acetonitrile

... A standardized second puff of cigarette smoke contains 0.31 mg acetonitrile. A smoker may absorb between 73 and 82% of this, depending on post smoking habits.

USDA APHIS Chemical Effects: collection=usda_chemeffect&query_type=synonym&query='^75-05-8$'

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acetonitrile, which has a vapor pressure of 88.8 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase acetonitrile is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 610 days(SRC), calculated from its rate constant of 2.63X10-14 cu cm/molecule-sec at 25 °C(3). Vapor-phase acetonitrile is also degraded in the atmosphere by reaction with ozone(SRC); the half-life for this reaction in air is estimated to be greater than or equal to 76 days(SRC), calculated from its rate constant of less than or equal to 1.5X10-19 cu cm/mole...

Acetonitrile has a reported measured Koc Value of 2.2(1). According to a classification scheme(2), this Koc value suggests that acetonitrile is expected to have very high mobility in soil(SRC).

ANAEROBIC: Results of anaerobic tests with acetonitrile suggest that anaerobic biodegradation is not effective for removing the compound from wastewater(1). Acetonitrile was classified as partially biodegradable under anaerobic conditions based on a calculated integrated assessment index (IAI) of 0.7286 in a study conducted in Beijing, China(1). The IAI relates to data collected from a model consisting of an initial acetonitrile concentration of 100 mg/L in an inorganic medium and anaerobic sludge from wastewater treatment digestor tanks in Beijing(2).

An estimated BCF of 3 was calculated in fish for acetonitrile(SRC), using a log Kow of -0.34(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for acetonitrile is 3.45X10-5 atm-cu m/mole(1). This Henry's Law constant indicates that acetonitrile is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 12 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 7.5 days(SRC). Acetonitrile's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Acetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 88.8 mm Hg(3).

The photochemical smog studies show that this compound is unreactive towards photochemically-generated free radicals(2). Due to nonreactivity of acetonitrile in the atmosphere, transport of the compound from troposphere to stratosphere is expected to occur(SRC) and acetonitrile has been detected in the stratosphere(1).

Acetonitrile was detected, not quantified in some milk products such as kefir culture(1).

Acetonitrile was detected in 35 surveyed samples of cow milk at concentrations ranging from 1.51 to 13.75 ng/mL (whole), 4.00 to 12.51 ng/mL (2% butterfat), and 4.03 to 12.74 ng/mL (1% butterfat). Average detected concentrations were 7.56 ng/mL (whole), 8.98 ng/mL (2% butterfat), and 7.10 ng/mL (1% butterfat). The samples represented 8 brands of pasteurized milk in Las Vegas, Nevada between January 2002 and February 2002(1).

Assuming the fossil fuel burned in Austria to be globally representative, acetonitrile emissions produced by fossil fuel burning have been calculated to contribute 6% of the total global contributing sources. The upper limit global rate of emission due to fuel burning was estimated as 5X10+10 g/year; the global rate of emission was estimated to be 2.7X10+11(1).

Environmental effects of the substance have been adequately investigated, but no significant effects have been found.

Acetonitrile occurs in coal tar in small amounts, has been detected in volcanic gases and quantified in emissions from the combustion of wood and other biomass.

RURAL/REMOTE: Acetonitrile was detected at a mean concentration of 0.024 ppb in two samples from a rural area(1). It was detected in air near ground levels in both urban and rural areas at a concentration of 2-7 ppb(2). Acetonitrile was reported to be present in the upper stratosphere(3). Acetonitrile was detected at a concentration of 0.2 nmol/mol in a series of 10 LBA-CLAIRE (Large-scale Biosphere-atmosphere experiment in Amazonia - Cooperative LBA Airborne Regional Experiment) measurement flights conducted over tropical rainforests in Surinam(4). Air was drawn and measured using a Proton-Transfer-Reaction Mass-Spectrometer at altitudes ranging from 0 to 12 km(4). An acetonitrile concentration of 94.1 ng/cu m was detected in air samples collected from a rural area of Arizona(5).

Acetonitrile's production and use in solvent extraction, reaction media, and as an intermediate in the preparation of pharmaceuticals and other organic chemicals(1,2) may result in its release to the environment through various waste streams(SRC). Acetonitrile is released during its manufacture and use, from some industrial operations like shale oil retorting and coal gasification and from combustion processes in gas turbines, ignition engines and automobile exhaust(3).

Blood cyanide concentrations exceeding 0.1 mg/L of plasma or urine thiocyanate exceeding 20 mg/L in workers exposed to acetonitrile are indicative of excessive exposure.

... A standardized second puff of cigarette smoke contains 0.31 mg acetonitrile.

Acetonitrile's production and use in solvent extraction, reaction media, and as an intermediate in the preparation of pharmaceuticals and other organic chemicals may result in its release to the environment through various waste streams. Acetonitrile occurs in coal tar in small amounts, has been detected in volcanic gases and quantified in emissions from the combustion of wood and other biomass. If released to air, a vapor pressure of 88.8 mm Hg at 25 °C indicates acetonitrile will exist solely as a vapor in the ambient atmosphere. Vapor-phase acetonitrile will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 610 days. Vapor-phase acetonitrile will also be degraded in the atmosphere by re...

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

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

...rabbits injected with acetonitrile excreted 27-35% of the dose as thiocyanate, while in thyroid-ectomized rabbits, the excretion decreased significantly (3-5% of the dose). Thiocyanate excretion increased notably upon feeding dessicated thyroid to these animals.

respiratory system, cardiovascular system, central nervous system, liver, kidneys

LD50: 3500 mg/kg (Subcutaneous, Rat) (T14) LD50: 1680 mg/kg (Intravenous, Rat) (T14) LD50: 269 mg/kg (Oral, Mouse) (T14) LC50: 2693 ppm over 1 hour (Inhalation, Mouse) (T14)

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

ACGIH Carcinogen - Not Classifiable.

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

Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also...

Oral Subchronic Chronic Reference Dose Reference: HEAST Current

No indication of carcinogenicity to humans (not listed by IARC).

Soil Saturation Concentration (mg/kg): 1.28e+05

A4: Not classifiable as a human carcinogen.

Soil Saturation Concentration (mg/kg): 1.28e+05

Reference: Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP