Nitric oxide

30.00610

29.99800

233-271-0

31C4KY9ESH

1311

1660

DTXSID1020938

COLORLESS GAS; BLUE LIQ|BLUISH-WHITE SNOW WHEN SOLID|Brown at high concn in air

R07AX|R - Respiratory system

17.07000

-0.44710

colourless gas turning brown upon exposure to air

1.269 g/cm³

-163.6 °C

-151.74 °C

Index of Refraction: 1.0002697 @ 25 °C

5%

IN GENERAL, MATERIALS WHICH ARE TOXIC AS STORED OR WHICH CAN DECOMP INTO TOXIC COMPONENTS SHOULD BE STORED IN A COOL, WELL-VENTILATED PLACE, OUT OF DIRECT RAYS OF SUN, AWAY FROM AREAS OF HIGH FIRE HAZARD, & SHOULD BE PERIODICALLY INSPECTED INCOMPATIBLE MATERIALS SHOULD BE ISOLATED .

34.2 atm

1.05 (vs air)

Nonflammable Gas, but will accelerate the burning of combustible materials.

Sharp, sweet odor

TROUTON CONSTANT: 27.1; CONTAINS ODD NUMBERS OF ELECTRONS & IS PARAMAGNETIC|CONVERSION FACTORS: 1 PPM IS EQUIVALENT TO 1.23 MG/CU M; 1 MG/CU M IS EQUIVALENT TO 0.813 PPM|HEAT OF FORMATION: -21.5 KCAL/MOLE AT 18 °C|COMBINES WITH OXYGEN TO FORM NITROGEN DIOXIDE (BROWN GAS) & WITH CHLORINE & BROMINE TO FORM NITROSYL HALIDES, SUCH AS NITROSYL CHLORIDE.|Ionization potential: 9.27 eV

Combines very rapidly with oxygen in the air to form nitrogen dioxide. Nitrogen dioxide reacts with water to form nitric acid and nitric oxide, reacts with alkalis to form nitrates and nitrites [Merck 11th ed. 1989].

Oxidizing Agents, Strong

Explosive

NITRIC OXIDE can serve as both an oxidizing agent and as a reducing agent. Sustains the combustion of powdered aluminum [Mellor 5:209-212. 1946-47]. Enflames or explodes when mixed with vapors of carbon disulfide [Mellor 8, Supp. 2:232. 1967]. Reacts vigorously with sodium monoxide above 100°C [Mellor 2, Supp. 2:629. 1961]. Reacts on contact with oxygen at room temperature to form brown gaseous nitrogen dioxide. Reacts with alkalis to form nitrates and nitrites [Merck 11th ed. 1989]. The liquid is very sensitive to detonation in the presence of water.

9.27 eV

Nonflammable Gas, but will accelerate the burning of combustible materials.

3.293 KCAL/MOLE

CRITICAL TEMP: -92.9 °C; CRITICAL PRESSURE: 64.6 ATM

2.3

UN 1660 2

1

R8

S17; S23; S36/37/39; S45

QX0525000

O; T

Fireproof if in building. Keep in a well-ventilated room.

Spontaneously reacts with oxygen in air to yield brown nitrogen dioxide. Reacts violently or explosively with ammonia and many organic materials.

P220, P244, P260, P264, P270, P271, P284, P304+P340, P307+P311, P310, P320, P321, P370+P376, P403, P403+P233, P405, P410+P403, P501

H270

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P076, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.|Nitric oxide is a poor candidate for incineration.

WILL REACT WITH WATER OR STEAM TO PRODUCE HEAT & CORROSIVE FUMES|CAN REACT VIGOROUSLY WITH REDUCING MATERIALS|Fluorine, combustible materials, ozone, ammonia, chlorinated hydrocarbons, metals, carbon disulfide [Note: Reacts with water to form nitric acid. Rapidly converted in air to nitrogen dioxide].|NITRIC OXIDE & CARBON DISULFIDE REACT EXPLOSIVELY WITH EMISSION OF LIGHT; MIXTURE OF NITRIC OXIDE & CHLORINE MONOXIDE CAN BE EXPLOSIVE; NITROGEN TRICHLORIDE EXPLODES ON CONTACT WITH NITRIC OXIDE; MIXTURES OF NITRIC OXIDE & OZONE EXPLODE EVEN WHEN QUANTITY OF OZONE IS SMALL.|For more Hazardous Reactivities and Incompatibilities (Complete) data for NITRIC OXIDE (10 total), please visit the HSDB record page.

Environment Canada; Tech Info for Problem Spills: Nitric Acid (Draft) (1985).|USEPA; Draft Criteria Document: Oxides of Nitrogen (1983).

