Oxygen Toxicity

Most divers know the NOAA Central Nervous System (CNS) oxygen exposure chart and the CNS tracker on your computer — telling you how long you can stay at a given partial pressure of oxygen. It’s a useful tool, but like most tables, it only tells part of the story.

Oxygen toxicity (OXTOX) is a funny topic. When we look at the CNS clock on our Shearwaters and see it exceed 100% on a routine dive it’s easy to think “these limits aren’t realistic”. It’s a logical conclusion. Why would I trust a metric that is exceeded routinely? The answer is simple – the variables in the risk of OXTOX are more than time+Po2. If we confine our thinking to those two variables, we are not doing a realistic risk assessment. In the same vein, we don’t need to be cutting edge scientists to mitigate our risk. The balance is reviewing the variables and adjusting our exposure.

A few realities:

  • OXTOX is a real risk of diving
  • Risk mitigation is never full proof
  • Good planning takes all variables into account.

What Is Oxygen Toxicity?

Oxygen toxicity happens when breathing oxygen at high partial pressures causes harm to the body. There are two main types:

  • CNS Oxygen Toxicity – the one divers worry about most. The most serious symptom is convulsions, which can obviously be fatal underwater.

  • Pulmonary Oxygen Toxicity – a slower, longer-term effect caused by breathing elevated oxygen for hours or days.

CNSOXTOX is rarely recoverable. There are a few fringe cases of divers who seized underwater that lived, but that’s rarely the case. The occurrence of CNSOXTOX in non-military divers is rare. It’s an example of a rare occurrence high consequence event. If it happens, you will most likely have no warning signs and die.

Pulmonary OXTOX requires a suspension of diving activities. Your lungs are “fried”. They will not work well for gas exchange.

Technical divers tend to focus on avoiding CNSOXTOX. To read more about these different manifestations, check out this DAN article. The primary method of avoiding risk is looking at PO2 and time. That’s the basis of the current tables.

Variables

Oxygen toxicity risk shifts with context.

  1. Workload and CO₂:
    Exercise increases CO₂ retention, and elevated CO₂ strongly amplifies risk. CO₂ lowers seizure thresholds [2]. “That guy didn’t seize for a really long time at a high Po2!” Yes, because he was scootering or on a drift dive – aka not working. (Also, he still seized).

  2. Wet vs. dry:
    Studies show that divers tolerate higher PO₂s longer in dry chamber conditions than in water [3]. This is important to associate with dry chamber studies using very high Po2 for long times. It’s also important for the underinformed age old adage of “well, in the chamber you’re at a 3.0 and don’t seize”.

  3. Temperature:
    Cold increases metabolic rate and accelerates CNS-OTOX onset [5]. Lower the PO2 in cold water.

  4. Individual variation:
    Fatigue, hydration, stress, and health all change susceptibility [5]. Don’t dive when you’re hungover with no sleep. At the least, don’t dive a high PO2.

  5. Gas density and breathing effort:
    Denser gases, increased breathing resistance, and CO₂ retention, all of which raise CNS risk [2]. Helium is awesome.

  6. Diet and metabolism:
    Diet can influence oxidative stress. [6]. Garbage in, garbage out.

Understanding these variables is required to reduce our risk. “It’s ok to have a CNS percentage of 150%” is a statement without context. It may have worked for scooter dives with a low workload in warm water etc. It may not work under different conditions. The punishment that OXTOX inflicts is rarely a recoverable situation.

ROS

Traditionally, the mechanism of oxygen toxicity has been described as a function of reactive oxygen species (ROS) – unstable oxygen byproducts like superoxide and peroxide cause oxidative stress and cellular damage. That’s still part of the story, but newer research adds an important twist.

Recent molecular studies show that molecular oxygen itself, not just its reactive derivatives, can directly attack certain critical proteins in cells. The main targets are iron-sulfur cluster (ISC)-containing proteins, which drive essential functions like energy production, DNA repair, and metabolism. Under high PO₂, oxygen oxidizes the iron and sulfur inside these proteins (a bit like rusting metal), destabilizing them and triggering a cascade of cellular failure independent of superoxide damage [1].

In short, oxygen toxicity isn’t just about free radicals. It’s also about oxygen overwhelming the body’s molecular machinery. This research invalidates theories of pushing high PO2s by eating blueberries and dark chocolate for the antioxidant powers because the ROS are not the sole culprits.

CO2 andPO2

Image from Arieli and Ertracht 1999. Latency to CNS oxygen toxicity in rats as a function of P CO2 and P O2. You can see the increase in seizure time when CO2 is introduced.

PO2 of 1.3

The current restrictions that are often disregarded come from the 1991 NOAA CNS table and clock. In 2025 a group of researchers did an evaluation to change the recommended exposure limits. The catalyst for this changed recommendation stemmed, in part, from people disregarding the recommendations and not believing oxygen restrictions to be important.

Every CCR diver should read Hoyt et. al 2025. I’ve listed a few interesting snippets here.

