Acrylonitrile

log Kow = 0.25

0.25

Practically odorless, or with a very slight odor of peach kernels

Sweet odor

Irritating odor

Unpleasant odor

Onion, garlic, pungent

0.8004 at 77 °F (EPA, 1998) - Less dense than water; will float

0.8007 at 25 °C

Relative density (water = 1): 0.8

0.81

0.806 @ 20°C

0.81

Clear, colorless liquid at room temperature

Colorless to pale-yellow liquid

10 to 50 mg/mL at 70.9 °F (NTP, 1992)

Solubility of water in acrylonitrile: 3.1 parts water/100 parts acrylonitrile

In water, 7.45X10+4 mg/L at 25 °C

Very soluble in ethanol, acetone, benzene, ether

Acrylonitrile is ... miscible with ethanol, carbon tetrachloride, ethyl acetate, ethylene cyanohydrin, liquid carbon dioxide, ... toluene, petroleum ether, and xylene.

Solubility in water, g/100ml at 20 °C: 7

32 °F (EPA, 1998)

-5 °C (23 °F) - closed cup

32 °F(0 °C)(open cup)

-1 °C c.c.

30 °F

30 °F

171 °F at 760 mmHg (EPA, 1998)

77.2 °C

77 °C

171 °F

77.3 °C @760 [mm Hg]

171 °F

Hazardous decomposition products formed under fire conditions - Carbon oxides, nitrogen oxides (NOx).

... When burned may decompose to free cyanide.

When heated to decomposition it emits toxic fumes of /nitrogen oxides and cyanides/.

-116 °F (EPA, 1998)

-83.51 °C

-84 °C

-116 °F

-83.48 °C

-116 °F

Danger

H225: Highly Flammable liquid and vapor [Danger Flammable liquids]；H301: Toxic if swallowed [Danger Acute toxicity, oral]；H311: Toxic in contact with skin [Danger Acute toxicity, dermal]；H315: Causes skin irritation [Warning Skin corrosion/irritation]；H317: May cause an allergic skin reaction [Warning Sensitization, Skin]；H318: Causes serious eye damage [Danger Serious eye damage/eye irritation]；H331: Toxic if inhaled [Danger Acute toxicity, inhalation]；H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]；H350: May cause cancer [Danger Carcinogenicity]；H411: Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P203, P210, P233, P240, P241, P242, P243, P261, P262, P264, P264+P265, P270, P271, P272, P273, P280, P301+P316, P302+P352, P303+P361+P353, P304+P340, P305+P354+P338, P316, P317, P318, P319, P321, P330, P332+P317, P333+P317, P361+P364, P362+P364, P370+P378, P391, P403+P233, P403+P235, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.2% (2 of 1097) of reports.

Chemical: 2-Propenenitrile；Specific Information Requirement: Obligations to provide information apply. These obligations are:；1. If the assessment report about the chemical recommends secondary notification of the chemical in particular circumstances and any of the circumstances occur in relation to the introduction (importation or manufacture) of the chemical by a person, then the person introducing this chemical must tell us in writing within 28 calendar days that the circumstances have occurred.；2. A person who introduces this chemical must tell us in writing within 28 calendar days if they become aware of any of the following circumstances, namely, that since the assessment under the Industrial Chemicals (Notification and Assessment) Act 1989:；a. the function or use of the chemical has changed, or is likely to change, significantly;；b. the amount of the chemical being introduced has increased, or is likely to increase, significantly;；c. in the case of a chemical not manufactured, or proposed to be manufactured, in Australia at the time of the assessment—it has begun to be manufactured in Australia;；d. the method of manufacture of the chemical in Australia has changed, or is likely to change, in a way that may result in an increased risk of an adverse effect of the chemical on occupational health and safety, public health or the environment;；e. additional information has become available to the person as to an adverse effect of the chemical on occupational health and safety, public health or the environment.

Hazard Traits - Carcinogenicity; Neurotoxicity; Respiratory Toxicity；Authoritative List - ATSDR Neurotoxicants; CA TACs; CWA 303(c); CWA 303(d); EC Annex VI CMRs - Cat. 1B; IARC Carcinogens - 1; IRIS Carcinogens - B1; NTP RoC - reasonable; OEHHA RELs; Prop 65；Report - regardless of intended function of ingredient in the product

2-Propenenitrile is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 2-Propenenitrile are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

TP - indicates a substance that is the subject of a proposed TSCA section 4 test rule.

Status: Active Update: 10-05-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/15561

2-Propenenitrile: HSNO Approval: HSR001082 Approved with controls

Materials are too dangerous to health to expose fire fighters. A few whiffs of vapor could cause death or vapor or liquid could be fatal on penetrating the fire fighter's normal full protective clothing. The normal full protective clothing and breathing apparatus available to the average fire department will not provide adequate protection against inhalation or skin contact with these materials. Explosion hazard is moderate. It is flammable and explosive at normal room temperatures. Can react violently with strong acids, amines, strong alkalis. Vapors may travel considerable distance to source of ignition and flash back. Dilute solutions are also hazardous (flash point of a solution of 2 percent in water is 70F). When heated or burned, toxic hydrogen cyanide gas and oxides of nitrogen are formed. Avoid strong acids, amines, alkalis. Incompatible with strong oxidizers (especially bromine) copper and copper alloys. Unstable, moderate hazard is possible when it is exposed to flames, strong acids, amines and alkalis. May polymerize spontaneously in the container, particularly in absence of oxygen or on exposure to visible light. If polymerization occurs in containers, there is a possibility of violent rupture. (EPA, 1998)

· HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames.；CAUTION: Methanol (UN1230) will burn with an invisible flame. Use an alternate method of detection (thermal camera, broom handle, etc.)；· Vapors may form explosive mixtures with air.；· Vapors may travel to source of ignition and flash back.；· Most vapors are heavier than air. They will spread along the ground and collect in low or confined areas (sewers, basements, tanks, etc.).；· Vapor explosion and poison hazard indoors, outdoors or in sewers.；· Those substances designated with a (P) may polymerize explosively when heated or involved in a fire.；· Runoff to sewer may create fire or explosion hazard.；· Containers may explode when heated.；· Many liquids will float on water.

