Hubbry Logo
Nitrous oxideNitrous oxideMain
Open search
Nitrous oxide
Community hub
Nitrous oxide
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Nitrous oxide
Nitrous oxide
Nitrous oxide
View on Wikipedia
from Wikipedia

Nitrous oxide
Nitrous oxide's canonical forms
Nitrous oxide's canonical forms
Ball-and-stick model with bond lengths
Ball-and-stick model with bond lengths
Space-filling model of nitrous oxide
Space-filling model of nitrous oxide
Names
IUPAC names
Nitrous oxide[1] (not recommended)[why?]
Dinitrogen oxide[2] (alternative name)
Systematic IUPAC name
Oxidodinitrogen(N—N)
Other names
  • Laughing gas
  • galaxy gas
  • sweet air
  • nitrous
  • nos
  • nang
  • nitrus[citation needed]
  • protoxide of nitrogen
  • hyponitrous oxide
  • dinitrogen oxide
  • dinitrogen monoxide
  • nitro
Identifiers
3D model (JSmol)
8137358
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.030.017 Edit this at Wikidata
E number E942 (glazing agents, ...)
2153410
KEGG
RTECS number
  • QX1350000
UNII
UN number 1070 (compressed)
2201 (liquid)
  • InChI=1S/N2O/c1-2-3 checkY
    Key: GQPLMRYTRLFLPF-UHFFFAOYSA-N checkY
  • InChI=1/N2O/c1-2-3
  • InChI=1/N2O/c1-2-3
    Key: GQPLMRYTRLFLPF-UHFFFAOYAP
  • N#[N+][O-]
  • [N-]=[N+]=O
Properties
N
2O
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)
Viscosity 14.90 μPa·s[3]
Structure
linear, C‹The template Smallsub is being considered for merging.› ∞v
0.166 D
Thermochemistry
219.96 J/(K·mol)
+82.05 kJ/mol
Pharmacology
N01AX13 (WHO)
Inhalation
Pharmacokinetics:
0.004%
5 minutes
Respiratory
Hazards
GHS labelling:
GHS03: Oxidizing
Danger
H270
P220, P244, P282, P317, P336, P370+P376, P403, P410+P403
NFPA 704 (fire diamond)
NFPA 704 four-colored diamondHealth 2: Intense or continued but not chronic exposure could cause temporary incapacitation or possible residual injury. E.g. chloroformFlammability 0: Will not burn. E.g. waterInstability 0: Normally stable, even under fire exposure conditions, and is not reactive with water. E.g. liquid nitrogenSpecial hazard OX: Oxidizer. E.g. potassium perchlorate
2
0
0
OX
Flash point Nonflammable
Safety data sheet (SDS) Ilo.org, ICSC 0067
Related compounds
Nitric oxide
Dinitrogen trioxide
Nitrogen dioxide
Dinitrogen tetroxide
Dinitrogen pentoxide
Related compounds
 Ammonium nitrate
Azide
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Nitrous oxide (dinitrogen oxide or dinitrogen monoxide), commonly known as laughing gas, nitrous, or factitious air, among others,[4] is a chemical compound, an oxide of nitrogen with the formula N
2O. At room temperature, it is a colourless non-flammable gas, and has a slightly sweet scent and taste.[4] At elevated temperatures, nitrous oxide is a powerful oxidiser similar to molecular oxygen.[4]

Nitrous oxide has significant medical uses, especially in surgery and dentistry, for its anaesthetic and pain-reducing effects,[5] and it is on the World Health Organization's List of Essential Medicines.[6] Its colloquial name, "laughing gas", coined by Humphry Davy, describes the euphoric effects upon inhaling it, which cause it to be used as a recreational drug inducing a brief "high".[5][7] When abused chronically, it may cause neurological damage through inactivation of vitamin B12. It is also used as an oxidiser in rocket propellants and motor racing fuels, and as a frothing gas for whipped cream.

Nitrous oxide is also an atmospheric pollutant, with a concentration of 333 parts per billion (ppb) in 2020, increasing at 1 ppb annually.[8][9] It is a major scavenger of stratospheric ozone, with an impact comparable to that of CFCs.[10] About 40% of human-caused emissions are from agriculture,[11][12] as nitrogen fertilisers are digested into nitrous oxide by soil micro-organisms.[13] As the third most important greenhouse gas, nitrous oxide substantially contributes to global warming.[14][15] Reduction of emissions is an important goal in the politics of climate change.[16]

Discovery and early use

[edit]

The gas was first synthesised in 1772 by English natural philosopher and chemist Joseph Priestley who called it dephlogisticated nitrous air (see phlogiston theory)[17] or inflammable nitrous air.[18] 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.[19]

"Living Made Easy": 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" (including 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".[20]

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,[clarification needed] 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.[20] 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.[21] Davy coined the name "laughing gas" for nitrous oxide.[22]

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.[23]

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.[24]

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.[25] 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.[26] 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.[27] 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.[20] Over the following three years, Colton and his associates successfully administered nitrous oxide to more than 25,000 patients.[28] 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. Instead, diethyl ether, being a stronger and more potent anaesthetic, was demonstrated and accepted for use in October 1846, along with chloroform in 1847.[20] When Joseph Thomas Clover invented the "gas-ether inhaler" in 1876, 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.[28] Although hospitals today use 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.

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.[29][30]

Chemical properties and reactions

[edit]

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

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

N
2O is inert at room temperature and has few reactions. At elevated temperatures, its reactivity increases. For example, nitrous oxide reacts with NaNH
2 at 187 °C (369 °F) to give NaN
3:

2 NaNH2 + N2O → NaN3 + NaOH + NH3

This reaction is the route adopted by the commercial chemical industry to produce azide salts, which are used as detonators.[31]

Mechanism of action

[edit]

The pharmacological mechanism of action of inhaled N
2O is not fully known. However, it has been shown to directly modulate a broad range of ligand-gated ion channels, which likely plays a major role. It moderately blocks NMDAR and [[CHRNB2|β‹The template Smallsub is being considered for merging.› 2-subunit]]-containing nACh channels, weakly inhibits AMPA, kainate, [[GABAA-rho receptor|GABA‹The template Smallsub is being considered for merging.› C]] and [[5-HT3 receptor|5-HT‹The template Smallsub is being considered for merging.› 3 receptors]], and slightly potentiates [[GABAA receptor|GABA‹The template Smallsub is being considered for merging.› A]] and glycine receptors.[32][33] It also has been shown to activate two-pore-domain K+
 channels.[34] While N
2O affects several ion channels, its anaesthetic, hallucinogenic and euphoriant effects are likely caused mainly via inhibition of NMDA receptor-mediated currents.[32][35] In addition to its effects on ion channels, N
2O may act similarly to nitric oxide (NO) in the central nervous system.[35] Nitrous oxide is 30 to 40 times more soluble than nitrogen.

The effects of inhaling sub-anaesthetic doses of nitrous oxide may vary unpredictably with settings and individual differences;[36][37] however, Jay (2008)[38] suggests that it reliably induces the following states and sensations:

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

A minority of users also experience uncontrolled vocalisations and muscular spasms. These effects generally disappear minutes after removal of the nitrous oxide source.[38]

Anxiolytic effect

[edit]

In behavioural tests of anxiety, a low dose of N
2O is an effective anxiolytic. This anti-anxiety effect is associated with enhanced activity of GABA‹The template Smallsub is being considered for merging.› A 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
2O.[39] Indeed, in humans given 30% N
2O, benzodiazepine receptor antagonists reduced the subjective reports of feeling "high", but did not alter psychomotor performance.[40][41]

Analgesic effect

[edit]

The analgesic effects of N
2O 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
2O.[42] Administration of antibodies that bind and block the activity of some endogenous opioids (not β-endorphin) also block the antinociceptive effects of N
2O.[43] Drugs that inhibit the breakdown of endogenous opioids also potentiate the antinociceptive effects of N
2O.[43] Several experiments have shown that opioid receptor antagonists applied directly to the brain block the antinociceptive effects of N
2O, but these drugs have no effect when injected into the spinal cord.

Apart from an indirect action, nitrous oxide, like morphine[44] also interacts directly with the endogenous opioid system by binding at opioid receptor binding sites.[45][46]

Conversely, [[alpha-2 adrenergic receptor|α‹The template Smallsub is being considered for merging.› 2-adrenoceptor]] antagonists block the pain-reducing effects of N
2O when given directly to the spinal cord, but not when applied directly to the brain.[47] Indeed, [[alpha-2B adrenergic receptor|α‹The template Smallsub is being considered for merging.› 2B-adrenoceptor]] knockout mice or animals depleted in norepinephrine are nearly completely resistant to the antinociceptive effects of N
2O.[48] Apparently N
2O-induced release of endogenous opioids causes disinhibition of brainstem noradrenergic neurons, which release norepinephrine into the spinal cord and inhibit pain signalling.[49] Exactly how N
2O causes the release of endogenous opioid peptides remains uncertain.

Production

[edit]

Various methods of producing nitrous oxide are used.[50]

Industrial methods

[edit]
Nitrous oxide production

Nitrous oxide is prepared on an industrial scale by carefully heating ammonium nitrate[50] at about 250 °C, which decomposes into nitrous oxide and water vapour.[51]

NH4NO3 → 2 H2O + N2O

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.[52]

Laboratory methods

[edit]

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:[53]

2 NaNO3 + (NH4)2SO4 → Na2SO4 + 2 N2O + 4 H2O

Another method involves the reaction of urea, nitric acid and sulfuric acid:[54]

2 (NH2)2CO + 2 HNO3 + H2SO4 → 2 N2O + 2 CO2 + (NH4)2SO4 + 2 H2O

Direct oxidation of ammonia with a manganese dioxide-bismuth oxide catalyst has been reported:[55] cf. Ostwald process.

