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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 200
CCOHS Chemical Name: Acrylonitrile

Synonyms:
Acrylonitrile monomer
Cyanoethylene
2-Propenenitrile
Propenoic acid nitrile
Vinyl cyanide
Cyanure de vinyle
Nitrile acrylique

Chemical Name French: Acrylonitrile
Chemical Name Spanish: Acrilonitrilo

Trade Name(s):
Acritet
Acrylon
Carbacryl

CAS Registry Number: 107-13-1
UN/NA Number(s): 1093
RTECS Number(s): AT5250000
EU EINECS/ELINCS Number: 203-466-5
Chemical Family: Unsaturated aliphatic nitrile / unsaturated aliphatic cyanide / alkenonitrile / alkenyl cyanide unsaturated aliphatic carboxylic acid nitrile / propenoic acid nitrile / methacrylic acid nitrile
Molecular Formula: C3-H3-N
Structural Formula: CH2=CH-C#N (# = triple bond)

SECTION 2. DESCRIPTION

Appearance and Odour:
Colourless, volatile, liquid with a slightly pungent odour similar to peach pit kernels, garlic or onion.(39) Lachrymator (vapour irritates the eyes and causes tears).(40)

Odour Threshold:
A wide range of values has been reported: 0.031 to 50.4 ppm.(2) An acceptable value is 1.6 ppm (3.4 mg/m3) (detection).(41)

Warning Properties:
NOT RELIABLE - odour threshold is about the same as the TLV.

Composition/Purity:
Acrylonitrile is available commercially in grades of purity of 99% and greater. Impurities may include dimethylformamide, acetonitrile, propionitrile, acetaldehyde, acetone, hydrogen peroxide, hydroxyanisole, methyl acrylate, phenyl-ether-biphenyl mixture, sodium metabisulfite, sulfur dioxide, sulfuric acid, and/or titanium dioxide. Commercial acrylonitrile contains hydroquinone monomethyl ether as an inhibitor at 35-50 mg/kg (ppm).(2,42,43,44)

Uses and Occurrences:
Acrylonitrile is used primarily in the manufacture of acrylic and modacrylic fibres. Other major uses include the production of acrylonitrile- butadiene-styrene (ABS) and styrene-acrylonitrile (SAN) resins, adiponitrile, acrylamide, nitrile rubbers and elastomers, and barrier resins (e.g. acrylonitrile-methyl acrylate-butadiene copolymer and styrene-containing nitrile copolymer). Other uses include the manufacture of carbon fibres, fatty amine amides (used in cosmetics, adhesives, corrosion inhibitors and water treatment resins), urethane polyether polymer polyols, fatty diamines, cyanoethylation of cotton and introduction of the cyanoethyl group in organic synthesis. It was historically used as a pesticide fumigant, but this use has been discontinued.(2,6,42,43,44)
Acrylonitrile does not occur as a natural product. It may be released into the air and wastewater during its production and use. During production, gaseous, liquid and solid wastes are produced. It may also enter the environment during storage, transport, transfer and end-use.(2)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Colourless, volatile, liquid with a slightly pungent odour similar to peach pit kernels, garlic or onion. Lachrymator. EXTREMELY FLAMMABLE LIQUID AND VAPOUR. Vapour is heavier than air and may spread long distances. Distant ignition and flash back are possible. DANGEROUSLY REACTIVE. Vapour or uninhibited liquid may polymerize explosively, if heated, or exposed to sunlight (ultraviolet light), pressure, peroxides, or other incompatible materials. Inhibited liquid may polymerize explosively at temperatures greater than 200 deg C. Closed containers may rupture violently when heated. VERY TOXIC. May be fatal if inhaled, absorbed through the skin or swallowed. Vapour is irritating to eyes and respiratory tract. High vapour concentrations may cause headache, nausea, dizziness, drowsiness, incoordination and confusion. More severe exposures can cause bluish discolouration of the skin, collapse and death. SKIN AND EYE IRRITANT. Causes severe skin and eye irritation. SKIN SENSITIZER. Can cause allergic skin reaction. POSSIBLE CANCER HAZARD - causes cancer based on animal information.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Acrylonitrile very rapidly forms high vapour concentrations at normal temperatures and is very toxic by inhalation. It therefore poses a serious inhalation hazard. Commonly reported symptoms include irritation of the nose and throat, headache, nausea, dizziness and vomiting. More severe exposure can cause tremors, bluish discolouration of the skin, collapse, convulsions and possibly death. However, no confirmed reports of deaths following acrylonitrile exposure were located. Acrylonitrile forms very toxic cyanide in the body, but to a lesser extent than some other nitriles.
One case report describes headache, dizziness, vomiting, tremors, uncoordinated movements and convulsions following exposure of a chemist to an unspecified concentration. Vomiting and nausea persisted for 24 hours. One day after exposure there was slight liver enlargement and congestion of the nasal area. After 4 days there were no kidney, liver, cardiac or respiratory abnormalities.(1,2-original in Italian) Another case report describes employees exposed to 16-100 ppm for 20-45 minutes. The most frequent symptoms reported included headaches, a feeling of fullness in the chest, irritation of the nose and throat, a feeling of apprehension and nervous irritation. All effects were reversed after exposure was stopped. Other exposures (considered mild but not specified) also reported nausea and vomiting, fatigue and diarrhea. In several cases, a mild jaundice (yellow colouring of the skin, indicative of liver injury) with a low grade anemia appeared, which resolved completely.(3,4)

Skin Contact:
Acrylonitrile is a severe irritant, based on human and animal information. Direct contact causes irritation, redness, blistering, peeling and slow healing. A burning tingling feeling in fingers and spreading to forearms has been reported. Acrylonitrile can cause allergic skin reactions (skin sensitization) in some people. Refer to "Effects of Long- Term (Chronic) Exposure" for additional information.
A review of 50 occupational case reports indicates that a burning sensation developed within 5 minutes to 24 hours. This was followed by reddening of the area, which often blistered after one day.(1,2-unconfirmed; original in German) Another case report describes an employee who splashed liquid acrylonitrile on his hands. After 1 day, there was diffuse redness of both hands and wrists. Blisters developed on the finger tips by the third day. The hands were slightly swollen, red, itchy and painful.(5) Some employees exposed to 16-100 ppm for 20-45 minutes reported intolerable itching of the skin with no obvious dermatitis. All effects reversed once exposure stopped.(3,4)
Acrylonitrile may be absorbed through the skin, based on animal and limited human information. Harmful effects, as described for "Inhalation" above, may develop. In one case, an employee was accidentally sprayed with acrylonitrile. Both skin contact and inhalation exposure would have occurred. Dizziness, flushing, nausea, vomiting and hallucinations resulted. Biochemical changes which may have indicated a reduced oxygen supply to body tissues were noted.(1,6)

Eye Contact:
The liquid is a moderate to severe irritant, based on animal information.
Irritation of the eyes has been reported in employees exposed to 16-100 ppm for 20-45 minutes.(3,4)

