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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 492
CCOHS Chemical Name: Acetonitrile

Synonyms:
ACN
Cyanomethane
Cyanure de méthyle
Ethanenitrile
Ethyl nitrile
Methanecarbonitrile
Methyl cyanide

Chemical Name French: Acétonitrile
CAS Registry Number: 75-05-8
UN/NA Number(s): 1648
RTECS Number(s): AL7700000
EU EINECS/ELINCS Number: 200-835-2
Chemical Family: Saturated aliphatic nitrile / saturated aliphatic cyanide / alkanonitrile / alkyl cyanide / acetic acid nitrile
Molecular Formula: C2-H3-N
Structural Formula: CH3-C#N (# = triple bond)

SECTION 2. DESCRIPTION

Appearance and Odour:
Volatile, colourless liquid with a sweet, ether-like odour.(2,10,53)

Odour Threshold:
Reported values vary widely; less than 40 ppm to 1161 ppm (detection).(8) Irritating concentration: 522 ppm (cited as 875 mg/m3).(58)

Warning Properties:
POOR - odour is detectable at concentrations greater than the TLV; irritation occurs at levels higher than the TLV. Olfactory fatigue can occur.

Composition/Purity:
Acetonitrile is readily available in several grades of purity.(59) It is also available in water solutions. Impurities present include propionitrile, allyl alcohol, unsaturated nitriles, such as acrylonitrile, aromatics and other heterocyclic compounds, some aldehydes and amines, and water.(53,59)

Uses and Occurrences:
Acetonitrile is widely used as an extractive distillation solvent in the petroleum industry for separating unsaturated hydrocarbons like butadiene; as a solvent for the extraction of fatty acids from fish, animal and vegetable oils; for removal of tars, phenols and colouring matter from petroleum hydrocarbons; as a solvent for polymers, spinning fibres, and casting and moulding plastics; as a solvent for the synthesis of DNA and peptide sequencing; in the purification of wool resin; in spectrophotometry, electrochemistry, and in high pressure liquid chromatography; for the extraction and refining of copper; in non-aqueous titrations; as a common laboratory solvent for crystallization of various chemicals like steroids; and as a non-aqueous solvent for inorganic salts. It is also used as the starting material for the synthesis of many chemicals like acetophenone and thiamine; as a medium for promoting reactions; as a catalyst and as a component in transition metal complexes catalysts; for dyeing textiles and in coating compositions; in the photographic industry; as a stabilizer for chlorinated solvents, particularly in the presence of aluminum; and in perfume manufacture.(2,53)
Acetonitrile may be formed by combustion of wood, straw and other vegetation. Small amounts can be found in coal tar. It is a by-product in the manufacture of acrylonitrile.(53)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Volatile, colourless liquid with a sweet, ether-like odour. FLAMMABLE LIQUID AND VAPOUR. Vapour burns with a luminous flame. Vapour is slightly heavier than air and may spread long distances. Distant ignition and flashback are possible. During a fire, extremely toxic and very flammable hydrogen cyanide and irritating and toxic nitrogen oxides may be generated. Closed containers may rupture violently if exposed to fire or excessive heat for a sufficient period of time. VERY TOXIC. May be fatal if inhaled, absorbed through the skin or swallowed. Early symptoms of toxicity may include anxiety and excitement, weakness, headache, nausea, vomiting, metallic taste, chest tightness, facial flushing, drowsiness, dizziness, rapid breathing, a rise in blood pressure and a decrease in pulse. More severe exposures can cause red skin colour, laboured breathing, convulsions, cardiovascular collapse, shock, fluid accumulation in the lungs and death. EYE IRRITANT. Causes severe eye irritation.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Acetonitrile very readily forms a high vapour concentration at room temperature and is very toxic if inhaled. It therefore poses a very serious inhalation hazard. The toxicity of acetonitrile is primarily due to the fact that it forms cyanide in the body.
The early symptoms of cyanide poisoning include anxiety and excitement, weakness, headache, nausea, vomiting, metallic taste, chest tightness, facial flushing, drowsiness, dizziness, irritation of the eyes, nose and throat, rapid breathing, a rise in blood pressure and a decrease in pulse. Laboured breathing, falling blood pressure, rapid, weak irregular heartbeat, unconsciousness, and convulsions follow these symptoms. In severe cases, cardiovascular collapse, shock, and fluid accumulation in the lungs (pulmonary edema) are followed by death.(29,30,44,45) With massive doses, many of the signs and symptoms may not be seen, and there is rapid onset of poisoning with convulsions, collapse, and death.(45) A characteristic sign of cyanide poisoning is the bright red colour of the blood, which may result in red skin colour.(44) For acetonitrile, appearance of these symptoms may be delayed for several hours after exposure.
There are many reports of cyanide poisoning from accidental, suicidal and homicidal exposure to hydrogen cyanide or its salts (most commonly potassium or sodium cyanide).
The majority of people who survive acute cyanide poisoning do not have long-lasting effects. However, depending on the degree of exposure, there may be enduring effects from low oxygen, including impaired memory and mathematical abilities, personality changes, and altered control and coordination of movement.(46)
There are several case reports of workers accidentally exposed to acetonitrile, with symptoms of cyanide poisoning developing several hours after exposure. Two men died.(23,24,25,47) In one case, a 35-year old male worker recovered following treatment for cyanide poisoning, but developed swollen and tender muscles with muscle wasting and kidney failure, which lasted for more than 3 months.(47)
Three male volunteers were exposed to 40 ppm acetonitrile for 4 hours. One man experienced a slight tightness in the chest that evening and a "cooling" sensation in the lungs the following morning, lasting for about 24 hours. The other 2 men reported no adverse effects. These 2 men were later exposed to 80 and 160 ppm for 4 hours. At 160 ppm, one man reported slight, temporary flushing of the face 2 hours after exposure and a slight feeling of tightness in the chest after 5 hours.(15)