Highly flammable. Gives off irritating or toxic fumes (or gases) in a fire. Vapour/air mixtures are explosive. Risk of fire and explosion on contact with strong bases or strong acids.

It is classified as very toxic. Probable oral lethal dose for human is 50-500 mg/kg (between 1 teaspoon and 1 oz.) for a 70 kg (150 lb.) person. Irritant skin dose -- 500 mg. Toxic concentrations have been reported at 16 ppm/20 min. Acute toxicity is similar to that due to cyanide poisoning, and the level of cyanide ion in blood is related to the level of poisoning. Inhalation or ingestion results in collapse and death due to tissue anoxia (lack of oxygen) and cardiac arrest (heart failure). (EPA, 1998)

· TOXIC; may be fatal if inhaled, ingested or absorbed through skin.；· Inhalation or contact with some of these materials will irritate or burn skin and eyes.；· Methyl chloroacetate (UN2295) is an eye irritant/lachrymator (causes flow of tears).；· Fire will produce irritating, corrosive and/or toxic gases.；· Vapors may cause dizziness or asphyxiation, especially when in closed or confined areas.；· Runoff from fire control or dilution water may cause environmental contamination.

Acrylonitrile is a colorless, liquid, man-made chemical with a sharp, onion- or garlic-like odor. It can be dissolved in water and evaporates quickly. Acrylonitrile is used to make other chemicals such as plastics, synthetic rubber, and acrylic fibers. A mixture of acrylonitrile and carbon tetrachloride was used as a pesticide in the past; however, all pesticide uses have stopped.

Exposure to acrylonitrile is primarily occupational: it is used in the manufacture of acrylic acid and modacrylic fibers. Acute (short-term) exposure of workers to acrylonitrile has been observed to cause mucous membrane irritation, headaches, dizziness, and nausea. No information is available on the reproductive or developmental effects of acrylonitrile in humans. Based on limited evidence in humans and evidence in rats, EPA has classified acrylonitrile as a probable human carcinogen (Group B1).

It is readily absorbed through GI, pulmonary, and skin routes; it's acute toxicity is due to the release of the cyanide ion in the body; Caused occupational fatalities in the past when it was used as a fumigant; [ACGIH] May cause redness and blisters when spilled on the skin. [ICSC] If left on clothes, can cause reddening of skin; [CHRIS] Allergic contact dermatitis reported in workers producing synthetic fibers; [Kanerva, p. 1746] In reproductive studies of experimental animals, acrylonitrile causes testicular damage and fetal skeletal abnormalities. [Frazier, p. 349-50] . . . when acrylonitrile exposures were less than those causing overt maternal toxicity, no developmental toxicity was observed. Decreased sperm counts were observed in 30 exposed workers, but the exposures were not quantified. [ACGIH] A lachrymator; [CHEMINFO] In summary, no mortality outcome of a priori interest, principally respiratory system cancer, is associated with increased AN exposure among fiber production workers over five decades of follow-up. [PMID 18469624] Acrylonitrile, stabilized (UN1093) has warning of explosive polymerization; [ERG 2016] See NITRILES.

1093 131P

1093 131P(inhibited)

In advanced or massive fires, fire fighting should be done from a safe distance or a protected location. Isolate for 1/2 mile in all directions if tank car or truck is involved in fire.；Small fires: dry chemical, carbon dioxide, water spray or foam. Large fires: water spray, fog or foam. Stay away from ends of tanks. Do not get water inside container. Cool containers that are exposed to flames with water from the side until well after fire is out. For massive fire in cargo area, use unmanned hose holder or monitor nozzles; if this is impossible, withdraw from area and let fire burn. Withdraw immediately in case of rising sound from venting safety device or any discoloration of tank due to fire. (EPA, 1998)

Use water spray, powder, alcohol-resistant foam, carbon dioxide. In case of fire: keep drums, etc., cool by spraying with water.

Fresh air, rest. Refer for medical attention.

First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again. Refer for medical attention .

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. Induce vomiting (ONLY IN CONSCIOUS PERSONS!). Refer for medical attention .

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.；· Keep unauthorized personnel away.；· Stay upwind, uphill and/or upstream.；· Ventilate closed spaces before entering, but only if properly trained and equipped.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.；· All equipment used when handling the product must be grounded.；· Do not touch or walk through spilled material.；· Stop leak if you can do it without risk.；· Prevent entry into waterways, sewers, basements or confined areas.；· A vapor-suppressing foam may be used to reduce vapors.；Small Spill；· Absorb with earth, sand or other non-combustible material and transfer to containers for later disposal.；· Use clean, non-sparking tools to collect absorbed material.；Large Spill；· Dike far ahead of liquid spill for later disposal.；· Water spray may reduce vapor, but may not prevent ignition in closed spaces.