Ingestion:
No reports of human ingestion were located. Animal toxicity values indicate that acrylonitrile is very toxic following ingestion. Signs and symptoms are expected to be similar to those produced following inhalation. Acrylonitrile forms very toxic cyanide in the body, but to a lesser extent than some other nitriles. Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

Nervous System:
Several studies have reported health effects following long-term occupational exposure, such as headache, insomnia, chest pains, general weakness, decreased working capacity, and increased irritability. The complaints of ill health are variable in nature and no consistent relationship with the extent of exposure appears to have been established.(2) Many of the studies are not available in English, therefore they cannot be evaluated. A thorough, exposure-based study has failed to detect any health effects following long-term exposure.(7)
Subjective symptoms were evaluated in a study of 504 employees at 7 manufacturing sites with exposures rated low, medium and high (1.8, 7.4 or 14.1 ppm). The mean values for length of exposure ranged from 5.6 to 8.6 years. Symptoms reported with significantly high prevalence were headache, tongue trouble, fatigability, general malaise, heavy arms and heavy sweating. There was no dose-response exposure relationship for any of the nervous system symptoms noted.(8)
Using the same factories as the study above, 12 years later (mean exposure of 17 years), a group of employees was classified with low and high exposures (0.19 and 1.13 ppm by personal sampling). Medical evaluation and tests showed no health effects compared to controls. Subjective symptoms reported with increased frequency in the high exposure group were: decreased sex drive, poor memory, and irritability.(9)
Acrylonitrile has caused nervous system effects (e.g. reduced nerve conduction) in animals exposed to very low concentrations, which have also been associated with the development of nervous system cancer.

Lungs/Respiratory System:
Subjective symptoms were evaluated in a study of 504 employees at 7 manufacturing sites with exposures rated low, medium and high (1.8, 7.4 or 14.1 ppm). The mean values for length of exposure ranged from 5.6 to 8.6 years. There was a dose-response exposure relationship for "choking lump in throat", which was considered to be related to the irritant properties of acrylonitrile.(8)
Inhalation of relatively low concentrations (20 ppm for 24 months) has caused degeneration and inflammatory changes in the nasal cavities of rats.

Skin Sensitization:
Acrylonitrile is an occupational skin sensitizer, based on animal and limited human information.
Repeated or prolonged skin contact can cause an allergic skin reaction in some individuals. Once a person is sensitized to a material, contact with even a small amount causes outbreaks of dermatitis with symptoms such as skin redness, itching, rash and swelling. This can spread from the hands or arms to other parts of the body. In one case, numbness, a prickling or tingling feeling and increased sensitivity (paresthesia) of the fingers was observed.
In one report, 5/10 employees with dermatitis had a relapse after return to work. Patch testing was positive to 0.1% acrylonitrile in all five individuals. Case reviews of 2 employees indicated that there was no personal or family history of skin allergy.(10) Another case report describes a 21-year-old woman, with no personal or family history of atopy, who developed dermatitis during her work with acrylonitrile in the laboratory of a synthetic fiber company. Patch testing showed a positive response to acrylonitrile.(64) Other reports describe skin reactions following exposure to liquid acrylonitrile and a finger splint made with an acrylonitrile-methyl methacrylate co-polymer. In the case of the reaction to the finger splint, allergy to acrylonitrile was confirmed by patch testing. There was no indication of whether either individual had a previous history of allergies.(1,2,65)
Positive results for skin sensitization have been reported in one well-conducted animal study.

Liver:
In one study, 102 employees with more than 5 years exposure in acrylic fiber factories were classified into 3 groups based on exposure assessed by personal sampling and biological monitoring. Mean exposures for the low, medium and high groups were 2.1, 7.4 and 14.1 ppm. Medical examination and further clinical chemistry measurements failed to show any health effects attributable to acrylonitrile. Slight liver changes were noted in the high exposure group, but this finding was not statistically significant.(7)
A group of employees from 7 manufacturing sites (mean exposure of 17 years) was classified with low and high exposures (0.19 and 1.13 ppm by personal sampling). Medical evaluation and tests showed no health effects compared to controls. When historical higher exposures were taken into account there were some changes in liver function tests.(9)

Eyes/Vision:
A group of employees from 7 manufacturing sites (mean exposure of 17 years) was classified with low and high exposures (0.19 and 1.13 ppm by personal sampling). Eye symptoms such as reddening, pain or tearing, decreased visual acuity, and blurred vision were reported with more frequency in exposed workers compared to controls. However, the eye effects were considered incidental, as they were related to only one factory.(9)

Carcinogenicity:

Acrylonitrile is carcinogenic, based on animal information. Exposure-related tumours have been observed in rats in ingestion and inhalation studies involving very low concentrations. The most common forms of cancer occurred in the central nervous system and in a gland of the ear canal (zymbal gland), which is found in certain rodent species. The types of tumours observed rarely occur spontaneously. Tumours of the mammary gland, tongue, small intestine and forestomach (oral exposure only) were less consistently seen.(1,69)
Human population studies carried out in the 1970's and 1980's suggested a possible increased risk of lung cancer among employees exposed to acrylonitrile. However, these studies were inconclusive because of one or more weaknesses in the study design. Consequently, larger and better studies were undertaken, in most cases building on the same employee groups that were studied initially. All the studies made some attempt to establish exposure levels and used different strategies for comparing exposed with unexposed. There was no significant risk for any type of cancer when all exposed employees were compared with unexposed employees, or with an external comparison population. Further, when employees were subdivided by levels of exposure, there was no increased risk for any site except lung. For lung cancer, employees with the highest exposures had increased risk (relative risk estimates greater than 1). This finding was strongest in the largest of the studies, but was not supported or only weakly supported by the other studies. The findings were not consistently significant and there was no dose-related response. Overall, the earlier indications of an increased risk of lung cancer among employees exposed to acrylonitrile are not confirmed by the recent, more informative studies. The International Agency for Research on Cancer (IARC) has determined that there is inadequate evidence for the carcinogenicity of acrylonitrile to humans. IARC has determined there is sufficient evidence for the carcinogenicity of acrylonitrile to experimental animals.(1)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is possibly carcinogenic to humans (Group 2B).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as a suspected human carcinogen (A2).

The US National Toxicology Program (NTP) has listed this chemical as reasonably anticipated to be a human carcinogen.

Teratogenicity and Embryotoxicity:
There is no human information available. Fetotoxicity, teratogenicity and embryotoxicity have been observed in the offspring of rats exposed by inhalation or ingestion, but only at doses that also produced significant maternal toxicity.

Reproductive Toxicity:
There is no human information available. There is insufficient animal information available to conclude that acrylonitrile is toxic to reproduction. In one study, reduced sperm count and testicular effects were observed in mice, but reproductive outcome was not assessed. Other reports lack sufficient information for evaluation.

