Nitrous oxide

Nitrous oxide, commonly known as laughing gas or nitrous,[1] is a chemical compound, an oxide of nitrogen with the formula N
. At room temperature, it is a colourless non-flammable gas, with a slight metallic scent and taste. At elevated temperatures, nitrous oxide is a powerful oxidiser similar to molecular oxygen. It is soluble in water.

Nitrous oxide has significant medical uses, especially in surgery and dentistry, for its anaesthetic and pain reducing effects. Its name "laughing gas", coined by Humphry Davy, is due to the euphoric effects upon inhaling it, a property that has led to its recreational use as a dissociative anaesthetic. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[2] It also is used as an oxidiser in rocket propellants, and in motor racing to increase the power output of engines.

Nitrous oxide occurs in small amounts in the atmosphere, but recently has been found to be a major scavenger of stratospheric ozone, with an impact comparable to that of CFCs. It is estimated that 30% of the N
in the atmosphere is the result of human activity, chiefly agriculture.[3]

Nitrous oxide
Nitrous oxide's canonical forms
Ball-and-stick model with bond lengths
Space-filling model of nitrous oxide
IUPAC name
Dinitrogen monoxide
Other names
Laughing gas, sweet air, protoxide of nitrogen, hyponitrous oxide
3D model (JSmol)
ECHA InfoCard 100.030.017
E number E942 (glazing agents, ...)
RTECS number QX1350000
UN number 1070 (compressed)
2201 (liquid)
Molar mass 44.013 g/mol
Appearance colourless gas
Density 1.977 g/L (gas)
Melting point −90.86 °C (−131.55 °F; 182.29 K)
Boiling point −88.48 °C (−127.26 °F; 184.67 K)
1.5 g/L (15 °C)
Solubility soluble in alcohol, ether, sulfuric acid
log P 0.35
Vapor pressure 5150 kPa (20 °C)
−18.9·10−6 cm3/mol
1.000516 (0 °C, 101,325 kPa)
linear, C∞v
0.166 D
219.96 J K−1 mol−1
+82.05 kJ mol−1
N01AX13 (WHO)
  • US: C (Risk not ruled out)
5 minutes
Safety data sheet, ICSC 0067
NFPA 704
Flash point Nonflammable
Related compounds
Nitric oxide
Dinitrogen trioxide
Nitrogen dioxide
Dinitrogen tetroxide
Dinitrogen pentoxide
Related compounds
Ammonium nitrate
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).


Rocket motors

Nitrous oxide may be used as an oxidiser in a rocket motor. This is advantageous over other oxidisers in that it is much less toxic, and due to its stability at room temperature is also easier to store and relatively safe to carry on a flight. As a secondary benefit, it may be decomposed readily to form breathing air. Its high density and low storage pressure (when maintained at low temperature) enable it to be highly competitive with stored high-pressure gas systems.[4]

In a 1914 patent, American rocket pioneer Robert Goddard suggested nitrous oxide and gasoline as possible propellants for a liquid-fuelled rocket.[5] Nitrous oxide has been the oxidiser of choice in several hybrid rocket designs (using solid fuel with a liquid or gaseous oxidiser). The combination of nitrous oxide with hydroxyl-terminated polybutadiene fuel has been used by SpaceShipOne and others. It also is notably used in amateur and high power rocketry with various plastics as the fuel.

Nitrous oxide also may be used in a monopropellant rocket. In the presence of a heated catalyst, N
will decompose exothermically into nitrogen and oxygen, at a temperature of approximately 1,070 °F (577 °C).[6] Because of the large heat release, the catalytic action rapidly becomes secondary, as thermal autodecomposition becomes dominant. In a vacuum thruster, this may provide a monopropellant specific impulse (Isp) of as much as 180 s. While noticeably less than the Isp available from hydrazine thrusters (monopropellant or bipropellant with dinitrogen tetroxide), the decreased toxicity makes nitrous oxide an option worth investigating.

Nitrous oxide is said to deflagrate at approximately 600 °C (1,112 °F) at a pressure of 309 psi (21 atmospheres).[7] At 600 psi, for example, the required ignition energy is only 6 joules, whereas N
at 130 psi a 2,500-joule ignition energy input is insufficient.[8][9]

Internal combustion engine

In vehicle racing, nitrous oxide (often referred to as just "nitrous") allows the engine to burn more fuel by providing more oxygen than air alone, resulting in a more powerful combustion. The gas is not flammable at a low pressure/temperature, but it delivers more oxygen than atmospheric air by breaking down at elevated temperatures. Therefore, it often is mixed with another fuel that is easier to deflagrate. Nitrous oxide is a strong oxidant, roughly equivalent to hydrogen peroxide, and much stronger than oxygen gas.

Nitrous oxide is stored as a compressed liquid; the evaporation and expansion of liquid nitrous oxide in the intake manifold causes a large drop in intake charge temperature, resulting in a denser charge, further allowing more air/fuel mixture to enter the cylinder. Sometimes nitrous oxide is injected into (or prior to) the intake manifold, whereas other systems directly inject, right before the cylinder (direct port injection) to increase power.

The technique was used during World War II by Luftwaffe aircraft with the GM-1 system to boost the power output of aircraft engines. Originally meant to provide the Luftwaffe standard aircraft with superior high-altitude performance, technological considerations limited its use to extremely high altitudes. Accordingly, it was only used by specialised planes such as high-altitude reconnaissance aircraft, high-speed bombers and high-altitude interceptor aircraft. It sometimes could be found on Luftwaffe aircraft also fitted with another engine-boost system, MW 50, a form of water injection for aviation engines that used methanol for its boost capabilities.

One of the major problems of using nitrous oxide in a reciprocating engine is that it can produce enough power to damage or destroy the engine. Very large power increases are possible, and if the mechanical structure of the engine is not properly reinforced, the engine may be severely damaged, or destroyed, during this kind of operation. It is very important with nitrous oxide augmentation of petrol engines to maintain proper operating temperatures and fuel levels to prevent "pre-ignition",[10] or "detonation" (sometimes referred to as "knock"). Most problems that are associated with nitrous oxide do not come from mechanical failure due to the power increases. Since nitrous oxide allows a much denser charge into the cylinder, it dramatically increases cylinder pressures. The increased pressure and temperature can cause problems such as melting the piston or valves. It also may crack or warp the piston or head and cause pre-ignition due to uneven heating.

Automotive-grade liquid nitrous oxide differs slightly from medical-grade nitrous oxide. A small amount of sulfur dioxide (SO
) is added to prevent substance abuse.[11] Multiple washes through a base (such as sodium hydroxide) can remove this, decreasing the corrosive properties observed when SO
is further oxidised during combustion into sulfuric acid, making emissions cleaner.

Aerosol propellant

N2O whippets
Food-grade N

The gas is approved for use as a food additive (also known as E942), specifically as an aerosol spray propellant. Its most common uses in this context are in aerosol whipped cream canisters and cooking sprays.

The gas is extremely soluble in fatty compounds. In aerosol whipped cream, it is dissolved in the fatty cream until it leaves the can, when it becomes gaseous and thus creates foam. Used in this way, it produces whipped cream four times the volume of the liquid, whereas whipping air into cream only produces twice the volume. If air were used as a propellant, oxygen would accelerate rancidification of the butterfat, but nitrous oxide inhibits such degradation. Carbon dioxide cannot be used for whipped cream because it is acidic in water, which would curdle the cream and give it a seltzer-like "sparkling" sensation.

The whipped cream produced with nitrous oxide is unstable, however, and will return to a more liquid state within half an hour to one hour.[12] Thus, the method is not suitable for decorating food that will not be served immediately.

During December 2016, some manufacturers reported a shortage of aerosol whipped creams in the United States due to an explosion at the Air Liquide nitrous oxide facility in Florida in late August. With a major facility offline, the disruption caused a shortage resulting in the company diverting the supply of nitrous oxide to medical clients rather than to food manufacturing. The shortage came during the Christmas and holiday season when canned whipped cream use is normally at its highest.[13]

Similarly, cooking spray, which is made from various types of oils combined with lecithin (an emulsifier), may use nitrous oxide as a propellant. Other propellants used in cooking spray include food-grade alcohol and propane.


N2O Medical Tanks
Medical-grade N
tanks used in dentistry

Nitrous oxide has been used in dentistry and surgery, as an anaesthetic and analgesic, since 1844.[14]

In the early days, the gas was administered through simple inhalers consisting of a breathing bag made of rubber cloth.[15] Today, the gas is administered in hospitals by means of an automated relative analgesia machine, with an anaesthetic vaporiser and a medical ventilator, that delivers a precisely dosed and breath-actuated flow of nitrous oxide mixed with oxygen in a 2:1 ratio.

Nitrous oxide is a weak general anaesthetic, and so is generally not used alone in general anaesthesia, but used as a carrier gas (mixed with oxygen) for more powerful general anaesthetic drugs such as sevoflurane or desflurane. It has a minimum alveolar concentration of 105% and a blood/gas partition coefficient of 0.46. The use of nitrous oxide in anaesthesia, however, can increase the risk of postoperative nausea and vomiting.[16][17][18]

Dentists use a simpler machine, that only delivers a N
mixture for the patient to inhale while conscious. The patient is kept conscious throughout the procedure, and retains adequate mental faculties to respond to questions and instructions from the dentist.[19]

Inhalation of nitrous oxide is used frequently to relieve pain associated with childbirth, trauma, oral surgery and acute coronary syndrome (includes heart attacks). Its use during labour has been shown to be a safe and effective aid for birthing women.[20] Its use for acute coronary syndrome is of unknown benefit.[21]

In Britain and Canada, Entonox and Nitronox are used commonly by ambulance crews (including unregistered practitioners) as a rapid and highly effective analgesic gas.