Skin Contact:
Acetonitrile is toxic if absorbed through the skin, based on animal information. Skin contact with the liquid or vapour can cause symptoms similar to those described under "Inhalation" above. Any skin contact will also involve significant inhalation exposure.
Acetonitrile is not a skin irritant, based on animal information. There is no human information available.

Eye Contact:
Acetonitrile is a very severe eye irritant, based on animal information. Permanent eye injury could result. There is no human information available.

Ingestion:
Acetonitrile is toxic if ingested, based on animal information. Its primary toxicity is due to the fact that it forms cyanide in the body. Symptoms of cyanide poisoning are described under "Inhalation" above. A few cases of Parkinsonism (a syndrome characterized by decreased mobility, muscular rigidity, and tremor) have been reported in survivors of acute oral cyanide poisoning. All case reports involved non-occupational exposure to high doses (where specified) of potassium or sodium cyanide.
Attempted suicides and accidental poisonings with acetonitrile have been reported in the literature. The individuals involved generally show delayed symptoms of cyanide poisoning.(48,49,50,51) Ingestion is not a typical route for occupational exposure.

Effects of Long-Term (Chronic) Exposure

There is no specific information available for acetonitrile. The short-term toxicity of acetonitrile is primarily caused by the fact that acetonitrile forms cyanide in the body.
Several human population studies have evaluated the potential health effects of long-term exposure to cyanide compounds. In general, these studies are limited by factors such as the small number of employees evaluated and the possibility of concurrent exposure to other potentially harmful chemicals (particularly in the electroplating industry). In addition, few studies report reliable measurements of cyanide exposures and even when airborne concentrations are reported, exposure may also have occurred by skin absorption. Despite these limitations, the available evidence suggests that long-term occupational cyanide exposure may be associated with harmful effects on the thyroid gland and the nervous system. Less consistently, there have been reports of effects on the respiratory and gastrointestinal systems, blood chemistry and the skin and eyes.
For more information on the available studies, refer to the CHEMINFO reviews of hydrogen cyanide, sodium cyanide and potassium cyanide.

Nervous System:
Limited information suggests that long-term exposure to cyanide compounds s may be associated with harmful effects on the nervous system. Some of the symptoms observed are non-specific (e.g. headaches) and could be associated with many causes. Nevertheless, there does seem to be an association between some nervous system symptoms and cyanide exposure. The types of nervous system symptoms observed in the available studies include: headaches, dizziness, weakness, and nervous instability.

Endocrine System:
Evidence from human and animal studies indicates that long-term exposure to cyanide compounds can result in impaired thyroid function and enlargement of the thyroid (goiter). Thiocyanate, the main metabolite of cyanide, is believed to cause these effects by inhibiting the uptake of iodine by the thyroid.

Carcinogenicity:

There is insufficient information available to conclude that acetonitrile is carcinogenic.
No conclusions can be drawn from a limited case-control study that investigated respiratory cancers in workers exposed to several chemicals while employed in a chemical company between 1943 and 1980. Forty-one respiratory cancer cases were identified. Matched controls (4/case) were selected from a group of employees who had ever worked at the same plant. Chemical exposures were classified as no contact, incidental contact and routine contact. A significantly elevated relative risk (8.2) was observed for workers with incidental contact to acetonitrile for 5 years or more. There were no significant differences for workers with routine contact with acetonitrile. When additional analysis of the data was done, the observed association was based on relatively recent employee exposures. In this case, there would not have been a long enough latency period for the acetonitrile exposure to cause the respiratory cancer. Virtually all respiratory cancer cases had a history of smoking. Smoking was also common among controls.(52) This study is limited by factors such as the small numbers of employees studied and concurrent exposures to other chemicals.
In a well-conducted animal study, inconclusive results were obtained for male rats that developed a non-significant increased in liver cancer. There was no evidence of carcinogenic activity in female rats or in male or female mice.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not classifiable as a human carcinogen (A4).