Mutagenicity:
Numerous tests have been conducted, but it is not possible to conclude that acrylonitrile is mutagenic. There was no difference in the incidence of chromosomal aberrations in the peripheral lymphocytes between 18 employees with exposure to acrylonitrile for an average of 15.3 years compared to 18 employees who had not been exposed. Exposure was estimated at 5 ppm for 11 years and 1.5 ppm for 3 years, but that did not include higher exposures that would have occurred during manual operations or incidents.(11) Biological monitoring of 10 employees at an acrylic textile fiber manufacturing facility showed that urine from exposed employees was negative for gene mutagenic potential with bacteria. However, there were highly significant differences in results of chromosome aberration analysis among maintenance workers. This study is limited by inadequate reporting of exposure and cytogenetic data.(1,12) Studies with cultured human cells have shown positive results in some tests (DNA strand breakage, gene mutations, sister chromatid exchanges), but not tests for unscheduled DNA synthesis or chromosomal aberrations.(1) Negative results have consistently been obtained in studies using live animals with relevant routes of exposure (inhalation and ingestion), except in one study where the dose was quite high.

Toxicologically Synergistic Materials:
Exposure to acrylonitrile often occurs in combination with exposure to dimethylformamide in fiber manufacturing plants. Investigations at 0, 7 and 20 months following the introduction of a new fiber-extruding technology with exposure to both chemicals showed significant increases in mutagenicity (chromosome aberrations, sister chromatid exchanges, unscheduled DNA synthesis, chromatid breaks and acentric fragments). Current smoking increased the genotoxicity and results showed that exposed non-smokers had higher chromosome aberrations and sister chromatid exchanges than did smokers. Continuous exposure held more risk than occasional exposure to temporary peaks. Clinical symptoms and hospitalizations due to dimethylformamide exposure were evident during the study.(13)

Potential for Accumulation:
Acrylonitrile is absorbed into the body following ingestion, skin contact or inhalation.(2,14) It is metabolized along two primary pathways, which undergo further reactions leading to a wide range of metabolites in the urine. At least 10 metabolites have been identified in animal urine. Acrylonitrile can bind to proteins and other macromolecules such as lipids or nucleic acids, or it can be directly conjugated to glutathione to form cyanoethylmercapturic acid, which is excreted in the urine. In the other pathway, acrylonitrile is converted to 2-cyanoethylene oxide (CEO), which can react directly with tissue macromolecules, or it can be conjugated with glutathione to form glutathionyl-1- cyanoethanol, which forms hydroxyethylmercapturic acids, cyanide and other products including thiodiglycolic acid. Cyanide is converted to thiocyanate, which is excreted in the urine. CEO itself is also further metabolized to cyanoacetic acid, 2-cyanoethanol, cyanide, thiocyanate and carbon dioxide, which iseliminated through the lungs.(1,2,6) Most of the breakdown products of acrylonitrile are removed from the body in the urine within 24 hours.(6)

Health Comments:
Acrylonitrile possesses some of the characteristics of poisoning by the cyanide ion, although there is a relatively low rate of conversion of acrylonitrile to cyanide (approximately 20% following oral exposure).(14)


SECTION 4. FIRST AID MEASURES

Inhalation:
This chemical is very toxic, a possible carcinogen and flammable. Take proper precautions to ensure your own safety before attempting rescue (e.g. remove any sources of ignition, wear appropriate protective equipment, use the buddy system). Move victim to fresh air. If breathing is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor's advice. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Immediately transport victim to an emergency care facility. See First Aid Comments below for antidote information.

Skin Contact:
Avoid direct contact. Wear chemical protective clothing, if necessary. As quickly as possible, flush with lukewarm, gently running water for at least 20 minutes, or until the chemical is removed. Under running water, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). If irritation persists, repeat flushing. Quickly transport victim to an emergency care facility. Discard contaminated clothing, shoes and leather goods. See First Aid Comments below for antidote information.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 20 minutes, or until the chemical is removed, while holding the eyelid(s) open. Take care not to rinse contaminated water into the non-affected eye. Quickly transport victim to an emergency care facility. See First Aid Comments below for antidote information.

Ingestion:
NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz) of water to dilute material in stomach. If breathing is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor's advice. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Quickly transport victim to an emergency care facility. See First Aid Comments below for antidote information.

First Aid Comments:
ANTIDOTE: Cyanide toxicity can occur following exposure to acrylonitrile. Amyl nitrite, which can be used as a first aid measure, is antidotal to cyanide toxicity. Consult with a doctor familiar with cyanide toxicity to determine the appropriateness of using amyl nitrite as first aid measure in your workplace and to arrange training for first aiders who may be required to administer amyl nitrite.

Provide general supportive measures (comfort, warmth, rest).
Some recommendations in the above sections may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

Note to Physicians:
There are antidotes available for cyanide toxicity, which can occur following exposure to acrylonitrile. Specific information on antidotes, which can be used as first aid and therapeutically in a medical setting, is available in references 66 and 67.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
-4.4 to -1.1 deg C (24.1 to 30 deg F) (closed cup) (2,39,45); less than 9 deg C (48 deg F) (5% w/v) (45); 21.1 deg C (70 deg F) (2% solution) (39)

Lower Flammable (Explosive) Limit (LFL/LEL):
3.0-3.1% (39,42,43)

Upper Flammable (Explosive) Limit (UFL/UEL):
17.0% (39,42,43)

Autoignition (Ignition) Temperature:
481 deg C (898 deg F) (39,42,43)

Sensitivity to Mechanical Impact:
No reports found of explosions caused by mechanical impact.

Sensitivity to Static Charge:
No information is available on the electrical conductivity of acrylonitrile. Mixtures of acrylonitrile vapour and air at concentrations in the flammable range may be ignited by a static charge of sufficient energy. Minimum ignition energy: 0.16 millijoules.(47,48)

Combustion and Thermal Decomposition Products:
Nitrogen oxides, hydrogen cyanide, carbon monoxide and other irritant and toxic gases.(39,42,46)

Fire Hazard Summary:
Extremely flammable and dangerously reactive liquid. Material will readily ignite at room temperature. Acrylonitrile has a very low ignition energy. Hazardous polymerization may occur under fire conditions. Acrylonitrile vapours are uninhibited and may polymerize explosively in a fire and may form polymers in vents and flame arresters, resulting in blockage of vents and/or the rupture of closed containers. Vapour is heavier than air and can travel a considerable distance to a source of ignition and flash back to a leak or open container. During a fire, irritating and toxic gases, such as hydrogen cyanide and nitrogen oxides, may be generated. Vapour can accumulate in confined spaces posing a toxicity and flammability hazard. Closed containers may rupture violently and suddenly release large amounts of product when exposed to fire or excessive heat for a sufficient period of time. Water solutions of acrylonitrile may be flammable.

Extinguishing Media:
Carbon dioxide, dry chemical powder, "alcohol resistant" foam, water fog or spray. Water may be ineffective because it will not cool acrylonitrile below its flash point. Fire fighting foams are the extinguishing agent of choice for most flammable liquid fires.(39) Foam manufacturers should be consulted for recommendations regarding types of foams and application rates.