Fifty per cent nitrous oxide can be considered for use by trained non-professional first aid responders in prehospital settings, given the relative ease and safety of administering 50% nitrous oxide as an analgesic. The rapid reversibility of its effect would also prevent it from precluding diagnosis.[22]

Recreational use

Doctor and Mrs Syntax, with a party of friends, experimentin Wellcome L0022227
Aquatint depiction of a laughing gas party in the nineteenth century
Nitrous oxide whippits used recreationally as a drug by Dutch youngsters near a school, Utrecht, 2017 - 1
Whippit remnants of recreational drug use, the Netherlands, 2017

Recreational inhalation of nitrous oxide, with the purpose of causing euphoria and/or slight hallucinations, began as a phenomenon for the British upper class in 1799, known as "laughing gas parties".

Starting in the nineteenth century, widespread availability of the gas for medical and culinary purposes allowed the recreational use to expand greatly throughout the world. In the United Kingdom, as of 2014, nitrous oxide was estimated to be used by almost half a million young people at nightspots, festivals and parties.[23] The legality of that use varies greatly from country to country, and even from city to city in some countries.

Widespread recreational use of the drug throughout the UK was featured in the 2017 Vice documentary Inside The Laughing Gas Black Market, in which journalist Matt Shea met with dealers of the drug who stole it from hospitals.[24]


The major safety hazards of nitrous oxide come from the fact that it is a compressed liquefied gas, an asphyxiation risk and a dissociative anaesthetic.

While relatively non-toxic, nitrous oxide has a number of recognised ill effects on human health, whether through breathing it in or by contact of the liquid with skin or eyes.

Nitrous oxide is a significant occupational hazard for surgeons, dentists and nurses. Because nitrous oxide is minimally metabolised in humans (with a rate of 0.004%), it retains its potency when exhaled into the room by the patient, and can pose an intoxicating and prolonged exposure hazard to the clinic staff if the room is poorly ventilated. Where nitrous oxide is administered, a continuous-flow fresh-air ventilation system or N
scavenger system is used to prevent a waste-gas buildup.

The National Institute for Occupational Safety and Health recommends that workers' exposure to nitrous oxide should be controlled during the administration of anaesthetic gas in medical, dental and veterinary operators.[25] It set a recommended exposure limit (REL) of 25 ppm (46 mg/m3) to escaped anaesthetic.[26]

Mental and manual impairment

Exposure to nitrous oxide causes short-term decreases in mental performance, audiovisual ability and manual dexterity.[27] These effects coupled with the induced spatial and temporal disorientation could result in physical harm to the user from environmental hazards.[28]

Neurotoxicity and neuroprotection

Like other NMDA antagonists, N
was suggested to produce neurotoxicity in the form of Olney's lesions in rodents upon prolonged (several hour) exposure.[29][30][31][32] New research has arisen suggesting that Olney's lesions do not occur in humans, however, and similar drugs such as ketamine are now believed not to be acutely neurotoxic.[33][34] It has been argued that, because N
has a very short duration under normal circumstances, it is less likely to be neurotoxic than other NMDA antagonists.[35] Indeed, in rodents, short-term exposure results in only mild injury that is rapidly reversible, and neuronal death occurs only after constant and sustained exposure.[29] Nitrous oxide also may cause neurotoxicity after extended exposure because of hypoxia. This is especially true of non-medical formulations such as whipped-cream chargers (also known as "whippets" or "nangs"),[36] which never contain oxygen, since oxygen makes cream rancid.[37]

Additionally, nitrous oxide depletes vitamin B12 levels. This can cause serious neurotoxicity if the user has preexisting vitamin B12 deficiency.[38]

Nitrous oxide at 75% by volume reduces ischemia-induced neuronal death induced by occlusion of the middle cerebral artery in rodents, and decreases NMDA-induced Ca2+ influx in neuronal cell cultures, a critical event involved in excitotoxicity.[39]

Oxygen deprivation

If pure nitrous oxide is inhaled without oxygen mixed in, this can eventually lead to oxygen deprivation resulting in loss of blood pressure, fainting and even heart attacks. This can occur if the user inhales large quantities continuously, as with a strap-on mask connected to a gas canister. It can also happen if the user engages in excessive breath-holding or uses any other inhalation system that cuts off a supply of fresh air.[40]

Vitamin B12 deficiency

Long-term exposure to nitrous oxide may cause vitamin B12 deficiency. It inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy and encephalopathy, may occur within days or weeks of exposure to nitrous oxide anaesthesia in people with subclinical vitamin B12 deficiency.

Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete.[41]

People with normal vitamin B12 levels have stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (nitrous oxide abuse). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anaesthesia.[42]

Prenatal development

Several experimental studies in rats indicate that chronic exposure of pregnant females to nitrous oxide may have adverse effects on the developing fetus.[43][43][44][45]

Chemical/physical risks

At room temperature (20 °C [68 °F]) the saturated vapour pressure is 50.525 bar, rising up to 72.45 bar at 36.4 °C (97.5 °F)—the critical temperature. The pressure curve is thus unusually sensitive to temperature.[46] Liquid nitrous oxide acts as a good solvent for many organic compounds; liquid mixtures may form shock sensitive explosives.

As with many strong oxidisers, contamination of parts with fuels have been implicated in rocketry accidents, where small quantities of nitrous/fuel mixtures explode due to "water hammer"-like effects (sometimes called "dieseling"—heating due to adiabatic compression of gases can reach decomposition temperatures).[47] Some common building materials such as stainless steel and aluminium can act as fuels with strong oxidisers such as nitrous oxide, as can contaminants that may ignite due to adiabatic compression.[48]

There also have been incidents where nitrous oxide decomposition in plumbing has led to the explosion of large tanks.[7]

Mechanism of action

The pharmacological mechanism of action of N
in medicine is not fully known. However, it has been shown to directly modulate a broad range of ligand-gated ion channels, and this likely plays a major role in many of its effects. It moderately blocks NMDA and β2-subunit-containing nACh channels, weakly inhibits AMPA, kainate, GABAC and 5-HT3 receptors, and slightly potentiates GABAA and glycine receptors.[49][50] It also has been shown to activate two-pore-domain K+
.[51] While N
affects quite a few ion channels, its anaesthetic, hallucinogenic and euphoriant effects are likely caused predominantly, or fully, via inhibition of NMDA receptor-mediated currents.[49][52] In addition to its effects on ion channels, N
may act to imitate nitric oxide (NO) in the central nervous system, and this may be related to its analgesic and anxiolytic properties.[52] Nitrous oxide is 30 to 40 times more soluble than nitrogen.

The effects of inhaling sub-anaesthetic doses of nitrous oxide have been known to vary, based on several factors, including settings and individual differences;[53][54] however, from his discussion, Jay (2008)[28] suggests that it has been reliably known to induce the following states and sensations:

  • Intoxication
  • Euphoria/dysphoria
  • Spatial disorientation
  • Temporal disorientation
  • Reduced pain sensitivity

A minority of users also will present with uncontrolled vocalisations and muscular spasms. These effects generally disappear minutes after removal of the nitrous oxide source.[28]

Euphoric effect

In rats, N
stimulates the mesolimbic reward pathway via inducing dopamine release and activating dopaminergic neurons in the ventral tegmental area and nucleus accumbens, presumably through antagonisation of NMDA receptors localised in the system.[55][56][57][58] This action has been implicated in its euphoric effects and, notably, appears to augment its analgesic properties as well.[55][56][57][58]

It is remarkable, however, that in mice, N
blocks amphetamine-induced carrier-mediated dopamine release in the nucleus accumbens and behavioural sensitisation, abolishes the conditioned place preference (CPP) of cocaine and morphine, and does not produce reinforcing (or aversive) effects of its own.[59][60] Effects of CPP of N
in rats are mixed, consisting of reinforcement, aversion and no change.[61] In contrast, it is a positive reinforcer in squirrel monkeys,[62] and is well known as a drug of abuse in humans.[63] These discrepancies in response to N
may reflect species variation or methodological differences.[60] In human clinical studies, N
was found to produce mixed responses, similarly to rats, reflecting high subjective individual variability.[64][65]

Anxiolytic effect

In behavioural tests of anxiety, a low dose of N
is an effective anxiolytic, and this anti-anxiety effect is associated with enhanced activity of GABAA receptors, as it is partially reversed by benzodiazepine receptor antagonists. Mirroring this, animals that have developed tolerance to the anxiolytic effects of benzodiazepines are partially tolerant to N
.[66] Indeed, in humans given 30% N
, benzodiazepine receptor antagonists reduced the subjective reports of feeling "high", but did not alter psychomotor performance, in human clinical studies.[67]

Analgesic effect

The analgesic effects of N
are linked to the interaction between the endogenous opioid system and the descending noradrenergic system. When animals are given morphine chronically, they develop tolerance to its pain-killing effects, and this also renders the animals tolerant to the analgesic effects of N
.[68] Administration of antibodies that bind and block the activity of some endogenous opioids (not β-endorphin) also block the antinociceptive effects of N
.[69] Drugs that inhibit the breakdown of endogenous opioids also potentiate the antinociceptive effects of N
.[69] Several experiments have shown that opioid receptor antagonists applied directly to the brain block the antinociceptive effects of N
, but these drugs have no effect when injected into the spinal cord.

Conversely, α2-adrenoceptor antagonists block the pain-reducing effects of N
when given directly to the spinal cord, but not when applied directly to the brain.[70] Indeed, α2B-adrenoceptor knockout mice or animals depleted in norepinephrine are nearly completely resistant to the antinociceptive effects of N
.[71] Apparently N
-induced release of endogenous opioids causes disinhibition of brainstem noradrenergic neurons, which release norepinephrine into the spinal cord and inhibit pain signalling.[72] Exactly how N
causes the release of endogenous opioid peptides remains uncertain.

Properties and reactions

Nitrous oxide is a colourless, non-toxic gas with a faint, sweet odour.