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
The available human and animal information suggests that acetonitrile does not cause developmental effects in the absence of significant maternal toxicity.
It is not possible to draw firm conclusions from a case-control study that did not show a strong association between acetonitrile exposure and the miscarriage rate in a group of Finnish women employed in laboratories.(56) While this study did not show an association, it is limited by the small number of cases (7 cases involved exposure to acetonitrile) and other factors, such as self-reporting biases and concurrent exposure to other chemicals.
Several well-conducted animal studies demonstrate that acetonitrile does not cause developmental toxicity at doses below those causing significant maternal toxicity.

Reproductive Toxicity:
There is no human information available. No reproductive effects (fertility cycle in females; testicular weight or sperm motility in males) were observed in rats and mice exposed by inhalation to acetonitrile for 13 weeks.

Mutagenicity:
There is no human information available. It is not possible to conclude that acetonitrile is mutagenic, based on the available animal evidence. A small, but significant, positive result was obtained for male mice exposed by inhalation to acetonitrile for 13 weeks. Negative results were obtained for females. Other tests using live animals did not use relevant routes of exposure. Short-term tests with mammalian cells have given both negative and positive results, and negative results have been obtained for point mutations in yeast and bacteria. Positive results have been obtained for aneuploidy in yeast and Drosophila (fruit flies).

Toxicologically Synergistic Materials:
In a case of suicide, a 22-year old female who ingested both acetonitrile and acetone did not show symptoms of cyanide toxicity for 24 hours. The concurrent exposure to acetone is believed to have delayed the metabolism of acetonitrile to cyanide.(51) Studies in animals have shown that acetone, acetophenone and dioxane potentiate the toxic effects of acetonitrile. A study with mice indicates that carbon tetrachloride decreases the toxicity of acetonitrile.

Potential for Accumulation:
Does not accumulate. Elimination occurs mainly through excretion in the urine as the unchanged compound, as free cyanide and as thiocyanate.(10)

Health Comments:
The toxicity of acetonitrile is due primarily to its delayed metabolism to cyanide. The cyanide ion binds with iron ions in the enzyme cytochrome oxidase, which prevents body cells from using oxygen. Thus, cyanide impairs the body's ability to use oxygen and the primary target organs for acute cyanide poisoning are the central nervous system and the heart.(27,28) Cyanides also inhibit other enzyme systems, especially those containing iron or copper, which contributes to the symptoms observed.(27,29,30)


SECTION 4. FIRST AID MEASURES

Inhalation:
This chemical is very toxic and flammable. Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the buddy system, remove any sources of ignition). Remove source of contamination or 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. Remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). As quickly as possible, flush with lukewarm, gently flowing water for at least 20 minutes or until the chemical is removed. Quickly transport victim to an emergency care facility. Discard contaminated clothing, shoes and leather goods. NOTE: This chemical is toxic by skin absorption. Any skin contact will also involve significant inhalation exposure. See "inhalation" for general procedures. 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 unaffected eye or onto the face. If irritation persists, repeat flushing. Quickly transport victim to an emergency care facility.

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:
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.

ANTIDOTE: Cyanide toxicity can occur following exposure to adiponitrile. 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.

NOTE: The onset of acetonitrile toxicity can be delayed several hours following exposure. Seek medical attention following any contact.

Note to Physicians:
There are antidotes available for cyanide toxicity, which can occur following exposure to adiponitrile. Specific information on antidotes which can be used as first aid and therapeutically in a medical setting is available in references 29 and 57.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
2.0 deg C (35.6 deg F) (closed cup) (62); also reported as 6 deg C (42.8 deg F) (open cup) (1)

Lower Flammable (Explosive) Limit (LFL/LEL):
3.0% (1); 4.4% (1,2,53)

Upper Flammable (Explosive) Limit (UFL/UEL):
16.0% (1,53); 17.0% (53)

Autoignition (Ignition) Temperature:
524 deg C (975 deg F) (1,53)

Sensitivity to Mechanical Impact:
Probably not sensitive. Stable material.

Sensitivity to Static Charge:
Acetonitrile has a very high electrical conductivity and will not accumulate static charge.(61) Mixtures of acetonitrile vapour and air at concentrations in the flammable range can be ignited by a static discharge of sufficient energy.

Electrical Conductivity:
7 X 10(8) pS/m at 20 deg C (61)

Minimum Ignition Energy:
Not available

Combustion and Thermal Decomposition Products:
Nitrogen oxides, hydrogen cyanide, carbon monoxide, carbon dioxide and other irritating and toxic fumes may be formed in a fire.(1,62) When heated to decomposition, acetonitrile emits very flammable and extremely toxic hydrogen cyanide and irritating and toxic nitrogen oxides.(62)

Fire Hazard Summary:
FLAMMABLE LIQUID AND VAPOUR. Can release vapours that form explosive mixtures with air at, or above, 2.0 deg C. Vapour burns with a luminous flame. Vapour is slightly heavier than air and may travel a considerable distance to a source of ignition and flash back to a leak or open container. During a fire, extremely toxic and very flammable hydrogen cyanide and irritating and toxic nitrogen oxides may be generated. Vapour can accumulate in confined spaces and low-lying areas resulting in 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.