Warning: Effects, including skin reactions, may be delayed. Caution is advised. Vital signs should be monitored closely. Heart palpitation may begin within minutes after exposure.；Note: Acrylonitrile is very readily absorbed through the skin.；Signs and Symptoms of Acrylonitrile Exposure: Signs and symptoms of acute exposure to acrylonitrile may include hypertension (high blood pressure) and tachycardia (rapid heart rate), followed by hypotension (low blood pressure) and bradycardia (slow heart rate). Cherry-red mucous membranes and blood, cardiac arrhythmias, and other cardiac abnormalities are common. Cyanosis (blue tint to the skin and mucous membranes) is not a consistent finding. Tachypnea (rapid respiratory rate) may be followed by respiratory depression. Lung hemorrhage and pulmonary edema may also occur. Headache, vertigo (dizziness), agitation, and giddiness may be followed by combative behavior, convulsions, paralysis, protruding eyeballs, dilated and unreactive pupils, and coma. Acrylonitrile is irritating to the skin and mucous membranes. Lacrimation (tearing) and a burning sensation of the mouth and throat are common. Excessive salivation, nausea, and vomiting may also occur.；Emergency Life-Support Procedures: Acute exposure to acrylonitrile may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination.；Inhalation Exposure:；1. Move victims to fresh air. Emergency personnel should avoid self-exposure to acrylonitrile.；2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. IMMEDIATELY begin administering 100% oxygen to all victims. Monitor victims for respiratory distress.Warning: To prevent self-poisoning, avoid mouth-to-mouth breathing; use a forced-oxygen mask. Direct oral contact with acrylonitrile-contaminated persons or their gastric contents may result in self-poisoning.；3. RUSH to a health care facility!；4. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.；Dermal/Eye Exposure:；1. Remove victims from exposure. Emergency personnel should avoid self-exposure to acrylonitrile.；2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. IMMEDIATELY begin administering 100% oxygen to all victims. Monitor victims for respiratory distress.Warning: To prevent self-poisoning, avoid mouth-to-mouth breathing; use a forced-oxygen mask. Direct oral contact with acrylonitrile-contaminated persons or their gastric contents may result in self-poisoning.；3. RUSH to a health care facility!；4. Remove contaminated clothing as soon as possible.；5. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes.；6. Wash exposed skin areas twice with soap and water.；7. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.；Ingestion Exposure:；1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. IMMEDIATELY begin administering 100% oxygen to all victims. Monitor victims for respiratory distress.Warning: To prevent self-poisoning, avoid mouth-to-mouth breathing; use a forced-oxygen mask. Direct oral contact with acrylonitrile-contaminated persons or their gastric contents may result in self-poisoning.；2. RUSH to a health care facility!

General First Aid:；· Call 911 or emergency medical service.；· Ensure that medical personnel are aware of the material(s) involved, take precautions to protect themselves and avoid contamination.；· Move victim to fresh air if it can be done safely.；· Administer oxygen if breathing is difficult.；· If victim is not breathing:；-- DO NOT perform mouth-to-mouth resuscitation; the victim may have ingested or inhaled the substance.；-- If equipped and pulse detected, wash face and mouth, then give artificial respiration using a proper respiratory medical device (bag-valve mask, pocket mask equipped with a one-way valve or other device).；-- If no pulse detected or no respiratory medical device available, provide continuous compressions. Conduct a pulse check every two minutes or monitor for any signs of spontaneous respirations.；· Remove and isolate contaminated clothing and shoes.；· For minor skin contact, avoid spreading material on unaffected skin.；· In case of contact with substance, remove immediately by flushing skin or eyes with running water for at least 20 minutes.；· For severe burns, immediate medical attention is required.；· Effects of exposure (inhalation, ingestion, or skin contact) to substance may be delayed.；· Keep victim calm and warm.；· Keep victim under observation.；· For further assistance, contact your local Poison Control Center.；· Note: Basic Life Support (BLS) and Advanced Life Support (ALS) should be done by trained professionals.；Specific First Aid:；· Wash skin with soap and water.

(General first aid procedures)；Eye: Irrigate immediately - If this chemical contacts the eyes, immediately wash (irrigate) the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately.；Skin: Water wash immediately - If this chemical contacts the skin, immediately wash the contaminated skin with water. If this chemical penetrates the clothing, immediately remove the clothing and wash the skin with water. If symptoms occur after washing, get medical attention immediately.；Breathing: Respiratory support；Swallow: Medical attention immediately - If this chemical has been swallowed, get medical attention immediately.

· Wear positive pressure self-contained breathing apparatus (SCBA).；· Wear chemical protective clothing that is specifically recommended by the manufacturer when there is NO RISK OF FIRE.；· Structural firefighters' protective clothing provides thermal protection but only limited chemical protection.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Use water spray to cool unopened containers.

Approach fire from upwind to avoid hazardous vapors and toxic decomposition products. Use water spray, dry chemical, "alcohol resistant" foam, or carbon dioxide. Use water spray to keep fire-exposed containers cool. Fight fire from protected location or maximum possible distance.

For more Fire Fighting Procedures (Complete) data for Acrylonitrile (7 total), please visit the HSDB record page.

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Recommended storage temperature 2 - 8 °C. Light sensitive. Storage class (TRGS 510): Flammable liquids.

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/

Isolate from alkalies and oxidizing materials. Inside storage should be in a standard flammable liquids storage warehouse, room, or cabinet. Outside or detached storage is preferred. Do not store uninhibited acrylonitrile.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Remove all sources of ignition. Evacuate personnel to safe areas. Beware of vapors accumulating to form explosive concentrations. Vapors can accumulate in low areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Contain spillage, and then collect with an electrically protected vacuum cleaner or by wet-brushing and place in container for disposal according to local regulations.