Nitrous oxide supports combustion by releasing the dipolar bonded oxygen radical, thus it can relight a glowing splint.

is inert at room temperature and has few reactions. At elevated temperatures, its reactivity increases. For example, nitrous oxide reacts with NaNH
at 460 K (187 °C) to give NaN

2 NaNH
+ N
+ NaOH + NH

The above reaction is the route adopted by the commercial chemical industry to produce azide salts, which are used as detonators.[73]


The gas was first synthesised in 1772 by English natural philosopher and chemist Joseph Priestley who called it phlogisticated nitrous air (see phlogiston theory)[74] or inflammable nitrous air.[75] Priestley published his discovery in the book Experiments and Observations on Different Kinds of Air (1775), where he described how to produce the preparation of "nitrous air diminished", by heating iron filings dampened with nitric acid.[76]

Early use

Laughing gas Rumford Davy
A satirical print from 1830 depicting Humphry Davy administering a dose of laughing gas to a woman

The first important use of nitrous oxide was made possible by Thomas Beddoes and James Watt, who worked together to publish the book Considerations on the Medical Use and on the Production of Factitious Airs (1794). This book was important for two reasons. First, James Watt had invented a novel machine to produce "Factitious Airs" (i.e. nitrous oxide) and a novel "breathing apparatus" to inhale the gas. Second, the book also presented the new medical theories by Thomas Beddoes, that tuberculosis and other lung diseases could be treated by inhalation of "Factitious Airs".[14]

Anaesthesia exhibition, 1946 Wellcome M0009908
Sir Humphry Davy's Researches chemical and philosophical: chiefly concerning nitrous oxide (1800), pages 556 and 557 (right), outlining potential anaesthetic properties of nitrous oxide in relieving pain during surgery

The machine to produce "Factitious Airs" had three parts: a furnace to burn the needed material, a vessel with water where the produced gas passed through in a spiral pipe (for impurities to be "washed off"), and finally the gas cylinder with a gasometer where the gas produced, "air", could be tapped into portable air bags (made of airtight oily silk). The breathing apparatus consisted of one of the portable air bags connected with a tube to a mouthpiece. With this new equipment being engineered and produced by 1794, the way was paved for clinical trials, which began in 1798 when Thomas Beddoes established the "Pneumatic Institution for Relieving Diseases by Medical Airs" in Hotwells (Bristol). In the basement of the building, a large-scale machine was producing the gases under the supervision of a young Humphry Davy, who was encouraged to experiment with new gases for patients to inhale.[14] The first important work of Davy was examination of the nitrous oxide, and the publication of his results in the book: Researches, Chemical and Philosophical (1800). In that publication, Davy notes the analgesic effect of nitrous oxide at page 465 and its potential to be used for surgical operations at page 556.[77] Davy coined the name "laughing gas" for nitrous oxide.[78]

Despite Davy's discovery that inhalation of nitrous oxide could relieve a conscious person from pain, another 44 years elapsed before doctors attempted to use it for anaesthesia. The use of nitrous oxide as a recreational drug at "laughing gas parties", primarily arranged for the British upper class, became an immediate success beginning in 1799. While the effects of the gas generally make the user appear stuporous, dreamy and sedated, some people also "get the giggles" in a state of euphoria, and frequently erupt in laughter.[79]

One of the earliest commercial producers in the U.S. was George Poe, cousin of the poet Edgar Allan Poe, who also was the first to liquefy the gas.[80]

Anaesthetic use

The first time nitrous oxide was used as an anaesthetic drug in the treatment of a patient was when dentist Horace Wells, with assistance by Gardner Quincy Colton and John Mankey Riggs, demonstrated insensitivity to pain from a dental extraction on 11 December 1844.[81] In the following weeks, Wells treated the first 12 to 15 patients with nitrous oxide in Hartford, Connecticut, and, according to his own record, only failed in two cases.[82] In spite of these convincing results having been reported by Wells to the medical society in Boston in December 1844, this new method was not immediately adopted by other dentists. The reason for this was most likely that Wells, in January 1845 at his first public demonstration to the medical faculty in Boston, had been partly unsuccessful, leaving his colleagues doubtful regarding its efficacy and safety.[83] The method did not come into general use until 1863, when Gardner Quincy Colton successfully started to use it in all his "Colton Dental Association" clinics, that he had just established in New Haven and New York City.[14] Over the following three years, Colton and his associates successfully administered nitrous oxide to more than 25,000 patients.[15] Today, nitrous oxide is used in dentistry as an anxiolytic, as an adjunct to local anaesthetic.

Nitrous oxide was not found to be a strong enough anaesthetic for use in major surgery in hospital settings, however. Instead, diethyl ether, being a stronger and more potent anaesthetic, was demonstrated and accepted for use in October 1846, along with chloroform in 1847.[14] When Joseph Thomas Clover invented the "gas-ether inhaler" in 1876, however, it became a common practice at hospitals to initiate all anaesthetic treatments with a mild flow of nitrous oxide, and then gradually increase the anaesthesia with the stronger ether or chloroform. Clover's gas-ether inhaler was designed to supply the patient with nitrous oxide and ether at the same time, with the exact mixture being controlled by the operator of the device. It remained in use by many hospitals until the 1930s.[15] Although hospitals today are using a more advanced anaesthetic machine, these machines still use the same principle launched with Clover's gas-ether inhaler, to initiate the anaesthesia with nitrous oxide, before the administration of a more powerful anaesthetic.

As a patent medicine

Colton's popularisation of nitrous oxide led to its adoption by a number of less than reputable quacksalvers, who touted it as a cure for consumption, scrofula, catarrh and other diseases of the blood, throat and lungs. Nitrous oxide treatment was administered and licensed as a patent medicine by the likes of C. L. Blood and Jerome Harris in Boston and Charles E. Barney of Chicago.[84][85]


Reviewing various methods of producing nitrous oxide is published.[86]

Industrial methods

Nitrous oxide production
Nitrous oxide production

Nitrous oxide is prepared on an industrial scale by careful heating of ammonium nitrate[86] at about 250 C, which decomposes into nitrous oxide and water vapour.[87]

→ 2 H
+ N

The addition of various phosphate salts favours formation of a purer gas at slightly lower temperatures. This reaction may be difficult to control, resulting in detonation.[88]

Laboratory methods

The decomposition of ammonium nitrate is also a common laboratory method for preparing the gas. Equivalently, it can be obtained by heating a mixture of sodium nitrate and ammonium sulfate:[89]

2 NaNO
+ (NH
+ 2 N
+ 4 H

Another method involves the reaction of urea, nitric acid and sulfuric acid:[90]

2 (NH2)2CO + 2 HNO
+ H
→ 2 N
+ 2 CO
+ (NH4)2SO4 + 2H

Direct oxidation of ammonia with a manganese dioxide-bismuth oxide catalyst has been reported:[91] cf. Ostwald process.

2 NH
+ 2 O
+ 3 H

Hydroxylammonium chloride reacts with sodium nitrite to give nitrous oxide. If the nitrite is added to the hydroxylamine solution, the only remaining by-product is salt water. If the hydroxylamine solution is added to the nitrite solution (nitrite is in excess), however, then toxic higher oxides of nitrogen also are formed:

Cl + NaNO
+ NaCl + 2 H

Treating HNO
with SnCl
and HCl also has been demonstrated:

+ 8 HCl + 4 SnCl
→ 5 H
+ 4 SnCl
+ N

Hyponitrous acid decomposes to N2O and water with a half-life of 16 days at 25 °C at pH 1–3.[92]

H2N2O2→ H2O + N2O

Atmospheric occurrence

Nitrous oxide is a minor component of Earth's atmosphere, currently with a concentration of about 0.330 ppm.[93]

Emissions by source

As of 2010, it was estimated that about 29.5 million tonnes of N
(containing 18.8 million tonnes of nitrogen) were entering the atmosphere each year; of which 64% were natural, and 36% due to human activity.[94][95]

Most of the N
emitted into the atmosphere, from natural and anthropogenic sources, is produced by microorganisms such as bacteria and fungi in soils and oceans.[96] Soils under natural vegetation are an important source of nitrous oxide, accounting for 60% of all naturally produced emissions. Other natural sources include the oceans (35%) and atmospheric chemical reactions (5%).[94]

The main components of anthropogenic emissions are fertilised agricultural soils and livestock manure (42%), runoff and leaching of fertilisers (25%), biomass burning (10%), fossil fuel combustion and industrial processes (10%), biological degradation of other nitrogen-containing atmospheric emissions (9%) and human sewage (5%).[97][98][99][100][101] Agriculture enhances nitrous oxide production through soil cultivation, the use of nitrogen fertilisers and animal waste handling. These activities stimulate naturally-occurring bacteria to produce more nitrous oxide. Nitrous oxide emissions from soil can be challenging to measure as they vary markedly over time and space, and the majority of a year's emissions may occur when conditions are favorable during "hot moments"[102] and/or at favorable locations known as "hotspots".[103]

Among industrial emissions, the production of nitric acid and adipic acid are the largest sources of nitrous oxide emissions. The adipic acid emissions specifically arise from the degradation of the nitrolic acid intermediate derived from nitration of cyclohexanone.[97][104][105]

Biological processes

Natural processes that generate nitrous oxide may be classified as nitrification and denitrification. Specifically, they include:

  • aerobic autotrophic nitrification, the stepwise oxidation of ammonia (NH
    ) to nitrite (NO
    ) and to nitrate (NO
  • anaerobic heterotrophic denitrification, the stepwise reduction of NO
    to NO
    , nitric oxide (NO), N
    and ultimately N
    , where facultative anaerobe bacteria use NO
    as an electron acceptor in the respiration of organic material in the condition of insufficient oxygen (O
  • nitrifier denitrification, which is carried out by autotrophic NH
    -oxidising bacteria and the pathway whereby ammonia (NH
    ) is oxidised to nitrite (NO
    ), followed by the reduction of NO
    to nitric oxide (NO), N
    and molecular nitrogen (N
  • heterotrophic nitrification
  • aerobic denitrification by the same heterotrophic nitrifiers
  • fungal denitrification
  • non-biological chemodenitrification

These processes are affected by soil chemical and physical properties such as the availability of mineral nitrogen and organic matter, acidity and soil type, as well as climate-related factors such as soil temperature and water content.