Extinguishing Media:
Carbon dioxide, dry chemical powder or appropriate foam.(1,62) Water may be effective for cooling, but may not be effective for extinguishing a fire because it may not cool acetonitrile below its flash point.(62) Fire fighting foams, such as multipurpose alcohol-resistant foams, are recommended for most flammable liquid fires. Foam manufacturers should be consulted for recommendations regarding types of foams and application rates.

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance. Approach fire from upwind to avoid hazardous vapours and very toxic decomposition products, such as hydrogen cyanide. Wear full protective gear if exposure is possible. See Protection of Firefighters.
Stop leak before attempting to stop the fire. If the leak cannot be stopped, and if there is no risk to the surrounding area, let the fire burn itself out. If the flames are extinguished without stopping the leak, vapours could form explosive mixtures with air and reignite. 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.
Closed containers may rupture violently when exposed to the heat of fire and suddenly release large amounts of products. Always stay away from ends of tanks, but be aware that flying material (shrapnel) from ruptured tanks may travel in any direction. If possible, isolate materials not yet involved in the fire and move containers from fire area if this can be done without risk. Protect personnel. Otherwise, cool fire-exposed containers, tanks or equipment by applying hose streams. Cooling should begin as soon as possible (within several minutes) and should concentrate on any unwetted portions of the container. Apply water from the side and a safe distance. Cooling should continue until well after the fire is out. If this is not possible, use unmanned monitor nozzles and immediately evacuate the area.
If a leak or spill has not ignited, use water spray in large quantities to disperse the vapours and to protect personnel attempting to stop the leak. Water spray can be used to flush spills away from ignition sources and to dilute spills to non-flammable mixtures. Dike fire control water for appropriate disposal. Solid streams of water may be ineffective and spread material.
For an advanced or massive fire in a large area, use unmanned hose holders or monitor nozzles; if this is not possible withdraw from fire area and allow fire to burn. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank.
After the fire has been extinguished, 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:
Acetonitrile can form extremely toxic and flammable hydrogen cyanide during a fire. Do not enter 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: 2 - Intense or continued (but not chronic) exposure could cause temporary incapacitation or possible residual injury.
NFPA - Flammability: 3 - Liquids and solids that can be ignited under almost all ambient temperature conditions.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 41.05

Conversion Factor:
1 ppm = 1.68 mg/m3; 1 mg/m3 = 0.595 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: -45.7 deg C (-50.3 deg F) (2,53); also reported as -43.8 deg C (-46.8 deg F) (59,63)
Boiling Point: 81.6 deg C (179 deg F) (2,60,63)
Relative Density (Specific Gravity): 0.786 at 20 deg C (2,63); 0.776 at 25 deg C (59) (water = 1)
Solubility in Water: Soluble in all proportions.(63,64)
Solubility in Other Liquids: Soluble in all proportions in ethanol, methanol, diethyl ether, acetone, ethyl acetate, methyl acetate, chloroform, carbon tetrachloride, ethylene chloride and many unsaturated hydrocarbons.(10,60,64) Immiscible with many saturated hydrocarbons (petroleum fractions).(10,60)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -0.34 (65)
pH Value: Probably near neutral. Nitriles are very weak acids.
Dissociation Constant: pKa = 25 (76)
Viscosity-Dynamic: 0.35 mPa.s (0.35 centipoises) at 20 deg C (2); 0.34 mPa.s (0.34 centipoises) at 25 deg C (59)
Surface Tension: 29.29 mN/m (29.29 dynes/cm) at 20 deg C (59,66); 28.66 mN/m (28.66 dynes/cm) at 25 deg C (66)
Vapour Density: 1.42 (air = 1) (calculated)
Vapour Pressure: 9.87 kPa (74 mm Hg) at 20 deg C (67); 11.84 kPa (88.8 mm Hg) at 25 deg C (59,68)
Saturation Vapour Concentration: 97400 ppm (9.74%) at 20 deg C; 116900 ppm (11.69%) at 25 deg C (calculated)
Evaporation Rate: 5.79 (n-butyl acetate = 1) (2)
Henry's Law Constant: 3.49 Pa.m3/mol (cited as 3.45 X 10(-5) atm.m3/mol) at 25 deg C (68); log H = -2.85 (dimensionless constant; calculated)

SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable.(69)

Hazardous Polymerization:
Does not occur.