Fire Fighting Instructions:
Use extreme caution since explosive polymerization may occur under fire conditions and may rupture containers. Evacuate area and fight fire from a protected, explosion-resistant location or maximum possible distance. Approach fire from upwind to avoid hazardous vapours and very toxic decomposition products. Wear full protective suit if exposure is possible. See Protection of Firefighters.
Water can extinguish the fire if used under favourable conditions and when hose streams are applied by experienced firefighters trained in fighting all types of flammable liquid fires.(46)
If a fire occurs in the vicinity of acrylonitrile, use unmanned monitors and hoseholders to keep cooling streams of water on fire- exposed containers, cylinders, tanks or pipelines until well after the fire is out, in order to protect their contents from the danger of polymerization. This should begin as soon as possible and should concentrate on any unwetted portions of the container. Stay away from ends of tanks, but be aware that flying material from ruptured cylinders or tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire.
In an advanced or massive fire, the area should be evacuated; use unmanned or monitor nozzles. If this is not possible, withdraw from the fire area and do not attempt to fight the fire.
If a leak or spill has not ignited, use water spray in large quantities to disperse the vapours. Water spray can also be used to dilute spills to non-flammable mixtures and to flush spills away from ignition sources. Dike fire control water for appropriate disposal. Solid streams of water may be ineffective and spread material.
Tanks, drums or other containers should not be approached directly after they have been involved in a fire until they have completely cooled down.
After the fire has been extinguished, explosive and toxic atmospheres may remain. Before entering such an area especially confined areas, check the atmosphere with an appropriate monitoring device while wearing full protective gear.

Protection of Fire Fighters:
Acrylonitrile is very toxic by inhalation and skin absorption and can form extremely toxic and flammable hydrogen cyanide gas during a fire. Do not enter fire area without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical protective suit with positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 4 - Very short exposure could cause death or major residual injury.
NFPA - Flammability: 3 - Liquids and solids that can be ignited under almost all ambient temperature conditions.
NFPA - Instability: 2 - Undergoes violent chemical change at elevated temperatures and pressures, or reacts violently with water, or may form explosive mixtures with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 53.06

Conversion Factor:
1 ppm = 2.17 mg/m3; 1 mg/m3 = 0.46 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: -83.55 deg C (-118.4 deg F) (2,43,52)
Boiling Point: 77.3 deg C (171.14 deg F) (42,43,52,53)
Relative Density (Specific Gravity): 0.806 at 20 deg C (water = 1) (42,43,53)
Solubility in Water: Moderately soluble (7.3 g/100 mL at 20 deg C (42,43); 7.4 g/100 mL at 25 deg C (52))
Solubility in Other Liquids: Soluble in all proportions in a wide range of organic solvents, including acetone, ethanol, methanol, benzene, carbon tetrachloride, diethyl ether, ethyl acetate, petroleum ether, toluene, some kerosenes and xylene.(42,43,44)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 0.25 (44,52,54)
pH Value: 5.5-7.5 (5% solution) (2); 6.0-7.5 (5% solution) (42)
Viscosity-Dynamic: 0.35 mPa.s (0.35 centipoise) at 20 deg C (53); 0.34 mPa.S (0.34 centipoise) at 25 deg C (42,43,53)
Viscosity-Kinematic: 0.434 mm2/s (0.434 centistokes) at 20 deg C (calculated)
Saybolt Universal Viscosity: 27.0 Saybolt Universal Seconds at 37.8 deg C (100 deg F) (calculated)
Surface Tension: 27.22 mN/m (27.22 dynes/cm) at 20 deg C; 26.63 mN/m (26.63 dynes/cm) at 25 deg C (56)
Vapour Density: 1.83 (air = 1) (43)
Vapour Pressure: 11.5 kPa (86.25 mm Hg) at 20 deg C (42); 13.33 kPa (100 mm Hg) at 23.6 deg C (2,52); 14.47 kPa (108.5 mm Hg) at 25 deg C (52)
Saturation Vapour Concentration: 113500 ppm (11.35%) at 20 deg C; 142800 ppm (14.28%) at 25 deg C (calculated)
Evaporation Rate: 4.54 (n-butyl acetate = 1) (44)

Other Physical Properties:
DIELECTRIC CONSTANT: 33 at 20 deg C (53)


SECTION 10. STABILITY AND REACTIVITY

Stability:
Acrylonitrile is stable in the presence of an inhibitor, when kept at normal temperatures and away from light and polymerization initiators. It is unstable (polymerizes readily) when moderately heated and exposed to light (ultraviolet or sunlight), even if inhibited.(47) Water improves the stability of acrylonitrile.(2)

Hazardous Polymerization:
Acrylonitrile polymerizes violently, in the absence of an inhibitor and oxygen, if initiated by heat, light, pressure, peroxides, azo compounds, radicals, "Redox" catalysts or strong bases and acids. Polymerization can occur in the liquid, solid and vapour phases.(42) Pure, undiluted acrylonitrile is generally stabilized with trace levels of hydroquinone monomethyl ether and water. Even when inhibited, it will polymerize exothermically (with generation of heat), at or above 200 deg C.(45)

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


STRONG BASES (e.g. sodium hydroxide or potassium hydroxide) or AMINES - polymerizes violently, whether stabilized or unstabilized. Polymerization is violent and exothermic, especially when heated above 60 deg C, the pressure is above atmospheric, and when heating is longer than 10 minutes.(45)
STRONG ACIDS (e.g. nitric or sulfuric acids) - unless well-chilled, contact may lead to vigorous exothermic or violent reactions. Can initiate violent or explosive polymerization. Acid contamination of closed containers has caused explosion and rupture of containers.(45,46)
HALOGENS (e.g. bromine or chlorine) - may cause a runaway exothermic reaction and violent polymerization, possibly catalyzed by hydrogen halide.(45,46)
OXIDIZING AGENTS (e.g. nitrates or perchlorates) - may react violently. Increased risk of fire and explosion.(47)
FORMALDEHYDE (as paraformaldehyde or trioxane) - may cause a runaway, violent, exothermic reaction under strong acid catalysis and in the presence of trace quantities of acetic anhydride.(45)
COPPER and COPPER ALLOYS - acrylonitrile is reported to attack copper and its alloys, which in turn decompose acrylonitrile.(39,40,47)
SILVER NITRATE - acrylonitrile containing undissolved silver nitrate can, on long standing, polymerize explosively and ignite.(45)
POLYMERIZATION INITIATORS - polymerization can be initiated by azoisobutyronitrile, dibenzoyl peroxide or di-tert-butyl peroxide. Explosion may occur at high pressures.(45)

Hazardous Decomposition Products:
None reported

Conditions to Avoid:
Heat, sparks, open flames, other ignition sources, sunlight, low inhibitor concentration, contamination.

