Hexandinitril

Nitrogen Compounds -> Nitriles

Flammable agents - 2nd degree

log Kow= -0.32

-0.32

0.965 at 68 °F (EPA, 1998) - Less dense than water; will float

0.9676 g/ml @ 20 °C

Relative density (water = 1): 0.97

0.97

0.963 @ 20°C

0.97

9.1 cP @ 20 °C; 2.6 cP @ 70 °C

58 mPa*s at 30 °C

NEEDLES FROM ETHER

Colorless liq

Water-white, oily liquid

50 to 100 mg/mL at 73 °F (NTP, 1992)

Sol in alc, chloroform

Sol in methanol, ethanol, chloroalkanes, and aromatics but has low solubility in carbon disulfide, ethyl ether, and aliphatic hydrocarbons.

In water, 8.0X10+4 mg/l @ 20 °C.

Solubility in water, g/l at 20 °C: 50-100 (good)

4.5%

199.4 °F (EPA, 1998)

93 °C

200 °F (93 °C) (OPEN CUP)

159 °C c.c.

199 °F (open cup)

(oc) 199 °F

563 °F at 760 mmHg (EPA, 1998)

295 °C @ 760 mm Hg

295 °C

563 °F

295 °C @760 [mm Hg]

563 °F

WHEN HEATED TO DECOMP RELEASES VAPORS CONTAINING HYDROCYANIC ACID.

When heated to decomp it emits highly toxic fumes of CN- /cyanides/.

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P260, P261, P264, P264+P265, P270, P271, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P317, P319, P320, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 224 reports by companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

Chemical: Hexanedinitrile

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

Status: Active Update: 12-05-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/14296

Adiponitrile: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Combustion products may contain hydrogen cyanide (hydrocyanic acid, HCN). Vapor may explode if ignited in an enclosed area. When heated to decomposition, it emits highly toxic fumes. Avoid oxidizing material. Hazardous polymerization may not occur. (EPA, 1998)

· Combustible material: may burn but does not ignite readily.

Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

This material is toxic by ingestion and inhalation. It produces disturbances of the respiration and circulation, irritation of the stomach and intestine, and loss of weight. It is irritating to skin and eyes. (EPA, 1998)

· TOXIC and/or CORROSIVE; inhalation, ingestion or skin contact with material may cause severe injury or death.

2205 153

2205 153

Kaplita PV and Smith RP; Toxicol Appl Pharmacol 84 (3): 533-540 (1986). Pathways for the bioactivation of aliphatic nitriles to free cyanide in mice.

Homan ER; Clinical and Experimental Toxicol of Cyanides, Bristol, UK 1-21 pages (1987). Reactions, industrial processes, and materials with potential for exposure to cyanide compounds were discussed in this overview on the toxicology of cyanides.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Hexanedinitrile is included on this list.

Wear chemical protective suit with self-contained breathing apparatus. Cool exposed containers with water.

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

Fresh air, rest. Administration of oxygen may be needed. No mouth-to-mouth artificial respiration. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Administration of oxygen may be needed. Refer immediately for medical attention.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer for medical attention.

Rinse mouth. Administration of oxygen may be needed. Give one or two glasses of water to drink. Refer for medical attention .

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

Warning: Effects may be delayed. Caution is advised. Vital signs should be monitored closely.

General First Aid:

(General first aid procedures)

USE WATER SPRAY, DRY CHEMICAL, FOAM OR CARBON DIOXIDE. USE WATER SPRAY TO KEEP FIRE-EXPOSED CONTAINERS COOL. APPROACH FIRE FROM UPWIND TO AVOID HAZARDOUS VAPORS AND TOXIC DECOMPOSITION PRODUCTS.

If material on fire or involved in fire: Use water in flooding quantities as fog. use foam, dry chemical, or carbon dioxide. Keep run-off water out of sewers and water sources. Cool all affected containers with flooding quantities of water. Apply water form as far a distance as possible.

Personal protection: complete protective clothing including self-contained breathing apparatus. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

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)

The toxic mechanism of nitriles (including adiponitrile) and the effect of metabolic modifiers in mice were studied in relation to their physicochemical properties. All the test nitriles liberated cyanide both in vivo and in vitro, with the exception of benzonitrile, although the extent of liberation and the effect of carbon tetrachloride pretreatment on the mortality of animals differed among nitriles. From these results, test compounds were tentatively divided into 3 groups. In group 1, acute toxicity was greatly reduced by carbon tetrachloride pretreatment, in group 2, toxicity was not significantly changed or was somewhat enhanced, and in group 3, benzonitrile only, toxicity was clearly enhanced. The amount of cyanide was higher at death in the brains of mice given group 1 compounds, the level being comparable to that found in mice killed by dosing with potassium cyanide. The relation between log (1/LD50) and log p for the compounds in group 1 fitted a parabolic plot, while that for compounds in group 2 was linear. For most nitriles, the in vitro metabolism was inhibited when the incubation mixture contained either SKF-525A, carbon monoxide, or microsomes from mice treated with carbon tetrachloride. When mice were closed with ethyl alcohol, metabolic enhancement of nitriles was seen compared with the control. However, ethyl alcohol, when added to the incubation mixture, inhibited the in vitro metabolism of nitriles.