2 NH3 + 2 O2 → N2O + 3 H2O

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:

NH3OHCl + NaNO2 → N2O + NaCl + 2 H2O

Treating HNO
3 with SnCl
2 and HCl also has been demonstrated:

2 HNO3 + 8 HCl + 4 SnCl2 → 5 H2O + 4 SnCl4 + N2O

Hyponitrous acid decomposes to N‹The template Smallsub is being considered for merging.› 2O and water with a half-life of 16 days at 25 °C at pH 1–3.[56]

H2N2O2 → H2O + N2O

Atmospheric occurrence

[edit]
Nitrous oxide (N2O) measured by the Advanced Global Atmospheric Gases Experiment (AGAGE) in the lower atmosphere (troposphere) at stations around the world. Abundances are given as pollution free monthly mean mole fractions in parts-per-billion.
Nitrous oxide atmospheric concentration since 1978
Annual growth rate of atmospheric nitrous oxide since 2000
Earth's nitrous oxide budget from the Global Carbon Project (2020)[57]

Nitrous oxide is a minor component of Earth's atmosphere and is an active part of the planetary nitrogen cycle. Based on analysis of air samples gathered from sites around the world, its concentration surpassed 330 ppb in 2017.[8] The growth rate of about 1 ppb per year has also accelerated during recent decades.[9] Nitrous oxide's atmospheric abundance has grown more than 20% from a base level of about 270 ppb in 1750.[58] Important atmospheric properties of N
2O are summarized in the following table:

Property Value
Ozone depletion potential (ODP) 0.017[10] (CCl3F = 1)
Global warming potential (GWP: 100-year) 273[59] (CO2 = 1)
Atmospheric lifetime 116 ± 9 years[60]

In 2022 the IPCC reported that: "The human perturbation of the natural nitrogen cycle through the use of synthetic fertilizers and manure, as well as nitrogen deposition resulting from land-based agriculture and fossil fuel burning has been the largest driver of the increase in atmospheric N2O of 31.0 ± 0.5 ppb (10%) between 1980 and 2019."[60]

Emissions by source

[edit]

17.0 (12.2 to 23.5) million tonnes total annual average nitrogen in N
2O was emitted in 2007–2016.[60] About 40% of N
2O emissions are from humans and the rest are part of the natural nitrogen cycle.[61] The N
2O emitted each year by humans has a greenhouse effect equivalent to about 3 billion tonnes of carbon dioxide: for comparison humans emitted 37 billion tonnes of actual carbon dioxide in 2019, and methane equivalent to 9 billion tonnes of carbon dioxide.[62]

Most of the N
2O emitted into the atmosphere, from natural and anthropogenic sources, is produced by microorganisms such as denitrifying bacteria and fungi in soils and oceans.[63] 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%).[64] Wetlands can also be emitters of nitrous oxide.[65][66] Emissions from thawing permafrost may be significant, but as of 2022 this is not certain.[60]

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%).[67][68][69][70][71] Agriculture enhances nitrous oxide production through soil cultivation, the use of nitrogen fertilisers and animal waste handling.[72] 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,[73] and the majority of a year's emissions may occur when conditions are favorable during "hot moments"[74][75] and/or at favorable locations known as "hotspots".[76]

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 the nitration of cyclohexanone.[67][77][78]

Biological processes

[edit]

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

  • aerobic autotrophic nitrification, the stepwise oxidation of ammonia (NH
    3    ) to nitrite (NO−
    2    ) and to nitrate (NO−
    3    )
  • anaerobic heterotrophic denitrification, the stepwise reduction of NO−
    3     to NO−
    2    , nitric oxide (NO), N
    2    O     and ultimately N
    2    , where facultative anaerobe bacteria use NO−
    3     as an electron acceptor in the respiration of organic material in the condition of insufficient oxygen (O
    2    )
  • nitrifier denitrification, which is carried out by autotrophic NH
    3    -oxidising bacteria and the pathway whereby ammonia (NH
    3    ) is oxidised to nitrite (NO−
    2    ), followed by the reduction of NO−
    2     to nitric oxide (NO), N
    2    O     and molecular nitrogen (N
    2    )
  • 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.[79]

Uses

[edit]

Rocket motors

[edit]

Nitrous oxide may be used as an oxidiser in a rocket motor. Compared to other oxidisers, it is much less toxic and more stable at room temperature, making it easier to store and safer to carry on a flight. Its high density and low storage pressure (when maintained at low temperatures) make it highly competitive with stored high-pressure gas systems.[80]

In a 1914 patent, American rocket pioneer Robert Goddard suggested nitrous oxide and gasoline as possible propellants for a liquid-fuelled rocket.[81] 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 may also be used as a monopropellant. In the presence of a heated catalyst at a temperature of 577 °C (1,071 °F), N
2O decomposes exothermically into nitrogen and oxygen.[82] 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 (I‹The template Smallsub is being considered for merging.› sp) up to 180 s. While noticeably less than the I‹The template Smallsub is being considered for merging.› sp available from hydrazine thrusters (monopropellant, or bipropellant with dinitrogen tetroxide), the decreased toxicity makes nitrous oxide a worthwhile option.

The ignition of nitrous oxide depends critically on pressure. It deflagrates at approximately 600 °C (1,112 °F) at a pressure of 309 psi (21 atmospheres).[83] At 600 psi, the required ignition energy is only 6 joules, whereas at 130 psi a 2,500-joule ignition energy input is insufficient.[84][85]

Internal combustion engine

[edit]
Main article: Nitrous oxide engine

In vehicle racing, nitrous oxide (often called "nitrous" in this context) increases engine power by providing more oxygen during combustion, thus allowing the engine to burn more fuel. It is an oxidising agent roughly equivalent to hydrogen peroxide, and much stronger than molecular oxygen. Nitrous oxide is not flammable at low pressure/temperature, but at about 300 °C (572 °F), its breakdown delivers more oxygen than atmospheric air. It often is mixed with another fuel that is easier to deflagrate.

Nitrous oxide is stored as a compressed liquid. In an engine intake manifold, the evaporation and expansion of the liquid causes a large drop in intake charge temperature, resulting in a denser charge and 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 it just before the cylinder (direct port injection).

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 nitrous oxide oxidant in a reciprocating engine is excessive power: if the mechanical structure of the engine is not properly reinforced, it may be severely damaged or destroyed. It is important with nitrous oxide augmentation of petrol engines to maintain proper and evenly spread operating temperatures and fuel levels to prevent pre-ignition (also called detonation or spark knock).[86] However, most problems associated with nitrous oxide come not from excessive power but from excessive pressure, since the gas builds up a much denser charge in the cylinder. The increased pressure and temperature can melt, crack, or warp the piston, valve, and cylinder head.

Automotive-grade liquid nitrous oxide differs slightly from medical-grade. A small amount of sulfur dioxide (SO
2) is added to prevent substance abuse.[87]

Aerosol propellant for food

[edit]
Food-grade N
2O whipped-cream chargers

The gas is approved for use as a food additive (E number: E942), specifically as an aerosol spray propellant. It is commonly used in aerosol whipped cream canisters and cooking sprays.

The gas is extremely soluble in fatty compounds. In pressurised aerosol whipped cream, it is dissolved in the fatty cream until it leaves the can, when it becomes gaseous and thus creates foam. This produces whipped cream four times the volume of the liquid, whereas whipping air into cream only produces twice the volume. Unlike air, nitrous oxide inhibits rancidification of the butterfat. 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 "sparkle".

Extra-frothed whipped cream produced with nitrous oxide is unstable, and will return to liquid within half an hour to one hour.[88] Thus, it is not suitable for decorating food that will not be served immediately.

In December 2016, there was a shortage of aerosol whipped cream in the United States, with canned whipped cream use at its peak during the Christmas and holiday season, due to an explosion at the Air Liquide nitrous oxide facility in Florida in late August. The company prioritized the remaining supply of nitrous oxide to medical customers rather than to food manufacturing.[89]

Also, cooking spray, made from various oils with lecithin emulsifier, may use nitrous oxide propellant, or alternatively food-grade alcohol or propane.

Medical

[edit]
Main article: Nitrous oxide (medication)
Medical-grade N
2O tanks used in dentistry

Nitrous oxide has been used in dentistry and surgery, as an anaesthetic and analgesic, since 1844.[20] In the early days, the gas was administered through simple inhalers consisting of a breathing bag made of rubber cloth.[28] 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 can increase the risk of postoperative nausea and vomiting.[90][91][92]

Dentists use a simpler machine which only delivers an N
2O/O
2 mixture for the patient to inhale while conscious but must still be a recognised purpose designed dedicated relative analgesic flowmeter with a minimum 30% of oxygen at all times and a maximum upper limit of 70% nitrous oxide. The patient is kept conscious throughout the procedure, and retains adequate mental faculties to respond to questions and instructions from the dentist.[93]

Inhalation of nitrous oxide is used frequently to relieve pain associated with childbirth, trauma, oral surgery and acute coronary syndrome (including heart attacks). Its use during labour has been shown to be a safe and effective aid for birthing women.[94] Its use for acute coronary syndrome is of unknown benefit.[95]

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

Fifty percent 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.[96]

Recreational

[edit]
Main article: Recreational use of nitrous oxide
Aquatint depiction of a laughing gas party in the nineteenth century, by Thomas Rowlandson
Street sign indicating ban of nitrous oxide use near the Poelestraat in Groningen
Whippit remnants (the small steel canisters) of recreational drug use, the Netherlands, 2017

Recreational inhalation of nitrous oxide, to induce euphoria and slight hallucinations, began with the British upper class in 1799 in gatherings known as "laughing gas parties".[97]

From the 19th century, the widespread availability of the gas for medical and culinary purposes allowed for recreational use to greatly expand globally. In the UK as of 2014, nitrous oxide was estimated to be used by almost half a million young people at nightspots, festivals and parties.[98]

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.[99]

A significant issue cited in London's press is the effect of nitrous oxide canister littering, which is highly visible and causes significant complaints from communities.[100]

Prior to 8 November 2023 in the UK, nitrous oxide was subject to the Psychoactive Substances Act 2016, making it illegal to produce, supply, import or export nitrous oxide for recreational use. The updated law prohibited possession of nitrous oxide, classifying it as a Class C drug under the Misuse of Drugs Act 1971.[101]

While nitrous oxide is understood by most recreational users to give a "safe high", many are unaware that excessive consumption may cause neurological harm which, if left untreated, can cause permanent neurological damage.[102] In Australia, recreation use became a public health concern following a rise in reports of neurotoxicity and emergency room admissions. In the state of South Australia, legislation was passed in 2020 to restrict canister sales.[103]

