Info Oxygen Toxicity Limits & Symptoms

Oxygen Toxicity Limits & Symptoms​

Oxygen toxicity limits can be very confusing, especially for PPO2 (Partial Pressure of Oxygen) levels above 1.6 ATA used in chamber-based hyperbaric treatment (recompression) and decompression tables. For example, here is a chart of one of the most common DCS (Decompression Sickness) treatment tables. Note that the PPO2 of pure oxygen at 60'/18.3M is 2.82 ATA — or more than twice the normal limits recreational divers observe.

U.S. Navy Diving Manual, Revision 7A, 30 April 2018.
Figure 17-4. Treatment Table 5, Page 17-43 (Page 899 in Acrobat file) ​

Some confusion comes from recreational diving courses that only teach the minimum subset necessary for that specialty. Hopefully this, plus contributions from other ScubaBoard members, will provide a more complete understanding.

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“ Why should anyone use high oxygen levels and risk oxygen toxicity? ”

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The "simple answer" for divers is twofold: Rapid removal of diluent gas (nitrogen and/or helium) from the body and reducing diluent gas absorption. Hyper-oxygenation can be the objective for non-diving HBOT (HyperBaric Oxygen Treatments) for CO poisoning, gangrene, burns, etc.

The following is an excerpt from the US Navy Diving Manual, with the following modifications:

I accentuated selected text from the manual with Bold to emphasize especially important points.

In addition, I included comments for added for context.

U.S. Navy Diving Manual, Revision 7A, Volume 1, 30 April 2018, starting on Page 3-42 or Acrobat Page 200

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3-9.2 Oxygen Toxicity. Exposure to a partial pressure of oxygen above that encountered in normal daily living may be toxic to the body. The extent of the toxicity is dependent upon both the oxygen partial pressure and the exposure time. The higher the partial pressure and the longer the exposure, the more severe the toxicity. The two types of oxygen toxicity experienced by divers are pulmonary oxygen toxicity and central nervous system (CNS) oxygen toxicity.

3‑9.2.1 Pulmonary Oxygen Toxicity. Pulmonary oxygen toxicity, sometimes called low pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 0.5 ata. A 12 hour exposure to a partial pressure of 1 ata will produce mild symptoms and measurable decreases in lung function. The same effect will occur with a 4 hour exposure at a partial pressure of 2 ata.

Long exposures to higher levels of oxygen, such as administered during Recompression Treatment Tables 4, 7, and 8, may produce pulmonary oxygen toxicity. The symptoms of pulmonary oxygen toxicity may begin with a burning sensation on inspiration and progress to pain on inspiration. During recompression treatments, pulmonary oxygen toxicity may have to be tolerated in patients with severe neurological symptoms to effect adequate treatment. In conscious patients, the pain and coughing experienced with inspiration eventually limit further exposure to oxygen. Unconscious patients who receive oxygen treatments do not feel pain and it is possible to subject them to exposures resulting in permanent lung damage or pneumonia. For this reason, care must be taken when administering 100 percent oxygen to unconscious patients even at surface pressure.

Return to normal pulmonary function gradually occurs after the exposure is terminated. There is no specific treatment for pulmonary oxygen toxicity.

The only way to avoid pulmonary oxygen toxicity completely is to avoid the long exposures to moderately elevated oxygen partial pressures that produce it. However, there is a way of extending tolerance. If the oxygen exposure is periodically interrupted by a short period of time at low oxygen partial pressure, the total exposure time needed to produce a given level of toxicity can be increased significantly.

A CNS OxTox hit is the primary concern for recreational divers due to the high probability of drowning when using a mouthpiece. A FFM is certainly much safer during a convulsion underwater but the ability to rapidly get the diver off a pure or high PPO2 mix is essential. Also note that nausea is an OxTox symptom and vomiting in a FFM can be very dangerous, especially if preceded by convulsion.

3‑9.2.2 Central Nervous System (CNS) Oxygen Toxicity. Central nervous system (CNS) oxygen toxicity, sometimes called high pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 1.3 ata in a wet diver or 2.4 ata in a dry diver. The reason for the marked increase in susceptibility in a wet diver is not completely understood. At partial pressures above the respective 1.3 ata wet and 2.4 ata dry thresholds, the risk of CNS toxicity is dependent on the oxygen partial pressure and the exposure time. The higher the partial pressure and the longer the exposure time, the more likely CNS symptoms will occur. This gives rise to partial pressure of oxygen-exposure time limits for various types of diving.