Corrosivity to Metals:
Undiluted acrylonitrile is not corrosive to copper and its alloys up to 93 deg C (57,58), whereas approximately 90% acrylonitrile in water is corrosive to copper and its alloys, and aluminum.(58) Pure, undiluted acrylonitrile is not corrosive to aluminum, Hastelloy, Inconel, Monel, type 304/347, 316, 400, 20 Cb 3 stainless steels, naval bronze, nickel and its alloys, tantalum, titanium or zirconium.(57,58)

Stability and Reactivity Comments:
Acrylonitrile attacks some plastics, such as CPVC, phenolic, polyesters, PVC, and vinyl ester, elastomers, such as butyl GR-1, Viton A, Nitrile Buna-N (NBR), polysulfides and silicone rubbers, and coal tar epoxy, epoxy, polyester and urethane coatings.(57)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (rat): 425 ppm (4-hour exposure) (15,16,17)

LD50 (oral, rat): 78 mg/kg (15,16-unconfirmed; original not in English)
LD50 (oral, rat): 81 mg/kg (18)
LD50 (oral, mouse): 27 mg/kg (15,16-unconfirmed; original not in English)

LD50 (dermal, male rat): 148 mg/kg (19)
LD50 (dermal, guinea pig): 202 mg/kg; cited as 0.25 mL/kg (20)

Eye Irritation:

Acrylonitrile is a moderate to severe eye irritant.

Application of 0.1 mL of undiluted acrylonitrile produced moderate irritation in rabbits (maximum score 35/110 at 24 hours). The irritation diminished slightly at 72 hours (score 22/110).(18) Application of 0.1 mL of undiluted acrylonitrile caused severe injury in rabbits (scored over 5 where 5 is severe injury; graded 4/10).(20) One hour after application of a single drop (0.05 mL), mild redness was observed in rabbits. No effects were evident after 24 hours.(21)

Skin Irritation:

Acrylonitrile is a severe skin irritant.

Application of 0.5 mL of undiluted acrylonitrile to intact or broken skin, under cover for 24 hours, produced severe injury in rabbits (scored 7.6/8). No significant difference was noted in the severity of irritation between the intact and abraded skin.(18) Application on a cotton pad for 15 minutes produced swelling of rabbit skin. A 20-hour exposure produced slight tissue death (necrosis).(1,2-unconfirmed; original not available in English)

Effects of Short-Term (Acute) Exposure:

Lethal inhalation or oral exposures with several different species have caused excitability and shallow, rapid breathing, changing to slow, gasping breathing followed by apnea and convulsions. Vomiting has occurred, particularly for cats, and marked reddening of the skin of the ears, nose and feet has been noted. Dogs appear to be significantly more susceptible than other species. Inhalation and oral exposure has caused tearing, nasal discharge and salivation. Oral exposure has caused incoordination and paralysis of hind limbs in rats.(1,5)

Inhalation:
Increased inhalation toxicity is observed with increasing concentration and/or duration of exposure. For example, high mortality was observed in rats following exposure to 320 ppm for 8 hours, 635 ppm for 4 hours, 1260 ppm for 2 hours or 2445 ppm for 1 hour.(5) Exposure of rats to 100 or 200 ppm for 4 hours has produced signs of mild kidney injury (altered urine chemistry and kidney changes).(22)

Ingestion:
Single oral exposure of rats to 20, 40 or 80 mg/kg has caused 2 phases of toxic symptoms. The initial response peaked within 0.5-1 hour with salivation, tearing of the eyes, abnormal contraction of the pupils, diarrhea, increased urination and dilation of blood vessels in the face, ears and extremities. The second phase produced central nervous system (CNS) effects including depression, convulsions and cyanosis starting 4 hours after administration.(23) Other studies have shown changes to red blood cells and hemoglobin in rats exposed to 80 mg/kg and gastrointestinal bleeding, which was shown not to be the result of direct irritating action, in rats exposed to 50 mg/kg.(24,25) In studies with rats, including doses that were lethal to some animals, there were only minimal effects on the liver. Rats were treated orally with 50, 75, 100, or 150 mg/kg for 1-3 days. Liver damage (tissue death) was observed at 150 mg/kg only, after 24 hours. Doses of 20, 100, or 500 ppm in drinking water for 21 days had no effect on the liver.(26)

Effects of Long-Term (Chronic) Exposure:

Acrylonitrile has caused harmful effects in the nervous systems of animals exposed by inhalation and ingestion to concentrations that are also capable of causing nervous system cancer. Inhalation of relatively low concentrations (20 ppm for 24 months) has also caused degeneration and inflammatory changes in the nasal cavities of rats.

Inhalation:
Male and female rats (100/group) were exposed by inhalation to 0, 20 or 80 ppm acrylonitrile for 24 months (6 hr/d; 5 d/wk). Mean body weights were significantly decreased in animals exposed to 80 ppm. More than 40 different organs and tissues were examined. Except for neoplastic findings, pathologic lesions showing dose-response relation to acrylonitrile exposure were observed only in the epithelium of the nasal mucosa. In animals inhaling 20 or 80 ppm, degeneration and inflammatory changes were observed in the respiratory epithelium of the nasal cavity. In male rats, the incidence of hyperplasia was slightly, but not significantly increased at 20 ppm, but was at 80 ppm. The incidence of hyperplasia of mucous secreting cells was significantly increased. In female rats, inflammatory findings in the mucosa and squamous transformation in the respiratory epithelium was significantly increased at 20 and 80 ppm. This study demonstrates that repeated exposure to 20 ppm causes chronic inflammation of the nasal mucosa in rats.(61, unconfirmed) Male rats (12/group) were exposed by inhalation to 25, 50 or 100 ppm for 24 weeks (6 hr/d; 5 d/wk). Mean body weights were significantly reduced in animals exposed to 100 ppm. Two rats in the high dose group died. None of the animals developed any weakness in the hindlimbs or disturbances in gait. Neurophysiological assessment of motor conduction velocity (MCV), sensory conduction velocity of the tail nerve (SCV), amplitudes of the sensory action potential (ASAP) and of the muscular action potential ((AMAP) were conducted. At 25 ppm, reductions in MCV were observed during the exposure period, but not with statistical significance until the 8-week follow-up; SCV was reduced at exposure week 24 and ASAP was reduced at week 16. At 50 ppm, MCV was reduced at week 24 of exposure and at the 8-week follow-up; SCV was significantly reduced at weeks 12 and 24 and ASAP was reduced at weeks 16, 20 and 24. At 100 ppm, significant MCV reductions were noted at weeks 16 and 24 of exposure; SCV was significantly reduced at weeks 12, 16, 20 and 24; and ASAP was reduced at weeks 16, 20, 24 and at the 8-week follow-up. In all cases, maximal deficits were observed at the last week of exposure.(29) Rats, guinea pigs, rabbits, cats and monkeys were exposed to 100 or 153 ppm for 8 weeks. Monkeys exposed to 153 ppm were more susceptible than other species. Rats, rabbits and guinea pigs tolerated the lower exposures with minimal effects. At 153 ppm, irritation of the eyes and nose, loss of appetite, gastrointestinal changes and reversible weakness of the hind limbs were observed. Autopsy showed kidney, spleen and liver changes (cats only).(27) Rats exposed by inhalation to 5, 10, 20 or 40 ppm for 52 weeks showed no changes in liver, kidneys or lungs.(28)

Skin Contact:
No conclusions can be drawn from a study in which 14 or 28 mg/kg for 2 months or 0.11, 0.56 or 2.8 mg/kg for 4.5 months was applied to the tails of rats.(19)