In 2024, under the street name "Galaxy Gas", nitrous oxide has exploded in popularity among young people for recreational use, partially driven by TikTok trends.[104][105]

Safety

[edit]

Nitrous oxide is a significant occupational hazard for surgeons, dentists and nurses. Because the gas 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 intoxicate the clinic staff if the room is poorly ventilated, with potential chronic exposure. A continuous-flow fresh-air ventilation system or N
2O scavenger system may be needed to prevent waste-gas buildup.[citation needed] 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.[106] It set a recommended exposure limit (REL) of 25 ppm (46 mg/m3) to escaped anaesthetic.[107]

Exposure to nitrous oxide causes short-term impairment of cognition, audiovisual acuity, and manual dexterity, as well as spatial and temporal disorientation,[108] putting the user at risk of accidental injury.[38]

Nitrous oxide is neurotoxic, and medium or long-term habitual consumption of significant quantities can cause neurological harm with the potential for permanent damage if left untreated.[103][102] It is believed that, like other NMDA receptor antagonists, N
2O produces Olney's lesions in rodents upon prolonged (several hour) exposure.[109][110][111][112] However, because it is normally expelled from the body rapidly, it is less likely to be neurotoxic than other NMDAR antagonists.[113] In rodents, short-term exposure results in only mild injury that is rapidly reversible, and neuronal death occurs only after constant and sustained exposure.[109] Nitrous oxide may also cause neurotoxicity after extended exposure because of hypoxia. This is especially true of non-medical formulations such as whipped-cream chargers ("whippits" or "nangs"),[114] which contain no oxygen gas.[115]

In reports to poison control centers, heavy users (≥400 g or ≥200 L of N2O gas in one session) or frequent users (regular, i.e., daily or weekly) have developed signs of peripheral neuropathy: ataxia (gait abnormalities) or paresthesia (perception of sensations such as tingling, numbness, or prickling, mostly in the extremities). Such early signs of neurological damage indicate chronic toxicity.[116]

Nitrous oxide might have therapeutic use in treating stroke. In a rodent model, nitrous oxide at 75% by volume reduced ischemia-induced neuronal death induced by occlusion of the middle cerebral artery, and decreased NMDA-induced Ca2+ influx in neuronal cell cultures, a cause of excitotoxicity.[113]

Occupational exposure to ambient nitrous oxide has been associated with DNA damage, due to interruptions in DNA synthesis.[117] This correlation is dose-dependent[118][119] and does not appear to extend to casual recreational use; however, further research is needed to confirm the level of exposure needed to cause damage.

Inhalation of pure nitrous oxide causes oxygen deprivation, resulting in low 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 or other inhalation system, or prolonged breath-holding.[120]

Long-term exposure to nitrous oxide may cause [[Vitamin B12 deficiency|vitamin B‹The template Smallsub is being considered for merging.› 12 deficiency]]. This can cause serious neurotoxicity if the user has preexisting vitamin B‹The template Smallsub is being considered for merging.› 12 deficiency.[121] It inactivates the cobalamin form of vitamin B‹The template Smallsub is being considered for merging.› 12 by oxidation. Symptoms of vitamin B‹The template Smallsub is being considered for merging.› 12 deficiency, including sensory neuropathy, myelopathy and encephalopathy, may occur within days or weeks of exposure to nitrous oxide anaesthesia in people with subclinical vitamin B‹The template Smallsub is being considered for merging.› 12 deficiency. Symptoms are treated with high doses of vitamin B‹The template Smallsub is being considered for merging.› 12, but recovery can be slow and incomplete.[122] People with normal vitamin B‹The template Smallsub is being considered for merging.› 12 levels have stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (nitrous oxide abuse). Vitamin B‹The template Smallsub is being considered for merging.› 12 levels should be checked in people with risk factors for vitamin B‹The template Smallsub is being considered for merging.› 12 deficiency prior to using nitrous oxide anaesthesia.[123]

Several experimental studies in rats indicate that chronic exposure of pregnant females to nitrous oxide may have adverse effects on the developing fetus.[124][125][126]

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.[127] 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).[128] 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.[129] There also have been incidents where nitrous oxide decomposition in plumbing has led to the explosion of large tanks.[83]

Environmental impact

[edit]

Global accounting of N
2O sources and sinks over the decade ending 2016 indicates that about 40% of the average 17 TgN/yr (teragrams, or million metric tons, of nitrogen per year) of emissions originated from human activity, and shows that emissions growth chiefly came from expanding agriculture.[11][12]

Trends in the atmospheric abundance of long-lived greenhouse gases

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 265 times the atmospheric heat-trapping ability of carbon dioxide (CO
2).[59] However, because of its low concentration (less than 1/1,000 of that of CO
2), its contribution to the greenhouse effect is less than one third that of carbon dioxide, and also less than methane.[130] On the other hand, since about 40% of the N
2O entering the atmosphere is the result of human activity,[67] control of nitrous oxide is part of efforts to curb greenhouse gas emissions.[131]

Most human caused nitrous oxide released into the atmosphere is a greenhouse gas emission from agriculture, when farmers add nitrogen-based fertilizers onto the fields, and through the breakdown of animal manure. Reduction of emissions can be a hot topic in the politics of climate change.[132]

Nitrous oxide is also released as a by-product of burning fossil fuel, though the amount released depends on which fuel was used. It is also emitted through the manufacture of nitric acid, which is used in the synthesis of nitrogen fertilizers. The production of adipic acid, a precursor to nylon and other synthetic clothing fibres, also releases nitrous oxide.[133]

A rise in atmospheric nitrous oxide concentrations has been implicated as a possible contributor to the extremely intense global warming during the Cenomanian-Turonian boundary event.[134]

Nitrous oxide has also been implicated in thinning the ozone layer. A 2009 study suggested that N
2O emission was the single most important ozone-depleting emission and it was expected to remain the largest throughout the 21st century.[10][135]

Legality

[edit]
Main article: Recreational use of nitrous oxide § Legal status

In India transfer of nitrous oxide from bulk cylinders to smaller, more transportable E-type, 1,590-litre-capacity tanks[136] is legal when intended for medical anaesthesia.

The New Zealand Ministry of Health has warned that nitrous oxide is a prescription medicine whose sale or possession without a prescription is an offense under the Medicines Act.[137] This would seemingly prohibit all non-medicinal uses of nitrous oxide, although it is implied that only recreational use will be targeted.

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.[138] In September 2023, the UK Government announced that nitrous oxide would be made illegal by the end of the year as a class C drug, with possession potentially carrying up to a two-year prison sentence or an unlimited fine.[139]

Possession of nitrous oxide is legal under United States federal law and is not subject to DEA purview.[140] 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 without a proper medical license. Many states have laws regulating the possession, sale and distribution of nitrous oxide. Such laws usually ban distribution to minors or limit the amount that may be sold without special license.[citation needed] For example, in California, possession for recreational use is prohibited and qualifies as a misdemeanor.[141]

See also

[edit]

References

[edit]

Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Nitrous oxide

View on Grokipedia
from Grokipedia
Nitrous oxide (N₂O) is a colorless, non-flammable gas with a slightly sweet odor and taste, consisting of two nitrogen atoms bonded to one oxygen atom in a linear molecular structure. Known as laughing gas for its euphoric effects when inhaled, it was first isolated by Joseph Priestley in 1772 and systematically studied by Humphry Davy in the late 1790s, who demonstrated its analgesic properties through self-experimentation. In medicine, nitrous oxide serves as an inhalational anesthetic and analgesic, particularly in dentistry and procedural sedation, owing to its rapid onset, minimal respiratory depression, and quick recovery profile. It is also employed as a propellant in food aerosols, such as whipped cream dispensers, and as an oxidizer to enhance combustion in rocket motors and automotive engines. Atmospherically, nitrous oxide acts as a long-lived greenhouse gas with a 100-year global warming potential of 265 to 298 times that of carbon dioxide and contributes to stratospheric ozone depletion by breaking down into nitric oxide in the upper atmosphere.

Chemical and Physical Properties

Molecular Structure and Basic Characteristics

Nitrous oxide (N₂O) is a linear triatomic molecule with the central nitrogen atom bonded to one terminal nitrogen and one oxygen atom. The molecule exhibits resonance, with the dominant structure represented as N≡N⁺–O⁻, featuring a triple bond between the nitrogens and a single bond to oxygen with formal charges, alongside a minor contribution from N⁻–N⁺≡O. This resonance hybridization results in bond lengths of approximately 1.13 Å (N-N) and 1.19 Å (N-O), reflecting partial double-bond character and contributing to the molecule's chemical stability and oxidizing properties due to the electrophilic nitrogen. The molar mass is 44.013 g/mol. At standard temperature and pressure, nitrous oxide exists as a colorless, odorless, nonflammable gas. It has a melting point of −90.86 °C and a boiling point of −88.48 °C. The gas density at 0 °C and 1 atm is 1.977 g/L, approximately 1.53 times that of air. Solubility in water is low, at 1.2 g/L (0.0012 g/mL) at 20 °C and 1 atm. Thermodynamic properties include a critical temperature of 36.4 °C and critical pressure of 72.5 atm (7.25 MPa). The ideal gas heat capacity at constant pressure (Cp) is approximately 38.6 J/mol·K at 25 °C, increasing with temperature as described by the Shomate equation for gas-phase conditions. These attributes underscore its utility in compressed form while highlighting phase behavior under varying pressures and temperatures.

