3,3'-Iminodipropiononitril

1.02 at 68 °F (NTP, 1992) - Denser than water; will sink

1.0165 @ 30 °C

greater than or equal to 100 mg/mL at 68 °F (NTP, 1992)

Sol in water, ethanol, acetone, benzene

230 °F (NTP, 1992)

110 °C

343 °F at 10 mmHg (NTP, 1992)

173 °C @ 10 mm Hg

BP: 205 °C @ 25 mm Hg

21 °F (NTP, 1992)

-5.50 °C

3.3 (NTP, 1992) - Heavier than air; will sink (Relative to Air)

4.2 (Air= 1)

1 mmHg at 284 °F (NTP, 1992)

0.00361 [mmHg]

Vapor pressure: 1 mm Hg @ 140 °C

Danger

H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]

P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P305+P354+P338, P317, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 44 reports by companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

A skin irritant; A severe eye irritant; May cause chronic cyanide poisoning after ingestion; [HSDB] Causes somnolence and convulsions in lethal dose inhalation studies of mice; [RTECS] An irritant; May cause serious eye injury; [MSDSonline] See NITRILES.

Nitriles, such as 3,3'-IMINODIPROPIONITRILE, may polymerize in the presence of metals and some metal compounds. They are incompatible with acids; mixing nitriles with strong oxidizing acids can lead to extremely violent reactions. Nitriles are generally incompatible with other oxidizing agents such as peroxides and epoxides. The combination of bases and nitriles can produce hydrogen cyanide. Nitriles are hydrolyzed in both aqueous acid and base to give carboxylic acids (or salts of carboxylic acids). These reactions generate heat. Peroxides convert nitriles to amides. Nitriles can react vigorously with reducing agents. Acetonitrile and propionitrile are soluble in water, but nitriles higher than propionitrile have low aqueous solubility. They are also insoluble in aqueous acids.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If you should spill this chemical, use absorbent paper to pick up all liquid spill material. Seal the absorbent paper, as well as any of your clothing which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Wash any surfaces you may have contaminated with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

THYROXINE HAS PROTECTIVE ACTION AGAINST BEHAVIORAL MANIFESTATIONS OF POISONING IN RATS WHICH IS EXERTED THROUGH AN ACTIVATION OF IDPN CONVERSION INTO ITS NONTOXIC CATABOLITE CYANOACETIC ACID. DETOXICATING MECHANISM BY WHICH THYROXINE PROTECTS AGAINST SUCH SUBSTANCES MAY BE COMMON TO ALL OF THEM, ESSENTIALLY CONSISTING IN THE DEAMINATION OF THOSE AMINO GROUPS LINKED TO THE CN RADICAL, EXISTING IN CERTAIN AMINO ACIDS OR IN COMBINATION, THAT RENDER THESE SUBSTANCES TOXIC.

SC ADMIN OF 0.2 MG/G TO MALE RATS INDUCED NEUROLOGICAL SYNDROME. HIGH-PROTEIN DIETS NET PROTEINS CALORIC VALUES OF 10.1, 6.2 OR 4.6 & SC INJECTIONS OF SODIUM 6-THYROXINE 1 MUG/G DELAYED DEVELOPMENT OF SYNDROME BUT DID NOT PREVENT ITS OCCURRENCE.

ADMIN OF LARGE DOSES OF IDPN TO RATS CAUSED RETINAL ANGIOPATHY & CENTRAL NERVOUS SYSTEM DISTURBANCE. ACTION OF 3 BIOFLAVONOIDS, 3',4',7-TRIHYDROXYETHYLRUTOSIDE; 3',4',5,7-TETRAHYDROXYETHYLRUTOSIDE & PAROVEN, A MIXTURE OF MONOHYDROXYETHYLRUTOSIDE, DIHYDROXYETHYLRUTOSIDE, TRIHYDROXYETHYLRUTOSIDE, & TETRAHYDROXYETHYLRUTOSIDE, ON EFFECTS OF IDPN WAS STUDIED. THE BIOFLAVONOIDS RETARDED DEVELOPMENT & AMELIORATED SEVERITY OF NEURAL & OCULAR SYMPTOMS PRODUCED BY LOW LEVELS OF IDPN, BUT THE PATHOLOGICAL CHANGES WERE NEVER COMPLETELY PREVENTED.

ADMIN OF IDPN TO RATS IN 5 DAILY SC INJECTIONS OF 30 MG, OR IN SINGLE SC INJECTION OF 100 MG/100 G, SEVERELY DAMAGED CENTRAL NERVOUS SYSTEM & RETINAL VASCULATURE. THESE CHANGES WERE PREVENTED BY DAILY IP INJECTION 6 DAYS PRETREATMENT & 8 DAYS TREATMENT SUBSEQUENTLY OF DL-ETHIONINE 24 MG/100 G.

MALE RATS WERE INJECTED SC DAILY WITH 20 MG IDPN FOR 6 DAYS. NEUROLOGICAL SYNDROMES WERE PREVENTED BY L-THYROXINE 200 GAMMA SC. BRAIN GAMMA-AMINOBUTYRIC ACID (GABA) LEVELS INCR SIGNIFICANTLY. BRAIN GLUTAMIC & ASPARTIC ACID LEVELS WERE ALSO INCR, BUT THESE INCR WERE PREVENTED BY L-THYROXINE.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from an measured log Kow of -1.34(2) and a regression-derived equation(3), indicates that beta,beta'-iminodipropionitrile is expected to have very high mobility in soil(SRC). Volatilization of beta,beta'-iminodipropionitrile from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.0X10-12 atm-cu m/mole(SRC), using a fragment constant estimation method(4). beta,beta'-Iminodipropionitrile is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.6X10-3 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation is not expected to be a rapid fate process based upon a theoretical BOD of 1-3% in 4 weeks using an activated sludge inoculum at 30 mg/l and the Japanese MITI test(2).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a measured log Kow of -1.34(2) and a regression-derived equation(3), indicates that beta,beta'-iminodipropionitrile is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 5.0X10-12 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low. Biodegradation is not expected to be a rapid fate process based upon a theoretical BOD of 1-3% in 4 weeks using an activated sludge inoculum at 30 mg/l and the Japanese MITI test(2).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), beta,beta'-iminodipropionitrile, which has an estimated vapor pressure of 3.6X10-3 mm Hg at 25 deg (SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase beta,beta'-iminodipropionitrile 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 6 days(SRC), calculated from its rate constant of 2.5X10-12 cu cm/molecule-sec at 25 °C(SRC) determined using a structure estimation method(3).

The Koc of beta,beta'-iminodipropionitrile is estimated as 4(SRC), using a measured log Kow of -1.34(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that beta,beta'-iminodipropionitrile is expected to have very high mobility in soil.

...INVESTIGATED PRINCIPALLY IN CONNECTION WITH LATHYRISM, A FORM OF SPASTIC PARAPLEGIA INDUCED...AS RESULT OF EATING SEEDS OF CERTAIN PLANTS OF LATHYRUS GROUP, BUT ONLY AFTER EATING THEM FOR A LONG TIME, & ONLY WHEN THEY CONSTITUTE THE PRINCIPAL NOURISHMENT.

A BCF range of 0.2-0.4 was measured using Orange-red killifish (Oryzias latipes) and a compound concn of 1 mg/l(1). According to a classification scheme(2), this BCF range suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for beta,beta'-iminodipropionitrile is estimated as 5.0X10-12 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that beta,beta'-iminodipropionitrile is expected to be essentially nonvolatile from water surfaces(2). beta,beta'-Iminodipropionitrile is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.6X10-3 mm Hg(SRC), determined from a fragment constant method(3).

The LD50 is greater than 3 g/kg when ... given orally to mice. ... Oral LD50 in rats is 2700 mg/kg. CNS damage was apparent in 3 days, & persisted for prolonged periods. Same symptoms were noted after skin application. Damage to lens of eye was noted after oral dosage, but not after skin contact.

Injection of 1-2 g/kg in rats, mice, birds & fish was followed in 2-10 days by great incr in motor activity, changes in behavioral patterns, backward walking & head twitching ... marked ... damage was found in brain.

IN RABBITS, SUBCUTANEOUS INJECTION HAS CAUSED REDUCTION OF INTRAOCULAR PRESSURE WITHIN A DAY, REVERSIBLY OR IRREVERSIBLY, DEPENDING ON DOSE. LATER THERE IS GRADUAL REDUCTION OF ELECTRORETINOGRAM. .../WHEN/ APPLIED TO RABBIT EYES /IT/ HAS SLIGHT INJURIOUS EFFECT.

.../WHEN/ ADMIN SUBCUTANEOUSLY TO MONKEYS...GUINEA PIGS...CATS, DOGS & HAMSTERS /IT/ INDUCES OCULAR LESIONS VARYING WITH SPECIES. IN MONKEYS, ORBITAL & PALPEBRAL EDEMA ARE ALWAYS PRONOUNCED, BUT RETINAL CHANGES ARE EXCEPTIONAL.

For more Non-Human Toxicity Excerpts (Complete) data for BETA,BETA'-IMINODIPROPIONITRILE (14 total), please visit the HSDB record page.