UN 1660 2

P220; P244; P260; P280; P303 + P361 + P353; P304 + P340 + P310; P305 + P351 + P338; P403 + P233; P410 + P403

Burns only when heated with hydrogen. With carbon disulfide, it reacts explosively with emission of light. When mixed with chlorine monoxide, can be explosive. Explodes on contact with nitrogen trichloride. When mixed with ozone, it will explode. Will react with water or steam to produce heat and corrosive fumes. Reacts vigorously with reducing materials. When heated to decomposition, highly toxic fumes of nitrogen oxides are emitted. May ignite other combustible materials (wood, paper, oil, etc.). Mixture with fuels may explode. Container may explode in heat of fire. Vapor explosion and poison hazard indoors, outdoors or in sewers. Reacts with oxygen to form poisonous nitrogen dioxide. Avoid storing in direct sunlight, or areas of high fire hazard. Incompatible with aluminum, boron, carbon disulfide, hypochlorite, chromium, fluorine, fuels, hydrocarbons, nitrogen trichloride, ozone, phosphorus, uns-dimethyl hydrazine, uranium, acetic anhydride, ammonia, barium oxide, boron trichloride, methyl chloride, 1,2-dichloroethane, dichloroethylene, ethylene, iron, magnesium, manganese, olefins, potassium, propylene, sodium, sulfur, trichloroethylene, 1,1,1-trichloroethane, uns-tetrachloroethaneand reducing agents. (EPA, 1998)|Not combustible but enhances combustion of other substances.|Reactive - 2nd degree

|Danger|H270 (100%): May cause or intensify fire; oxidizer [Danger Oxidizing gases]|P220, P244, P260, P261, P264, P271, P280, P284, P301+P330+P331, P303+P361+P353, P304+P340, P305+P351+P338, P310, P311, P314, P320, P321, P363, P370+P376, P403, P403+P233, P405, P410+P403, and P501|Aggregated GHS information provided by 281 companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H270: May cause or intensify fire; oxidizer [Danger Oxidizing gases]|P220, P244, P260, P264, P270, P271, P284, P304+P340, P307+P311, P310, P320, P321, P370+P376, P403, P403+P233, P405, P410+P403, and P501|P220, P244, P260, P261, P264, P270, P271, P304+P340, P307+P311, P311, P321, P370+P376, P403, P403+P233, P405, P410+P403, and P501

Wear positive pressure breathing apparatus and full protective clothing. Move container from fire area if you can do so without risk. Stay away from ends of tanks. Spray cooling water on containers that are exposed to flames until well after fire is out. For massive fire in cargo area, use unmanned hose holder or monitor nozzles; if this is impossible, withdraw from area and let fire burn. For small fires, use dry chemical or carbon dioxide. For large fires, use water spray, fog, or foam. (EPA, 1998)|In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep cylinder cool by spraying with water. Combat fire from a sheltered position.

Excerpt from ERG Guide 124 [Gases - Toxic and/or Corrosive - Oxidizing]: As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions. SPILL: See ERG Table 1 - Initial Isolation and Protective Action Distances on the UN/NA 1660 datasheet. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

Excerpt from ERG Guide 124 [Gases - Toxic and/or Corrosive - Oxidizing]: Fully encapsulating, vapor-protective clothing should be worn for spills and leaks with no fire. Do not touch or walk through spilled material. Keep combustibles (wood, paper, oil, etc.) away from spilled material. Stop leak if you can do it without risk. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Do not direct water at spill or source of leak. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. Isolate area until gas has dispersed. Ventilate the area. (ERG, 2016)

Skin: No recommendation is made specifying the need for personal protective equipment for the body. Eyes: No recommendation is made specifying the need for eye protection. Wash skin: No recommendation is made specifying the need for washing the substance from the skin (either immediately or at the end of the work shift). Remove: No recommendation is made specifying the need for removing clothing that becomes wet or contaminated. Change: No recommendation is made specifying the need for the worker to change clothing after the work shift. (NIOSH, 2016)|Vendor recommendations concerning the protective qualities of materials are as follows: Butyl and polyvinyl chloride received excellent or good ratings from less than three vendors, no fair or poor ratings, good or fair ratings with good ratings predominating, from several vendors.|Recommendations for respirator selection. Max concn for use: 100 ppm. Respirator Class(es): Any supplied-air respirator operated in a continuous-flow mode. May require eye protection. Any chemical cartridge respirator with a full facepiece and cartridge(s) providing protection against the compound of concern. Only nonoxidizable solvents allowed (not charcoal). Any powered, air-purifying respirator with cartridge(s) providing protection against the compound of concern. Only nonoxidizable solvents allowed (not charcoal). May require eye protection. Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. Only nonoxidizable solvents allowed (not charcoal). Any supplied-air respirator. May require eye protection. Any self-contained breathing apparatus with a full facepiece.|Recommendations for respirator selection. Condition: Emergency or planned entry into unknown concn or IDLH conditions: Respirator Class(es): Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode. Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode in combination with an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive-pressure mode.|Recommendations for respirator selection. Condition: Escape from suddenly occurring respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. Only nonoxidizable sorbents allowed (not charcoal). Any appropriate escape-type, self-contained breathing apparatus.|(See protection codes)