Reactivity and Stability

Nitrous oxide demonstrates high stability at standard temperature and pressure, showing minimal reactivity with air, water, or most organic materials, which distinguishes it from more labile nitrogen oxides. This inertness arises from its linear molecular structure and weak polarity, rendering it non-corrosive and suitable for long-term storage in compatible materials like steel or aluminum. However, it functions as a mild oxidizing agent, comparable in strength to hydrogen peroxide but superior to dioxygen, capable of supporting the combustion of flammable substances without igniting itself. Thermal decomposition represents the dominant reactivity pathway, proceeding via the endothermic dissociation 2N2O→2N2+O22\mathrm{N_2O} \rightarrow 2\mathrm{N_2} + \mathrm{O_2} with a standard enthalpy change of ΔH=+164\Delta H = +164 kJ/mol (or +82 kJ/mol per mole of N₂O), driven by the release of stable N₂. This reaction initiates appreciably above 500 °C under atmospheric pressure, with rates increasing exponentially; for instance, significant decomposition occurs between 600–850 °C in the absence of catalysts. Metal surfaces, such as iron or copper, or certain contaminants like oils, can catalyze this process, lowering the activation energy and accelerating decomposition at reduced temperatures through surface-mediated oxygen atom abstraction. Nitrous oxide engages in limited direct reactions, including slow oxidation with alkali metals like sodium or potassium, where the metal atom abstracts an oxygen from N₂O, forming metal oxide and N₂; this proceeds via a collinear transition state with barriers around 10–20 kcal/mol depending on the metal. Such reactivity underscores its role as an oxygen donor rather than a reducing agent. Despite baseline stability, nitrous oxide exhibits sensitivity to extreme conditions, where rapid decomposition can generate explosive pressures from the evolved oxygen and heat—up to 20-fold volume expansion. Contaminants, including hydrocarbons or halocarbons, lower the decomposition threshold dramatically, sometimes to below 300 °C or even ambient temperatures in confined spaces, as impurities facilitate chain-propagating radicals. This hazard necessitates rigorous purification and temperature controls in storage cylinders to prevent autoignition or rupture.

Historical Development

Discovery and Initial Characterization

Joseph Priestley first isolated nitrous oxide in 1772 by heating a mixture involving ammonium nitrate, producing what he termed "nitrous air" or "phlogisticated nitrous air," though he did not fully characterize its properties or effects. Priestley's empirical method involved thermal decomposition, yielding the gas alongside other nitrogen oxides, but his observations focused primarily on its reactivity with reducing agents rather than its physiological impacts. In 1799, Humphry Davy systematically studied the gas at the Pneumatic Institution in Bristol, purifying it through repeated distillation and conducting self-experiments by inhaling it via inhalation bags. Davy named it "nitrous oxide" to distinguish it from nitric oxide and documented its euphoric effects, describing sensations of intense pleasure, heightened vividness of ideas, and muscular excitement during respiration trials from 1799 to 1800. These experiments, detailed in his 1800 publication Researches, Chemical and Philosophical, linked the gas to respiration studies, noting its potential to induce giddiness and emotional elevation without immediate toxicity when briefly inhaled. Early characterizations also revealed nitrous oxide's asphyxiant nature, as prolonged inhalation displaced oxygen, leading to hypoxia despite initial invigorating perceptions; Davy's trials highlighted this dual aspect, with subjects experiencing convulsions or unconsciousness in extended exposures. By the early 19th century, chemical analyses confirmed its molecular formula as N₂O through volumetric and gravimetric methods, solidifying its identity as a distinct oxide of nitrogen.

Early Industrial and Medical Applications

Horace Wells, an American dentist, pioneered the medical application of nitrous oxide on December 10, 1844, after attending a public demonstration by Gardner Quincy Colton in Hartford, Connecticut, where he observed a participant injure himself without apparent pain under the gas's influence. Wells self-administered nitrous oxide the following day for the extraction of his own molar, experiencing no pain, and subsequently used it successfully on several patients for dental procedures. Although an attempt to demonstrate it publicly in Boston shortly thereafter failed due to improper administration and patient movement, this event marked the initial clinical use of nitrous oxide for analgesia in dentistry. By the 1860s, nitrous oxide achieved broader adoption in surgical and dental practices across the United States, driven by Colton's promotion through lectures, clinics, and training of over 15,000 practitioners, which facilitated its integration into routine extractions and minor operations. Efficacy remained variable, however, as pure nitrous oxide often induced incomplete anesthesia or hypoxia from oxygen displacement, limiting its reliability without adjuncts like ether and contributing to sporadic failures in early applications. This variability stemmed from inadequate dosing and delivery systems, yet the gas's rapid onset and short duration positioned it as a practical alternative to ether for short procedures where flammability risks were a concern. Industrial production of nitrous oxide scaled in the late 19th century to meet growing medical demand, with facilities established for thermal decomposition of ammonium nitrate, enabling reliable supply for clinical use. Early non-medical applications included experimental use as an oxidizer in engines, though significant deployment occurred during World War II, when the German Luftwaffe incorporated nitrous oxide in the GM-1 system to boost aircraft engine power by up to 100 horsepower through enhanced oxygen supply, compensating for fuel limitations without raising detonation risks. This wartime innovation highlighted nitrous oxide's utility as a monopropellant for temporary performance gains in piston engines. Post-World War II refinements standardized medical administration as mixtures with oxygen, typically 50% nitrous oxide and 50% oxygen (Entonox), to avert hypoxia while preserving analgesic effects, improving safety margins and enabling wider surgical adoption. These mixtures addressed earlier limitations by maintaining adequate oxygenation, with production processes optimized for purity to minimize contaminants that could exacerbate variability.

Production Processes

Industrial Synthesis

The primary industrial method for synthesizing nitrous oxide (N₂O) entails the controlled thermal decomposition of ammonium nitrate (NH₄NO₃). This process involves heating an aqueous solution of ammonium nitrate, typically at concentrations of 80–93%, to temperatures between 250–280 °C, yielding N₂O and water vapor via the exothermic reaction NH₄NO₃ → N₂O + 2H₂O. Precise temperature control is essential to prevent uncontrolled decomposition or detonation risks inherent to ammonium nitrate. The resulting gas mixture, containing N₂O along with impurities such as water vapor, nitric oxide (NO), and nitrogen dioxide (NO₂), undergoes purification. This includes condensation to remove water, alkaline scrubbing to eliminate nitrogen oxides, and fractional distillation to achieve purities exceeding 99%. Byproduct management focuses on capturing and recycling unreacted ammonium nitrate or neutralizing acidic effluents, with typical material efficiency requiring 1.8–2 kg of ammonium nitrate per kg of N₂O produced. Alternative methods, such as decomposition in chloride-containing nitric acid solutions or recovery as a byproduct from adipic acid or nitric acid production, exist but are less prevalent due to lower yields and higher complexity compared to the ammonium nitrate route. Global production capacity supports an estimated annual output of approximately 0.5 million metric tons of commercial-grade N₂O as of 2023, scaled by market demand for medical, food, and propulsion applications. The process's scalability stems from its exothermic nature, minimizing external energy inputs beyond initial heating and compression for liquefaction, contributing to production costs around $0.50–1.00 per kg at scale, primarily driven by raw material expenses.

Laboratory Preparation

Nitrous oxide is commonly prepared in laboratories through the controlled thermal decomposition of dry ammonium nitrate, following the reaction NH₄NO₃ → N₂O + 2H₂O. This process requires heating the reagent to temperatures between 170°C and 270°C in a suitable apparatus, such as a distillation flask equipped with a condenser, to generate the gas while minimizing side reactions that could produce nitrogen or nitric oxide at higher temperatures. The resulting gas is typically collected by displacement of water or air, then purified via fractional distillation under reduced pressure or by passing through drying agents like concentrated sulfuric acid to remove moisture and impurities, ensuring high purity suitable for analytical or educational purposes. This batch-wise approach allows for precise control over reaction conditions in glassware setups, differing from industrial continuous-flow processes by prioritizing small-scale yield optimization—often achieving 80-90% efficiency through careful temperature regulation—and enabling immediate spectroscopic verification of product identity. Safety protocols are critical, as ammonium nitrate decomposition can accelerate explosively if overheated beyond 300°C or contaminated, necessitating operations in a well-ventilated fume hood with remote heating and pressure relief mechanisms. An alternative laboratory route involves the reaction of sulfamic acid with nitric acid, which generates nitrous oxide via intermediate formation of nitrosylsulfamic acid, though this method carries risks of uncontrolled gas evolution and is less favored for routine use due to its hazardous nature.

Natural Occurrence and Biogeochemical Cycle

Atmospheric concentrations of nitrous oxide (N₂O) prior to the Industrial Revolution were approximately 270 parts per billion (ppb), based on ice core records spanning the past 800,000 years where levels rarely exceeded 280 ppb. By May 2025, global average concentrations reached 338.66 ppb, reflecting a roughly 25% increase since pre-industrial times, as measured by the NOAA Global Monitoring Laboratory at sites like Mauna Loa. The long-term trend shows a steady rise driven by anthropogenic emissions outpacing natural removal processes, with N₂O's atmospheric lifetime estimated at 116 ± 9 years, primarily due to stratospheric photolysis and oxidation. This accumulation contributes about 6% to the total radiative forcing from long-lived anthropogenic greenhouse gases since 1750. Annual growth rates have averaged 0.8–1 ppb per year over recent decades but accelerated post-2020, reaching 1.32 ppb in 2020 and 1.29 ppb in 2021—the highest observed since systematic monitoring began in the late 1970s—consistent with intensified global nitrogen inputs enhancing net production. Isotopic analysis of the ¹⁵N/¹⁴N ratio in atmospheric N₂O provides a tracer for distinguishing emission origins and transformation pathways, revealing shifts toward lighter signatures (more depleted in ¹⁵N) that align with increased microbial production under elevated nitrogen availability. These site preference and bulk δ¹⁵N values, derived from high-precision measurements, confirm that recent trend accelerations reflect imbalances in the global N₂O budget rather than changes in atmospheric sinks.

