of two intermediate metabolites, diethylene cyanohydrin and cyanoacetic acid.

The liberation of cyanide from succinonitrile has been studied to obtain information on the cellular systems responsible for the release of this metabolite. sing isolated endoplasmic reticulum preparations a complex between succinonitrile and cyt. P450 has been detected. This finding together with the inhibition of cyanide liberation by SKF-525A in liver slices indicates that the endoplasmic reticulum is involved in the early stages of succinonitrile metabolism. The decreased metabolism of succinonitrile which was observed after addition of inhibitors of oxidative phosphorylation indicates that an energy-dependent mitochondrial step might be involved in the subsequent steps. ...Cyanide liberation from succinonitrile is a multistep process in which the mitochondrial membrane and the endoplasmic reticulum are involved.

Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)

...The excretion of succinonitrile and its metabolites in urine and feces of mice, following a single injection of succinonitrile /was reported/. The cumulative excretion of succinonitrile and metabolites in urine and feces measured 60% by 24 hours and 83% by 72 hours. In the first multiple-dose experiment in which mice received three doses of unlabeled succinonitrile and one dose of radioactive succinonitrile, 52% of the radioactivity was excreted in urine in 24 hours. In the second multiple-dose experiment, in which mice received four doses of radioactive succinonitrile, 50% of the radioactivity was excreted in each 24 hr period.

...The fate of 14C-labeled succinonitrile in male mice /was investigated/. ...A mean of 53% of the total succinonitrile injected ip in each animal in single and multiple dose studies was eliminated in the first 24 hours post-treatment and 88% of this eliminated succinonitrile was excreted as metabolites. In a single dose study, 7% of the 14C-labeled succinonitrile was excreted as thiocyanate and 36% as intermediate metabolites in 24 hours. In the multiple dose study, 18% thiocyanate and 24% intermediate metabolites were excreted.

Used to make plastics and nitron fibers; [HSDB]

Used in the production of plastics and nitron fibers.

Interaction of ethylene dibromide and potassium cyanide in the presence of alcohol.

Succinonitrile is obtained by addition of hydrogen cyanide to acrylonitrile.