The emission of the gas to the atmosphere is limited greatly by its consumption inside the cells, by a process catalysed by the enzyme nitrous oxide reductase.[106]

Environmental impact

Greenhouse effect

Major greenhouse gas trends
Greenhouse gas trends

Nitrous oxide has significant global warming potential as a greenhouse gas. On a per-molecule basis, considered over a 100-year period, nitrous oxide has 298 times the atmospheric heat-trapping ability of carbon dioxide (CO
);[107][108] however, because of its low concentration (less than 1/1,000 of that of CO
),[93] its contribution to the greenhouse effect is less than one third that of carbon dioxide, and also less than water vapour and methane. On the other hand, since 38% or more of the N
entering the atmosphere is the result of human activity,[97] and its concentration has increased 15% since 1750,[93][109] control of nitrous oxide is considered part of efforts to curb greenhouse gas emissions.[110]

A 2008 study by Nobel Laureate Paul Crutzen suggests that the amount of nitrous oxide release attributable to agricultural nitrate fertilisers has been seriously underestimated, most of which presumably, would come under soil and oceanic release in the Environmental Protection Agency data.[111]

Globally, about 40 per cent of total N2O emissions come from human activities. Nitrous oxide is emitted from agriculture, transportation and industry activities, described below.

  • Agriculture. Nitrous oxide can result from various agricultural soil management activities, such as synthetic and organic fertiliser application and other cropping practices, the management of manure, or burning of agricultural residues. Agricultural soil management is the largest source of N2O emissions in the United States, accounting for about 77 per cent of total U.S. N2O emissions in 2016.
  • Fuel Combustion. Nitrous oxide is emitted when fuels are burned. The amount of N2O emitted from burning fuels depends on the type of fuel and combustion technology, maintenance and operating practices.
  • Industry. Nitrous oxide is generated as a byproduct during the production of nitric acid, which is used to make synthetic commercial fertiliser, and in the production of adipic acid, which is used to make fibres, like nylon and other synthetic products.[112]

Ozone layer depletion

Nitrous oxide also has been implicated in thinning of the ozone layer. A new study suggests that N
emission currently is the single most important ozone-depleting substance (ODS) emission and is expected to remain the largest throughout the twenty-first century.[3][113]


In the United States, possession of nitrous oxide is legal under federal law and is not subject to DEA purview.[114] It is, however, regulated by the Food and Drug Administration under the Food Drug and Cosmetics Act; prosecution is possible under its "misbranding" clauses, prohibiting the sale or distribution of nitrous oxide for the purpose of human consumption. Many states have laws regulating the possession, sale and distribution of nitrous oxide. Such laws usually ban distribution to minors or limit the amount of nitrous oxide that may be sold without special license. For example, in the state of California, possession for recreational use is prohibited and qualifies as a misdemeanour.[115]

In August 2015, the Council of the London Borough of Lambeth (UK) banned the use of the drug for recreational purposes, making offenders liable to an on-the-spot fine of up to £1,000.[116]

In New Zealand, the Ministry of Health has warned that nitrous oxide is a prescription medicine, and its sale or possession without a prescription, is an offense under the Medicines Act.[117] This statement would seemingly prohibit all non-medicinal uses of nitrous oxide, although it is implied that only recreational use will be targeted legally.

In India, transfer of nitrous oxide from bulk cylinders to smaller, more transportable E-type, 1,590-litre-capacity tanks,[118] is legal when the intended use of the gas is for medical anaesthesia.