Emission Sources and Biological Pathways

Nitrous oxide (N₂O) emissions arise predominantly from microbial processes in the nitrogen cycle, where bacteria and fungi in soils, sediments, and aquatic systems produce the gas as a byproduct or intermediate. Nitrification, an aerobic oxidation of ammonium (NH₄⁺) to nitrate (NO₃⁻), generates N₂O primarily during the partial oxidation of hydroxylamine (NH₂OH) to nitrite (NO₂⁻) by ammonia-oxidizing organisms such as Nitrosomonas species. Denitrification, an anaerobic dissimilatory process, reduces NO₃⁻ stepwise to N₂, releasing N₂O when enzymes like nitrous oxide reductase are substrate-limited or inhibited, often under low oxygen and high nitrate conditions; this pathway dominates in waterlogged soils and oxygen minimum zones (OMZs) of oceans. These processes are regulated by environmental factors including temperature, pH, oxygen levels, and nitrogen availability, with incomplete denitrification yielding higher N₂O yields under fluctuating redox conditions. Chemodenitrification—abiotic reactions of reduced nitrogen compounds like NO₂⁻ with soil organics or metals—and nitrifier denitrification (hybrid aerobic reduction by nitrifiers) contribute smaller fractions globally. Global N₂O emissions totaled approximately 18 Tg N yr⁻¹ during 2010–2019, with natural sources comprising 65% (11.8 Tg N yr⁻¹) and anthropogenic sources 35% (6.5 Tg N yr⁻¹). Natural emissions stem chiefly from unfertilized soils (6.4 Tg N yr⁻¹), where microbial nitrification and denitrification occur in forest, grassland, and wetland ecosystems, modulated by organic matter decomposition and precipitation patterns. Oceanic sources add about 4.7 Tg N yr⁻¹ (open ocean 3.5 Tg N yr⁻¹ plus shelves 1.2 Tg N yr⁻¹), concentrated in tropical OMZs via denitrification and nitrifier activity amid upwelling nutrient-rich waters. Anthropogenic emissions, while representing a minority of the total, have risen 40% since 1980 due to intensified nitrogen cycling. Agricultural soils account for the largest share, with direct emissions from synthetic fertilizers and manure (3.6 Tg N yr⁻¹) stimulating excess nitrification and denitrification in cropped fields, where excess ammonium and nitrate applications exceed plant uptake. This sector comprises 56% of anthropogenic emissions, as nitrogen inputs amplify microbial rates beyond natural baselines. Industrial sources, including nitric acid production for fertilizers and adipic acid synthesis for nylon, contribute under 0.5 Tg N yr⁻¹ (<5% of anthropogenic total), via side reactions like ammonium nitrate decomposition. Minor anthropogenic fluxes arise from fossil fuel combustion (~0.2 Tg N yr⁻¹), biomass burning, and wastewater, where incomplete denitrification in anaerobic digesters releases N₂O. Indirect emissions from atmospheric nitrogen deposition and leaching (1.2 Tg N yr⁻¹) further enhance natural soil and aquatic processes. Temperature increases from climate change accelerate soil microbial respiration, elevating N₂O production rates via higher enzyme kinetics in both nitrification (Q₁₀ ~1.5–2) and denitrification (Q₁₀ up to 3), fostering positive feedback where warming boosts emissions by 10–50% per °C in many ecosystems. Enhanced fertilizer application efficiencies, such as precision timing and slow-release formulations, however, reduce N₂O yield per unit nitrogen input by limiting substrate excess for microbial processes.

Industrial and Technical Applications

Propulsion and Performance Enhancement

Nitrous oxide functions as an oxidizer in propulsion systems by decomposing exothermically into nitrogen and oxygen, thereby supplying additional oxygen for combustion and releasing heat that augments thrust. This property makes it suitable for hybrid rocket motors, where it is vaporized and injected over a solid fuel grain, such as hydroxyl-terminated polybutadiene (HTPB), to control the regression rate and achieve throttlable performance. In rocketry, nitrous oxide enabled the SpaceShipOne spacecraft to complete the first private crewed suborbital flight on June 21, 2004, using a hybrid motor that generated sufficient thrust—estimated at around 76,000 pounds-force at peak—to propel the vehicle to an altitude of 367,441 feet. Hybrid configurations with nitrous oxide typically deliver specific impulses of 200 to 250 seconds at sea level, benefiting from the oxidizer's self-pressurizing characteristics that simplify feed systems compared to cryogenic alternatives. The decomposition reaction enhances effective thrust by providing both mass flow and thermal energy, potentially increasing performance over pure oxidizer-fuel systems, though actual gains depend on mixture ratio and chamber pressure. Despite these advantages, nitrous oxide's use in rocketry carries detonation risks from uncontrolled decomposition, which can escalate to explosion if triggered by contaminants like iron oxide or elevated temperatures exceeding 565°C, leading to pressure spikes that rupture tanks. Relative to liquid oxygen (LOX), nitrous oxide offers non-cryogenic storage and lower handling complexity, reducing boil-off losses, but yields lower specific impulse due to its higher molecular weight exhaust products and demands careful mixture ratio control to avoid efficiency drops. LOX, while requiring cryogenic infrastructure, supports higher performance in bipropellant systems but introduces risks like frostbite and oxygen fires. In automotive applications, nitrous oxide injection systems—branded as NOS—deliver the gas into the engine intake manifold, where it decomposes to enrich oxygen content, permitting up to 50-200% more fuel to be burned and boosting horsepower by 50 to 250 units in typical street setups. This oxygen augmentation allows internal combustion engines to exceed their naturally aspirated limits temporarily, with power gains scaling by injection volume: a 100-horsepower shot might add 100 horsepower, while larger 500-horsepower kits suit high-output racing engines. The technique traces to World War II German Luftwaffe aircraft experiments for high-altitude power, but gained prominence in U.S. drag racing from the late 1940s, where early adopters like those in Southern California hot rod circles achieved quarter-mile elapsed times under 12 seconds, outpacing supercharged rivals. By the 1970s, commercialized NOS kits from innovators like Mike Thermos dominated classes such as Pro Modified, enabling consistent sub-7-second runs and solidifying nitrous as a cost-effective, bolt-on enhancer for drag-and-drive events. Systems require precise solenoid timing and bottle pressure management (typically 900-1,100 psi) to prevent backfires or uneven delivery, with popularity enduring due to affordability—kits starting under $500—versus turbocharging or supercharging.

Food Processing and Aerosol Uses

Nitrous oxide functions as a propellant in whipped cream dispensers, where its high solubility in the fat content of cream—greater than that of nitrogen or oxygen—enables it to dissolve under pressure (typically 5-10 bar), forming stable microbubbles upon release that expand the foam volume up to four times the original liquid. This solubility follows Henry's law, with the dissolved gas concentration proportional to its partial pressure, ensuring uniform dispersion without acidic off-flavors from alternatives like carbon dioxide. The U.S. Food and Drug Administration authorizes nitrous oxide for direct food use in applications such as whipped cream production, deeming it safe when employed as a propellant in contained systems. Global annual sales of nitrous oxide cream chargers surpass 250 million units, predominantly for culinary foaming in the food industry. In modified atmosphere packaging (MAP), nitrous oxide supplements common gases like nitrogen and carbon dioxide by displacing oxygen to curb oxidation, microbial growth, and produce respiration, extending shelf life for items such as fresh fruits and vegetables. Food-grade nitrous oxide demand underscores its role in preservation, with the sector driving significant market volume amid controlled release that limits atmospheric emissions.

Medical and Pharmacological Applications

Clinical Uses in Anesthesia and Pain Management

Nitrous oxide serves as an adjunct in general anesthesia for surgical procedures, where concentrations of 50-70% in oxygen mixtures accelerate the onset of other inhaled anesthetics via the second gas effect and provide mild analgesia with rapid equilibration (onset within 2-5 minutes). Due to its high minimum alveolar concentration (approximately 104%), it lacks sufficient potency for standalone anesthesia and must be combined with potent agents like opioids or volatiles to achieve adequate depth, reducing overall requirements for these adjuvants by 20-30% in balanced techniques. In dentistry, nitrous oxide-oxygen mixtures (30-70%) are widely used for conscious sedation during procedures such as extractions and restorations, effectively reducing patient anxiety and procedural pain scores on visual analog scales by 20-50% compared to placebo or alternative sedatives like midazolam. Success rates for completing dental interventions under this sedation exceed 90% in pediatric and adult populations, with self-administration minimizing overdose risks. For labor analgesia, a fixed 50% N₂O/50% O₂ mixture, self-administered intermittently via demand valve mask, offers moderate pain relief, decreasing VAS scores by 3-5 points on a 10-point scale without impairing maternal mobility or fetal outcomes. Efficacy is comparable to systemic opioids but inferior to neuraxial blocks, with 40-60% of users reporting satisfactory relief despite higher dissatisfaction rates than epidural alternatives. Employed clinically since the 1840s, nitrous oxide maintains a favorable safety profile in controlled settings, with serious adverse events below 1% and mostly mild effects like nausea (rates <5-8%) resolving post-discontinuation. Recent advancements include portable, IoT-enabled delivery devices for ambulatory and emergency use, enabling real-time monitoring of gas flow, patient vitals, and automated safety cutoffs to enhance precision and reduce exposure variability as of 2025.

Mechanism of Action

Nitrous oxide exerts its primary pharmacological effects through central nervous system interactions, acting as a non-competitive antagonist at N-methyl-D-aspartate (NMDA) glutamate receptors, which inhibits excitatory neurotransmission and contributes to analgesia and mild anesthesia. This NMDA blockade occurs at clinically relevant concentrations, reducing ionic currents and protecting against excitotoxic damage without significantly potentiating inhibitory gamma-aminobutyric acid type A (GABAA) receptors, distinguishing it from other inhalational agents. Additionally, nitrous oxide modulates endogenous opioid systems by stimulating opioid peptide release in the periaqueductal gray matter of the midbrain, which activates descending noradrenergic inhibitory pathways to enhance antinociception and anxiolysis. It also influences dopaminergic pathways, potentially amplifying reward and analgesic responses, though these effects are secondary to NMDA antagonism. Unlike volatile anesthetics, nitrous oxide produces minimal respiratory depression at subanesthetic doses used for analgesia, preserving ventilatory drive due to its weak potency and selective neural targeting. The potency of nitrous oxide is quantified by its minimum alveolar concentration (MAC) of approximately 104%, indicating the alveolar partial pressure required to prevent movement in 50% of subjects to surgical stimulus, which underscores its role as an adjunct rather than a sole agent. Effects correlate directly with inhaled partial pressure, with rapid onset and equilibration facilitated by its low blood:gas partition coefficient of 0.47, allowing quick diffusion across the blood-brain barrier and minimal accumulation in tissues. This low solubility contrasts with more lipid-soluble volatiles, enabling faster induction and emergence without prolonged hangover effects. Nitrous oxide undergoes negligible metabolism in humans, with less than 0.004% biotransformed, primarily via cytochrome P450 enzymes under hypoxic conditions; the vast majority is exhaled unchanged through the lungs, supporting swift recovery proportional to alveolar ventilation. This pharmacokinetic profile minimizes accumulation and active metabolites, differentiating it from agents prone to hepatic processing or tissue redistribution, and aligns its central effects tightly with exposure duration.