Remove solutions containing acrylonitrile by vacuum cleaning to prevent an increase in airborne concentrations.

Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents. Apply "universal" gelling agent to immobilize spill.

Environmental considerations: Air spill: Apply water spray or mist to knock down vapors. Combustion products include corrosive or toxic vapors.

For more Cleanup Methods (Complete) data for Acrylonitrile (8 total), please visit the HSDB record page.

Excerpt from ERG Guide 131 [Flammable Liquids - Toxic; polymerization hazard]:；ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor-suppressing foam may be used to reduce vapors.；SMALL SPILL: Absorb with earth, sand or other non-combustible material and transfer to containers for later disposal. Use clean, non-sparking tools to collect absorbed material.；LARGE SPILL: Dike far ahead of liquid spill for later disposal. Water spray may reduce vapor, but may not prevent ignition in closed spaces. (ERG, 2024)

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U009, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Product: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Acrylonitrile is a waste chemical stream constituent which may be subjected to ultimate disposal by controlled incineration. Nitrogen oxides removed from effluent gas by scrubbers and/or thermal devices.

For more Disposal Methods (Complete) data for Acrylonitrile (16 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)

Gastrointestinal；Nervous；Respiratory

[brain tumors, lung & bowel cancer]

Pre-treatment with cyanide was found to greatly enhance the toxicity of acrylonitrile, and to cause a three-fold increase in the cyanide level in the blood of treated rats.

Rats chronically exposed to acrylonitrile (ACN) have shown a dose-dependent increase in the incidence of astrocytomas in the brain. The mechanism(s) by which ACN induces cancer in rodents has not been established. ACN does not appear to be directly genotoxic in the brain and thus a nongenotoxic mode of action has been proposed. Inhibition of gap junctional intercellular communication (GJIC) has been shown to be a property of many nongenotoxic carcinogens. The present study examined the effects of ACN on GJIC in a rat astrocyte transformed cell line, DI TNC1 cells (a target cell for ACN carcinogenicity) and primary cultured hepatocytes (a nontarget cell for ACN carcinogenicity). ACN inhibited GJIC in rat astrocytes in a dose-dependent manner. Inhibition of GJIC was observed following 2 h treatment with 0.10 mmol/L and 1.00 mmol/L ACN. However, in primary cultured hepatocytes, ACN exposed did not result in inhibition of GJIC even after 48 h of continued treatment. In the astrocytes, GJIC inhibition plateaued after 4 h of treatment and remained blocked throughout the entire experimental period examined. Inhibition of GJIC in DI TNC1 cells was reversed by removal of ACN from the culture medium after 4 or 24 h of treatment. Cotreatment of astrocytes with vitamin E reduced the effect of ACN-induced inhibition of GJIC. Similarly, inhibition of GJIC was prevented by treatment with 2-oxothiazolidine-4-carboxylic acid (OTC), a precursor of glutathione synthesis. Decreasing cellular glutathione by treatment with buthionine sulfoxamine alone (without ACN) did not affect GJIC in astrocytes. Collectively, these results demonstrate that treatment with ACN caused a selective inhibition of GJIC in rat DI TNC1 astrocytes (the target cell type), but not in rat hepatocytes (a nontarget tissue). Inhibition of GJIC in astrocytes was reversed by treatment with antioxidants and suggests a potential role for oxidative stress in ACN-induced carcinogenesis.

Some of the more striking expressions of toxicity are the tremors and seizures observed approximately 100 min after exposure of rats to an acutely toxic dose of acrylonitrile (AN). ... For AN, at least two chemical entities could produce these toxic effects, namely the parent AN molecule, the metabolically-released cyanide, or both. Which of these two agents is responsible for each of the symptoms of acute intoxication is not known. To help dissect the toxicity, it was anticipated that an effective inhibitor of the oxidative metabolism of AN to cyanide could help ... to understand which toxic symptoms might be associated with each agent. Three inhibitors of oxidative metabolism were tested, namely SKF-525A, 1-benzylimidazole and metyrapone and one alternative substrate, ethanol. As compared to SKF-525A and metyrapone, both 1-benzylimidazole and ethanol were highly effective in reducing blood cyanide levels to insignificant levels in rats treated with an LD90 dose of AN. In addition, both agents abolished the early seizure activity, suggesting that this first phase of seizures is due to cyanide and not the parent molecule. 1-Benzylimidazole did not prevent the severe clonic convulsive phase preceding death, suggesting that these terminal convulsions are due to the toxic effects of the parent AN molecule. The CNS depressant ethanol was only partially effective in attenuating the terminal convulsions. None of these agents affected the incidence of AN-induced mortality, clearly establishing that, even in the absence of cyanide, the parent AN molecule is acutely toxic. The partial effectiveness of ethanol suggested that anticonvulsants might be of benefit. Both phenobarbital and phenytoin protected rats from both the early and terminal convulsions, while valproic acid was ineffective. These effects were not related to a reduction in blood cyanide levels but rather due to their inherent anticonvulsant activity.

Hydrogen cyanide and carbon monoxide enhance acrylonitrile toxicity in experimental animals.