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)

TLm Pimephales promelas (fathead minnow) 820 mg/l/96 hr (hard water) /Conditions of bioassay not specified/

TLm Pimephales promelas (fathead minnow) 1250 mg/l/96 hr (soft water) /Conditions of bioassay not specified/

TLm Bluegill sunfish 1250 mg/l/24 hr (soft water) /Conditions of bioassay not specified/

TLm Guppies 775 mg/l/96 hr (soft water) /Conditions of bioassay not specified/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 16(SRC), determined from a log Kow of -0.32(2) and a regression-derived equation(3), indicates that adiponitrile is expected to have very high mobility in soil(SRC). Volatilization of adiponitrile from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.21X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 6.79X10-4 mm Hg(4), and water solubility, 8.00X10+4 mg/l(5). Adiponitrile is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). In water, adiponitrile had a 5-day theoretical BOD of 40% in a river die-away study using unacclimated Ohio River water, 0.5-10 mg/l substrate concn and sewage inocula(6); the 12-day theoretical BOD was >100%(6); negligible degradation was observed after 2 days(6). In addition, microorganisms (Aeromonas sp.) isolated from soil were able to use adiponitrile as its sole source of carbon(7). Thus, adiponitrile may be expected to biodegrade in soil systems(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 16(SRC), determined from a log Kow of -0.32(2) and a regression-derived equation(3), indicates that adiponitrile 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 1.21X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 6.79X10-4 mm Hg(4), and water solubility, 8.00X10+4 mg/l(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Adiponitrile had a 5-day theoretical BOD of 40% in a river die-away study using unacclimated Ohio River water, 0.5-10 mg/l substrate concn and sewage inocula(8); the 12-day theoretical BOD was >100%(8); negligible degradation was observed after 2 days(8). Thus, adiponitrile is expected to biodegrade in aquatic systems(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), adiponitrile, which has a vapor pressure of 6.79X10-4 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere(SRC). Vapor-phase adiponitrile 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 23 days(SRC), calculated from its rate constant of 7.12X10-13 cu cm/molecule-sec at 25 °C(SRC) determined using a structure estimation method(3).

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

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

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 known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)

Headache. Vomiting. Dizziness. Nausea. Laboured breathing. Confusion. Convulsions.

MAY BE ABSORBED! Redness. Pain.

Redness. Blurred vision.

Abdominal pain. Further see Inhalation.

irritation eyes, skin, respiratory system; headache, dizziness, lassitude (weakness, exhaustion), confusion, convulsions; blurred vision; dyspnea (breathing difficulty); abdominal pain, nausea, vomiting

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)

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Hexanedinitrile is included on this list.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Adiponitrile is produced, as an intermediate or a final product, by process units covered under this subpart.

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Adiponitrile is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 1000 lbs.

... In guinea pigs ... it is hydrolyzed to hydrogen cyanide in the body giving rise to thiocyanate in urine.

Male ddY mice were pretreated with carbon tetrachloride or olive oil and administered adiponitrile orally in concentrations sufficient to determine its median lethal dose (LD50). Brain cyanide concentrations were determined. The distribution coefficient (P) for partitioning adiponitrile between water and n-octanol was measured. Mice were pretreated as before and dosed with adiponitrile at 3 to 5 times its LD50. Mean survival times were determined. Hepatic microsomes were obtained from mice pretreated with carbon tetrachloride or olive oil and incubated with adiponitrile. The rate of release of free cyanide was investigated. The oral LD50 for animals pretreated with olive oil was 1.592 mmol/kg. The LD50 for the carbon tetrachloride treated mice was 2.652 mmol/kg. Brain cyanide concentrations in olive oil pretreated mice ranged from 0.35 to 0.74 ug/g. Carbon tetrachloride pretreatment lengthened survival and reduced brain cyanide concentrations. Dinitriles are metabolized to cyanides in vivo and in vitro.

Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)

Seventy nine percent of dose /about 50 mg/kg sc admin to guinea pigs/ was eliminated as thiocyanate in urine. ... Skin penetration was suggested by incr in thiocyanate in urine ... after application to depilated skin. Greater quantities were absorbed when skin was abraded.

The concentrations of thiocyanate in the blood and urine of guinea pigs injected with adiponitrile were proportional to the doses administered. Following administration of adiponitrile, 79% was eliminated as thiocyanate in the urine of guinea pigs. Of the cyanide antidotes, thiosulfate was most effective. However, on the basis of the ratio between administered adiponitrile dose and quantity of cyanide detected, /it was/ concluded that a greater part of the dose was metabolized to cyanide.

Used to manufacture hexamethylenediamine that is used to make nylon 66; [HSDB]

Intermediate in the manufacture of nylon; organic synthesis

Preparation of adipoquanamine; extractant for aromatic hydrocarbons

2023: 1,000,000,000 - <2,500,000,000 lb

(1972) 3.6X10+11 GRAMS

(1991) 1415 million lb (capacity)

U.S. production capacity = 625,000 metric tons in 1992

Chlorination of butadiene to dichlorobutylene, which is reacted with 35% sodium cyanide soln to yield 1,4-dicyanobutylene; which is hydrogenated to adiponitrile. Also by electroorganic synthesis from acrylonitrile.

Reaction of adipic acid with ammonia (either liquid or vapor phase) produces adipamide as intermediate, which is subsequently dehydrated to adiponitrile.

Prepared by dimerization of acrylonitrile at the cathode of an electrolytic cell (propionitrile and bis(cyanoethyl) ether are by-products).

Prepared by direct addition of hydrogen cyanide to butadiene catalyzed by soluble, air and moisture sensitive, triarylphosphite nickel(0) complexes.

All Other Basic Organic Chemical Manufacturing

Hexanedinitrile: ACTIVE