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 OXIDIZING AGENTS (e.g. hypochlorites, nitrates, peroxides, perchlorates (e.g. lanthanide perchlorate or iron(III) perchlorate), or dinitrogen tetraoxide ) - react violently. Risk of fire and explosion.(69,70)
STRONG ACIDS (e.g. hydrochloric acid, chlorosulfonic acid, sulfuric acid or oleum) - may react vigorously or violently to form acetic acid, ammonia and hydrogen cyanide. The reaction may be violent with increased temperature and pressure.(53,70,71) For example, a mixture of acetonitrile and sulfuric acid, on heating, underwent an uncontrollable reaction to 160 deg C. The presence of 28 mol% of sulfur trioxide reduces the initiation temperature to about 15 deg C.(69) Fuming nitric acid, perchloric acid, and lanthanide perchlorate form potentially explosive mixtures.(6,69)
DIPHENYL SULFOXIDE, TRICHLOROSILANE - may explode.(69)
FUMING NITRIC ACID, PERCHLORIC ACID, N-FLUORO COMPOUNDS (e.g. tetrafluorourea) or NITRATING AGENTS (e.g. 2-cyano-2-propyl nitrate) - form potentially explosive mixtures.(6,69)
STRONG BASES (e.g. sodium and potassium hydroxide) - can vigorously hydrolyze acetonitrile to acetic acid and ammonia in the presence of water.(70,71)
REDUCING AGENTS (e.g. metal hydrides, such as lithium aluminum hydride or borane, or tin chloride) - can react violently.(62)

Hazardous Decomposition Products:
Acetic acid and ammonia are formed very slowly on reaction with water, but not in hazardous amounts.

Conditions to Avoid:
Open flames, sparks, electrostatic discharge, heat, hot surfaces and other ignition sources.

Corrosivity to Metals:
Acetonitrile is not corrosive to the common metals, such as carbon steel (types 1010 and 1020), cast iron (unspecified), stainless steel (such as 300 series, 400 series, 17-4PH, and Carpenter 20Cb-3), aluminum (type 3003), nickel-base alloys, such as Incolloy, and tantalum.(72,73)

Corrosivity to Non-Metals:
Acetonitrile attacks plastics, such as acrylonitrile-butadiene-styrene (ABS), chlorinated polyvinyl chloride (CPVC), polyesters, polystyrene, polysulfone and vinyl ester; elastomers, such as nitrile-Buna-N (NBR), Viton A (FKM), and flexible polyvinyl chloride (PVC). It does not attack plastics, such as nylon, Teflon and other fluorocarbons, and polypropylene; elastomers, such as butyl rubber (isobutene isoprene), chloroprene, ethylene-propylene-diene, fluorocarbons, such as Chemraz and Kalrez and isoprene.(73,74,75)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (mouse): 1347 ppm (4-hour exposure); cited as 2693 ppm (1-hour exposure) (13)
LC50 (male rabbit): 2828 ppm (4-hour exposure) (15)
LC50 (mouse): 3587 ppm (4-hour exposure) (4)
LC50 (guinea pig): 5655 ppm (4-hour exposure) (15)

LD50 (oral, mouse): 269 mg/kg (cited as 6.550 mMol/kg) (14)
LD50 (oral, mouse): 617 mg/kg (4)
LD50 (oral, 14-day old rat): 157 mg/kg (cited as 0.2 mL/kg) (17)
LD50 (oral, young adult rat): 3060 mg/kg (cited as 3.9 mL/kg) (17)
LD50 (oral, adult rat): 3460 mg/kg (cited as 4.4 mL/kg) (17)
LD50 (oral, male guinea pig): 139 mg/kg (cited as 0.177 mL/kg) (15)
Note: There is a considerable variation in toxicity between species, and the toxicity is higher in younger (14-day old) rats than in older rats.

LD50 (dermal, male rabbit): 980 mg/kg (cited as 1.25 mL/kg) (15)
LD50 (dermal, rabbit): greater than 2000 mg/kg (4)

Eye Irritation:

Acetonitrile is a very severe eye irritant and is capable of producing irreversible eye injury.

Application of 0.1 mL undiluted acetonitrile caused a marked opacity of more than half the cornea, and severe reddening, swelling and discharge within 24 hours in rabbits. After 21 days, there were still mild effects on the cornea and mild to moderate irritation in some animals. The maximum average irritation score was 46/110 at 24 hours.(4) Application of 0.02 mL of undiluted acetonitrile caused severe injury (scored over 5 where 5 is severe injury; graded 5/10).(12)

Skin Irritation:

Acetonitrile is not irritating to the skin.

Application of 0.5 mL of undiluted acetonitrile, under a semi-occlusive patch for 4 hours, caused no irritation in rabbits (irritation score 0.0/8 according to Draize scale).(4)

Effects of Short-Term (Acute) Exposure:

The toxic effects of acetonitrile are primarily due to the formation of cyanide in the body. However, cyanide is formed more slowly from acetonitrile than for other nitriles, allowing more efficient detoxification and lower toxicity.(9,10) Cyanide toxicity is primarily caused by the cyanide ion binding with iron ions in the enzyme cytochrome oxidase, thereby preventing cells from using oxygen. The primary target organs for acute cyanide poisoning are the central nervous system (CNS) and the heart, because they are the most sensitive to oxygen deprivation.(27,28) Cyanide also inhibits other enzyme systems, especially those containing iron or copper, which contributes to the symptoms observed.(28,29,30)