... For most nitriles, the in vitro metabolism was inhibited when the incubation mixture contained either SKF-525A, carbon monoxide, or microsomes from mice treated with carbon tetrachloride. When mice were dosed with ethyl alcohol, metabolic enhancement of nitriles was seen compared with the control. However, ethyl alcohol, when added to the incubation mixture, inhibited the in vitro metabolism of nitriles. /Nitriles/

Cancer, Developmental (effects during periods when organs are developing), Gastrointestinal (Stomach and Intestines, part of the digestive system), Neurological (Nervous System), Respiratory (From the Nose to the Lungs)

Respiratory

Eyes, skin, cardiovascular system, liver, kidneys, central nervous system

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)

LC50; Species: Pimephales promelas (fathead minnow); Conditions: static bioassay; Concentration: 2600 ug/L for 30 days

LC50; Species: /Lagodon rhomboides/ (Pinfish); Conditions: saltwater, static bioassay; Concentration: 24,500 ug/L for 24 hr

LC50; Species: Lepomis macrochirus (bluegill); Conditions: static bioassay; Concentration: 11,800 ug/L for 96 hr

LC50; Species: Pimephales promelas (fathead minnow); Conditions: flow through; Concentration: 10,100 ug/L for 96 hr

For more Ecotoxicity Values (Complete) data for Acrylonitrile (24 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 29(SRC), determined from a log Kow of 0.25(2) and a regression-derived equation(3), indicates that acrylonitrile is expected to have very high mobility in soil(SRC). Volatilization of acrylonitrile from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 1.38X10-4 atm-cu m/mole(4). Acrylonitrile is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 109 mm Hg at 25 °C(5). Complete biodegradation of a low concentration of acrylonitrile was <2 days to 6 days depending on soil type with slow degradation reported in unacclimated soils exposed to high concentrations of acrylonitrile(6); these findings suggest that biodegradation may be an important environmental fate process in soil under certain conditions(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 29(SRC), determined from a log Kow of 0.25(2) and a regression-derived equation(3), indicates that acrylonitrile is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon a Henry's Law constant of 1.38X10-4 atm-cu m/mole(5). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 7 hrs and 4 days, respectively(SRC). According to a classification scheme(6), a BCF of 48(7) suggests bioconcentration in aquatic organisms is moderate(SRC). Acrylonitrile was stable to aqueous hydrolysis in the pH range of 4-10 over a 10-day observation period(8) suggesting that hydrolyis is not important under environmental conditions (pH 5 to 9). Complete degradation in 6-20 days using various freshwater inoculums(8,9) suggests that biodegradation may be an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acrylonitrile, which has a vapor pressure of 109 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase acrylonitrile 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 1.5 hours(SRC), calculated from its rate constant of 1.11X10-11 cu cm/molecule-sec at 25 °C(3). The half-life for reaction with ozone in air is estimated to be 83 days(SRC), calculated from its rate constant of 1.38X10-19 cu cm/molecule-sec at 25 °C(4). Acrylonitrile does not absorb UV light at wavelengths >290 nm(5) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Other Poison - Chemical Asphyxiant；Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.；Dermatotoxin - Skin burns.；Lacrimator (Lachrymator) - A substance that irritates the eyes and induces the flow of tears.；Skin Sensitizer - An agent that can induce an allergic reaction in the skin.；IARC Carcinogen - Class 3: Chemicals are not classifiable by the International Agency for Research on Cancer.；NTP Carcinogen - Reasonably anticipated to be a human carcinogen.；ACGIH Carcinogen - Confirmed Animal.

The substance can be absorbed into the body by inhalation of its vapour, through the skin and by ingestion.

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

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

IDENTIFICATION AND USE: Acrylonitrile is a clear, colorless liquid at room temperature. Acrylonitrile is used as a monomer for acrylic and modacrylic fibers and whiskers, in copolymers with styrene and butadiene (ABS resins), in the manufacture of adiponitrile, and in nitrile rubbers. Acrylonitrile is no longer used as a fumigant and nitrile resins made with acrylonitrile are no longer used to make beverage bottles. HUMAN STUDIES: Dermal exposure to acrylonitrile causes irritation, burns, and blisters. Additionally, dermal exposure to acrylonitrile can lead to systemic toxicity and lethality. Chronic effects can also occur after exposure to acrylonitrile vapors or liquid. 576 Japanese workers exposed to 5-20 ppm acrylonitrile over 10 yr showed headache, fatigue, nausea, and weakness with symptoms of anemia, jaundice, conjunctivitis, and abnormal whole blood and serum specific gravity, cholinesterase, urobilinogen, bilirubin, urinary protein, and sugar values, indicative of liver injury and a general toxic effect. In cultured human bronchial epithelial cells acrylonitrile induced cytotoxicity, sister chromatid exchanges and DNA single strand breaks. Acrylonitrile affected semen quality among exposed workers. Acrylonitrile or its metabolites could induce reproductive defects as an in vivo multipotent genotoxic agent by inducing DNA strand breakage and sex chromosome non-disjunction in spermatogenesis. Exposure to acrylonitrile in pregnant workers caused increasing risk of preterm delivery and birth defects. ANIMAL STUDIES: After a single oral dose of 46.5 mg/kg bw acrylonitrile, moderate to marked hyperplasia of the Clara cells lining the bronchioles was observed in male rats. A 10% aqueous solution administered to the eyes of a rabbit caused a trace of pain and slight conjunctival irritation immediately following contact. There was no corneal injury at any time. The conjunctiva was completely normal within 24 hours. Intraperitoneal injection of 50 mg/kg bw acrylonitr

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)