BURNS ONLY WHEN HEATED WITH HYDROGEN

1) VENTILATE AREA OF LEAK OR RELEASE TO DISPERSE GAS. 2) STOP FLOW OF GAS. IF SOURCE ... IS CYLINDER & LEAK CANNOT BE STOPPED IN PLACE, REMOVE ... CYLINDER TO SAFE PLACE IN OPEN AIR, & REPAIR LEAK OR ALLOW ... TO EMPTY.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emmissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.|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.

/GUIDE 124: GASES - TOXIC AND/OR CORROSIVE - OXIDIZING/ Health: TOXIC; may be fatal if inhaled or absorbed through skin. Fire will produce irritating, corrosive and/or toxic gases. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Runoff from fire control may cause pollution. /Nitric oxide; Nitric oxide, compressed/|/GUIDE 124: GASES - TOXIC AND/OR CORROSIVE - OXIDIZING/ Fire or Explosion: Substance does not burn but will support combustion. Vapors from liquefied gas are initially heavier than air and spread along ground. These are strong oxidizers and will react vigorously or explosively with many materials including fuels. May ignite combustibles (wood, paper, oil, clothing, etc.). Some will react violently with air, moist air and/or water. Cylinders exposed to fire may vent and release toxic and/or corrosive gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket. /Nitric oxide; Nitric oxide, compressed/|/GUIDE 124: GASES - TOXIC AND/OR CORROSIVE - OXIDIZING/ Public Safety: CALL Emergency Response Telephone Number ... . As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 `feet) in all directions. Keep unauthorized personnel away. Stay upwind. Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks). Keep out of low areas. Ventilate closed spaces before entering. /Nitric oxide; Nitric oxide, compressed/|/GUIDE 124: GASES - TOXIC AND/OR CORROSIVE - OXIDIZING/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. /Nitric oxide; Nitric oxide, compressed/|For more DOT Emergency Guidelines (Complete) data for NITRIC OXIDE (8 total), please visit the HSDB record page.

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./|The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.|The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

Irritation of eyes, nose & throat.|/HAZARD WARNING:/ Only slightly irritating to upper respiratory tract and eyes ... dangerous amounts of fumes may ... be inhaled before any discomfort is noticed.|Higher concentrations (60-150 ppm) cause immediate irritation of the nose and throat, with coughing and burning in the throat and chest. These symptoms often clear upon breathing fresh air, and the worker may feel well for several hours. Some 6-24 hours after exposure, a sensation of tightness and burning in the chest develops, followed by shortness of breath, sleeplessness, and restlessness.

Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 25 ppm (30 mg/cu m).

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 25 ppm (30 mg/cu m).

Personal protection: gas-tight chemical protection suit including self-contained breathing apparatus. Shut off cylinder if possible. Isolate the area until the gas has dispersed.

Fireproof if in building. Keep in a well-ventilated room.

A harmful concentration of this gas in the air will be reached very quickly on loss of containment.

Inhalation of high concentrations of the gas may cause damage to the lungs.

Repeated or prolonged inhalation may cause effects on the lungs.

NO contact with combustible substances.

STRICT HYGIENE!

Use ventilation.

Wear safety goggles or eye protection in combination with breathing protection.

| 3 - Materials that, under emergency conditions, can cause serious or permanent injury.| 0 - Materials that will not burn under typical fire conditions, including intrinsically noncombustible materials such as concrete, stone, and sand.| 0 - Materials that in themselves are normally stable, even under fire conditions.|OX - Oxidizer: Materials that possess oxidizing properties.

P076; An acute hazardous waste when a discarded commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).|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. Nitric oxide is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 100 lbs.

P076; As stipulated in 40 CFR 261.33, when nitric oxide, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).