See also


  1. ^ Tarendash, Albert S. (2001). Let's review: chemistry, the physical setting (3rd ed.). Barron's Educational Series. p. 44. ISBN 978-0-7641-1664-3.
  2. ^ "WHO Model List of Essential Medicines 20th List (March 2017)" (PDF). Geneva, Switzerland: World Health Organization. March 2017. Retrieved 24 August 2017.
  3. ^ a b Ravishankara, A. R.; Daniel, J. S.; Portmann, R. W. (2009). "Nitrous Oxide (N2O): The Dominant Ozone-Depleting Substance Emitted in the 21st Century". Science. 326 (5949): 123–5. Bibcode:2009Sci...326..123R. doi:10.1126/science.1176985. PMID 19713491.
  4. ^ Berger, Bruno (5 October 2007). "Is nitrous oxide safe?" (PDF). Swiss Propulsion Laboratory. pp. 1–2. ...Self pressurizing (Vapor pressure at 20°C is ~50.1 bar...Nontoxic, low reactivity -> rel. safe handling (General safe ???)...Additional energy from decomposition (as a monopropellant: ISP of 170 s)...Specific impulse doesn’t change much with O/F...[page 2] N2O is a monopropellant (as H2O2 or Hydrazine...)
  5. ^ Goddard, R. H. (1914) "Rocket apparatus" U.S. Patent 1,103,503
  6. ^ Nitrous Oxide Safety. Space Propulsion Group (2012)
  7. ^ a b Munke, Konrad (2 July 2001) Nitrous Oxide Trailer Rupture, Report at CGA Seminar "Safety and Reliability of Industrial Gases, Equipment and Facilities", 15–17 October 2001, St. Louis, Missouri
  8. ^ "Scaled Composites Safety Guidelines for N
    (PDF). Scaled Composites. 17 June 2009. Retrieved 29 December 2013. For example, N2O flowing at 130 psi in an epoxy composite pipe would not react even with a 2500 J ignition energy input. At 600 psi, however, the required ignition energy was only 6 J.
  9. ^ FR-5904. Pratt & Whitney Aircraft.
  10. ^ Cline, Allen W. (January 2000) "Engine Basics: Detonation and Pre-Ignition". CONTACT! Magazine
  11. ^ "Holley performance products, FAQ for Nitrous Oxide Systems". Holley. Retrieved 18 December 2013.
  12. ^ "Explora Science | Nitrous use as a propellant and in cooking". Retrieved 19 February 2019.
  13. ^ Dewey, Caitlin (21 December 2016). "The real reason grocery stores are running out of whipped cream this Christmas". The Washington Post. Retrieved 22 December 2016.
  14. ^ a b c d e Sneader W (2005). Drug Discovery –A History. (Part 1: Legacy of the past, chapter 8: systematic medicine, pp. 74–87). John Wiley and Sons. ISBN 978-0-471-89980-8. Retrieved 21 April 2010.
  15. ^ a b c Miller AH (1941). "Technical Development of Gas Anesthesia". Anesthesiology Journal. 2 (4): 398–409. doi:10.1097/00000542-194107000-00004. Archived from the original on 19 December 2014.
  16. ^ Divatia, Jigeeshu V.; Vaidya, Jayant S.; Badwe, Rajendra A.; Hawaldar, Rohini W. (1996). "Omission of Nitrous Oxide during Anesthesia Reduces the Incidence of Postoperative Nausea and Vomiting". Anesthesiology. 85 (5): 1055–1062. doi:10.1097/00000542-199611000-00014.
  17. ^ Hartung, John (1996). "Twenty-Four of Twenty-Seven Studies Show a Greater Incidence of Emesis Associated with Nitrous Oxide than with Alternative Anesthetics". Anesthesia & Analgesia. 83 (1): 114–116. doi:10.1213/00000539-199607000-00020.
  18. ^ Tramèr, M.; Moore, A.; McQuay, H. (February 1996). "Omitting nitrous oxide in general anaesthesia: meta-analysis of intraoperative awareness and postoperative emesis in randomized controlled trials". British Journal of Anaesthesia. 76 (2): 186–193. doi:10.1093/bja/76.2.186. PMID 8777095.
  19. ^ Council on Clinical Affairs (2013). "Guideline on use of nitrous oxide for pediatric dental patients" (PDF). Reference Manual V37. 6: 206–210.
  20. ^ Copeland, Claudia. "Nitrous Oxide Analgesia for Childbirth". Archived from the original on 25 May 2011.
  21. ^ O'Connor RE; Brady W; Brooks SC; Diercks, D.; Egan, J.; Ghaemmaghami, C.; Menon, V.; O'Neil, B. J.; et al. (2010). "Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18 Suppl 3): S787–817. doi:10.1161/CIRCULATIONAHA.110.971028. PMID 20956226.
  22. ^ Faddy, S. C.; Garlick, S. R. (1 December 2005). "A systematic review of the safety of analgesia with 50% nitrous oxide: can lay responders use analgesic gases in the prehospital setting?". Emergency Medicine Journal. 22 (12): 901–908. doi:10.1136/emj.2004.020891. PMC 1726638. PMID 16299211.
  23. ^ "Warning over laughing gas misuse". The Guardian. London. Press Association. 9 August 2014. Retrieved 9 August 2014.
  24. ^ VICE (7 February 2017), Inside The Laughing Gas Black Market, retrieved 29 March 2019
  25. ^ NIOSH Alert: Controlling Exposures to Nitrous Oxide During Anesthetic Administration. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 94-100
  26. ^ "CDC – NIOSH Pocket Guide to Chemical Hazards – Nitrous oxide". Retrieved 21 November 2015.
  27. ^ Criteria for a recommended standard: occupational exposure to waste anesthetic gases and vapors. Cincinnati, OH: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, DHEW (NIOSH) Publication No. 77B140.
  28. ^ a b c Jay, Mike (1 September 2008). "Nitrous oxide: recreational use, regulation and harm reduction". Drugs and Alcohol Today. 8 (3): 22–25. doi:10.1108/17459265200800022.
  29. ^ a b Jevtovic-Todorovic V, Beals J, Benshoff N, Olney JW; Beals; Benshoff; Olney (2003). "Prolonged exposure to inhalational anesthetic nitrous oxide kills neurons in adult rat brain". Neuroscience. 122 (3): 609–16. doi:10.1016/j.neuroscience.2003.07.012. PMID 14622904.CS1 maint: Multiple names: authors list (link)
  30. ^ Nakao S; Nagata A; Masuzawa M; Miyamoto, E; Yamada, M; Nishizawa, N; Shingu, K (2003). "NMDA receptor antagonist neurotoxicity and psychotomimetic activity". Masui. The Japanese Journal of Anesthesiology (in Japanese). 52 (6): 594–602. PMID 12854473.
  31. ^ Jevtovic-Todorovic V, Benshoff N, Olney JW; Benshoff; Olney (2000). "Ketamine potentiates cerebrocortical damage induced by the common anaesthetic agent nitrous oxide in adult rats". British Journal of Pharmacology. 130 (7): 1692–8. doi:10.1038/sj.bjp.0703479. PMC 1572233. PMID 10928976.CS1 maint: Multiple names: authors list (link)
  32. ^ Jevtovic-Todorovic V, Carter LB; Carter (2005). "The anesthetics nitrous oxide and ketamine are more neurotoxic to old than to young rat brain". Neurobiology of Aging. 26 (6): 947–56. doi:10.1016/j.neurobiolaging.2004.07.009. PMID 15718054.
  33. ^ Slikker, W.; Zou, X.; Hotchkiss, C. E.; Divine, R. L.; Sadovova, N.; Twaddle, N. C.; Doerge, D. R.; Scallet, A. C.; Patterson, T. A.; Hanig, J. P.; Paule, M. G.; Wang, C. (2007). "Ketamine-Induced Neuronal Cell Death in the Perinatal Rhesus Monkey". Toxicological Sciences. 98 (1): 145–158. doi:10.1093/toxsci/kfm084. PMID 17426105.
  34. ^ Sun, Lin; Qi Li; Qing Li; Yuzhe Zhang; Dexiang Liu; Hong Jiang; Fang Pan; David T. Yew (November 2012). "Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys". Addiction Biology. 19 (2): 185–94. doi:10.1111/adb.12004. PMID 23145560.
  35. ^ Abraini JH, David HN, Lemaire M; David; Lemaire (2005). "Potentially neuroprotective and therapeutic properties of nitrous oxide and xenon". Annals of the New York Academy of Sciences. 1053 (1): 289–300. Bibcode:2005NYASA1053..289A. doi:10.1196/annals.1344.025. PMID 16179534.CS1 maint: Multiple names: authors list (link)
  36. ^ De Vasconcellos, K.; Sneyd, J. R. (2013). "Nitrous oxide: Are we still in equipoise? A qualitative review of current controversies". British Journal of Anaesthesia. 111 (6): 877–85. doi:10.1093/bja/aet215. PMID 23801743.
  37. ^ Middleton, Ben (2012). Physics in anaesthesia. Banbury, Oxfordshire, UK: Scion Pub. Ltd. ISBN 978-1-904842-98-9.
  38. ^ Flippo, T. S.; Holder Jr, W. D. (1993). "Neurologic Degeneration Associated with Nitrous Oxide Anesthesia in Patients with Vitamin B12 Deficiency". Archives of Surgery. 128 (12): 1391–5. doi:10.1001/archsurg.1993.01420240099018. PMID 8250714.
  39. ^ Abraini, Jacques H.; David, Hélène N.; Lemaire, Marc (2008). "Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon". Annals of the New York Academy of Sciences. 1053: 289–300. doi:10.1111/j.1749-6632.2005.tb00036.x. PMID 16179534.
  40. ^ Dangers of Nitrous Oxide. Just Say N2O
  41. ^ Giannini, A.J. (1999). Drug Abuse. Los Angeles: Health Information Press. ISBN 978-1-885987-11-2.
  42. ^ Conrad, Marcel (4 October 2006). "Pernicious Anemia". Retrieved 2 June 2008.
  43. ^ a b Vieira, E.; Cleaton-Jones, P.; Austin, J.C.; Moyes, D.G.; Shaw, R. (1980). "Effects of low concentrations of nitrous oxide on rat fetuses". Anesthesia and Analgesia. 59 (3): 175–7. doi:10.1213/00000539-198003000-00002. PMID 7189346.
  44. ^ Vieira, E. (1979). "Effect of the chronic administration of nitrous oxide 0.5% to gravid rats". British Journal of Anaesthesia. 51 (4): 283–7. doi:10.1093/bja/51.4.283. PMID 465253.
  45. ^ Vieira, E; Cleaton-Jones, P; Moyes, D. (1983). "Effects of low intermittent concentrations of nitrous oxide on the developing rat fetus". British Journal of Anaesthesia. 55 (1): 67–9. doi:10.1093/bja/55.1.67. PMID 6821624.
  46. ^ Nitrous oxide. Air Liquide Gas Encyclopedia.
  47. ^ "Vaseline triggered explosion of hybrid rocket".
  48. ^ "Safetygram 20: Nitrous Oxide" (PDF). Archived from the original (PDF) on 1 September 2006.
  49. ^ a b Yamakura T, Harris RA; Harris (2000). "Effects of gaseous anaesthetics nitrous oxide and xenon on ligand-gated ion channels. Comparison with isoflurane and ethanol". Anesthesiology. 93 (4): 1095–101. doi:10.1097/00000542-200010000-00034. PMID 11020766.
  50. ^ Mennerick S, Jevtovic-Todorovic V, Todorovic SM, Shen W, Olney JW, Zorumski CF; Jevtovic-Todorovic; Todorovic; Shen; Olney; Zorumski (1998). "Effect of nitrous oxide on excitatory and inhibitory synaptic transmission in hippocampal cultures". Journal of Neuroscience. 18 (23): 9716–26. doi:10.1523/JNEUROSCI.18-23-09716.1998. PMID 9822732.CS1 maint: Multiple names: authors list (link)
  51. ^ Gruss M, Bushell TJ, Bright DP, Lieb WR, Mathie A, Franks NP; Bushell; Bright; Lieb; Mathie; Franks (2004). "Two-pore-domain K+ channels are a novel target for the anesthetic gases xenon, nitrous oxide, and cyclopropane". Molecular Pharmacology. 65 (2): 443–52. doi:10.1124/mol.65.2.443. PMID 14742687.CS1 maint: Multiple names: authors list (link)
  52. ^ a b Emmanouil DE, Quock RM; Quock (2007). "Advances in Understanding the Actions of Nitrous Oxide". Anesthesia Progress. 54 (1): 9–18. doi:10.2344/0003-3006(2007)54[9:AIUTAO]2.0.CO;2. PMC 1821130. PMID 17352529.
  53. ^ Atkinson, Roland M.; Green, J. DeWayne; Chenoweth, Dennis E.; Atkinson, Judith Holmes (1 October 1979). "Subjective Effects of Nitrous Oxide: Cognitive, Emotional, Perceptual and Transcendental Experiences". Journal of Psychedelic Drugs. 11 (4): 317–330. doi:10.1080/02791072.1979.10471415.
  54. ^ Walker, Diana J.; Zacny, James P. (1 September 2001). "Within- and between-subject variability in the reinforcing and subjective effects of nitrous oxide in healthy volunteers". Drug and Alcohol Dependence. 64 (1): 85–96. doi:10.1016/s0376-8716(00)00234-9. PMID 11470344.
  55. ^ a b Sakamoto S, Nakao S, Masuzawa M, Inada T, Maze M, Franks NP, Shingu K (2006). "The differential effects of nitrous oxide and xenon on extracellular dopamine levels in the rat nucleus accumbens: a microdialysis study". Anesthesia and Analgesia. 103 (6): 1459–63. CiteSeerX doi:10.1213/01.ane.0000247792.03959.f1. PMID 17122223.
  56. ^ a b Benturquia N, Le Marec T, Scherrmann JM, Noble F; Le Marec; Scherrmann; Noble (2008). "Effects of nitrous oxide on dopamine release in the rat nucleus accumbens and expectation of reward". Neuroscience. 155 (2): 341–4. doi:10.1016/j.neuroscience.2008.05.015. PMID 18571333.CS1 maint: Multiple names: authors list (link)
  57. ^ a b Lichtigfeld FJ, Gillman MA; Gillman (1996). "Role of dopamine mesolimbic system in opioid action of psychotropic analgesic nitrous oxide in alcohol and drug withdrawal". Clinical Neuropharmacology. 19 (3): 246–51. doi:10.1097/00002826-199619030-00006. PMID 8726543.
  58. ^ a b Koyanagi S, Himukashi S, Mukaida K, Shichino T, Fukuda K; Himukashi; Mukaida; Shichino; Fukuda (2008). "Dopamine D2-like receptor in the nucleus accumbens is involved in the antinociceptive effect of nitrous oxide". Anesthesia and Analgesia. 106 (6): 1904–9. CiteSeerX doi:10.1213/ane.0b013e318172b15b. PMID 18499630.CS1 maint: Multiple names: authors list (link)