Chemical: 2-Propenenitrile；Specific Information Requirement: Obligations to provide information apply. These obligations are:；1. If the assessment report about the chemical recommends secondary notification of the chemical in particular circumstances and any of the circumstances occur in relation to the introduction (importation or manufacture) of the chemical by a person, then the person introducing this chemical must tell us in writing within 28 calendar days that the circumstances have occurred.；2. A person who introduces this chemical must tell us in writing within 28 calendar days if they become aware of any of the following circumstances, namely, that since the assessment under the Industrial Chemicals (Notification and Assessment) Act 1989:；a. the function or use of the chemical has changed, or is likely to change, significantly;；b. the amount of the chemical being introduced has increased, or is likely to increase, significantly;；c. in the case of a chemical not manufactured, or proposed to be manufactured, in Australia at the time of the assessment—it has begun to be manufactured in Australia;；d. the method of manufacture of the chemical in Australia has changed, or is likely to change, in a way that may result in an increased risk of an adverse effect of the chemical on occupational health and safety, public health or the environment;；e. additional information has become available to the person as to an adverse effect of the chemical on occupational health and safety, public health or the environment.

Hazard Traits - Carcinogenicity; Neurotoxicity; Respiratory Toxicity；Authoritative List - ATSDR Neurotoxicants; CA TACs; CWA 303(c); CWA 303(d); EC Annex VI CMRs - Cat. 1B; IARC Carcinogens - 1; IRIS Carcinogens - B1; NTP RoC - reasonable; OEHHA RELs; Prop 65；Report - regardless of intended function of ingredient in the product

2-Propenenitrile is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 2-Propenenitrile are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

TP - indicates a substance that is the subject of a proposed TSCA section 4 test rule.

Status: Active Update: 10-05-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/15561

2-Propenenitrile: HSNO Approval: HSR001082 Approved with controls

U009; As stipulated in 40 CFR 261.33, when acrylonitrile, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

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. Acrylonitrile is produced, as an intermediate or a final product, by process units covered under this subpart.

Acrylonitrile has been designated as a hazardous air pollutant under section 112 of the Clean Air Act.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Acrylonitrile is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Acrylonitrile is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 10,000 lbs.

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations.

Acrylonitrile is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

The levels for acrylonitrile through ingestion of contaminated water and contaminated aquatic organisms ... which may result in incremental increase of cancer risk over the lifetime are estimated at 1X10-5, 1X10-6, and 1X10-7. The corresponding criteria are 0.58 ug/L, 0.058 ug/L, and 0.006 ug/L, respectively. For consumption of aquatic organisms only, excluding consumption of water, the levels are 6.5 ug/L, 0.65 ug/L, and 0.065 ug/L, respectively.

Acrylonitrile

1

10000

Flammable chemical that can be released at a facility.

(AZ) ARIZONA 0.15 ug/L

(FL) FLORIDA 8 ug/L

(NH) NEW HAMPSHIRE 0.06 ug/L

(ME) MAINE 0.6 ug/L

Acrylonitrile (AN) is a vinyl monomer used in the production of synthetic fibers, rubber and plastics. AN is acutely toxic but its mechanism of toxicity remains to be established. AN is metabolized to cyanide in vivo but cyanide production alone cannot explain acute AN toxicity. Previous work ... has shown that AN can alkylate highly reactive cysteine residues in proteins. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a critical enzyme involved in glycolysis, has a catalytically active cysteine 149 in its active site. ... AN irreversibly inhibits GAPDH with second-order rate constants, at pH 7.4, of 3.7 and 9.2 M(-1) s(-1) at 25 and 37 degrees C, respectively. A combination of matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) and electrospray ionization-mass spectrometry-mass spectrometry (ESI-MS-MS) was used to show that AN inactivates GAPDH by covalently binding to cysteine 149 in the active site of the enzyme. Inactivation of GAPDH by AN would be expected to impair glycolytic ATP production and when coupled with the inhibition of mitochondrial ATP synthesis by the AN metabolite cyanide would result in metabolic arrest. The brain can withstand metabolic arrest for only a few minutes thus these combined actions may account for the acute toxicity of AN in vivo.

The interaction of acrylonitrile (VCN) with rat blood has been investigated at the molecular level in an attempt to understand the possible mechanism of its toxicity. ... Up to a maximum of 94% of (14)C from VCN in erythrocytes was detected covalently bound to cytoplasmic and membrane proteins. ... Determination of specific activity showed that binding occurred more in vivo than in vitro which indicated that the VCN molecule was bioactivated inside erythrocytes. These results indicate that ... VCN, which binds to cytoplasmic and membrane proteins, may cause damage to red cells by mechanisms other than release of CN-.

Acrylonitrile (AN) is an organic compound produced in large quantities by the chemical industry and is acutely toxic. One mechanism proposed to explain the toxicity of AN is metabolism by P450 into cyanide (CN). Although blood and brain levels of CN in rats following an LD90 dose of AN are consistent with acute toxicity, blocking CN formation with P450 inhibitors does not prevent lethality. Another mechanism implicated in toxicity is covalent binding of AN to cysteine residues in tissue proteins. Previous work ... has shown that AN can irreversibly inactivate the catalytically active cysteine-149 in glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Inactivation of GAPDH by AN would be expected to impair glycolytic ATP production and, when coupled to the inhibition of mitochondrial ATP synthesis by the AN metabolite CN, would result in metabolic arrest, particularly in brain. ... /Researchers/ measured the high energy metabolites phosphocreatine (PCr), ATP, ADP and AMP by HPLC and compared their levels in the brains of rats treated with an LD90 dose of AN, when respiration ceased, vs. controls. Two methods of rapid brain freezing in liquid nitrogen were used: funnel freezing (FF) and head immersion (HI). AN administration resulted in large decreases in PCr of 74% (FF) and 80% (HI) but relatively minor decreases in ATP of 5% (FF) and 21% (HI) and Energy Charge of 6% (FF) and 10% (HI). Thus, although substantial depletion of PCr was observed, possibly due to inhibition of creatine kinase by AN, we found no evidence that brain ATP is depleted when respiration ceases in AN-intoxicated rats.