IN TERMS OF AMT OF MATERIAL EMITTED ANNUALLY INTO AIR, FIVE MAJOR POLLUTANTS ACCOUNT FOR CLOSE TO 98% OF POLLUTION. ... NITROGEN OXIDES (6%). /NITROGEN OXIDES/

IDENTIFICATION: Nitric oxide is a colorless, odorless gas that is only slightly soluble in water. The main sources of nitrogen oxides (including nitric oxide) emissions are combustion processes. Fossil fuel power stations, motor vehicles and domestic combustion appliances emit nitrogen oxides, mostly in the form of nitric oxide. Nitric oxide can be present at significant concentrations in ambient air and in indoor air. HUMAN EXPOSURE: Human exposure to nitrogen oxides varies from indoors to outdoors, from cities to the countryside, and with the time of day and season. Nitric oxide is readily oxidized to nitrogen dioxide and peroxidation then occurs. Because of the concurrent exposure to some nitrogen dioxide in nitric oxide exposures, it is difficult to discriminate nitric oxide effects from nitrogen dioxide. Nitric oxide functions as an intracellular second messenger modulating a wide variety of essential enzymes, and it inhibits its own production (e.g., negative feedback). Nitric oxide activates guanylate cyclase which in turn increases intracellular cGMP levels. Nitric oxide is acknowledged as an important endogenous second messenger within several organ systems. At certain levels, inhaled nitric oxide concentrations can cause vasodilation in the pulmonary circulation without affecting the systemic circulation. The lowest effective concentration is not established. Information on pulmonary function and lung host defenses consequent to nitric oxide exposure are too limited for any conclusions to be drawn. Relatively high concentrations have been used in clinical applications for brief periods without reported adverse effects. ANIMAL STUDIES: The toxicological database for nitric oxide is small, relative to nitrogen dioxide. It is often difficult to obtain pure nitric oxide in air without some contamination with nitrogen dioxide. Endogenous nitric oxide synthesis occurs by nitric oxide formation from physiological substrate in cells of many of the organ systems such as nerve tissue, blood vessels and the immune system. Nitric oxide may be more potent than nitrogen dioxide in introducing certain changes in lung morphology. In a study examining the effects of nitric oxide on bacterial defenses, there were no statistically significant effects for either sex at any of the time points studied. In vitro data indicate that nitric oxide stimulates guanylate cyclase and leads to smooth muscle relaxation and vasodilation and functional effects on the nervous system. These effects are probably responsible for vasodilation in the pulmonary circulation and an acute bronchodilator effect of inhaled nitric oxide. Nitric oxide has an affinity for haem-bound iron which is two times higher than that of carbon monoxide. This affinity leads to the formation of methaemoglobin and the stimulation of guanylate cyclase. Furthermore, nitric oxide reacts with thiol-associated iron in enzymes and eventually displaces the iron. This is a possible mechanism for the cytotoxic effects of nitric oxide. Nitric oxide can deaminate DNA, evoke DNA chain breaks, and inhibit DNA polymerase and ribonucleotide reductase. It might be antimitogenic and inhibit T cell proliferation in rat spleen cells.

Nitric oxide (NO) is produced both by macrophages in vivo as a physiological response to infection and by a variety of cell types as an intercellular messenger. In addition, NO and nitrogen dioxide (NO2) are significant components of many combustion processes. The ubiquitous exposure of humans to nitrogen oxides (NOx), both endogenously and exogenously, may play a significant role in the carcinogenic process due to nitrosation of amines by NOx. We report here that exposure to low concentrations of NO, alone or in combination with NO2, results in significantly enhanced mutation in Salmonella typhimurium TA1535 using a modified Ames Salmonella reversion assay. The observed mutagenicity requires that the bacteria be actively dividing at the time of exposure to NO or NO2, suggesting that the nitrogen oxides, or their reaction products, function as direct-acting mutagens and that the induced lesion is easily repairable by non-dividing cells. Exposure to NO resulted in a time- and dose-dependent increase in the number of revertants approximately proportional to the square of the NO concentration from 0 to 20 ppm. NO was a more effective mutagen relative to NO2, however, the observed requirement for O2 suggests limited oxidation of NO (presumably to NO2) is necessary. Numerous lipid- and aqueous-phase inhibitors of nitrosation, as well as a number of other general antioxidants and free-radical trapping agents, were examined for their effectiveness in blocking the mutagenic effects of NO. The mutagenic activity of NO was most effectively inhibited by beta-carotene and tocopherols. BHT, dimethyl sulfoxide and mannitol also blocked the mutagenic effects of NOx but appeared less effective than beta-carotene or vitamin E, while ascorbate was ineffective as an inhibitor of mutation resulting from NO exposure.|... THE MECHANISM OF NITRIC OXIDE INTOXICATION SUGGESTS THAT IN MIXTURES WITH CARBON MONOXIDE, AS WELL AS NITROGEN DIOXIDE, ADDITIVE EFFECTS SHOULD BE ASSUMED.|The effects of nitric oxide (NO) and carbon monoxide on discrimination learning and brain activity were studied in rats. Male Long-Evans rats surgically instrumented with prefrontal and parietal electroencephalographic electrodes were exposed to 0, 100, or 500 ppm carbon monoxide or 10 or 50 ppm NO alone or in combination for 180 min. Effects on behavior (lever press task) and response to auditory stimulation were examined. Response to auditory stimulation was assessed by recording auditory evoked potentials. At the end of exposure, the rats were killed and blood carboxyhemoglobin and methemoglobin were determined. There was no significant difference between blood auditory evoked potential concn after exposure to 100 or 500 ppm carbon monoxide or 100 or 500 ppm carbon monoxide plus 10 or 50 ppm NO. Methemoglobin concn were significantly higher after exposure to 10 ppm NO plus 100 ppm carbon monoxide than after 10 ppm NO alone. Exposure to 50 ppm NO reduced the number of correct trials and the total number of lever presses significantly. Exposure to 500 ppm carbon monoxide decr the number of correct trials nonsignificantly and the total number of lever presses significantly. Combined carbon monoxide and NO exposure caused synergistic decr in number of correct trials and total number of trials. Carbon monoxide or NO caused increased amplitudes and prolonged latencies in early auditory evoked potential peaks. NO prolonged the latency of late auditory evoked potential peaks. Carbon monoxide incr the amplitude of the N150 peak, whereas NO decr its amplitude. The 10 ppm NO plus 100 ppm carbon monoxide exposure induced a combination effect that was less than additive. The 50 ppm NO plus 500 ppm carbon monoxide exposure induced an additive or synergistic effect on auditory evoked potential peak response. /It was concluded/ that NO plays a dominant role during intoxication with NO and carbon monoxide.|It as shown that preincubation of pancreatic islet cells with alpha-tocopherol significantly improves their resistance to toxic doses of nitric oxide. No protection was afforded by other antioxidants such as vitamin C or glutathione-monoethyl ester. The pathway of NO induced islet cell death involves DNA damage and excessive activation of poly(ADP-ribose)polymerase leading to irreversible depletion of intracellular NAD+. alpha-Tocopherol was found to interfere at early steps of this pathway, by preventing the occurrence of DNA strand breaks. This indicates that alpha-tocopherol directly interacts with nitric oxide or its reactive intermediates. Alpha-tocopherol is not only part of the cellular defence system against oxygen radicals but also protects eukaryotic cells from nitric oxide toxicity.

