79-46-9

Colorless liquid with a mild fruity odor. May float on or sink in water.

2-NITROPROPANE(79-46-9) is sensitive to heat. Can react with amines/heavy metal oxides, strong acids, strong alkalis, and chlorosulfonic acid. . The heat of adsorption of this compound on carbon, such as that found in cartridge respirators, is extremely high. Metal oxide catalysts, such as copper oxide or manganese oxide, can initiate ignition, therefore carbon respirators should not be used in environments that have a high vapor concentration of this material.

Highly flammable.

Flammable, dangerous fire risk, moderate explosion hazard when shocked or heated. Liver damage and liver cancer. Possible carcinogen.

Inhalation causes respiratory tract irritation, headache, dizziness, nausea, and diarrhea. Ingestion causes irritation of mouth and stomach. Contact with liquid irritates eyes and causes mild irritation of skin.

2-Nitropropane is used as a solvent for polymers, organic compounds; cellulose, esters; gums,vinyl resins; waxes, epoxy resins, fats, dyes, and chlorinated rubber; as a stabilizer. Its combustion properties have made it useful as a rocket propellant and as a gasoline and diesel fuel additive. 2-Nitropropane also has limited use as a paint and varnish remover. It serves as an intermediate in organic synthesis of some pharmaceuticals; dyes, insecticides, and textile chemicals.

Special Hazards of Combustion Products: Toxic oxides of nitrogen may form in fire.

If this chemical gets into the eyes, remove any contact lenses at once and irrigate immediately for at least 15 minutes, occasionally lifting upper and lower lids. Seek medical attention immediately. If this chemical contacts the skin, remove contaminated clothing and wash immediately with soap and water. Seek medical attention immediately. If this chemical has been inhaled, remove from exposure, begin rescue breathing (using universal precautions, including resuscitation mask) if breathing has stopped and CPR if heart action has stopped. Transfer promptly to a medical facility. When this chemical has been swallowed, get medical attention. Give large quantities of water and induce vomiting. Do not make an unconscious person vomit.

UN2608 Nitropropanes, Hazard Class: 3; Labels: 3-Flammable liquid.

1-Nitropropane, a nitroparaffin compound, forms explosive mixture with air. Contact with heavy metal oxides may cause decomposition. Mixtures with hydrocarbons are extremely flammable. Attacks some plastics, rubber and coatings. May explode on heating. Violent reaction with strong bases; strong acids and metal oxides. Shock-sensitive compounds are formed with acids, amines, inorganic bases and heavy metal oxides. Incompatible with strong oxidizers, combustible materials. 2-Nitropropane reacts with activated carbon causing decomposition. This reaction may occur in activated carbon respirator filters.

2-Nitropropane exists in equilibrium with 2-propane nitronic acid (HSDB 1988). A 0.01 M aqueous solution has a pH of 6.2. 2-Nitropropane reacts with inorganic bases and amines to form salts which are flammable when dry. 2-Nitropropane is sensitive to detonation when mixed with oxidizers and a mixture of the chemical with ammonium nitrate is a commercial explosive.

2-Nitropropane(2-NP) is an aliphatic nitro compound. It is a colorless, oily, and flammable liquid with a mild fruity odor. Soluble in water 1.7 mL/100 mL (20C); solubility of water in 2-nitropropane 0.6 cc/100 cc (20C); miscible with organic solvents.
As other nitroalkane, 2-NP exists in tautomeric equilibrium with its nitronic acid isomers (protonated and anionic aci forms).The aci form is amphoterically reactive, the protonated form being electrophilic and the anionic form being nucleophilic.

Incineration: large quantities of material may require nitrogen oxide removal by catalytic or scrubbing processes. Dilute with pure kerosene and burn with care as it is potentially explosive. Consult with environmental regulatory agencies for guidance on acceptable disposal practices. Generators of waste containing this contaminant (≥100 kg/mo) must conform with EPA regulations governing storage, transportation, treatment, and waste disposal.

Colorless, oily liquid with a mild, fruity odor. 2-Nitropropane was detected in two studies at concentrations of 3.1 and 5.2 ppm_v (Crawford et al., 1984).