Recreational Use and Associated Risks

Patterns of Abuse

Non-medical inhalation of nitrous oxide, often termed "whippits," typically involves discharging gas from small whipped cream charger canisters into balloons for inhalation or direct mouth inhalation using makeshift devices. Direct inhalation from canisters risks frostbite from the expanding gas reaching temperatures up to -40°C, potentially damaging lips, nose, throat, and vocal cords. Users commonly obtain canisters marketed for food preparation, with brands like Galaxy Gas gaining popularity through social media platforms such as TikTok starting around 2023, promoting flavored variants and party uses that facilitated wider diversion. Prevalence data indicate significant lifetime exposure among youth, with a 2010 U.S. adolescent survey reporting 15.8% lifetime use, while the 2023 National Survey on Drug Use and Health documented over 13 million Americans with lifetime misuse. Self-reported surveys highlight episodic patterns, particularly among those aged 16-24, driven by accessibility and social normalization at events. Recreational motivations center on short-lived euphoria and dissociative effects achieved via inhalation volumes equivalent to 1-2 liter balloons, producing sensations of floating or altered perception lasting seconds to minutes. Use patterns skew toward infrequent, social contexts like music festivals and nightclubs, where balloons are shared among groups, often alongside other substances, though some individuals exhibit repeated dosing in sessions. Over-the-counter availability of culinary chargers has sustained supply, with the global nitrous oxide cream charger market valued at approximately $510 million in 2025 and projected to reach $1 billion by 2035 at a 6.9% CAGR, reflecting demand growth that indirectly supports diversion despite emerging age-based sales restrictions in select U.S. states. Recreational nitrous oxide abuse primarily causes neurological damage through irreversible oxidation of vitamin B12's cobalt ion, disrupting methionine synthase and methylmalonyl-CoA mutase activity, which impairs myelin synthesis and leads to subacute combined degeneration (SCD) of the spinal cord. This manifests as progressive sensory ataxia, paresthesia, and weakness, often mimicking B12 deficiency syndromes, with case studies reporting myeloneuropathy in heavy users after weeks to months of inhalation. Peripheral neuropathy affects sensory and motor nerves, predominantly axonal, with electrophysiologic evidence of slowed conduction velocities in chronic abusers. While exact prevalence varies, series indicate neuropathy or myelopathy in a substantial fraction of documented chronic cases, estimated at 20-50% based on aggregated clinical reports of persistent users inhaling hundreds of canisters weekly. Long-term sequelae include dorsal column degeneration visible on spinal MRI as T2 hyperintensities, potentially progressing to irreversible paraplegia or cognitive impairment if untreated, though early cessation and high-dose B12 supplementation can reverse symptoms in milder instances via restored enzyme function. Psychiatric effects, such as psychosis or mood disturbances, arise from combined hypoxic and metabolic disruptions, with some users experiencing hallucinations or dependency after prolonged exposure. Severe cases report permanent disability, underscoring causality from B12 inactivation rather than direct toxicity, as confirmed by elevated homocysteine and methylmalonic acid levels in affected individuals. Acute risks stem from hypoxia and asphyxia during inhalation, as nitrous oxide displaces oxygen, causing symptoms including dizziness, chest tightness, weakness, coordination issues, nausea, and vomiting; severe cases lead to fainting, seizures, asphyxiation, or sudden death. Users may also experience acute hallucinations, illusions, sensory distortions, disorientation, and reduced muscle control, heightening injury risk. In the United States, deaths attributed to nitrous oxide poisoning rose from 23 in 2010 to 156 in 2023 among ages 15-74, a 578% increase, totaling 1,240 fatalities over the period, with asphyxia and acute neurological events predominant mechanisms. This surge correlates with wider availability of small canisters for recreational use, amplifying overdose potential in unsupervised settings, though underreporting may inflate true trends given reliance on death certificate data.

Safety and Toxicity Profile

Acute and Chronic Exposure Effects

Acute exposure to nitrous oxide primarily manifests as central nervous system depression and acts as a simple asphyxiant, with symptoms including dizziness, chest tightness, weakness, loss of coordination, nausea, vomiting, headache, and euphoria at concentrations above 50% when inhaled without supplemental oxygen. Higher levels, exceeding 70-80%, can lead to loss of consciousness, seizures, and death due to hypoxia from oxygen displacement rather than direct cellular toxicity. Direct inhalation from high-pressure canisters poses an additional risk of frostbite to the lips, nose, throat, and vocal cords due to the extreme cold of the expanding gas, which can reach temperatures as low as -40°C. Animal lethality data underscore its relatively low inherent toxicity, with median lethal concentrations (LC50) in rodents requiring prolonged exposure to near-pure gas (e.g., 20-30% for hours), emphasizing anoxic mechanisms over chemical poisoning. The dose-response threshold for acute effects aligns with partial pressure equivalents; brief exposures below 25% with adequate oxygenation typically produce reversible analgesia without significant toxicity, but unsupervised high-dose inhalation risks rapid deoxygenation and cardiovascular instability. Chronic exposure, often occupational, inactivates vitamin B12-dependent methionine synthase, potentially leading to megaloblastic bone marrow depression, leukopenia, and neurological deficits such as peripheral neuropathy or subacute combined degeneration after months to years at elevated levels without folate supplementation. Hematologic changes, including reduced leukocyte motility and chemotaxis, have been observed in exposed healthcare workers, indirectly impairing immunity, though subclinical effects predominate at trace concentrations. Reproductive outcomes remain debated; early studies linked unscavenged occupational exposure (e.g., >75 ppm) in female dental assistants to increased spontaneous abortions and reduced fertility, but confounding factors like co-anesthetics and poor ventilation limit causality, with modern scavenged environments showing no consistent deficits. Regulatory thresholds mitigate risks: NIOSH recommends a 25 ppm time-weighted average (TWA) over 10 hours for waste anesthetic gas exposure to avert chronic effects, while ACGIH suggests 50 ppm TWA, with medical protocols emphasizing continuous monitoring, ventilation, and oxygen co-administration to maintain margins below these limits.

Occupational and Handling Hazards

Nitrous oxide poses risks as a simple asphyxiant in occupational settings, particularly in confined spaces where it can displace oxygen and lead to suffocation without warning symptoms due to its colorless, odorless nature. Exposure to high concentrations can cause dizziness, unconsciousness, and death by hypoxia. As a strong oxidizing agent, it supports combustion more vigorously than atmospheric oxygen, increasing fire and explosion hazards when in contact with flammable contaminants like oils, greases, or organic materials in cylinders or equipment. In production and handling, cylinder failures have occurred due to overpressurization, contamination, or improper storage, with notable incidents including a 2010s workplace explosion from a venting nitrous oxide-saline mixture that injured multiple workers. Such events underscore the need for purity standards to prevent decomposition reactions that generate pressure and heat. In medical environments like dentistry and surgery, chronic low-level exposure to unscavenged waste gases has been associated with potential reproductive and neurological effects in older studies, but meta-analyses of modern practices with exposure limits below 25 ppm show no consistent deficits when engineering controls are applied. Mitigation relies on engineering controls such as scavenging systems, local exhaust ventilation, and leak detection to maintain ambient levels below recommended thresholds like the NIOSH 25 ppm guideline or health-based limits of 20 mg/m³ (approximately 14 ppm) as an 8-hour time-weighted average. Personal protective equipment includes chemical-resistant gloves, eye protection meeting ANSI/ISEA Z87.1 standards, and self-contained breathing apparatus for high-risk handling or emergencies. Training emphasizes secure cylinder storage away from heat sources, compatibility with non-combustible materials, and protocols to avoid oil contamination during maintenance. Incidents remain rare with adherence to these standards, highlighting the efficacy of proactive purity and pressure management.

Environmental Impacts

Contribution to Climate Change

Nitrous oxide (N₂O) acts as a long-lived greenhouse gas, absorbing infrared radiation primarily in the 7.7–8.0 μm and 16–17 μm spectral regions, contributing to atmospheric warming through enhanced radiative forcing. Its global warming potential (GWP) is 273 relative to CO₂ over a 100-year timescale, reflecting its potency despite lower concentrations compared to CO₂ or methane (CH₄). This metric accounts for N₂O's radiative efficiency and atmospheric lifetime of approximately 109–121 years, during which it persists until photolysis or reaction with atomic oxygen in the stratosphere breaks it down. Anthropogenic N₂O emissions contribute about 6.4% to the total effective radiative forcing from well-mixed greenhouse gases since 1750, a share dwarfed by CO₂ (around 66%) and CH₄ (about 16%). Human activities generate roughly 40% of global N₂O emissions, with the remainder from natural sources like soils and oceans; within anthropogenic emissions, agriculture dominates at 70–75%, driven by microbial denitrification and nitrification in fertilized soils and manure management, while medical, industrial, and fuel combustion sources each comprise less than 1–3%. This sectoral imbalance underscores N₂O's climate role as tied predominantly to agronomic nitrogen inputs rather than dispersed industrial processes. Atmospheric N₂O concentrations reached 338.0 ppb in 2024, up 1.0 ppb from 2023, with a multidecadal growth rate of approximately 0.8–1.0 ppb per year that has remained linearly consistent without observed tipping points or nonlinear accelerations. Observed trends align with emission inventories, showing no deviation from steady-state increases attributable to expanding agricultural nitrogen use.