Ingestion:
Rats (48/sex/exposure group; 80/sex/control group) were exposed to 0, 35, 100 or 300 ppm acrylonitrile in their drinking water for up to 2 years. Interim necropsy was conducted on an additional 10 rats/sex/group at 1 year. Reported doses were 0, 3.4, 8.5 and 21.3 mg/kg/day for males and 0, 4.4, 10.8 and 25.0 mg/kg/day for females. Decreased water consumption, feed consumption and body weight suppression occurred within days of the study initiation and persisted throughout the study for all treatment groups. Non-tumorous and tumorous lesions were found at an increased and/or decreased rate in a number of tissues of both sexes at all treatment levels. The primary non-tumorous histopathologic effects occurred in the forestomach, with changes suggestive of chronic irritation occurring in a dose-related manner, and in the central nervous system, with gliosis in low and mid-dose females and in males, without statistical significance, but considered treatment related. The CNS lesions were interpreted to be a tumour precursor.(62) Male rats (12/group) were exposed orally to 12.5, 25 or 50 mg/kg acrylonitrile dissolved in olive oil for 12 weeks (5 d/wk). An olive oil control group was used. Mean body weights were significantly reduced in animals exposed to 25 or 50 mg/kg. At 50 mg/kg, one rat died and 5 rats developed weakness in the hindlimbs, which abated during the recovery period. Neurophysiological assessment of motor conduction velocity (MCV), sensory conduction velocity of the tail nerve (SCV), amplitudes of the sensory action potential (ASAP) and of the muscular action potential ((AMAP) were conducted. Significant deficits were observed for SCV from the 6th-12th week in animals exposed to 50 mg/kg. In the 8-week recovery period, the deficit in SCV persisted. Reductions in ASAP were observed throughout the study, but were not observed with statistical significance until the end of 8-week recovery period in animals exposed to 50 mg/kg.(29) Rats were exposed to 0, 100, 500 or 2000 ppm (approximately 8, 40, or 160 mg/kg/day) in drinking water or to an equivalent dose once daily by gavage for 7, 21 or 60 days. There was degeneration of the adrenal glands and levels of some steroids in the blood were reduced, with a greater effect noted with gavage dosing. Increased cell growth in the stomach and duodenum was noted.(30) In a 2-year study, rats were exposed to 0, 20 ppm (0.002%), 100 ppm (0.01%) or 500 ppm (0.05%) (approximately 2, 10, or 50 mg/kg/day) in drinking water. Increased mortality was noted at 500 ppm.(31) Rats exposed orally to 5 mg/kg 3 times per week for 52 weeks showed no changes in liver, kidneys or lungs.(28)

Skin Sensitization:
Positive results were obtained in the Guinea Pig Maximization Test (GPMT), using Freund's Complete Adjuvant. Challenge tests with 0.2%, 0.5% and 1% acrylonitrile (minimum purity 99.5%) in water produced positive results in 80%, 85% and 95% of the animals tested.(10,63)

Carcinogenicity:
The International Agency for Research on Cancer (IARC) has concluded that there is sufficient evidence for the carcinogenicity of acrylonitrile to experimental animals.(1)
Exposure-related tumours have been observed in rats in ingestion and inhalation studies involving very low concentrations in well-conducted studies. The most common forms of cancer occurred in the central nervous system and in a gland of the ear canal (zymbal gland), which is found in certain rodent species. The types of tumours observed rarely occur spontaneously. Tumours of the mammary gland, tongue, small intestine and forestomach (oral exposure only) were less consistently seen.(1,69)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
Fetotoxicity, teratogenicity and embryotoxicity have been observed in the offspring of rats, but only at doses that also produced significant maternal toxicity.
Rats were exposed orally in drinking water (0, 10, 25 or 65 mg/kg) or by inhalation (0, 40 or 80 ppm) from days 6-15 of pregnancy. At 10 mg/kg and 20 ppm, there was no embryotoxicity or teratogenicity observed. Teratogenic and embryotoxic effects were seen at higher doses that also produced maternal toxicity (e.g. decreased weight gain, increased excitability and excessive salivation).(32) Rats were exposed by inhalation to 0, 35, 25, 50 or 100 ppm on days 6-20 of pregnancy. At 25 ppm and higher, there was fetotoxicity (reduced body weight) with overt signs of maternal toxicity (depressed body weight gain). No significant teratogenicity was observed.(33) Rats exposed orally to 0 or 5 mg/kg on days 5-21 of pregnancy showed no significant effects in the offspring. Minor changes in neurological chemistry were noted. There were no effects on the mothers.(34)

Reproductive Toxicity:
There is insufficient information available to conclude that acrylonitrile is toxic to reproduction. In two studies, reduced sperm count and testicular effects were observed, but reproductive outcome was not assessed. Other reports lack sufficient information for evaluation.
Oral exposure of male mice to 0, 1 or 10 mg/kg, daily for 60 days, caused no overt signs of toxicity. Both doses caused reduced sperm counts, with statistical significance at 10 mg/kg. Also at 10 mg/kg, there were changes in the testes (degeneration of tubules) and in enzyme activity.(35) In another study reported in an abstract, male rats were exposed to 0, 11.5, 23 or 46 mg/kg for 2 and 4 weeks. A dose-dependant decrease in body and testis weight was observed. Sperm count and sperm motility were significantly decreased.(36) Reproductive outcome was not assessed in either study. Exposure of rats to 500 ppm led to decreased fertility and decreased viability of the young. Females developed progressive muscular weakness in the hind legs about 16-19 weeks after weaning of the second litter.(1,5 citing an unpublished report) There are no further details available for evaluation. In an unpublished 3-generation reproduction study, rats were exposed to 0, 106 or 522 ppm in drinking water. At 522 ppm (70 mg/kg/day), reduced viability and lactation were observed in all generations. These effects were attributed to decreased water intake of the mothers. There were no changes in reproductive capacity at 106 ppm.(6,37)