  59. ^ David HN, Ansseau M, Lemaire M, Abraini JH; Ansseau; Lemaire; Abraini (2006). "Nitrous oxide and xenon prevent amphetamine-induced carrier-mediated dopamine release in a memantine-like fashion and protect against behavioral sensitization". Biological Psychiatry. 60 (1): 49–57. doi:10.1016/j.biopsych.2005.10.007. PMID 16427030.CS1 maint: Multiple names: authors list (link)
  60. ^ a b Benturquia N, Le Guen S, Canestrelli C, Lagente V, Apiou G, Roques B, Noble F (2007). "Specific blockade of morphine- and cocaine-induced reinforcing effects in conditioned place preference by nitrous oxide in mice". Neuroscience. 149 (3): 477–86. doi:10.1016/j.neuroscience.2007.08.003. PMID 17905521.
  61. ^ Ramsay DS, Watson CH, Leroux BG, Prall CW, Kaiyala KJ; Watson; Leroux; Prall; Kaiyala (2003). "Conditioned place aversion and self-administration of nitrous oxide in rats". Pharmacology Biochemistry and Behavior. 74 (3): 623–33. doi:10.1016/S0091-3057(02)01048-1. PMID 12543228.CS1 maint: Multiple names: authors list (link)
  62. ^ Wood RW, Grubman J, Weiss B; Grubman; Weiss (1977). "Nitrous oxide self-administration by the squirrel monkey". The Journal of Pharmacology and Experimental Therapeutics. 202 (3): 491–9. PMID 408480.CS1 maint: Multiple names: authors list (link)
  63. ^ Zacny JP, Galinkin JL; Galinkin (1999). "Psychotropic drugs used in anesthesia practice: abuse liability and epidemiology of abuse". Anesthesiology. 90 (1): 269–88. doi:10.1097/00000542-199901000-00033. PMID 9915336.
  64. ^ Dohrn CS, Lichtor JL, Coalson DW, Uitvlugt A, de Wit H, Zacny JP; Lichtor; Coalson; Uitvlugt; De Wit; Zacny (1993). "Reinforcing effects of extended inhalation of nitrous oxide in humans". Drug and Alcohol Dependence. 31 (3): 265–80. doi:10.1016/0376-8716(93)90009-F. PMID 8462415.CS1 maint: Multiple names: authors list (link)
  65. ^ Walker DJ, Zacny JP; Zacny (2001). "Within- and between-subject variability in the reinforcing and subjective effects of nitrous oxide in healthy volunteers". Drug and Alcohol Dependence. 64 (1): 85–96. doi:10.1016/S0376-8716(00)00234-9. PMID 11470344.
  66. ^ Emmanouil, D. E., Johnson, C. H. & Quock, R. M.; Johnson; Quock (1994). "Nitrous oxide anxiolytic effect in mice in the elevated plus maze: mediation by benzodiazepine receptors". Psychopharmacology. 115 (1–2): 167–72. doi:10.1007/BF02244768. PMID 7862891.CS1 maint: Multiple names: authors list (link)
  67. ^ Zacny, J.P., Yajnik, S., Coalson, D., Lichtor, J.L., Apfelbaum, J.L., Rupani, G., Young, C., Thapar, P. & Klafta, J.; Yajnik; Coalson; Lichtor; Apfelbaum; Rupani; Young; Thapar; Klafta (1995). "Flumazenil may attenuate some subjective effects of nitrous oxide in humans: a preliminary report". Pharmacology Biochemistry and Behavior. 51 (4): 815–9. doi:10.1016/0091-3057(95)00039-Y. PMID 7675863.CS1 maint: Multiple names: authors list (link)
  68. ^ Berkowitz, B. A., Finck, A. D., Hynes, M. D. & Ngai, S. H.; Finck; Hynes; Ngai (1979). "Tolerance to nitrous oxide analgesia in rats and mice". Anesthesiology. 51 (4): 309–12. doi:10.1097/00000542-197910000-00006. PMID 484891.CS1 maint: Multiple names: authors list (link)
  69. ^ a b Branda, E. M., Ramza, J. T., Cahill, F. J., Tseng, L. F. & Quock, R. M.; Ramza; Cahill; Tseng; Quock (2000). "Role of brain dynorphin in nitrous oxide antinociception in mice". Pharmacology Biochemistry and Behavior. 65 (2): 217–21. doi:10.1016/S0091-3057(99)00202-6.CS1 maint: Multiple names: authors list (link)
  70. ^ Guo, T. Z., Davies, M. F., Kingery, W. S., Patterson, A. J., Limbird, L. E. & Maze, M.; Davies; Kingery; Patterson; Limbird; Maze (1999). "Nitrous oxide produces antinociceptive response via alpha2B and/or alpha2C adrenoceptor subtypes in mice". Anesthesiology. 90 (2): 470–6. doi:10.1097/00000542-199902000-00022. PMID 9952154.CS1 maint: Multiple names: authors list (link)
  71. ^ Sawamura, S., Kingery, W. S., Davies, M. F., Agashe, G. S., Clark, J. D., Koblika, B. K., Hashimoto, T. & Maze, M.; Kingery; Davies; Agashe; Clark; Kobilka; Hashimoto; Maze (2000). "Antinociceptive action of nitrous oxide is mediated by stimulation of noradrenergic neurons in the brainstem and activation of [alpha]2B adrenoceptors". J. Neurosci. 20 (24): 9242–51. doi:10.1523/JNEUROSCI.20-24-09242.2000. PMID 11125002.CS1 maint: Multiple names: authors list (link)
  72. ^ Maze M, Fujinaga M; Fujinaga (2000). "Recent advances in understanding the actions and toxicity of nitrous oxide". Anaesthesia. 55 (4): 311–4. doi:10.1046/j.1365-2044.2000.01463.x. PMID 10781114.
  73. ^ Housecroft, Catherine E. & Sharpe, Alan G. (2008). "Chapter 15: The group 15 elements". Inorganic Chemistry (3rd ed.). Pearson. p. 464. ISBN 978-0-13-175553-6.
  74. ^ Keys, T.E. (1941). "The Development of Anesthesia". Anesthesiology. 2 (5): 552–574. Bibcode:1982AmSci..70..522D. doi:10.1097/00000542-194109000-00008. Archived from the original on 12 January 2014.
  75. ^ McEvoy, J. G. (6 March 2015). "Gases, God and the balance of nature: a commentary on Priestley (1772) 'Observations on different kinds of air'". Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences. 373 (2039): 20140229. Bibcode:2015RSPTA.37340229M. doi:10.1098/rsta.2014.0229. PMC 4360083. PMID 25750146.
  76. ^ Priestley J (1776). "Experiments and Observations on Different Kinds of Air". 2 (3).
  77. ^ Davy H (1800). Researches, chemical and philosophical –chiefly concerning nitrous oxide or dephlogisticated nitrous air, and its respiration. Printed for J. Johnson.
  78. ^ Hardman, Jonathan G. (2017). Oxford Textbook of Anaesthesia. Oxford University Press. p. 529. ISBN 9780199642045.
  79. ^ Brecher EM (1972). "Consumers Union Report on Licit and Illicit Drugs, Part VI – Inhalants and Solvents and Glue-Sniffing". Consumer Reports Magazine. Retrieved 18 December 2013.
  80. ^ "George Poe is Dead". Washington Post. 3 February 1914. Retrieved 29 December 2007.
  81. ^ Erving, H. W. (1933). "The Discoverer of Anæsthesia: Dr. Horace Wells of Hartford". The Yale Journal of Biology and Medicine. 5 (5): 421–430. PMC 2606479. PMID 21433572.
  82. ^ Wells H (1847). A history of the discovery, of the application of nitrous oxide gas, ether, and other vapours, to surgical operations. J. Gaylord Wells.
  83. ^ Desai SP, Desai MS, Pandav CS (2007). "The discovery of modern anaesthesia-contributions of Davy, Clarke, Long, Wells and Morton". Indian J Anaesth. 51 (6): 472–8.
  84. ^ "Alleged Forgery". The Inter Ocean. 28 September 1877. p. 8. Retrieved 26 October 2015.
  85. ^ "A Man of Ominous Name". The Inter Ocean. 19 February 1890. Retrieved 26 October 2015.
  86. ^ a b Parmon, V. N.; Panov, G. I.; Uriarte, A.; Noskov, A. S. (2005). "Nitrous oxide in oxidation chemistry and catalysis application and production". Catalysis Today. 100 (2005): 115–131. doi:10.1016/j.cattod.2004.12.012.
  87. ^ Holleman, A. F.; Wiberg, E. (2001). Inorganic Chemistry. San Diego: Academic Press. ISBN 978-0-12-352651-9.
  88. ^ "Nitrous oxide plant". Sanghi Organization. Archived from the original on 27 November 2013. Retrieved 18 December 2013.
  89. ^ "Nitrogen Family".
  90. ^ "Preparation of Nitrous Oxide from Urea, Nitric Acid and Sulfuric Acid".
  91. ^ Suwa T, Matsushima A, Suziki Y, Namina Y (1961). "Synthesis of Nitrous Oxide by Oxidation of Ammonia". Kohyo Kagaku Zasshi, Showa Denka Ltd. 64 (11): 1879–1888. doi:10.1246/nikkashi1898.64.11_1879.
  92. ^ Egon Wiberg, Arnold Frederick Holleman (2001) Inorganic Chemistry, Elsevier ISBN 0-12-352651-5
  93. ^ a b c US Environmental Protection Agency, "Climate Change Indicators: Atmospheric Concentrations of Greenhouse Gases" Web document, accessed on 2017-02-14
  94. ^ a b US Environmental Protection Agency (2010), "Methane and Nitrous Oxide Emissions from Natural Sources". Report EPA 430-R-10-001.
  95. ^ "2011 U.S. Greenhouse Gas Inventory Report | Climate Change – Greenhouse Gas Emissions | U.S. EPA". Retrieved 11 April 2011.
  96. ^ Sloss, Leslie L. (1992). Nitrogen Oxides Control Technology Fact Book. William Andrew. p. 6. ISBN 978-0-8155-1294-3.
  97. ^ a b c K. L. Denman, G. Brasseur, et al.(2007), "Couplings Between Changes in the Climate System and Biogeochemistry". In Fourth Assessment Report of the Intergovernmental Panel on Climate Change, Cambridge University Press.
  98. ^ Steinfeld, H.; Gerber, P.; Wassenaar, T.; Castel, V.; Rosales, M. & de Haan, C. (2006). "Livestock's long shadow – Environmental issues and options". Retrieved 2 February 2008.
  99. ^ "Nitrous Oxide Emissions". U.S. Environmental Protection Agency. 23 December 2015. Retrieved 31 March 2016.
  100. ^ "Sources and Emissions – Where Does Nitrous Oxide Come From?". U.S. Environmental Protection Agency. 2006. Retrieved 2 February 2008.
  101. ^ IPCC. 2013. Climate change: the physical basis (WG I, full report). p. 512.
  102. ^ Molodovskaya, M.; Singurindy, O.; Richards, B. K.; Warland, J. S.; Johnson, M.; Öberg, G.; Steenhuis, T. S. (2012). "Temporal variability of nitrous oxide from fertilized croplands: hot moment analysis". Soil Science Society of America Journal. 76 (5): 1728–1740. Bibcode:2012SSASJ..76.1728M. doi:10.2136/sssaj2012.0039.
  103. ^ Mason, C.W.; Stoof, C.R.; Richards, B.K.; Das, S.; Goodale, C.L.; Steenhuis, T.S. (2017). "Hotspots of nitrous oxide emission in fertilized and unfertilized perennial grasses on wetness-prone marginal land in New York State". Soil Science Society of America Journal. 81 (3): 450–458. Bibcode:2017SSASJ..81..450M. doi:10.2136/sssaj2016.08.0249.
  104. ^ Reimer R. A.; Slaten C. S.; Seapan M.; Lower M. W.; Tomlinson P. E. (1994). "Abatement of N2O emissions produced in the adipic acid industry". Environmental Progress. 13 (2): 134–137. doi:10.1002/ep.670130217.
  105. ^ Shimizu, A.; Tanaka, K. & Fujimori, M. (2000). "Abatement of N2O emissions produced in the adipic acid industry". Chemosphere – Global Change Science. 2 (3–4): 425–434. Bibcode:2000ChGCS...2..425S. doi:10.1016/S1465-9972(00)00024-6.
  106. ^ Schneider, Lisa K.; Wüst, Anja; Pomowski, Anja; Zhang, Lin and Einsle, Oliver (2014). "Ch. 8 No Laughing Matter: The Unmaking of the Greenhouse Gas Dinitrogen Monoxide by Nitrous Oxide Reductase". In Kroneck, Peter M. H. and Sosa Torres, Martha E. (ed.). The Metal-Driven Biogeochemistry of Gaseous Compounds in the Environment. Metal Ions in Life Sciences. 14. Springer. pp. 177–210. doi:10.1007/978-94-017-9269-1_8. ISBN 978-94-017-9268-4. PMID 25416395.CS1 maint: Multiple names: authors list (link)
  107. ^ "40 CFR Part 98 – Revisions to the Greenhouse Gas Reporting Rule and Final Confidentiality | U.S. EPA" (PDF). Environmental Protection Agency. 15 November 2013. Retrieved 19 March 2014.
  108. ^ "Overview of Greenhouse Gases – Nitrous Oxide" (PDF). US EPA. 10 June 2014. Page 164 (document header listing). Retrieved 19 March 2014.
  109. ^ "Climate Change 2007: The Physical Sciences Basis". IPCC. Archived from the original on 1 May 2007. Retrieved 30 April 2007.
  110. ^ "4.1.1 Sources of Greenhouse Gases". IPCC TAR WG1 2001. Archived from the original on 29 October 2012. Retrieved 21 September 2012.
  111. ^ Crutzen, P. J.; Mosier, A. R.; Smith, K. A.; Winiwarter, W. (2008). "N2O release from agro-biofuel production negates global warming reduction by replacing fossil fuels". Atmospheric Chemistry and Physics. 8 (2): 389–395. doi:10.5194/acp-8-389-2008.
  112. ^ </
  113. ^ Grossman, Lisa (28 August 2009). "Laughing gas is biggest threat to ozone layer". New Scientist.
  114. ^ "US Nitrous Oxide Laws (alphabetically) Based on a search of online free legal databases. Conducted May 2002". Center for Cognitive Liberty and Ethics.
  115. ^ "CAL. PEN. CODE § 381b : California Code – Section 381b".
  116. ^ "Lambeth Council bans laughing gas as recreational drug". BBC News. 17 August 2015. Retrieved 17 August 2015.
  117. ^ Anderton, Jim (26 June 2005). "Time's up for sham sales of laughing gas". Archived from the original on 8 January 2015.
  118. ^ "Ohio Medical" (PDF).