Ozone Layer Interactions and Broader Ecosystem Effects

In the stratosphere, nitrous oxide (N₂O) serves as the primary source of nitrogen oxides (NOx), which catalyze ozone (O₃) destruction through a series of reactions. N₂O, with an atmospheric lifetime of approximately 116 years, reaches the stratosphere largely intact and undergoes destruction primarily via photolysis or reaction with excited oxygen atoms (O(¹D)), producing nitric oxide (NO): N₂O + O(¹D) → 2NO. The NO then participates in catalytic cycles, such as NO + O₃ → NO₂ + O₂ followed by NO₂ + O → NO + O₂, resulting in net ozone loss: O₃ + O → 2O₂. These processes occur most efficiently in the middle stratosphere, where NOx from N₂O contributes significantly to ozone depletion. Following the phase-out of chlorofluorocarbons (CFCs) and other synthetic ozone-depleting substances under the Montreal Protocol, anthropogenic N₂O has emerged as the dominant ozone-depleting emission, accounting for the largest ongoing threat to stratospheric ozone recovery. Natural N₂O emissions provide a baseline, but human activities have increased concentrations by about 20% since pre-industrial levels, sustaining depletion pressures despite reductions in halocarbons. Without controls on N₂O, projections indicate it will remain the primary anthropogenic contributor through the 21st century. Beyond stratospheric effects, N₂O emissions disrupt terrestrial and aquatic ecosystems through linkages in the nitrogen cycle. Excess nitrogen inputs from agriculture, such as fertilizers, drive denitrification processes that emit N₂O while contributing to eutrophication via nitrate runoff and atmospheric deposition of NOx precursors derived from related microbial pathways. In eutrophic waters, high nitrate levels promote incomplete denitrification, elevating N₂O yields and exacerbating hypoxia and algal blooms. Soil microbial communities, particularly denitrifying bacteria, respond to warming by accelerating N₂O production, creating feedbacks where elevated temperatures enhance emissions from thawing permafrost and fertilized soils, potentially amplifying nitrogen losses.

Regulatory Framework and Debates

Nitrous oxide is not scheduled as a controlled substance under United Nations conventions on psychotropic substances or narcotic drugs, remaining legal for legitimate industrial, medical, agricultural, and culinary uses across all countries. However, many jurisdictions monitor its distribution to prevent recreational misuse, with restrictions typically targeting sales for human inhalation rather than commodity applications. International trade in nitrous oxide for non-recreational purposes encounters no blanket prohibitions, though exports of related agricultural precursors like ammonium nitrate may face national security or environmental controls in select cases. In the United States, nitrous oxide holds no federal scheduling under the Drug Enforcement Administration's Controlled Substances Act, permitting its production and sale as an unregulated chemical commodity for industrial and food uses. The Food and Drug Administration oversees its purity and labeling for medical anesthesia and propellant applications, while twelve states explicitly ban sales or possession intended for recreational inhalation. The United Kingdom classified nitrous oxide as a Class C drug under the Misuse of Drugs Act 1971 effective November 8, 2023, criminalizing possession, supply, production, import, or export for purposes other than authorized uses like industry or medicine. In the European Union, no unified ban exists, but member states enforce varying controls; for instance, the Netherlands prohibited possession, import, and sale for recreational purposes starting January 1, 2023. Australia deems the sale of nitrous oxide for human consumption a criminal offense under federal law, with states imposing additional limits such as age restrictions on purchases and prohibitions on non-therapeutic supply. Western Australia amended its Medicines and Poisons Regulations 2016 effective October 31, 2024, to bar public access for non-legitimate ends, while Victoria reclassified non-therapeutic products as Schedule 6 poisons from October 1, 2022.

Controversies Over Bans and Mitigation Strategies

Proponents of recreational bans emphasize nitrous oxide's role in public health crises, including neurological damage and fatalities from heavy misuse, which prompted the UK government's classification of the substance as a Class C drug effective November 8, 2023, with penalties up to two years imprisonment for repeat possession offenses intended for inhalation. This measure addressed rising antisocial use and hospital admissions, yet critics, including medical experts and harm reduction advocates, contend it disproportionately burdens law enforcement while discouraging affected users from seeking timely treatment, as fear of prosecution may delay diagnosis of reversible deficiencies like vitamin B12 depletion. Post-ban analyses reveal enforcement challenges, with historical precedents showing that restrictions since 2016 on non-medical sales merely shifted supply to informal networks without reducing prevalence, suggesting causal inefficacy in altering demand-driven behaviors absent education or alternatives. Environmental mitigation debates center on medical sector emissions, which represent a negligible share—less than 1% of global anthropogenic nitrous oxide—compared to agriculture's 70-75% contribution from fertilizers and manure management. The American Society of Anesthesiologists advocated in October 2024 for deactivating piped delivery systems in hospitals, transitioning to portable cylinders to curb venting losses that amplify the gas's 265-298 times greater warming potential over carbon dioxide, a strategy yielding over 50% emissions cuts in adopting facilities like those in NYC Health + Hospitals. However, scalability hinges on infrastructure costs and clinical workflow disruptions, with destruction technologies like catalytic converters facing feasibility hurdles due to nitrous oxide's chemical stability; empirical prioritization thus favors agricultural precision fertilization over medical curbs, as the latter yields marginal climate gains without broader soil and livestock reforms. Regulatory skeptics invoke individual liberties and market dynamics, projecting the nitrous oxide industry's expansion to $2.3 billion by 2030 amid rising medical and automotive demands, arguing that overreach stifles innovation without proportional benefits. Pro-ban advocates cite dual health and climate imperatives, but evidence from prohibition models indicates limited long-term efficacy, as usage persists via diversion and without tackling agricultural dominance, underscoring that mitigation success demands data-driven tradeoffs over punitive universality.