MAIN SOURCE OF URBAN NITRIC OXIDE ... IS COMBUSTION OF FOSSIL FUELS. ESCAPE OF ... GASES FROM INDUSTRIAL PROCESSES WHERE NITRIC OXIDE IS MADE OR USED, OR FROM FERTILIZER OR EXPLOSIVE FACTORIES, CAN BE IMPORTANT IN LOCAL AREA & IN PLANTS THEMSELVES. IN GENERAL, HIGHER COMBUSTION TEMP YIELD MORE NITROGEN OXIDES.|IN MOST URBAN AREAS THE CAR IS SINGLE LARGEST PRODUCER OF NITRIC OXIDE, WHICH MOVES SO RAPIDLY FROM ENGINE CYLINDER TO COOLER EXHAUST PIPES THAT IT IS PREVENTED FROM DECOMP ...|Volatile organics and nitrogen oxides are emitted by transportation and industrial sources. Oxides of nitrogen are emitted in the combustion of fossil fuels. /Nitrogen oxides/|... RELEASED IN REACTION BETWEEN NITRIC ACID & ANY ORG MATERIAL; IN EXHAUST FROM METAL CLEANING ... FROM ELECTRIC ARC WELDING; IN ELECTROPLATING, ENGRAVING, & PHOTOGRAVURE OPERATIONS; IN DYNAMITE BLASTING ... IN DIESEL ENGINE EXHAUST; IN BURNING OF NITROCELLULOSE ... & IN COMBUSTION OF SOME SHOE POLISHES. /NITROGEN OXIDES/

NITRIC OXIDE IS CONVERTED SPONTANEOUSLY IN AIR TO NITROGEN DIOXIDE, HENCE SOME OF LATTER GAS IS INVARIABLY PRESENT WHENEVER NITRIC OXIDE IS FOUND IN AIR. AT CONCN BELOW 50 PPM ... THIS REACTION IS SLOW ... & FREQUENTLY SUBSTANTIAL CONCN ... MAY OCCUR WITH NEGLIGIBLE QUANTITIES OF NITROGEN DIOXIDE ... .|PHOTOCHEMICAL AIR POLLUTION ARISES FROM A SERIES OF ATMOSPHERIC REACTIONS. THE MAIN COMPONENTS ARE OZONE, OXIDES OF NITROGEN, ALDEHYDES, PEROXYACETYL NITRATES, AND HYDROCARBONS. ... THEY ENTER INTO THE CHEMICAL REACTIONS THAT LEAD TO FORMATION OF PHOTOCHEMICAL SMOG. /OXIDES OF NITROGEN/