External links

Aerated chocolate

Aerated chocolate is a type of chocolate which has been turned into a foam via the addition of gas bubbles. The process for manufacturing it was invented by Rowntree's in 1947. During manufacturing the fluid chocolate mass is foamed with a propellant, and then cooled in a low pressure environment. As the bubbles of gas expand they cool and help set the chocolate. This helps to maintain an even bubble distribution within the chocolate. Due to the isolating effect of the bubbles, air chocolate melts differently from compact bar chocolate — the mouthfeel is fragile-short at first, then as the chocolate is chewed it melts rapidly due to its bigger surface area. This intensifies the perception of taste.

Nitrogen, argon, carbon dioxide and nitrous oxide are often used as propellants for air chocolate. Air itself is not used as a propellant because it contains oxygen which speeds up rancidification of the chocolate. A survey funded by Nestlé, conducted at the University of Reading, revealed that chocolate foamed with nitrogen — and especially with nitrous oxide — has the most intense taste. The researchers found that this was due to the larger bubbles which these gases produce. Further research by Nestlé has concluded that "[t]he existing technology to control bubble size and distribution is difficult," which has led to experiments involving the creation of foams under zero-gravity conditions.In 2013, Chinese scientists announced results from a study using phospholipids derived from soybeans to aerate cocoa butter.

Alcohol detoxification

Alcohol detoxification, or detox, for individuals with alcohol dependence, is the abrupt cessation of alcohol intake, a process often coupled with substitution of cross-tolerant drugs that have effects similar to the effects of alcohol in order to prevent alcohol withdrawal.

Anaesthetic machine

An anaesthetic machine (British English) or anesthesia machine (American English; see spelling differences) is a medical device used to generate and mix a fresh gas flow of medical gases and inhalational anaesthetic agents for the purpose of inducing and maintaining anaesthesia.

The machine is commonly used together with a mechanical ventilator, breathing system, suction equipment, and patient monitoring devices; strictly speaking, the term "anaesthetic machine" refers only to the component which generates the gas flow, but modern machines usually integrate all these devices into one combined freestanding unit, which is colloquially referred to as the "anaesthetic machine" for the sake of simplicity. In the developed world, the most frequent type in use is the continuous-flow anaesthetic machine or "Boyle's machine", which is designed to provide an accurate supply of medical gases mixed with an accurate concentration of anaesthetic vapour, and to deliver this continuously to the patient at a safe pressure and flow. This is distinct from intermittent-flow anaesthetic machines, which provide gas flow only on demand when triggered by the patient's own inspiration.

Simpler anaesthetic apparatus may be used in special circumstances, such as the Triservice anaesthetic apparatus, a simplified anaesthesia delivery system invented for the British Defence Medical Services, which is light and portable and may be used effectively even when no medical gases are available. This device has unidirectional valves which suck in ambient air, which can be enriched with oxygen from a cylinder, with the help of a set of bellows. A large number of draw-over type of anaesthesia devices are still in use in India for administering an air-ether mixture to the patient, which can be enriched with oxygen.

Concentration effect

In the study of inhaled anesthetics, the concentration effect is the increase in the rate that the Fa(alveolar concentration)/Fi(inspired concentration) ratio rises as the alveolar concentration of that gas is increased. In simple terms, the higher the concentration of gas administered, the faster the alveolar concentration of that gas approaches the inspired concentration. In modern practice is only relevant for nitrous oxide since other inhaled anesthetics are delivered at much lower concentrations due to their higher potency.


Denitrification is a microbially facilitated process where nitrate (NO3−) is reduced and ultimately produces molecular nitrogen (N2) through a series of intermediate gaseous nitrogen oxide products. Facultative anaerobic bacteria perform denitrification as a type of respiration that reduces oxidized forms of nitrogen in response to the oxidation of an electron donor such as organic matter. The preferred nitrogen electron acceptors in order of most to least thermodynamically favorable include nitrate (NO3−), nitrite (NO2−), nitric oxide (NO), nitrous oxide (N2O) finally resulting in the production of dinitrogen (N2) completing the nitrogen cycle. Denitrifying microbes require a very low oxygen concentration of less than 10%, as well as organic C for energy. Since denitrification can remove NO3−, reducing its leaching to groundwater, it can be strategically used to treat sewage or animal residues of high nitrogen content. Denitrification can leak N2O, which is an ozone-depleting substance and a greenhouse gas that can have a considerable influence on global warming.

The process is performed primarily by heterotrophic bacteria (such as Paracoccus denitrificans and various pseudomonads), although autotrophic denitrifiers have also been identified (e.g., Thiobacillus denitrificans). Denitrifiers are represented in all main phylogenetic groups. Generally several species of bacteria are involved in the complete reduction of nitrate to N2, and more than one enzymatic pathway has been identified in the reduction process.Direct reduction from nitrate to ammonium, a process known as dissimilatory nitrate reduction to ammonium or DNRA, is also possible for organisms that have the nrf-gene. This is less common than denitrification in most ecosystems as a means of nitrate reduction. Other genes known in microorganisms which denitrify include nir (nitrite reductase) and nos (nitrous oxide reductase) among others; organisms identified as having these genes include Alcaligenes faecalis, Alcaligenes xylosoxidans, many in the genus Pseudomonas, Bradyrhizobium japonicum, and Blastobacter denitrificans.

Fink effect

The Fink effect, also known as "diffusion anoxia", "diffusion hypoxia",

or the "third gas effect",

is a factor that influences the pO2 (partial pressure of oxygen) within the alveolus. When water-insoluble gases such as anesthetic agent N2O (nitrous oxide) are breathed in large quantities they can be dissolved in body fluids rapidly. This leads to a temporary increase in both the concentrations and partial pressures of oxygen and carbon dioxide in the alveolus.

The effect is named for Bernard Raymond Fink (1914–2000), whose 1955 paper first explained it.