References

  1. https://pubchem.ncbi.nlm.nih.gov/compound/Nitrous-Oxide
  2. https://pubmed.ncbi.nlm.nih.gov/30829177/
  3. https://www.ncbi.nlm.nih.gov/books/NBK532922/
  4. https://cameochemicals.noaa.gov/chemical/8909
  5. https://www.epa.gov/ghgemissions/nitrous-oxide-emissions
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3408851/
  7. https://chemistry.stackexchange.com/questions/29657/what-are-the-correct-resonance-structures-of-nitrous-oxide
  8. https://topblogtenz.com/nitrous-oxide-n2o-resonance-structures/
  9. https://webbook.nist.gov/cgi/cbook.cgi?ID=C10024972
  10. https://encyclopedia.airliquide.com/nitrous-oxide
  11. https://webbook.nist.gov/cgi/cbook.cgi?ID=C10024972&Mask=1
  12. https://webbook.nist.gov/cgi/cbook.cgi?ID=C10024972&Mask=1EFF
  13. https://royalsocietypublishing.org/doi/10.1098/rspa.1934.0057
  14. https://pubs.acs.org/doi/10.1021/jp0307295
  15. https://www.csb.gov/assets/1/20/airgas_investigation_report_-_final_-_2017-02-28.pdf
  16. https://apps.dtic.mil/sti/tr/pdf/ADA489459.pdf
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC6637098/
  18. https://www.woodlibrarymuseum.org/museum/nitrous-oxide/
  19. https://www.sciencedirect.com/science/article/pii/S0007091217468309/pdf?md5=b24902e55248b9b60d482c8f0ba100d1&pid=1-s2.0-S0007091217468309-main.pdf
  20. https://publicdomainreview.org/collection/the-nitrous-oxide-experiments-of-humphry-davy/
  21. https://www.open.edu/openlearn/history-the-arts/history-science-technology-medicine/humphry-davy-laughing-gas-and-the-era-self-experimentation
  22. https://www.sciencedirect.com/science/article/abs/pii/S095281800900258X
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC11566315/
  24. https://pubmed.ncbi.nlm.nih.gov/23962967/
  25. https://connecticuthistory.org/horace-wells-discovers-pain-free-dentistry/
  26. https://cerritosdentalsurgery.com/2014/02/04/a-brief-history-of-nitrous-oxide/
  27. https://data.isiscb.org/isis/citation/CBB001561406/
  28. https://www.pistonheads.com/news/ph-features/ph-origins-nitrous-oxide-injection/37769
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC3821266/
  30. https://academic.oup.com/bmb/article/125/1/103/4925059
  31. https://www.hitechgas.com/nitrous-oxide/nitrous-oxide-plants/how-nitrous-oxide-plant-works/
  32. https://asiaiga.org/uploaded_docs/en_AIGA_080_16_safe_practices_for_the_production_of_nitrous_oxide_from_ammonium_nitrate.pdf
  33. https://melscience.com/US-en/articles/methods-synthesis-nitrous-oxide/
  34. https://www.sciencedirect.com/science/article/pii/S0007091217519595
  35. https://www.eiga.eu/ct_documents/doc191-pdf/
  36. https://patents.google.com/patent/US4154806A/en
  37. https://www.ghgonline.org/nitrousindustry.htm
  38. https://finance.yahoo.com/news/nitrous-oxide-industry-report-2024-093800412.html
  39. https://www.researchnester.com/reports/nitrous-oxide-market/6406
  40. https://thundersaidenergy.com/downloads/nitric-acid-production-costs/
  41. https://pubs.acs.org/doi/pdf/10.1021/ja01202a507
  42. https://www.thoughtco.com/make-nitrous-oxide-or-laughing-gas-608280
  43. https://essd.copernicus.org/articles/16/2543/2024/
  44. https://www.epa.gov/climate-indicators/climate-change-indicators-atmospheric-concentrations-greenhouse-gases
  45. https://gml.noaa.gov/ccgg/trends_n2o/
  46. https://agupubs.onlinelibrary.wiley.com/doi/abs/10.1002/2015jd023267
  47. https://futureearth.org/2024/06/25/global-carbon-project-led-study-shows-nitrous-oxide-emissions-soared-40-percent-from-1980-to-2020-accelerating-climate-change/
  48. https://agupubs.onlinelibrary.wiley.com/doi/full/10.1029/2018JD029008
  49. https://acp.copernicus.org/articles/20/6495/2020/
  50. https://www.sciencedirect.com/topics/earth-and-planetary-sciences/nitrous-oxide-production
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC3682742/
  52. https://www.ghgonline.org/nitrousoceans.htm
  53. https://iiasa.ac.at/news/jun-2024/global-nitrous-oxide-budget-2024
  54. https://www.sciencedirect.com/science/article/pii/S1674927824000170
  55. https://www.sciencedirect.com/science/article/pii/S0016236125027619
  56. https://www.mdpi.com/2226-4310/12/5/372
  57. https://arc.aiaa.org/doi/10.2514/1.B39710
  58. https://www.ibb.ch/publication/N2O/zakirov.pdf
  59. https://www.spacesafetymagazine.com/aerospace-engineering/rocketry/hybrid-rocket-overview-part-2/
  60. https://shop.advanceautoparts.com/r/advice/car-truck-mods/everything-you-need-to-know-about-nitrous-oxide
  61. https://www.hotrod.com/features/the-facts-about-nitrous-oxide-injection-january-1984-982-1218-22-1
  62. https://www.v8buick.com/index.php?threads/nitrous-history.338439/
  63. https://journal.classiccars.com/2020/07/31/meet-the-father-of-nos-mike-thermos/
  64. https://www.sickthemagazine.com/news/nitrous-oxide-systems-continues-to-remain-a-popular-power-adder-choice
  65. https://fast-gas.com/nitrous-oxide-science/
  66. https://www.quora.com/Whipped-cream-use-nitrous-oxide-instead-of-nitrogen-gas-What-can-be-the-reason
  67. https://edepot.wur.nl/206766
  68. https://www.fda.gov/food/alerts-advisories-safety-information/fda-advises-consumers-not-inhale-nitrous-oxide-products
  69. https://www.archivemarketresearch.com/reports/nitrous-oxide-cream-charger-164310
  70. https://www.sciencedirect.com/science/article/abs/pii/S0963996918309773
  71. https://www.verifiedmarketresearch.com/product/food-grade-nitrous-oxide-market/
  72. https://clinicalview.gehealthcare.com/article/use-or-not-use-nitrous-oxide-anesthesia-providers-decision-when-nitrous-oxide-should-be
  73. https://www.openanesthesia.org/keywords/nitrous-oxide/
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC8637914/
  75. https://jdapm.org/DOIx.php?id=10.17245/jdapm.2025.25.3.161
  76. https://journals.lww.com/ebp/fulltext/2024/02000/is_nitrous_oxide_an_effective_monotherapy_for.22.aspx
  77. https://www.asahq.org/about-asa/governance-and-committees/asa-committees/committee-on-obstetric-anesthesia/nitrous-oxide
  78. https://onlinelibrary.wiley.com/doi/10.1155/2019/4618798
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC7755562/
  80. https://publications.aap.org/pediatrics/article/121/3/e528/72826/High-Concentration-Nitrous-Oxide-for-Procedural
  81. https://www.linkedin.com/pulse/how-medical-nitrous-oxide-works-one-simple-flow-2025-thrive-wellx-gsw5f/
  82. https://www.verifiedmarketreports.com/product/nitrous-oxide-sedation-machine-market/
  83. https://pubmed.ncbi.nlm.nih.gov/9546794/
  84. https://www.pnas.org/doi/full/10.1073/pnas.0402825101
  85. https://pubmed.ncbi.nlm.nih.gov/11936558/
  86. https://journals.lww.com/anesthesia-analgesia/fulltext/1995/04000/opioid_effects_of_psychotropic_analgesic_nitrous.57.aspx
  87. https://www.sciencedirect.com/science/article/pii/S1521689601901673
  88. https://emedicine.medscape.com/article/1413427-overview
  89. https://www.nejm.org/doi/full/10.1056/NEJMicm2502232
  90. https://www.addictioncenter.com/community/galaxy-gas/
  91. https://injury.research.chop.edu/blog/posts/dangerous-trend-galaxy-gas
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC2921531/
  93. https://olemiss.edu/news/2025/04/nitrous-oxide-abuse-study/index.html
  94. https://www.bmj.com/content/378/bmj.o2155
  95. https://adf.org.au/drug-facts/nitrous-oxide/
  96. https://pubmed.ncbi.nlm.nih.gov/26912510/
  97. https://pmc.ncbi.nlm.nih.gov/articles/PMC9517250/
  98. https://www.wiseguyreports.com/reports/nitrous-oxide-cream-charger-market
  99. https://www.linkedin.com/pulse/nitrous-oxide-cream-charger-market-application-jh26e
  100. https://pmc.ncbi.nlm.nih.gov/articles/PMC7366039/
  101. https://pmc.ncbi.nlm.nih.gov/articles/PMC11590355/
  102. https://thejcn.com/DOIx.php?id=10.3988/jcn.2023.19.1.44
  103. https://pn.bmj.com/content/23/3/222
  104. https://shmabstracts.mystagingwebsite.com/abstract/n2o-laughing-matter-nitrous-oxide-induced-vitamin-b12-myelopathy/
  105. https://www1.racgp.org.au/ajgp/2021/november/recreational-nitrous-oxide-neurotoxicity
  106. https://www.ajnr.org/content/ajnr/19/5/894.full.pdf
  107. https://americanaddictioncenters.org/inhalant-abuse/nitrous-oxide-whippets
  108. https://pmc.ncbi.nlm.nih.gov/articles/PMC12311712/
  109. https://www.newsweek.com/deaths-one-drug-spike-more-500-2106883
  110. https://nj.gov/health/eoh/rtkweb/documents/fs/1399.pdf
  111. https://oxfordtreatment.com/prescription-drug-abuse/nitrous-oxide/overdose/
  112. https://www.ncbi.nlm.nih.gov/books/NBK614263/
  113. https://go.drugbank.com/drugs/DB06690
  114. https://www.cdc.gov/niosh/npg/npgd0465.html
  115. https://www.sciencedirect.com/science/article/pii/S1521689602902648
  116. https://pmc.ncbi.nlm.nih.gov/articles/PMC5661723/
  117. https://www.nejm.org/doi/full/10.1056/NEJM199210013271405
  118. https://pmc.ncbi.nlm.nih.gov/articles/PMC9354063/
  119. https://archive.cdc.gov/www_cdc_gov/niosh/topics/nitrousoxide/default.html
  120. https://chemicalsafety.ilo.org/dyn/icsc/showcard.display?p_card_id=0067
  121. https://louisville.edu/micronano/files/documents/safety-data-sheets-sds/NitrousOxide.pdf
  122. https://www.osha.gov/ords/imis/accidentsearch.accident_detail?id=14308787
  123. https://www.csb.gov/assets/1/20/airgas_investigation_report_-_final_-_2017-02-28.pdf?15808
  124. https://www.bjanaesthesia.org/article/S0007-0912%2819%2930063-7/fulltext
  125. https://pmc.ncbi.nlm.nih.gov/articles/PMC9719248/
  126. https://www.osha.gov/waste-anesthetic-gases/workplace-exposures-guidelines
  127. https://pure.au.dk/portal/files/274787293/1_s2.0_S0013935121008690_main.pdf
  128. https://nationaldepressionhotline.org/safety-gear-used-nitrous-oxide/
  129. https://www.airgas.com/msds/001042.pdf
  130. https://www.eiga.eu/uploads/documents/DOC176.pdf
  131. https://www.ajronline.org/doi/full/10.2214/ajr.177.1.1770027?src=recsys
  132. https://www.ipcc.ch/report/ar6/wg1/chapter/chapter-7/
  133. https://www.epa.gov/ghgemissions/understanding-global-warming-potentials
  134. https://www.igsd.org/wp-content/uploads/2024/10/IGSD-N2O-Primer.pdf
  135. https://publications.jrc.ec.europa.eu/repository/handle/JRC134363
  136. https://www.carbonbrief.org/agriculture-major-driver-of-rise-in-nitrous-oxide-emissions-over-past-40-years/
  137. https://wmo.int/sites/default/files/2025-10/GHG-21_en.pdf
  138. https://agupubs.onlinelibrary.wiley.com/doi/full/10.1002/2015GL065702
  139. https://pmc.ncbi.nlm.nih.gov/articles/PMC3306630/
  140. https://www.unep.org/news-and-stories/press-release/rise-nitrous-oxide-emissions-endangers-pathway-15degc-ozone-layer
  141. https://www.aaas.org/news/science-nitrous-oxide-emissions-now-most-significant-threat-ozone
  142. https://agupubs.onlinelibrary.wiley.com/doi/full/10.1029/2024JG008510
  143. https://www.sciencedirect.com/science/article/abs/pii/S1001074225001640
  144. https://www.eesi.org/articles/view/laughing-gas-is-no-joke-the-forgotten-greenhouse-gas
  145. https://cdn.who.int/media/docs/default-source/46th-ecdd/nitrous-oxide_46th-ecdd_critical-review_public-version.pdf?sfvrsn=f6dcf08d_1
  146. https://www.sciencedirect.com/science/article/pii/S2949916X25000143
  147. https://www.networkforphl.org/news-insights/nothing-to-laugh-about-nitrous-oxide-misuse-and-the-need-for-a-public-health-response/
  148. https://mostpolicyinitiative.org/science-note/nitrous-oxide/
  149. https://www.gov.uk/government/publications/nitrous-oxide-ban/nitrous-oxide-ban-guidance
  150. https://www.bbc.com/news/health-67346032
  151. https://www.health.wa.gov.au/Articles/N_R/nitrous-oxide
  152. https://www.health.vic.gov.au/aod-treatment-services/responsible-sale-of-solvents
  153. https://www.bbc.com/news/uk-66660760
  154. https://www.bmj.com/content/380/bmj.p723
  155. https://transformdrugs.org/blog/why-criminalising-nitrous-oxide-is-a-mistake
  156. https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667%2824%2900298-6/fulltext
  157. https://pmc.ncbi.nlm.nih.gov/articles/PMC10714631/
  158. https://www.asahq.org/standards-and-practice-parameters/statement-on-deactivating-central-piped-nitrous-oxide-to-mitigate-avoidable-health-care-pollution
  159. https://www.nychealthandhospitals.org/pressrelease/nyc-health-hospitals-cuts-annual-anesthesia-related-carbon-emissions-by-over-50-through-deactivation-of-central-piped-nitrous-oxide-systems/
  160. https://www.sciencedirect.com/science/article/pii/S2468266724002986
  161. https://www.grandviewresearch.com/press-release/global-nitrous-oxide-market
  162. https://www.drugscience.org.uk/today-s-ban-on-laughing-gas-is-wrong-prof-david-nutt
Add your contribution
Related Hubs
User Avatar
No comments yet.