Nangs, SCUBA diving, and paraquat – when nitrogen and oxygen turn deadly.

Recently, I gave evidence about nitrogen narcosis. As a former commercial diver and a toxicologist, it was an unusual overlap between two very different parts of my background. I was then asked to consider when oxygen and nitrogen might be lethal to humans.

What is nitrogen, what is oxygen?

Nitrogen and oxygen are both elements, and together they make up almost all of the air we breathe. Ordinary air is approximately 78% nitrogen and 21% oxygen.

Under normal conditions, neither gas is harmful in ordinary air. Oxygen is essential for life, and nitrogen is largely inert at surface pressure. But under the wrong conditions, the same familiar gases can become dangerous. In diving, nitrogen can cause narcosis. At increased partial pressures, oxygen can become toxic. And in toxicology, chemicals containing nitrogen and oxygen can cause harm through entirely different mechanisms.

Nangs

What is a nang?

“Nangs” are small metal cylinders containing nitrous oxide, N₂O. Nitrous oxide has legitimate uses, including in catering and medicine. It is also widely misused recreationally, and some distributors make that fairly obvious by advertising after-hours delivery, “discreet” service, and delivery patterns that have little to do with baking. No baker needs a discreet delivery to a Surfers Paradise apartment at 10 pm.

Nitrous oxide has a rapid onset and offset because it has low blood solubility. In simple terms, it spreads quickly between the lungs, blood, and brain. That is why the effects can come on within seconds and fade quickly once the drug user returns to breathing normal air.¹ 

The current pharmacological explanation for the “high” is not one single mechanism, but a combination of effects. Nitrous oxide acts, at least in part, as an antagonist at the N-methyl-D-aspartate (NMDA) receptor². NMDA receptor antagonism is associated with dissociation, altered perception, impaired sensory integration, and the “floaty” effect users describe.

Nitrous oxide also appears to affect reward pathways. NMDA receptor antagonism can indirectly alter dopamine signalling, which helps explain euphoria and the desire to redose².

That does not make nitrous oxide pharmacologically identical to alcohol or opioids, just that it causes a similar ‘high’.

Why is it so dangerous?

Nitrous oxide is used in medicine, where it is given with oxygen and appropriate clinical supervision. A common medical preparation is Entonox, which contains 50% nitrous oxide and 50% oxygen. It is used for short-term analgesia in settings such as emergency medicine, dentistry, and paramedic practice.

Nangs are different. A person inhaling nitrous oxide from chargers is not receiving a controlled oxygen mixture. If they repeatedly inhale nitrous oxide instead of air, they can reduce the oxygen available in the lungs, causing hypoxaemia (lack of oxygen in the blood) and tissue hypoxia (lack of oxygen in the tissues). The brain is particularly sensitive to oxygen deprivation. In severe cases, this can cause collapse, traumatic injury, brain injury, or death.

There is also a separate neurological risk from repeated nitrous oxide use. Nitrous oxide can inactivate vitamin B12, causing a functional B12 deficiency even when measured serum B12 is not obviously low. This can impair methionine synthase activity and damage myelin, leading to numbness, weakness, gait disturbance, peripheral neuropathy, spinal cord injury, and sometimes irreversible neurological harm.³

SCUBA diving

When SCUBA diving, both nitrogen and oxygen can become toxic in their own way.

Oxygen becomes dangerous when its partial pressure becomes too high. In diving, a commonly used upper limit is a partial pressure of oxygen of about 1.6 atmospheres absolute. On normal air, this occurs at approximately 66 metres of seawater. At these pressures, oxygen is no longer simply the gas keeping you alive. It can become a central nervous system toxin.

Central nervous system oxygen toxicity is particularly dangerous because it can cause twitching, visual changes, nausea, dizziness, anxiety, confusion, and, most importantly, seizures. On land, a seizure is serious. Underwater, a seizure is almost certainly fatal, because the diver may lose the regulator, inhale water, and drown. The risk is not just determined by oxygen pressure, but also by exposure time, exertion, carbon dioxide retention, cold, stress, and individual susceptibility.

Oxygen can also injure the lungs. This is a different form of oxygen toxicity, usually associated with longer exposures rather than the sudden seizure risk seen with high-pressure oxygen underwater. Pulmonary oxygen toxicity can cause chest discomfort, coughing, airway irritation, and reduced lung function. This is why oxygen is both essential and dangerous: the dose, pressure, and duration matter.

Nitrogen causes a different problem. At increasing depth, the partial pressure of nitrogen rises. Nitrogen is usually described as inert, but under pressure it becomes narcotic. Around 30 metres, many divers begin to experience nitrogen narcosis. The diver may feel relaxed, euphoric, slowed, overconfident, or “drunk”. Judgment, reaction time, memory, attention, coordination, and problem-solving can deteriorate. This is something my team trained for at the Wesley Hospital in the hyperbaric chamber when I was a commercial diver, we would be brought up to those levels and taught to ‘push through’ the intoxication.