INDUSTRIAL EXPOSURES CAN TAKE PLACE WHEREVER NITRIC ACID IS MADE OR USED & HAS OCCURRED MOST COMMONLY WHERE METALS ARE DIPPED IN ACID BATHS. ELECTRIC ARC WELDING, & TO LESSER EXTENT GAS WELDING, CAN GENERATE HAZARDOUS CONCN. FERMENTATION OF SILAGE PRODUCES HIGH CONCN, & POISONINGS OF FARMERS HAVE OCCURRED.|APPROX 1.5 MILLION USA WORKERS ARE EXPOSED DIRECTLY OR INDIRECTLY TO OXIDES OF NITROGEN (NITRIC OXIDE, NITROGEN DIOXIDE, NITRIC ACID) THROUGH OCCUPATIONS INVOLVING WELDING, SILO FILLING & EXPLOSIVE MANUFACTURE. /FROM TABLE/

For the treatment of term and near-term (>34 weeks) neonates with hypoxic respiratory failure|INOmax, in conjunction with ventilatory support and other appropriate active substances, is indicated:for the treatment of newborn infants ≥34 weeks gestation with hypoxic respiratory failure associated with clinical or echocardiographic evidence of pulmonary hypertension, in order to improve oxygenation and to reduce the need for extracorporeal membrane oxygenation;as part of the treatment of peri- and post-operative pulmonary hypertension in adults and newborn infants, infants and toddlers, children and adolescents, ages 0-17 years in conjunction to heart surgery, in order to selectively decrease pulmonary arterial pressure and improve right ventricular function and oxygenation.|Other pulmonary heart disease, Persistent Pulmonary Hypertension

Bronchodilator Agents; Free Radical Scavengers; Vasodilator Agents|Although its use still is considered experimental, nitric oxide has been used successfully in some patients with persistent fetal circulation, pulmonary hypertension secondary to cardiac dysfunction or surgery, or with the adult respiratory distress syndrome.

Persistent pulmonary hypertension of the newborn (PPHN) occurs as a primary developmental defect or as a condition secondary to other diseases such as meconium aspiration syndrome (MAS), pneumonia, sepsis, hyaline membrane disease, congenital diaphragmatic hernia (CDH), and pulmonary hypoplasia. In these states, pulmonary vascular resistance (PVR) is high, which results in hypoxemia secondary to right-to-left shunting of blood through the patent ductus arteriosus and foramen ovale. In neonates with PPHN, Nitric oxide improves oxygenation (as indicated by significant increases in PaO2). Nitric oxide appears to increase the partial pressure of arterial oxygen (PaO2) by dilating pulmonary vessels in better entilated areas of the lung, redistributing pulmonary blood flow away from lung regions with low ventilation/perfusion (V/Q) ratios toward regions with normal ratios.

Agents that cause an increase in the expansion of a bronchus or bronchial tubes. (See all compounds classified as Bronchodilator Agents.)|Substances used for their pharmacological actions on any aspect of neurotransmitter systems. Neurotransmitter agents include agonists, antagonists, degradation inhibitors, uptake inhibitors, depleters, precursors, and modulators of receptor function. (See all compounds classified as Neurotransmitter Agents.)|Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN. (See all compounds classified as Endothelium-Dependent Relaxing Factors.)|Substances that eliminate free radicals. Among other effects, they protect PANCREATIC ISLETS against damage by CYTOKINES and prevent myocardial and pulmonary REPERFUSION INJURY. (See all compounds classified as Free Radical Scavengers.)|Endogenously produced lipid-soluble gaseous molecules which function as neurotransmitters and signal mediators targeting ION CHANNELS and transporters. (See all compounds classified as Gasotransmitters.)

Nitric oxide is absorbed systemically after inhalation.|Nitrate has been identified as the predominant nitric oxide metabolite excreted in the urine, accounting for >70% of the nitric oxide dose inhaled.|ABSORPTION IS BY WAY OF LUNG.|ON INHALATION, CONSIDERABLE PORTION ... IS ABSORBED IN UPPER RESP TRACT.|Most of the inhaled nitric oxide is eventually eliminated from the body as nitrate.|... it is efficiently (>80%) absorbed via inhalation ...|When seven volunteers inhaled 0.33, 0.5, 1, or 5 ppm, 85% to 93% of the inspired nitric oxide was retained.

via pulmonary capillary bed|The biotransformation of nitric oxide (NO) and its intermed metabolites, nitrite and nitrate ions, was reviewed: absorption and conversion of NO in blood, metabolism and excretion of inhaled NO, and conversion of nitrite and nitrate in the digestive system. ... The major proportion of inhaled NO reaches the deeper portion of the lung and reacts with hemoglobin in erythrocytes to form nitrosylhemoglobin which is converted immediately to nitrite and nitrate. The nitrate and nitrite are then transferred to the serum, and the greater part of the nitrate is excreted into the urine through the kidney. ... Part of the nitrate in the blood is secreted into the oral cavity through saliva and is converted to nitrite by oral bacteria, part of the nitrite that reaches the stomach is converted to nitrogen gas with the proteins of the diet and disappears, the intestinal nitrate transferred from the blood and stomach is converted to ammonia or unknown compounds through nitrite by the intestinal bacteria, the thus produced ammonia is absorbed through the intestinal wall into the body, and this ammonia is metabolized to urea through the urea cycle and excreted into the urine.