Inhalation:
Rats exposed to 2800 ppm for 5 days (2 hrs/d) experienced difficulty breathing, reduced urination, diarrhea and paralysis of the extremities. One death was observed.(16) Female mice were exposed to 0, 100, 200 or 400 ppm over 14 days (6 hr/d; 5 d/wk) and studied for effects on the immune system. No significant signs of toxicity or decreases in body weight were noted. Atrophy of the thymus was noted at 200 and 400 ppm. Concentration-related effects were noted in many blood parameters, including hematocrit, hemoglobin, and red and white blood cell count, with most reaching significance at 200 ppm. A significant concentration-related decrease in immunoglobulin (IgG) levels was seen at all concentrations. No significant differences were noted with other immunity assays, however trends indicated some immune suppression.(11) Rats were exposed daily to 0, 620, 1850 and 6240 ppm (cited as 0, 1038, 3104 or 10485 mg/m3) acetonitrile for 1 month (6-hr/d; 5-d/wk). Irritation to the eyes and/or nose, decreases in body weight, mild anemia, respiratory difficulties, various nervous system effects and death were observed at 1850 and/or 6240 ppm. No effects were noted at 620 ppm.(54, unconfirmed) This study is reported by abstract and there are no further details available.

Ingestion:
Male rats given a single dose of 2460 mg/kg developed signs of toxicity similar to those produced by hydrogen cyanide, i.e. central nervous system depression, convulsion and respiratory failure. This study indicates that the toxicity of acetonitrile is due primarily to the liberation of the cyanide ion. Substantial concentrations of cyanide were found in the liver, kidneys and brain.(55) Male rats given acetonitrile in their drinking water at concentrations of 40 or 80 mMolar (reported doses 60 and 114 mg/kg/day) for up to 4 weeks developed a dose-related decrease in body weight, but no signs of nervous system damage.(22)

Effects of Long-Term (Chronic) Exposure:

Inhalation:
Rats were exposed to 0, 100, 200, 400, 800 or 1600 ppm for 13 weeks (6 hrs/d; 5 d/wk). At 1600 ppm, 6/10 males and 3/10 females died, body weight gain and thymus weight were decreased, liver, kidney and heart weights were increased in females, the thyroid hormone T3 (triiodothyronine) was decreased in females and there was evidence of anemia in both sexes. At 800 ppm, 1/10 males died and decreased thymus weights and anemia were observed in females. Mice were similarly exposed to the same concentrations. All animals exposed to 1600 ppm died. At 800 ppm, 1/10 males and 4/10 females died. At 400 ppm, 1/10 females died. Body weights of all groups of treated males were slightly less than controls, with significance at 800 ppm. Relative liver weights were increased at 100 ppm and higher in males, and 400 ppm and higher for females. Lesions in the stomach were observed at 200 ppm and higher for females and 400 ppm and higher for males.(10) Rats were exposed to 0, 100, 200 or 400 ppm and mice were exposed to 0, 50, 100 or 200 ppm for 2 years (6 hrs/d; 5 d/wk). There were no treatment effects on body weight, organ weights, blood chemistry, behaviour or general health in either species. Detailed tissue examination in male rats showed signs of liver injury at 200 and 400 ppm. In mice, there was a dose-related thickening of the lining of the forestomach, which was significant at 100 ppm in females and at 200 ppm in males.(10) Rats were exposed to 0, 166, 330 or 655 ppm for 90 days (7 hrs/d; 5 d/wk). No effects were noted on body or organ weights and there were no treatment-related deaths. At 655 ppm, statistically significant inflammation and/or swelling in the lower respiratory tract and swelling in the kidneys and liver were noted.(15)

Skin Sensitization:
Negative results were obtained in guinea pigs in study using the Buehler test.(4)

Carcinogenicity:
Rats were exposed to 0, 100, 200 or 400 ppm and mice were exposed to 0, 50, 100 or 200 ppm for 2 years (6 hrs/d; 5 d/wk). A non-significant increase in carcinogenic effects in the liver (hepatocellular carcinomas and adenomas) was observed in male rats exposed to 400 ppm. It was concluded that, under the conditions of this study, there was equivocal evidence of carcinogenic activity of acetonitrile in male rats. There was no evidence of carcinogenic activity in female rats or in male or female mice.(10)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
Acetonitrile is not toxic to the offspring at doses below those causing maternal toxicity. There are several well-conducted studies that support this conclusion.
Rats were exposed by inhalation to 0, 100, 400, or 1200 ppm acetonitrile from days 6-19 of pregnancy (6-hrs/d; 7-d/wk). At 1200 ppm, 2/33 mothers died and at 400 ppm, 1/33 mothers died. The only effect observed in the offspring was a slight, exposure-related, increase in the incidence of extra ribs.(31) This effect is considered to have low biological significance. Rats were exposed orally to 0, 50, 150, 300 or 500 mg/kg/day from days 7-21 of pregnancy. At 300 and 500 mg/kg/day, 12/22 and 16/20 mothers died. No significant effects were noted for pregnancy rates, fetal weight, live pups/litter, resorptions, or postnatal survival of pups to day 4.(32) Rats were exposed by inhalation to 0, 900, 1200, 1500 or 1800 ppm from days 6-20 of pregnancy (6-hrs/d). At 1800 ppm, 8/20 mothers died. At 1500 ppm, there was a significant decrease in body weight gain (corrected for uterine weight). There was a significant increase in embryotoxicity (a significant increase in the mean percentage of non-surviving implants and early embryonic resorptions) at 1800 ppm, but no significant reductions in fetal weight or other developmental effects.(33) Rabbits were dosed orally with 0, 2, 15 and 30 mg/kg/day from days 6-18 of pregnancy. Maternal weight gain was significantly decreased at 15 and 30 mg/kg/day. Other maternal effects observed at 30 mg/kg/day included deaths (5/25 animals), incoordination, decreased motor activity, laboured breathing and impaired righting reflex. At 30 mg/kg/day, there was a significant decrease in the average number of live fetuses and in the incidence of an extra ossification site in the parietal bones. No significant fetal effects were noted at lower doses.(34) Rats were orally exposed to 0, 125, 190 or 275 mg/kg/day to acetonitrile on days 6-19 of pregnancy. At 275 mg/kg/day, 2/25 mothers died and there was a non-statistically significant increase in embryotoxicity (post-implantation loss) and a slight, non-significant increase in incomplete skeletal ossification. At 190 mg/kg/day and lower, no maternal or developmental toxicity was noted.(20) No conclusions can be drawn from other studies (21,35) that are limited by the small number of animals used and/or the fact that only a single dose was administered.