The rate constant for the vapor-phase reaction of beta,beta'-iminodipropionitrile with photochemically-produced hydroxyl radicals has been estimated as 2.5X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 6 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). beta,beta'-Iminodipropionitrile is not expected to undergo hydrolysis in the environment due to the absence of hydrolyzable functional groups(2). Direct photolysis is not expected due to the lack of absorption in the environmental UV spectrum (>290 nm).

IDPN INDUCES MUCH OF ITS NEUROFILAMENT & AXONAL PATHOLOGY BY WAY OF A SELECTIVE INHIBITION OF SLOW AXOPLASMIC TRANSPORT.

(3)H-URIDINE WAS SC INJECTED INTO MICE & AUTORADIOGRAPHS OF SPINAL GANGLIONS AT DIFFERENT INTERVALS PREPD. BY STATISTICAL ANALYSIS OF GRAIN COUNTS IT WAS FOUND THAT, IN NORMAL MICE 1 HR AFTER INJECTION OF PRECURSOR, MOST OF GRAINS WERE LOCALIZED OVER NUCLEUS, 24 HR LATER THEY HAD MIGRATED INTO CYTOPLASM. WHEN MICE RENDERED HYPERACTIVE BY IDPN, THERE WAS INCR LABELLING OF NUCLEAR & CYTOPLASMIC RNA AFTER 1 HR & DECR LABELLING AFTER 24 HR. STATE OF HYPERACTIVITY IS APPARENTLY ASSOC WITH INCR SYNTH & DISAPPEARANCE OF RNA FROM NEURONAL CELL BODIES.

BIOGENIC AMINE MOST AFFECTED BY ADMIN TO RATS IN IP DAILY DOSES OF 300 MG/KG FOR 7 DAYS WAS SEROTONIN (5-HT). ON DAY 7, STRIATAL 5-HT LEVELS INCR & ITS METAB, 5-HYDROXYINDOLEACETIC ACID (5-HIAA) LEVELS DECR WHILE IN MEDULLA & MIDBRAIN, 5-HIAA LEVELS INCR. ON DAY 14, SIGNIFICANT REDUCTIONS IN BOTH 5-HT, THE MIDBRAIN, STRIATUM & CORTEX, & 5-HIAA, IN ALL REGIONS EXCEPT THE CORTEX WERE OBSERVED. NOREPINEPHRINE (NE) WAS MARKEDLY INCR IN MEDULLA, MIDBRAIN & STRIATUM ON DAY 7, WHEREAS ON DAY 14 IT WAS WITHIN NORMAL RANGE IN THESE SAME REGIONS. WITH EXCEPTION OF SLIGHT, BUT SIGNIFICANT, INCR IN CORTEX ON DAY 7, DOPAMINE LEVELS IN ALL REGIONS WERE RELATIVELY UNAFFECTED ON DAY 7 & 14.

MALE RATS WERE INJECTED SC DAILY WITH 20 MG IDPN FOR 6 DAYS. NEUROLOGICAL SYNDROMES WERE PREVENTED BY L-THYROXINE 200 GAMMA SC. BRAIN GAMMA-AMINOBUTYRIC ACID (GABA) LEVELS INCR SIGNIFICANTLY. BRAIN GLUTAMIC & ASPARTIC ACID LEVELS WERE ALSO INCR, BUT THESE INCR WERE PREVENTED BY L-THYROXINE.

For more Mechanism of Action (Complete) data for BETA,BETA'-IMINODIPROPIONITRILE (7 total), please visit the HSDB record page.

BIOTRANSFORMATION IN RATS...AFFORDS BETA-AMINOPROPIONITRILE, CYANOACETIC ACID & BETA-ALANINE. SINCE CYANOACETIC ACID IS NOT LATHYROGENIC, ITS PRODN REPRESENTS DETOXICATION... /IT IS SUGGESTED THAT BETA-ALANINE/ AROSE THROUGH HYDROLYSIS OF BETA-AMINOPROPIONITRILE.../& THAT/ THIS METAB PATHWAY ALSO REPRESENTS DETOXICATION.

IDPN IS METABOLIZED, IN PART, TO BETA-AMINOPROPIONITRILE (BAPN). MUCH OF THE CONNECTIVE TISSUE DISRUPTION WITH IDPN MAY THUS RESULT FROM A DEFICIT IN COLLAGEN CROSS-LINKING SECONDARY TO INHIBITION OF LYSYLOXIDASE BY BAPN.

Used in medical research (neurotoxin) and as a chemical intermediate; [HSDB]

For Beta, beta'-iminodipropionitrile (USEPA/OPP Pesticide Code: 600004) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

CHEM INT FOR 3,3'-IMINOBISPROPYLAMINE (PROBABLE USE)

Medical research - neurotoxicant