Acrylonitrile-induced adrenal necrosis is associated with the early depletion of adrenal glutathione and elevation of adrenal dopamine. These biochemical events could result in increased susceptibility to free radical-mediated lipid peroxidation which may play a role in pathogenesis of adrenal injury caused by acrylonitrile.

Administered intraperitoneally to rats at a dose of 100 mg/kg bw, acrylonitrile inhibits non-competitively the activity of brain, kidney and liver cytochrome oxidase; when injected subcutaneously at a dose of 100-120 g/kg bw it decreases the ratio between oxidized and reduced nucleotides in the brain and blood; when given as an intravenous dose of 150 mg/kg bw, it reduces the content of glutathione in liver, lung, kidneys, adrenals and brain of rats.

Blood: 8 hours; [TDR, p. 50]

/Acrylonitrile has a/ half-life in /bluegill/ tissue between 4 and 7 days.

The metabolism of acrylonitrile to the epoxide, 2-cyanoethylene oxide (ANO) was examined in rat liver microsomes, lung microsomes, and isolated enriched lung cell preparations. GC/high resolution MS was used to quantitate ANO in microsomal and cellular extracts by monitoring the fragment ion C2H3N (m/z 41.0265). The limit of detection was 0.05 pmol of ANO/0.5 microliter of standard solution, microsomal extract, or cellular extract injected onto the column, and the linear range of analysis was 0.05 to 12.5 pmol of ANO. Kinetic parameters of Vmax, V/K, and Km were calculated for microsomal ANO formation. Liver microsomes were quantitatively more active than lung microsomes on a mg of protein basis. The Vmax (pmol of ANO formed/min/mg of protein) was 666.61 for liver and 45.07 for lung microsomes. The V/K (pmol of ANO/min/mg of protein/microM) was 12.83 for liver and 0.02 for lung microsomes. The apparent Km was 51.93 uM and 1853.83 uM for liver and lung microsomes, respectively. When calculated as nmol of ANO formed/min/nmol of microsomal P-450, the Vmax for lung was equivalent to the Vmax for liver. ANO formation in the rat lung was cell specific. The rates of metabolism in the Clara cell-enriched fraction, the alveolar type II cell-enriched fraction, and the cell suspension were 2.55, 0.38, and 0.67 pmol of ANO formed/min/mg of protein, respectively. No metabolism was observed in the endothelial (small) cell-enriched fraction or in the alveolar macrophages. The results suggest that the lung contributes to the metabolism and disposition of inhaled acrylonitrile.

... Acrylonitrile was administered by gavage at 0, 2.5, 10, or 20 mg/kg/day, 5 days per week, for 2 years. Urinary thiocyanate and N-acetyl-S-(2-cyanoethyl)-L-cysteine were measured as markers of exposure to acrylonitrile. In general, there were dose-related increases in urinary thiocyanate and N-acetyl-S-(2-cyanoethyl)-L-cysteine concentrations in all dosed groups of mice and at all time points. ...

Acrylonitrile is metabolized to cyanide. Interestingly, the overall amount of acrylonitrile metabolism is substantially less in humans than in rodents, and the amount of cyanide produced as a result is greater in rodents than humans.

In liver fractions from Sprague-Dawley rats, the metabolism of acrylonitrile (VCN) to cyanide (CN-) was localized the microsomal fraction and required NADPH and O2 for maximal activity. The biotransformation of VCN to CN- was characterized with respect to time, microsomal protein concentration, pH, and temperature. Metabolism of VCN was increased in microsomes obtained from phenobarbital-, Aroclor 1254-, or 3-methylcholanthrene-treated rats (479%, 414%, and 142% of control, respectively) and decreased with CoCl2 treatment (54% of control). The KM estimated for VCN with the phenobarbital (54.8 +/- 9.5 mM) or Aroclor 1254 (40.9 +/- 4.1 mM) preparation was lower than the control (190.7 +/- 19.7 mM). Addition of SKF 525-A or CO to incubation mixtures inhibited VCN metabolism. Addition of the epoxide hydratase inhibitor, 1,1,1-trichloropropane 2,3-oxide, decreased the formation of CN- from VCN. Addition of glutathione, cysteine, D-penicillamine, or 2-mercaptoethanol enhanced the release of CN- from VCN. These findings indicate that VCN is metabolized to CN- via a cytochrome P-450-dependent mixed-function oxidase system.

For more Metabolism/Metabolites (Complete) data for Acrylonitrile (19 total), please visit the HSDB record page.

Acrylonitrile has known human metabolites that include Cyanoethylene oxide.

Acrylonitrile is readily absorbed from the respiratory and gastrointestinal tracts and through the intact skin.

Fat tissue accumulation of acrylonitrile may also occur. While the high solubility of acrylonitrile in water (7.35 percent at 20 °C) would permit the excretion of the unchanged compound in the urine, the urinary detection 72 hours after exposure in the rabbit strongly suggests either fat storage or reversible protein binding.

After intravenous injection of a lethal dose of acrylonitrile (75 mg/kg bw) in rabbits, the hydrogen cyanide concentration in the blood rose steadily until the death of the animals; the thiocyanate concentration in the blood increased slightly during this period. After a single intravenous injection of 15 mg/kg bw, about 3% of the dose was expired for about 1 hr, and approximately 10% of the total dose was gradually excreted in the urine for more than 48 hr after its injection. The total amount of thiocyanate (formed from hydrogen cyanide) excreted in the urine over 24 hr after the injection of acrylonitrite was equivalent to about 14% of the dose.

In guinea pigs, elimination of acrylonitrile in urine was demonstrated within 24 hr and 30 hr after oral and sc admin, respectively. ... In rats given doses of 26-40 mg/kg body wt, elimination of thiocyanate in urine was over 20% of dose after oral admin, 2-5% after ip or sc injection and 1% after iv admin. Greater amt of acrylonitrile is transformed into thiocyanate after oral than after ip admin in hamsters and mice.

For more Absorption, Distribution and Excretion (Complete) data for Acrylonitrile (13 total), please visit the HSDB record page.

Acrylonitrile is primarily used in the manufacture of acrylic and modacrylic fibers. It is also used as a raw material in the manufacture of plastics (acrylonitrile-butadiene-styrene and styrene-acrylonitrile resins), adiponitrile, acrylamide, and nitrile rubbers and barrier resins.

Used as a monomer in the production of acrylic fibers and acrylonitrile-butadiene-styrene resins; Also used to produce adiponitrile; Was used in the past as a fumigant and to make nitrile resins for beverage bottles; [ACGIH] Used in the plastics, coatings, and adhesive industries; [Merck Index]

No longer used as a fumigant in the U.S. [EPA Pesticides]

Working with Glues and Adhesives [Category: Other]；Firefighting [Category: Other]；Burning Synthetic Polymers [Category: Burn]

For acrylonitrile (USEPA/OPP Pesticide Code: 000601) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

... Cyanoethylation of cotton; synthetic soil blocks (acrylonitrile polymerized wood pulp); ... monomer for a semiconductive polymer that can be used like inorganic oxide catalysts in dehydrogenation of tert-butanol to isobutylene and water.

The major impurity is water, which is usually present at a maximum of 0.5%.

Acetone, 300 ppm max; acetonitrile, 500 ppm max; aldehydes, 100 ppm max; hydrogen cyanide, 10 ppm max; hydroquinone monomethyl ether (inhibitor), 35-50 ppm; iron, 0.10 ppm max; nonvolatile matter, 100 ppm max; peroxides, 0.5 ppm max; water, 1.3882-1.3892 wt% max.

(1978) 1.09X10+11 G

(1983) 3.88X10+11 G

(1977) 109,000 million tons

(1985) 4.28X10+11 g

For more U.S. Exports (Complete) data for Acrylonitrile (6 total), please visit the HSDB record page.

(1977) 8.54X10+7 G

(1982) 1.00X10+6 G

(1985) 2.00X10+5 g

Negligible

2023: 1,000,000,000 - <2,500,000,000 lb；2022: 1,000,000,000 - <2,500,000,000 lb；2021: 2,500,000,000 - <4,000,000,000 lb；2020: 1,000,000,000 - <2,500,000,000 lb

(1983) 9.53X10+11 G

(1978) 7.95X10+11 G

(1977): 745,000 million tons

(1985) 1.06X10+12 g

For more U.S. Production (Complete) data for Acrylonitrile (16 total), please visit the HSDB record page.

COMONOMER FOR ACRYLIC & MODACRYLIC FIBERS, 51%; COMONOMER FOR ACRYLONITRILE-BUTADIENE-STYRENE RESINS, 18%; CHEM INT FOR ADIPONITRILE, 13%; CHEM INT FOR ACRYLAMIDE, 6%; COMONOMER FOR NITRILE ELASTOMERS, 3%; COMONOMER FOR STYRENE-ACRYLONITRILE RESINS, 2%; OTHER USES, 7% (1983)

In 1976, 282 million kg were used to make acrylic and modacrylic fibers.

Acrylic & modacrylic fibers, 45%; acrylonitrile butadiene styrene copolymer resins, 20%; styrene acrylonitrile polymer resins, 9%; adiponitrile, 13%; acrylamide, 6%; miscellaneous, 7% (1984)

CHEMICAL PROFILE: Acrylonitrile. Exports, 43%; acrylic and modacrylic fibers, 28%; acrylonitrile-butadiene-styrene and styrene-acrylonitrile resins, 15%; adiponitrile, 7%; acrylamide, 4%; miscellaneous, including nitrile rubber and barrier resins, 3%.

For more Consumption Patterns (Complete) data for Acrylonitrile (8 total), please visit the HSDB record page.

Acrylonitrile is produced commercially by the catalytic vapor-phase propylene ammoxidation process developed by SOHIO. ... The commercial process uses a fluidized bed reactor in which propylene, ammonia, and air contact a solid catalyst at 400-510 °C and 50-200 kPa gauge. The process uses a stoichiometric excess of ammonia and oxygen (as air). It is a single-pass process with about 98% conversion of propylene that typically consumes about 1.1 kg of propylene per kilogram of acrylonitrile produced or less with the recent generations of highly selective catalysts.

Technical grade acrylonitrile is a highly purified product with greater than 99% purity.

Acritet = 34% acrylonitrile, 60% CCl4; ventox = acritet; carbacryl: equal volumes of acrylonitrile and CCl4; acrylofume: 3.95% acrylonitrile, 30% CCl4, 30% chloroform, 0.5% chloropicrin.