When a patient is recovering from N2O anaesthesia, large quantities of this gas cross from the blood into the alveolus (down its concentration gradient) and so for a short period of time, the O2 and CO2 in the alveolus are diluted by this gas. A sufficiently large decrease in the partial pressure of oxygen leads to hypoxia. The decrease in CO2 pressure can also potentiate this effect when ventilation is suppressed, leading to potential hypoxaemia. Nonetheless, this effect only lasts a couple of minutes and hypoxia can be avoided by increasing the fractional inspired oxygen concentration when recovering from N2O anaesthesia.

It is for this reason that Entonox, a 50:50 combination of nitrous oxide and oxygen, is suitable for use by para-medical staff such as ambulance officers: it provides sufficient nitrous oxide for pain relief with sufficient oxygen to avoid hypoxia.


Inhalants are a broad range of household and industrial chemicals whose volatile vapors or pressurized gases can be concentrated and breathed in via the nose or mouth to produce intoxication (called "getting high" in slang), in a manner not intended by the manufacturer. They are inhaled at room temperature through volatilization (in the case of gasoline or acetone) or from a pressurized container (e.g., nitrous oxide or butane), and do not include drugs that are sniffed after burning or heating. For example, amyl nitrite (poppers), nitrous oxide and toluene – a solvent widely used in contact cement, permanent markers, and certain types of glue – are considered inhalants, but smoking tobacco, cannabis, and crack are not, even though these drugs are inhaled as smoke.While a small number of inhalants are prescribed by medical professionals and used for medical purposes, as in the case of inhaled anesthetics and nitrous oxide (an anxiolytic and pain relief agent prescribed by dentists), this article focuses on inhalant use of household and industrial propellants, glues, fuels and other products in a manner not intended by the manufacturer, to produce intoxication or other psychoactive effects. These products are used as recreational drugs for their intoxicating effect. According to a 1995 report by the National Institute on Drug Abuse, the most serious inhalant abuse occurs among homeless children and teens who "... live on the streets completely without family ties." Inhalants are the only substance which is used more by younger teens than by older teens. Inhalant users inhale vapor or aerosol propellant gases using plastic bags held over the mouth or by breathing from a solvent-soaked rag or an open container. The practices are known colloquially as "sniffing", "huffing" or "bagging".

The effects of inhalants range from an alcohol-like intoxication and intense euphoria to vivid hallucinations, depending on the substance and the dose. Some inhalant users are injured due to the harmful effects of the solvents or gases or due to other chemicals used in the products that they are inhaling. As with any recreational drug, users can be injured due to dangerous behavior while they are intoxicated, such as driving under the influence. In some cases, users have died from hypoxia (lack of oxygen), pneumonia, cardiac failure or arrest, or aspiration of vomit. Brain damage is typically seen with chronic long-term use of solvents as opposed to short-term exposure.Even though many inhalants are legal, there have been legal actions taken in some jurisdictions to limit access by minors. While solvent glue is normally a legal product, a Scottish court has ruled that supplying glue to children is illegal if the store knows the children intend to abuse the glue. In the US, thirty-eight of 50 states have enacted laws making various inhalants unavailable to those under the age of 18, or making inhalant use illegal.

Inhalational anaesthetic

An inhalational anaesthetic is a chemical compound possessing general anaesthetic properties that can be delivered via inhalation. They are administered through a face mask, laryngeal mask airway or tracheal tube connected to an anaesthetic vaporiser and an anaesthetic delivery system. Agents of significant contemporary clinical interest include volatile anaesthetic agents such as isoflurane, sevoflurane and desflurane, as well as certain anaesthetic gases such as nitrous oxide and xenon.

Music for Nitrous Oxide

Music for Nitrous Oxide is the first studio album released by Stars of the Lid on Sedimental Records in 1995. The album features minimal, droning compositions of varying length. The press release from Sedimental Records read: “Sedimental announces the first CD from Austin drone stars Stars of the Lid, an amazing 4-track recording that is created in the spirit of Eno, Main and Spacemen 3. Produced without keyboards, this lo-fi ambient journey employs predominately [sic] guitar, avoiding typical rock elements while still possessing the ‘home’ recorded feel of so much independent music.”In 2009 Sedimental Records released a remastered version featuring updated artwork by Craig McCaffrey.Adamord features an excerpt of a letter written by Alcoholics Anonymous co-founder Lois W., addressed to her husband.

Track four features an audio clip of Brent Spiner from the seventh season Star Trek: The Next Generation episode "Force of Nature". Spiner's character Data is shown attempting to train his cat Spot not to jump onto his keyboard while he is working. Track four also contains a snippet of Chopin's Prelude Op.28, No.7.

Track five features a clip from the film Apocalypse Now during which Frederic Forrest's character Jay 'Chef' Hicks suffers a nervous breakdown aboard a boat after encountering a tiger in the Cambodian jungle. This clip is interspersed with one of an unknown sci-fi program discussing extraterrestrials.

Track seven features an audio clip of C.H. Evans who played Jack in Hap's Diner, in David Lynch's film Twin Peaks: Fire Walk with Me. Evans' line is: "Now, her name is Irene and it is night. Don't take it any further than that. There's nothin' good about it."

Nitrous-oxide reductase

In enzymology, a nitrous oxide reductase also known as nitrogen:acceptor oxidoreductase (N2O-forming) is an enzyme that catalyzes the final step in bacterial denitrification, the reduction of nitrous oxide to dinitrogen.

N2O + 2 reduced cytochome c ⇌ N2 + H2O + 2 cytochrome cIt plays a critical role in preventing release of a potent greenhouse gas into the atmosphere.

Nitrous oxide (medication)

Nitrous oxide, sold under the brand name Entonox among others, is an inhaled gas used as a pain medication and together with other medications for anesthesia. Common uses include during childbirth, following trauma, and as part of end of life care. Onset of effect is typically within half a minute and lasts for about a minute.There are few side effects, other than vomiting, with short term use. With long term use anemia or numbness may occur. It should always be given with at least 21% oxygen. It is not recommended in people with a bowel obstruction or pneumothorax. Use in the early part of pregnancy is not recommended. Breastfeeding can occur following use.Nitrous oxide was discovered between 1772 and 1793 and used for anesthesia in 1844. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. It often comes as a 50/50 mixture with oxygen. Devices with a demand valve are available for self-administration. The setup and maintenance is relatively expensive for developing countries.

Nitrous oxide engine

A nitrous oxide engine is an internal combustion engine in which oxygen for burning the fuel comes from the decomposition of nitrous oxide, N2O, rather than air. The system increases the engine's power output by allowing fuel to be burned at a higher-than-normal rate, because of the higher partial pressure of oxygen injected with the fuel mixture. Nitrous injection systems may be "dry", where the nitrous oxide is injected separately from fuel, or "wet" in which additional fuel is carried into the engine along with the nitrous. Nitrous oxide systems may not be permitted for street or highway use, depending on local regulations. Nitrous oxide use is permitted in certain classes of auto racing. Reliable operation of an engine with nitrous injection requires careful attention to the strength of engine components and to the accuracy of the mixing systems, otherwise destructive detonations or exceeding engineered component maximums may occur. Nitrous oxide injection systems were applied as early as World War II for certain aircraft engines.

Nitrous oxide fuel blend

Nitrous Oxide Fuel Blend propellants are a class of liquid rocket propellants that were intended in the early 2010s to be able to replace hydrazine as the standard storable rocket propellent in some applications.

In nitrous-oxide fuel blends, the fuel and oxidizer are blended and stored; this is sometimes referred to as a mixed monopropellant. Upon use, the propellant is heated or passed over a catalyst bed and the nitrous oxide decomposes into oxygen-rich gasses. Combustion then ensues. Special care is needed in the chemical formulation and engine design to prevent detonating the stored fuel.


Pro FWD is a class in drag racing. The E.T. Bracket categories are no-electronics classes. Delay devices, throttle stops, air shifters, transbrakes, etc. or any device that transmits real-time, on-track data to the driver or any remote location are prohibited. All applicable NHRA rules apply based on elapsed time.

E.T. Bracket classes use a .5-second, full-countdown Tree.

Recreational use of nitrous oxide

Recreational use of nitrous oxide is the inhalation of nitrous oxide gas for its euphoriant effects.

The gas is sometimes called Whippets, Laughing Gas, the Epiphany Drug, or Hippy Crack.

In Australia, nitrous oxide bulbs are known as nangs.

Relative analgesia machine

A relative analgesia machine is used by dentists to induce inhalation sedation in their patients. It delivers a mixture of nitrous oxide ("laughing gas") and oxygen. A relative analgesia machine is simpler than an anaesthetic machine, as it does not feature the additional medical ventilator and anaesthetic vaporiser, which are only needed for administration of general anesthetics. Instead the relative analgesia machine is designed for the light form of anaesthesia with nitrous oxide, where the patient is less sensitive to pain but remains fully conscious.

Second gas effect

During induction of general anesthesia, when a large volume of a gas (e.g. nitrous oxide) is taken up from alveoli into pulmonary capillary blood, the concentration of gases remaining in the alveoli is increased. This results in effects known as the "concentration effect" and the second gas effect. These effects occur because of the contraction of alveolar volume associated with the uptake of the nitrous oxide. Previous explanations by Edmond I. Eger and Robert K. Stoelting have appealed to an extra-inspired tidal volume due to a potential negative intrapulmonary pressure associated with the uptake of the nitrous oxide.

There are two extreme breathing patterns and the extra-inspired tidal volume is an artificial construct associated with one of these patterns. Thus it is the volume change that actually causes the effects.

Whipped-cream charger

A whipped cream charger (sometimes colloquially called a whippit, whippet, nossy, nang, Johnson or charger) is a steel cylinder or cartridge filled with nitrous oxide (N2O) that is used as a whipping agent in a whipped cream dispenser. The narrow end of a charger has a foil covering which is broken to release the gas. This is usually done by a sharp pin inside the whipped cream dispenser. The nitrous oxide in chargers is also used as an oxidizer in hybrid model rocket engines. It is also a popular recreational drug.

The associated kitchen appliance which receives the charger is commonly known as a whipping siphon.

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