The synthesis of 2-nitropropane can be accomplished directly by nitration of 2-halopropanes with sodium nitrite. With 2-iodopropane, the reaction is carried out in dry DMF in the presence of urea. For the slower reacting 2-bromopropane, a longer reaction time and the presence of phloroglucinol as a nitrite ester scavenger is required.
Like 1-nitropropane, 2-nitropropane is also produced by vapor-phase nitration of propane with nitric acid at elevated temperature and pressure (Baker and Bollmeier 1978).

Like 1-nitropropane, 2-nitropropane is produced by vapor-phase nitration of propane with nitric acid at elevated temperature and pressure (Baker and Bollmeier 1978). U.S. production in 1977 was put at 30 million pounds (Finklea 1977). Amounts in use have been greatly reduced in recent times because of concern about its carcinogenic potential.

Solvent systems containing 2-nitropropane are used in various coatings, including vinyl, epoxy paints, nitrocellulose and chlorinated rubber, printing inks and adhesives. When mixed with oxidizers, it is used in explosives (HSDB 1988).

2-Nitropropane is reasonably anticipated to be a human carcinogenbased on sufficient evidence of carcinogenicity from studies in experimental animals.

Photolytic. Anticipated products from the reaction of 2-nitropropane with ozone or OH radicals in the atmosphere are formaldehyde and acetaldehyde (Cupitt, 1980).

After exposure of male Sprague-Dawley rats to 2-nitropropane (200 p.p.m. by inhalation, or 50 mg/kg intraperitoneally) the major pathway of elimination was by exhalation. Carbon dioxide, acetone and isopropanol were the major metabolites. Exhalation was also the major route of elimination after a dose of 10 mg/kg to chimpanzees (Muller et al 1983). Nonlinear elimination of 2-nitropropane was suggested by studies in which male Sprague-Dawley rats were exposed by inhalation to doses of 20 or 154 p.p.m. radiolabeled 2-nitropropane for 6 h (Nolan et al 1982). Average blood 2-nitropropane concentrations immediately following the 20 and 154 p.p.m. exposures were 0.6 and 7.1 μg/ml, respectively. Furthermore, raising the dose from 20 to 154 p.p.m. caused a greater fraction of the radioactivity to be excreted as unchanged 2-nitropropane. The dose-dependent changes in the elimination of 2-nitropropane may account, at least in part, for the increase in toxicity observed in rats exposed to large concentrations of 2-nitropropane (Lewis et al 1979).
Analysis of incubations of 2-nitropropane with liver microsomes of phenobarbital or 3-methylcholanthrene pretreated male Sprague-Dawley rats indicated that oxidative denitrification of 2-nitropropane produced acetone and nitrite (Ullrich et al 1978). This effect seems not to be dependent on pretreatment with a cytochrome P-450 inducer in other species or strains, since the hepatic microsomes from 5 strains of untreated mice all showed significant, but variable, NADPH-dependent ability to release nitrite from 2-nitropropane (Marker and Kulkarni 1985). Ullrich and coworkers (1978) considered that the reduction of the nitro group of 2-nitropropane to form 2-aminopropane was unlikely, at least in vitro, since the rate of oxidative denitrification of 2-nitropropane was unaltered in microsomal incubations under reduced oxygen tension. Whether any significant nitro group reduction of 2-nitropropane occurs in vivo to produce potentially reactive metabolites is unknown. Speck et al (1982), however, have shown that 2-aminopropane is not mutagenic in Salmonella tester strains.

Purify it as for nitromethane. [Beilstein 1 IV 230.]

DNA damage can cause 2-NP metabolites such as N-isopropyl hydroxylamine (IPHA) and hydroxylamine-O-sulfonic (HAS) acid by a reactive oxygen generating process that can be inhibited by free hydroxyl radical scavengers, catalase, and deferoxamine mesylate, an iron chelating agent. IPHA causes DNA damage at thymine and HAS most frequently induces DNA damage at 5'-TG-3', 5'-GG-3', and 5' -GGG-3' sequences. Formation of 8-oxodesoxyguanine by IPHA or HAS increased in the presence of metal ions.DNA damage caused by 2-NP metabolites plays an important role in mutagenicity and carcinogenicity of 2-NP. The liver damage induced by 2-NP is related to oxidative damage and reduction in catalase (CAT) activity.