Reproductive Toxicity:
Rats and mice exposed by inhalation to 0, 100, 200 or 400 ppm for 13 weeks had no effects on the reproductive cycle in females or on testicular weight or sperm motility in males.(36) No other reproductive toxicity studies were located.

Mutagenicity:
It is not possible to conclude that acetonitrile is mutagenic, based on the available information. Both weak positive and negative results have been obtained for in vivo micronucleus tests in mice. In vitro tests using mammalian cells have given both negative and positive results and negative results have been obtained for point mutations in yeast and bacteria. Positive results have been obtained for aneuploidy in yeast and Drosophila (fruit flies).
A small, but significant, increase in micronuclei was observed in peripheral blood of male mice, but not in female mice, exposed by inhalation to 400 ppm for 13 weeks (6-hr/d; 5-d/wk).(10) A negative result was obtained in a micronucleus test in bone marrow and peripheral blood in mice receiving intraperitoneal doses of 100 or 125 mg/kg.(37) In a similar study, mice received intraperitoneal doses reported as 40 and 60% of the LD50 (probably 70 and 105 mg/kg). Results were a small, but significant, increase in the formation of micronuclei in bone marrow cells after 24 hours, at the higher dose.(38) Intraperitoneal injection is not considered a relevant route of exposure for assessing occupational effects.
A negative result (sister chromatid exchange) was obtained in mammalian cells with activation, and a weak positive result without activation. A small increase in chromosome aberrations was obtained in mammalian cells with activation, and a negative result without activation.(10,26) Negative results (gene mutation) were obtained in yeast and bacteria, with and without metabolic activation.(10,19,38) A positive result (aneuploidy) was obtained in yeast.(19,39)
A positive result (aneuploidy) was obtained in Drosophila (fruit flies).(40,41)

Toxicological Synergisms:
In two studies, orally administered acetone increased the toxicity of orally administered acetonitrile in rats.(42,43) The same result was obtained following inhalation exposure to these chemicals.(43) The oral LD50s of acetonitrile mixed equally with each of 26 other chemicals were determined. When mixed with acetone, acetophenone or dioxane, the mixtures were more than 3 times as toxic (that is the effects were more than additive).(18) Pretreatment with an intraperitoneal injection of carbon tetrachloride reduced the toxicity of orally administered acetonitrile.(14)