Mutagenicity:
Numerous mutagenicity tests have been conducted, but none clearly show conclusively that acrylonitrile is mutagenic.
In studies using live animals and routes of exposure relevant to human, test results have been negative (unscheduled DNA synthesis, chromosomal aberrations and dominant lethal effects), in all but one study.(1) In this study, unscheduled DNA synthesis was observed in the livers of rats orally dosed with 50 mg/kg. However, this dose is expected to have produced significant other toxicity in the animals.(38) Binding to proteins (DNA, RNA and nucleotides) has been demonstrated in live animals following single oral doses in rats. However, conclusions cannot be drawn due to weaknesses in the test protocol.(1)
In cultured mammalian cells, acrylonitrile has induced DNA strand breakage, gene mutation, sister chromatid exchanges and chromosomal aberrations, but not aneuploidy or unscheduled DNA synthesis. Positive results have been obtained in tests using bacteria, usually but not exclusively in the presence of metabolic activation. Positive and negative results have been obtained in tests using fungi.(1)
Positive (somatic cell mutation and aneuploidy) and negative (sex-linked recessive lethal mutations or genetic crossing over) have been obtained in fruit flies.(1)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
(1) International Agency for Research on Cancer (IARC). Acrylonitrile. In: IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 71, parts 1, 2 and 3. Re-evaluation of some organic chemicals, hydrazine and hydrogen peroxide. World Health Organization, 1999. p. 43-108
(2) International Programme on Chemical Safety (IPCS). Acrylonitrile. Environmental Health Criteria; 28. World Health Organization, 1983
(3) Wilson, R.H. Health hazards encountered in the manufacture of synthetic rubber. Journal of the American Medical Association. Vol. 124, no. 11 (1944). p. 701-703
(4) Wilson, R.H., et al. Medical problems encountered in the manufacture of American-made rubber. Industrial Medicine. Vol. 17, no. 6 (June 1948). p. 199-207
(5) Dudley, H.C., et al. Toxicology of acrylonitrile (vinyl cyanide). I. A study of acute toxicity. Journal of Industrial Hygiene and Toxicology. Vol. 24, no. 2 (Feb. 1942). p. 27-36
(6) Toxicological Profile for Acrylonitrile. TP-90-02. Agency for Toxic Substances and Disease Registry (ATSDR), Public Health Service, US Department of Health and Human Services, 1990
(7) Sakurai, H., et al. Health effects of acrylonitrile in acrylic fiber factories. British Journal of Industrial Medicine. Vol. 35, no. 3 (1978). p. 219-225
(8) Kaneko, K., et al. Effect of chronic exposure to acrylonitrile on subjective symptoms. Keio Journal of Medicine. Vol. 41, no. 1 (Mar. 1992). p. 25-32
(9) Muto T., et al. Health profiles of workers exposed to acrylonitrile. Keio Journal of Medicine. Vol. 41, no. 3 (1992). p. 154-160
(10) Bakker, J.G., et al. Occupational contact dermatitis due to acrylonitrile. Contact Dermatitis. Vol. 24, no. 1 (1991). p. 50-53
(11) Thiess, A.M., et al. Analysis of chromosomes of workers exposed to acrylonitrile. Archives of Toxicology. Vol. 41, no. 2 (1978). p. 149-152
(12) Borba, H., et al. Evaluation of some biomonitoring markers in occupationally exposed populations to acrylonitrile. Teratogenesis, Carcinogenesis, and Mutagenesis. Vol. 16, no. 4 (1996). Part I of II. p. 205- 218
(13) Major J., et al. Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers. Environmental and Molecular Mutagenesis. Vol. 31, no. 4 (1998). p. 301-310
(14) Hartung, R. Cyanides and nitriles: acrylonitrile. In Patty's industrial hygiene and toxicology. 4th ed. Edited by G.D. Clayton, et al. Vol. II. Toxicology. Part D. John Wiley and Sons, 1994. p. 3119-3124, 3137- 3139, 3168-3172
(15) RTECS database record for acrylonitrile. Last updated: 1999-12
(16) Willhite, C.C. Toxicology updates: acrylonitrile. Journal of Applied Toxicology. Vol. 2, no. 1 (1982). p. 54-56
(17) Jaeger, R.J., et al. Toxicity and biochemical changes in rats after inhalation exposure to 1,1-dichlorethylene, bromobenzene, styrene, acrylonitrile or 2-chlorobutadiene. Abstract. Toxicology and Applied Pharmacology. Vol. 29 (1974). p. 81
(18) Vernon, P.A., et al. Acute toxicological evaluation of acrylonitrile. Journal of the American College of Toxicology. Part B. Vol. 1 (1990). p. 114- 115
(19) Zotova, L.V. The toxic effect of acrylonitrile on the organism of experimental animals when administered through the skin . Gigiyena i Sanitariya. Vol. 10 (1976). p. 103-105. (English translation: OSHA-76-1310)
(20) Smyth, H.F., Jr., et al. Further experience with the range finding test in the industrial toxicology laboratory. Journal of Industrial Hygiene and Toxicology. Vol. 30, no. 1 (1948). p. 63-68
(21) McOmie, W.A. Comparative toxicity of methacrylonitrile and acrylonitrile. Journal of Industrial Hygiene and Toxicology. Vol. 31, no. 2 (Mar. 1949). p. 113-116
(22) Rouisse, L., et al. Acute nephrotoxic potential of acrylonitrile in Fischer-344 rats. Research Communications in Chemical Pathology and Pharmacology. Vol. 53, no. 3 (Sept. 1986). p. 347-360
(23) Ghanayem, B.I., et al. Assessment of the acute acrylonitrile-induced neurotoxicity in rats. Neurotoxicology and Teratology. Vol. 13, no. 5 (1991). p. 499-502
(24) Farooqui, M.Y.H., et al. The effects of acrylonitrile on hemoglobin and red cell metabolism. Journal Of Toxicology and Environmental Health. Vol. 12, no. 4 (1983). p. 695-707
(25) Ghanayem, B.I., et al. Acrylonitrile-induced gastrointestinal hemorrhage and the effects of metabolism modulation in rats. Toxicology and Applied Pharmacology. Vol. 68, no. 2 (1983). p. 290-296
(26) Silver, E.H., et al. Limited hepatotoxic potential of acrylonitrile in rats. Toxicology and Applied Pharmacology. Vol. 64, no. 1 (1982). p. 131-139
(27) Dudley, H.C., et al. Toxicology of acrylonitrile (vinyl cyanide). II. Studies of effects of daily inhalation. Journal of Industrial Hygiene and Toxicology. Vol. 24, no. 9 (Nov. 1942). p. 255-258
(28) Maltoni, C., et al. Carcinogenicity bioassays on rats of acrylonitrile administered by inhalation and by ingestion. La Medicina del Lavoro. Vol. 68, no. 6 (Nov.-Dec. 1977). p. 401-411
(29) Gagnaire, F., et al. Relative neurotoxicological properties of five unsaturated aliphatic nitriles in rats. Journal of Applied Toxicology. Vol. 18, no. 1 (1998). p. 25-31
(30) Szabo, S., et al. Subacute and chronic action of acrylonitrile on adrenals and gastrointestinal tract: biochemical, functional and ultrastructural studies in the rat. Journal of Applied Toxicology. Vol. 4, no. 3 (1984). p. 131-140
(31) Gallagher, G.T., et al. Neoplasms in rats ingesting acrylonitrile for two years. Journal of the American College of Toxicology. Vol. 7, no. 5 (1988). p. 603-615
(32) Murray, F.J., et al. Teratogenicity of acrylonitrile given to rats by gavage or by inhalation. Food and Cosmetics Toxicology. Vol. 16, (1978). p. 547-551
(33) Saillenfait, A.M., et al. Relative developmental toxicities of inhaled aliphatic mononitriles in rats. Fundamental and Applied Toxicology. Vol. 20, no. 3 (1993). p. 365-375
(34) Khanna, V.K., et al. Biochemical and developmental effects in rats following in utero exposure to acrylonitrile: a preliminary report. Industrial Health. Vol. 26, no. 4 (1988). p. 251-255
(35) Tandon, R., et al. Testicular effects of acrylonitrile in mice. Toxicology Letters. Vol. 42, no. 1 (1988). p. 55-63
(36) Abdel Naim, A.B., et al. Acrylonitrile (VCN)-induced testicular toxicity in the rat. (Abstract). Toxicologist. Vol. 14, no. 1 (1994). p. 87
(37) IRIS (Integrated Risk Information System) database record for acrylonitrile. (URL: www.epa.gov/ngispgm3/iris/subst/0206.htm.) Last revised: 1993-07-01
(38) Hogy, L.L., et al. In vivo interaction of acrylonitrile and 2- cyanoethylene oxide with DNA in rats. Cancer Research, Vol. 46, no. 8 (1986). p. 3932-3938
(39) Emergency action guide for acrylonitrile. Association of American Railroads, Jan. 1988
(40) Sigma-Aldrich Canada Ltd. (URL: http://www.sigma- aldrich.com/saws.nsf/Pages/Main?EditDocument - Password required)
(41) Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, 1989. p. 12, 44
(42) Brazdil, J.F. Acrylonitrile. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 1. John Wiley and Sons, 1991. p. 352-369
(43) Langvardt, P.W. Acrylonitrile. In: Ullmann's encyclopedia of industrial chemistry. 5th rev. ed. Vol. A 1. VCH Publishers, 1985. p. 177- 184
(44) HSDB record for acrylonitrile. Last revision date: 2000/03/13
(45) Urben, P.G., ed. Bretherick's reactive chemical hazards database (CD ROM). 6th ed. Version 3.0. Butterworth-Heinemann Ltd., 1999
(46) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325; NFPA 49; NFPA 491
(47) Acrylonitrile. In: Chemical safety sheets: working safely with hazardous chemicals. Kluwer Academic Publishers, 1991. p. 20
(48) Haase, H. Electrostatic hazards: their evaluation and control. Translated by M. Wald. Verlag Chemie, 1997. p. 108
(49) Acrylonitrile. In: NIOSH pocket guide to chemical hazards. National Institute for Occupational Safety and Health, June 1997
(50) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(51) blank
(52) CHEMFATE database. (URL: http://esc- plaza.syrres.com/efdb/Chemfate.htm)
(53) Dean, J.A. Lange's handbook of chemistry. 14th ed. McGraw-Hill, Inc., 1992. p. 1.80, 5.92, 6.134
(54) On-line LogP (octanol/water partition coefficient) database, including experimental data (Interactive LogKow (KowWin)) (URL: http://esc- plaza.syrres.com/interkow/kowdemo.htm)
(55) Daubert, T.E., et al. Data compilation tables of properties of pure compounds. American Institute of Chemical Engineers, 1985
(56) Jasper, J.J. Surface tension of pure liquid compounds. In: Compilation of data of some 2200 pure liquid compounds. Journal of Physical and Chemical Reference Data. Vol. 1, no. 4 (1972). p. 889
(57) Schweitzer, P.A. Corrosion resistance tables: metals, nonmetals, coatings, mortars, plastics, elastomers and linings, and fabrics. 4th ed. Part A, A-D. Marcel Dekker, Inc., 1995. p. 77-80
(58) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 4-10 to 5-10
(59) European Communities (EC). Commission Directive 2004/73/EC. Apr. 29, 2004
(60) Report on Carcinogens. 11th ed. US Department of Health and Human Services, Public Health Service, National Toxicology Program
(61) Sakurai, H. Carcinogenicity and other health effects of acrylonitrile with reference to occupational exposure limit. Industrial Health. Vol. 38, no. 2 (2000). p. 165-180
(62) Quast, J.F. Two-year toxicity and oncogenicity study with acrylonitrile incorporated in the drinking water of rats. Toxicology Letters. Vol. 132, no. 3 (June 2002). p. 153-196
(63) Koopmans, M.J.E., et al. Skin sensitization to acrylonitril in the Albino guinea pig (maximization-test). Unpublished report. Study 012972 of RCC NOTOX B.V. The Netherlands, by order of DSM Chemicals B.V. June 23, 1989
(64) Chu, C.-Y., et al. Allergic contact dermatitis from acrylonitrile. American Journal of Contact Dermatitis. Vol. 12, no. 2 (June 2001). p. 113-114
(65) Balda, B.-R. Allergic contact dermatitis due to acrylonitrile. Contact Dermatitis Newsletter (London). (1970). p. 219
(66) Beasley, D.M.G., et al. Cyanide poisoning: pathophysiology and treatment recommendations. Occupational Medicine. Vol. 48, no. 7 (1998). p. 427-431
(67) IPCS/CEC Evaluation of Antidotes Series. Vol. 2. Antidotes for poisoning by cyanide. Edited by T.J. Meredith, et al. Published by Cambridge University Press on behalf of the World Health Organization and of the Commission of European Communities. Cambridge University Press, 1993. Also available from the World Wide Web: <http://www.inchem.org/pages/antidote.html>
(68) European Chemical Industry Council (CEFIC). Acrylonitrile Sector Group. Guidelines for the distribution of acrylonitrile: revision 3. Jan. 2003. Available from World Wide Web: <http://www.petrochemistry.net/ftp/pressroom/Acryl2.pdf>
(69) Acrylonitrile. Priority Existing Chemical Assessment Report No. 10. Australia National Industrial Chemicals Notification and Assessment Scheme. Feb. 2000. Available on the World Wide Web at <http://www.nicnas.gov.au/publications/car/pec/pecindex.htm>
(70) Occupational Safety and Health Administration (OSHA). Acrylonitrile. In: OSHA Analytical Methods Manual. Revision Date: Oct. 31, 2001. Available at: <www.osha-slc.gov/dts/sltc/methods/toc.html>
(71) National Institute for Occupational Safety and Health (NIOSH). Acrylonitrile. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113. Aug. 1994. Available at: <www.cdc.gov/niosh/nmam/nmammenu.html>