Pharmacologically, nitrogen narcosis is not fully explained by one receptor mechanism. The older explanation is the Meyer-Overton relationship: gases that dissolve more readily into lipid membranes tend to be more narcotic.⁴ Modern explanations are more nuanced and include effects on neuronal membranes, ion channels, neurotransmission, and altered signalling in the central nervous system. In practical terms, the result is simple: the deeper you go on air, the less reliable your brain becomes.

This matters because nitrogen narcosis does not have to knock a diver unconscious to be dangerous. It only has to make the diver careless. A narcotised diver may ignore their depth, misread gauges, forget a plan, fail to notice gas consumption, make a poor ascent decision, or respond badly to a minor problem.⁴ Underwater, small errors can become fatal quickly.

Nitrogen also causes decompression sickness. As a diver descends, increased pressure causes more nitrogen to dissolve into the blood and body tissues. The deeper and longer the dive, the more nitrogen is absorbed. During ascent, pressure decreases and that dissolved nitrogen must leave the body gradually through the lungs. If the diver ascends too quickly, misses decompression stops, or exceeds safe limits, nitrogen can come out of solution as bubbles.

Those bubbles can form in tissues and blood vessels. They can cause joint pain, skin changes, numbness, weakness, dizziness, paralysis, breathing difficulty, collapse, and death. This is the condition divers call “the bends”. It is not poisoning in the usual sense. It is a pressure-driven gas injury: nitrogen was harmless while dissolved under pressure, but dangerous when bubbles formed during decompression.

So in diving, nitrogen and oxygen are dangerous for different reasons. Nitrogen can make you drunk at depth and form bubbles on ascent. Oxygen can provoke seizures at high partial pressure and injure the lungs with prolonged exposure. Both gases are ordinary parts of the air we breathe, but underwater the pressure changes the pharmacology and physiology completely.

Paraquat: when giving oxygen can make things worse

Paraquat (N,N′-dimethyl-4,4′-bipyridinium dichloride… we’ll stick to paraquat…) is a herbicide, it is also infamous in Australia for being a common way for farmers to commit suicide, but toxicologically it is most famous for what it does to the lungs. After ingestion, paraquat is actively taken up into lung tissue, particularly the alveolar cells. This means the lung can concentrate paraquat to levels much higher than the blood.

Once inside cells, paraquat undergoes a process called redox cycling.⁵ In simple terms, paraquat accepts an electron from normal cellular reducing systems, forming a paraquat radical. It then passes that electron to molecular oxygen, regenerating paraquat and producing superoxide, a reactive oxygen species.

That is the lethal trick: paraquat is regenerated and can repeat the cycle again and again. It behaves less like a simple poison that is used up, and more like a chemical engine for producing oxidative stress.

The more oxygen available, the more substrate there is for this reaction. Giving high-concentration oxygen can therefore increase the production of reactive oxygen species, worsening lipid peroxidation, cell injury, inflammation, alveolitis, and ultimately pulmonary fibrosis.

This creates one of the cruel paradoxes of paraquat poisoning. The patient may be dying of lung injury and hypoxia, but giving oxygen can accelerate the very oxidative damage causing the respiratory failure. For that reason, supplemental oxygen is generally avoided unless there is significant hypoxaemia, and even then clinicians aim to use the lowest oxygen concentration necessary.

This does not mean oxygen is “never” given. If a patient is severely hypoxic, oxygen may be unavoidable because the brain and heart still need oxygen to survive. But paraquat is one of the classic poisonings where oxygen is treated as a drug with a dangerous dose-response relationship, not as a harmless supportive measure.

Conclusion

In normal air, nitrogen and oxygen keep us alive. In a nang, nitrous oxide can displace oxygen and injure the nervous system. Underwater, pressure turns nitrogen into a narcotic and oxygen into a potential convulsant. In paraquat poisoning, oxygen can become the fuel for lethal free-radical chemistry.

The lesson is simple: the body does not care whether something sounds harmless, natural, medical, or familiar. Under the wrong conditions, even the gases we breathe can become toxic.

REFERENCES

¹V. Cornelio et al., ‘Impact of Nitrous Oxide on Neuropsychiatric Impairment in Adolescents: A Scoping Review’, Cureus, vol. 17, no. 8, 2025.

²T. Brunt, W. Van den Brink, and J. Van Amsterdam, ‘Mechanisms Involved in the Neurotoxicity and Abuse Liability of Nitrous Oxide: A Narrative Review’, International Journal of Molecular Sciences, vol. 23, no. 23, 2022, pp. 1046-1050.

³E. Porruvecchio et al., ‘Functional Vitamin B12 Deficiency in Association With Nitrous Oxide Inhalation’, Cureus, vol. 14, no. 1, 2022.

⁴P. Kirkland et al., ‘Nitrogen Narcosis In Diving’, StatPearls, St. Petersburg, Florida (USA), 2023, ncbi.nlm.nih.gov/books/NBK470304/, (accessed 29 June 2026).

⁵R. Dinis-Oliveira et al., ‘Paraquat poisonings: mechanisms of lung toxicity, clinical features, and treatment’, Critical Review in Toxicology, vol. 38, no. 1, 2008, pp. 13-71.