2–6 seconds

Nitric oxide is a compound produced by many cells of the body. It relaxes vascular smooth muscle by binding to the heme moiety of cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of cyclic guanosine 3',5'-monophosphate, which then leads to vasodilation. When inhaled, nitric oxide produces pulmonary vasodilation.|The effect of nitric oxide (NO) on blood hemoglobin was studied in vitro. Previously deoxygenated human blood was equilibrated with a continuous flow of 1,000 ppm NO, 5.6% carbon dioxide in nitrogen for 3 hours, and flushed for 30 min with 5.6% carbon dioxide in nitrogen. Nitrosylhemoglobin containing blood was equilibrated for various lengths of time with 21% oxygen and 5.6% carbon dioxide in nitrogen or 100% carbon monoxide for 1 hr. Methemoglobin was measured with an anaerobic method. Carboxyhemoglobin was measured. Anaerobic nitrosylhemoglobin blood/buffer solution was equilibratd with carbon monoxide and nitrogen. Acid/base blood changes in nitrosylhemoglobin and methemoglbin formation were determined after 1 hr of nitrogen equilibration, after 3 hr of NO equilibration, and after air exposure. The amount of methemoglobin formed was monitored by spectrophotometric changes of the anaerobic nitrosylhemoglobin solution after being exposed to air. Nitrosylhemoglobin exposure to oxygen incr the methemoglobin formation, with 59% and 78% of the total hemoglobin oxidized in the first 15 min and after 120 min of oxygen exposure, respectively. No significant methemoglobin was formed with nitrosylhemoglobin exposure to carbon dioxide. A total of 42% total hemoglobin in the nitrosylhemoglobin in the nitrosylhemoglobin blood/buffer solution was converted to methemoglobin after 30 min of air exposure and to 55% after 60 min of air exposure. NO exposure significantly decr the pH and base excess after 3 hr of exposure to NO. There were no significant changes after air exposure. ... /It was concluded/ that only under strict anaerobic conditions can NO combine with hemoglobin as nitrosylhemoglobin without any methemoglobin. NO is not a hemoglobin oxidant, it needs the presence of oxygen.

Can cause death or permanent injury after a very short exposure to small quantities. Irritant of eyes, nose, throat; can cause unconsciousness. Nitric oxide forms acids in the respiratory system which are irritating and cause congestion in the lungs. Concentrations of 60-150 ppm cause immediate irritation of the nose and throat with coughing and burning in the throat and chest. 6-24 hours after exposure, labored breathing and unconsciousness may result. Concentrations of 100-150 ppm are dangerous for short exposure of 30-60 minutes. Concentrations of 200-700 ppm may be fatal after very short exposure. (EPA, 1998)

Warning: Can cause permanent injury after very short exposure to small quantities. Delayed pulmonary edema can occur even following minimal early symptoms. Caution is advised. Signs and Symptoms of Nitric Oxide Exposure: Acute exposure to nitric oxide may result in changes of the pulmonary system including pulmonary edema, pneumonitis, bronchitis, bronchiolitis and emphysema. Mild or violent coughing, hyperpnea (rapid, deep breathing), and dyspnea (difficult or labored breathing) may occur. Fatigue, drowsiness, restlessness, anxiety, mental confusion, nausea and abdominal pain may be seen. Also weak rapid pulse, dilated heart, circulatory collapse, and loss of consciousness may be noted. Emergency Life-Support Procedures: Acute exposure to nitric oxide may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination. Inhalation Exposure: 1. Move victims to fresh air. Emergency personnel should avoid self-exposure to nitric oxide. 2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer 100% humidified oxygen or other respiratory support. 3. Obtain authorization and/or further instructions from the local hospital for performance of other invasive procedures. 4. Rush to a health care facility. Dermal/Eye Exposure: 1. Remove victims from exposure. Emergency personnel should avoid self-exposure to nitric oxide. 2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer 100% humidified oxygen or other respiratory support. 3. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes. 4. Obtain authorization and/or further instructions from the local hospital for performance of other invasive procedures. 5. Rush to a health care facility. Ingestion Exposure: Note: Ingestion of nitric oxide gas is not expected to be a significant route of exposure. 1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer 100% humidified oxygen or other respiratory support. 2. Obtain authorization and/or further instructions from the local hospital for performance of other invasive procedures. 3. Rush to a health care facility. (EPA, 1998)|(See procedures)