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 2000-10-03

Revision Indicators:
ERPG 2001-03-01
EU classification 2002-02-01
EU risks 2002-02-01
EU safety 2002-02-01
EU comments 2002-02-01
Critical temperature 2002-02-18
Critical pressure 2002-02-18
Other physical properties 2002-02-18
US transport 2002-12-23
Personal hygiene 2003-05-26
Short-term skin contact 2003-07-07
Toxicological info 2003-07-07
Long-term exposure 2003-07-07
WHMIS detailed classification 2003-07-07
WHMIS health effects 2003-07-07
Emergency overview 2003-07-07
Protection of fire fighters 2003-07-07
First aid inhalation 2003-07-07
First aid skin 2003-07-07
First aid ingestion 2003-07-07
First aid comments 2003-07-07
Note to physicians 2003-07-07
Engineering controls 2003-07-07
Handling 2003-07-07
Storage 2003-07-07
Short-term inhalation 2003-07-08
Carcinogenicity 2003-07-08
Fire fighting instructions 2003-07-08
Disposal 2003-07-11
Resistance of materials for PPE 2004-04-08
EU classification 2005-01-05
EU comments 2005-01-05
Bibliography 2005-02-02
Bibliography 2005-03-30
Passive Sampling Devices 2005-03-30
Sampling/analysis 2005-03-30
PEL-TWA final 2006-05-17
PEL-STEL final 2006-05-17
PEL-C final 2006-05-17
PEL final comments 2006-05-17



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