SECTION 16. OTHER INFORMATION

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(3) European Communities (EC). Commission Directive 2001/59/EC. Aug. 6, 2001
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(5) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
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(8) Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, 1989. p. 12, 43
(9) Freeman, J.J., et al. The metabolism of acetonitrile to cyanide by isolated rat hepatocytes. Fundamental and Applied Toxicology. Vol. 8, no. 2 (1987). p. 263-271
(10) US National Toxicology Program (NTP). Toxicology and carcinogenesis studies of acetonitrile (CAS No. 75-05-8) in F344/N rats and B6C3F1 mice (inhalation studies). Technical report series no. 447. NIH Publication 96-3363. US Department of Health and Human Services, 1996
(11) Bowles, C.A., et al. Limited toxicity of inhaled acetonitrile on the immune system of mice with cover letter dated 01/26/84 and EPA acknowledgement dated 03/09/84. ImmuQuest Laboratories Inc., 1984. EPA/OTS FYI-OTS-0284-0292
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(13) Willhite, C.C. Inhalation toxicology of acute exposure to aliphatic nitriles. Clinical Toxicology. Vol. 18, no. 8 (1981). p. 991-1003
(14) Tanii, H., et al. Studies on the mechanism of acute toxicity of nitriles in mice. Archives of Toxicology. Vol. 55, no. 1 (Mar. 1984). p. 47-54
(15) Pozzani, U.C., et al. The investigation of the mammalian toxicity of acetonitrile. Journal of Occupational Medicine. Vol. 1 (Dec. 1959). p. 634-642
(16) Haguenor, J.-M., et al. Intoxications experimentales par l'acetonitrile. 2 note: intoxications aigues par voie pulmonaire. (French). European Journal of Toxicology. Vol. 8, no. 2 (Mar.-Apr. 1975). p. 102-106
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(18) Smyth, Jr., H.F., , et al. An exploration of joint toxic action: twenty-seven industrial chemicals intubated in rats in all possible pairs. Toxicology and Applied Pharmacology. Vol. 14 (1969). p. 340-347
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(20) Johanssen, F.R., et al. Evaluation of the teratogenic potential of three aliphatic nitriles in the rat. Fundamental and Applied Toxicology. Vol. 7, no. 1 (July 1986). p. 33-40
(21) Willhite, C.C. Developmental toxicology of acetonitrile in the Syrian golden hamster. Teratology. Vol. 27, no. 3 (1983). p. 313-325
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(24) Dequidt, J., et al. Intoxication with acetonitrile with regard to a fatal case. European Journal of Toxicology and Environmental Hygiene. Vol. 7, no. 2 (Mar.-Apr. 1974)
(25) Grabois, B. Fatal exposure to methyl cyanide. New York State Department of Labor, Division of Industrial Hygiene, Monthly Review. Vol. 34, no. 1 (Jan. 1955). p. 1-4
(26) Galloway, S.M., et al. Chromosome aberrations and sister chromatid exchanges in Chinese hamster ovary cells. Vol. 10, suppl. 10 (1987). p. 1-175
(27) Basu, D.K., et al. Drinking water criteria document for cyanides (final draft). US Environmental Protection Agency, 1985
(28) Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for cyanide (update). US Department of Health and Human Services, 1997
(29) Beasley, D.M.G., et al. Cyanide poisoning: pathophysiology and treatment recommendations. Occupational Medicine. Vol. 48, no. 7 (1998). p. 427-431
(30) Consensus report for hydrogen cyanide, sodium cyanide and potassium cyanide. Scientific Basis for Swedish Occupational Standards XXII. Edited by J. Montelius. Arbete Och Halsa. No. 20 (2001). p. 43-59
(31) Mast, T.J., et al. Inhalation developmental toxicology studies: acetonitrile in rats. Final report. Feb. 1994. Contract No. NIH-Y01-ES-70153. NTIS Technical Report. NTIS/DE94-0082722) Smith, M.K., et al. Developmental toxicity of halogenated acetonitriles: drinking water by-products of chlorine disinfection. Toxicology. Vol. 46, no. 1 (Oct. 1987). p. 83-93
(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) Argus Research Laboratories. Embryo-fetal toxicity and teratogenicity study of acetonitrile in New Zealand white rabbits (segment II evaluation) project No. H19-001 with cover letter to Timm G. Standard Oil Co., 1984. EPA/OTS 40-8446070. NTIS/OTS0507279
(35) Saillenfait, A.M., et al. Comparative developmental toxicities of aliphatic nitriles: in vivo and in vitro. Toxicology and Applied Pharmacology. Vol. 163, no. 2 (Mar. 2000). p. 149-163
(36) Morrissey, R.E., et al. Evaluation of rodent sperm vaginal cytology and reproductive organ weight data from National Toxicology Program 13-week studies. Fundamentals of Applied Toxicology. Vol. 11, no. 2 (1988). p. 343-358
(37) Jones, E., et al. The mutagenic potential of acetonitrile in the bone marrow and peripheral blood of the mouse. Mutagenesis. Vol. 16, no. 2 (Mar. 2001). p. 151-154
(38) Schlegelmilch, R., et al. Mutagenic activity of acetonitrile and fumaronitrile in three short term assays with special reference to autoinduction. Journal of Applied Toxicology. Vol. 8, no. 3 (1988). p. 201-209
(39) Whittaker, S.G., et al. Detection of induced mitotic chromosome loss in Saccharomyces cerevisiae - an interlaboratory study. Mutation Research. Vol. 224, no. 1 (1989). p. 31-78
(40) Osgood, C., et al. Aneuploidy in Drosophila, II. Further validation of the FIX and ZESTE genetic test systems employing female Drosophila melanogaster. Mutation Research. Vol. 259, no. 2 (Feb. 1991). p. 147-163
(41) Osgood, C., et al. Aneuploidy in Drosophila, IV. Inhalation studies on the induction of aneuploidy by nitriles. Mutation Research. Vol. 259, no. 2 (Feb. 1991). p. 165-176
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(43) Pozzani, U.C., et al. The toxicological basis of threshold limit values: 5. The experimental inhalation of vapor mixtures by rats, with notes upon the relationship between single dose inhalation and single oral dose data. Industrial Hygiene Journal. Vol. 20 (1959). p. 364-369
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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: 2005-03-29



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