  • The 1991 recommendations were focused on test data for higher PO2,1.6-2.5ATA. Lower Po2s did not have significant data. “these limits were based on best judgement from extensive experience, not on the statistical analysis of quantitative data”
  • “the Navy also imposed an arbitrary time limit of 240 min at 1.3 atm because of potential onset of pulmonary oxygen toxicity”
  • The new limits increase the maximum time for a PO2 of 1.3. The Navy dataset for oxygen diving found an extremely low risk of seizure at that Po2.
  • The new limits further delineate a lower risk factor, with increased time, for resting/decompression during a dive.
  • “It is acknowledged that this reported experience with 1.3 atm PO2 exposures does not inform the risk assessment for either lower or higher setpoints. It can be expected that any duration limit deemed acceptable for a 1.3 atm PO2 setpoint would result in a lower CNS toxicity risk at lower inspired PO2 values, but there are insufficient data to generate limits that take the form of the progressively longer existing NOAA table limits”

This change of limits is well backed by experimental data. It also identifies fallacies about the risk of oxygen toxicity. It is an important, well done, and interesting paper.

While the paper increases limits for PO2s of 1.3 and below, effectively invalidating the CNS clock on our dive computers for those PO2s – it absolutely does not condone longer times at PO2s above 1.3. The data at higher PO2s is not trivial, and while the same variables that affect lower PO2s are in play, the buffer doesn’t exist in these ranges. I fear, and have witnessed, people using this paper to ramp PO2s beyond 1.3 on working portions of the dive. “If 1.3 is ok, then higher is probably ok too.” That is inappropriate.

Lipid Peroxidation

When we talk about oxygen toxicity, especially at the cellular level, lipid peroxidation is one of the key processes doing the real damage. It’s basically what happens when oxygen and free radicals start attacking the fats (lipids) that make up our cell membranes. It’s a chemical chain reaction that spreads fast and wrecks the structure of cells.

Lipid peroxidation starts when a reactive oxygen species (ROS) or a free radical steals a hydrogen atom from a fatty acid molecule, especially from polyunsaturated fats like arachidonic acid or linoleate. That theft creates a new radical, which then reacts with oxygen to form a peroxyl radical. That radical can attack the next lipid in line. The result is a self-sustaining chain reaction, with oxygen feeding the process.

Lipid peroxidation is part of the downstream cascade of oxygen toxicity. The initial insult may begin when molecular oxygen directly damages iron–sulfur cluster (ISC) proteins, kicking off a chain of metabolic disruption. From there, ROS production ramps up, and lipid peroxidation spreads the damage.

Ketosis

One of the more interesting areas of oxygen toxicity research looks at how ketosis — the metabolic state your body enters when burning fat instead of carbs — might actually help protect against CNS oxygen toxicity (CNS-OTOX).

Studies on animals show that inducing ketosis, either through a ketogenic diet or by taking ketone esters (like BD-AcAc₂, a β-hydroxybutyrate precursor), can delay the onset of oxygen toxicity seizures during hyperbaric oxygen exposure. In one experiment, rats given BD-AcAc₂ lasted about 58 minutes before seizing, compared to only 9–11 minutes in non-ketotic controls,  a more than fivefold increase in tolerance.

Most people associate ketosis with the fad diet of ~10 years ago. Keto is a very effective antiseizure diet and has been used for controlled seizures since the 70s, they even made a movie about it. [7]

This doesn’t mean divers should start chugging ketone drinks before dives. I am not on the keto diet and have no desire to be. These studies are a reminder that physiology is a complex and complicated system. Addressing oxygen risk as a two-factor system is not appropriate.

D’Agostino et al 2013. Increase of time with the ketone ester is C.

Practical Takeaways for Divers

Oxygen toxicity is a multi-factor problem. Don’t dismiss the limits because some of them were literally made up (I know, that’s a wild thing to say). Take big bites of the information to have the knowledge needed to increase or decrease exposure.

  • Understand what shifts your tolerance — workload, CO₂, immersion, and temperature are important variables. If you can’t control those variables, be more conservative with PO2.

  • Keep working PO₂ modest.

  • Don’t dismiss the limits just because someone else got away with it.

  • Hacks like eating antioxidants aren’t a substantiated method for reducing risk.

  • Physiology is complicated. Being healthy is probably a good idea to reduce risk.

References

    1. [Molecular Cell, 2023] Oxygen toxicity causes cyclic damage by destabilizing specific Fe-S cluster-containing protein complexes
    2. [European Journal of Applied Physiology and Occupational Physiology, 1999] Latency to CNS oxygen toxicity in rats as a function of PCO2 and PO2
    3. [Donald, 1992] Oxygen and the Diver
    4. [Shykoff & Florian, 2018] Immersion increases pulmonary and CNS oxygen toxicity symptoms in oxygen-breathing divers.
    5. [StatPearls, 2023] Oxygen Toxicity
    6. [Nature, 2018] Effects of the Ketogenic diet in overweight divers breathing Enriched Air Nitrox.
    7. [Nature 1976] Ketonemia and Seizures: Metabolic and Anticonvulsant Effects of Two Ketogenic Diets in Childhood Epilepsy