Fresh air, rest.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Basic treatment: Establish a patent airway. Suction if necessary. Aggressive airway management may be needed. Encourage patient to take deep breaths. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuosly with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. ... /Nitrogen oxides (NOX) and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or in respiratory arrest. Early intubation at the first signs of upper airway obstruction may be necessary. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W TKO /SRP: "To keep open", minimal flow rate/. Consider drug therapy for pulmonary edema ... . Consider the use of vasopressors to treat hypotension without signs of hypovolemia ... . Administer 1% solution methylene blue if patient is symptomatic with severe hypoxia, cyanosis, and cardiac compromise not responding to oxygen. ... . Use proparacaine hydrochloride to assist eye irrigation. /Nitrogen oxides (NOX) and related compounds/

CHIEF TOXIC EFFECT ... ASCRIBED TO FORMATION OF METHEMOGLOBIN & SUBSEQUENT ACTION ON CNS.|SYMPTOMATOLOGY: 1. Usually no symptoms occur at the time of exposure, with the exception of a slight cough and perhaps fatigue and nausea. Exposure to low concn may result in impaired pulmonary defense mechanisms (macrophages, cilia) with complications. ... 2. Only very concn nitrous fumes produce prompt coughing, choking, headache, nausea, abdominal pain, and dyspnea (tightness and burning pain in the chest). 3. A symptom-free period follows exposure and lasts for 5-72 hr. 4. Fatigue, uneasiness, restlessness, cough, hyperpnea, and dyspnea appear insidiously, as the adult respiratory distress syndrome gradually develops. /Nitrogen oxides/|SYMPTOMATOLOGY: 5. Increasingly rapid and shallow respirations, cyanosis, mild or violent coughing with frothy expectoration and physical signs of pulmonary edema (for example rales and rhonchi). The vital capacity is rapidly reduced. A serous exudate may develop in the pleural cavity, but its volume is usually small. 6. Anxiety, mental confusion, lethary and finally loss of consciousness. 7. A weak, rapid pulse, dilated heart, venous congestion, intense cyanosis and severe hemoconcentration. Circulatory collapse is secondary to anoxia and hemoconcentration. 8. An asphyxial death due to blockade of gas exchange in the lungs. Death commonly occurs within a few hours after the first evidence of pulmonary edema. /Nitrogen oxides/|SYMPTOMATOLOGY: 9. Sometimes a second acute phase follows the initial pulmonary reaction after a quiescent period of several weeks. Cough, tachypnea, dyspnea, fever, tachycardia and cyanosis at this stage are usually due to bronchiolitis obliterans. The relapse may be abrupt and fulminating, leading either to death or a slow convalescence. 10. In nonfatal cases, convalescence may be complicated by infectious bronchitis, bronchiolitis obliterans, pneumonia and general asthenia. Rarely diffuse pulmonary fibrosis may develop. /Nitrogen oxides/|For more Human Toxicity Excerpts (Complete) data for NITRIC OXIDE (11 total), please visit the HSDB record page.

Endogenous Nitrate Vasodilator

The substance can be absorbed into the body by inhalation.|inhalation

irritation eyes, wet skin, nose, throat; drowsiness, unconsciousness; methemoglobinemia

Cough. Shortness of breath.

Redness.

Eyes, skin, respiratory system, blood, central nervous system

Grade: Pure, 99%

Nitrogen oxide (NO): ACTIVE|NITRIC OXIDE ... IS FORMED WHEN COMBUSTION TAKES PLACE AT HIGH ENOUGH TEMP TO CAUSE REACTION BETWEEN AIR'S NITROGEN & OXYGEN.

NITRITE ION (NO2-) DETECTED IN AIR BY SPECTROPHOTOMETRIC ANALYSIS AT 540 NM AFTER OXIDATION TO NITROGEN DIOXIDE, COLLECTION ON TRIETHANOLAMINE-COATED MOLECULAR SIEVE & DESORPTION WITH TRIETHANOLAMINE. RANGE 11.1 TO 48 PPM IN 1.5 L AIR SAMPLE.|CHEMILUMINESCENT METHOD DEPENDS ON REACTION BETWEEN NITRIC OXIDE & OZONE, WHICH EMITS LIGHT THAT CAN BE MEASURED. ... COMMERCIAL INSTRUMENTS ... DEVELOPED THAT ARE STABLE, SENSITIVE & DURABLE. ... GAS-PHASE TITRATION IS USED TO ATTAIN SATISFACTORY PRECISION: JONES W & RIDGIK T, AM IND HYG ASSOC J 41: 433 (1980).

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