Note that many of these factors are eliminated or mitigated by relaxing in a chamber.

3‑9.2.2.1 Factors Affecting the Risk of CNS Oxygen Toxicity. A number of factors are known to influence the risk of CNS oxygen toxicity:

Individual Susceptibility. Susceptibility to CNS oxygen toxicity varies markedly from person to person. Individual susceptibility also varies markedly from time to time and for this reason divers may experience CNS oxygen toxicity at exposure times and pressures previously tolerated. Individual variability makes it difficult to set oxygen exposure limits that are both safe and practical.

CO2 Retention. Hypercapnia greatly increases the risk of CNS toxicity probably through its effect on increasing brain blood flow and consequently brain oxygen levels. Hypercapnia may result from an accumulation of CO2 in the inspired gas or from inadequate ventilation of the lungs. The latter is usually due to increased breathing resistance or a suppression of respiratory drive by high inspired ppO2. Hypercapnia is most likely to occur on deep dives and in divers using closed and semi-closed circuit rebreathers.

Exercise. Exercise greatly increases the risk of CNS toxicity, probably by increasing the degree of CO2 retention. Exposure limits must be much more conservative for exercising divers than for resting divers.

Immersion in Water. Immersion in water greatly increases the risk of CNS toxicity. The precise mechanism for the big increase in risk over comparable dry chamber exposures is unknown, but may involve a greater tendency for diver CO2 retention during immersion. Exposure limits must be much more conservative for immersed divers than for dry divers.

Depth. Increasing depth is associated with an increased risk of CNS toxicity even though ppO2 may remain unchanged. This is the situation with UBAs that control the oxygen partial pressure at a constant value, like the MK 16. The precise mechanism for this effect is unknown, but is probably more than just the increase in gas density and concomitant CO2 retention. There is some evidence that the inert gas component of the gas mixture accelerates the formation of damaging oxygen free radicals. Exposure limits for mixed gas diving must be more conservative than for pure oxygen diving.

The MK 16 is a mixed gas rebreather built for the US Navy. UBA = Underwater Breathing Apparatus.

Intermittent Exposure. Periodic interruption of high ppO2 exposure with a 5-15 min exposure to low ppO2 will reduce the risk of CNS toxicity and extend the total allowable exposure time to high ppO2. This technique is most often employed in hyperbaric treatments and surface decompression.

Because of these modifying influences, allowable oxygen exposure times vary from situation to situation and from diving system to diving system. In general, closed and semi-closed circuit rebreathing systems require the lowest partial pres3- sure limits, whereas surface-supplied open-circuit systems permit slightly higher limits. Allowable oxygen exposure limits for each system are discussed in later chapters.

3‑9.2.2.2 Symptoms of CNS Oxygen Toxicity. The most serious direct consequence of oxygen toxicity is convulsions. Sometimes recognition of early symptoms may provide sufficient warning to permit reduction in oxygen partial pressure and prevent the onset of more serious symptoms. The warning symptoms most often encountered also may be remembered by the mnemonic VENTIDC:

V: Visual symptoms. Tunnel vision, a decrease in diver’s peripheral vision, and other symptoms, such as blurred vision, may occur.​

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E: Ear symptoms. Tinnitus, any sound perceived by the ears but not resulting from an external stimulus, may resemble bells ringing, roaring, or a machinery-like pulsing sound.​

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N: Nausea or spasmodic vomiting. These symptoms may be intermittent.​

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T: Twitching and tingling symptoms. Any of the small facial muscles, lips, or muscles of the extremities may be affected. These are the most frequent and clearest symptoms.​

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I: Irritability. Any change in the diver’s mental status including confusion, agitation, and anxiety.​

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D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.​

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C: Convulsions. The first sign of CNS oxygen toxicity may be convulsions that occur with little or no warning.​

Note that "air breaks" are built-in to most treatment tables used on recreational divers. It just means that the patient removes their BIBS (Built In Breathing System) oral-nasal mask and breathes air from the chamber atmosphere.

Edit 15 November 2021: Updated links for Version 7A of the US Navy Diving Manual and changed the use of colors for compatibility with different ScubaBoard Styles.

 

[Doppler]

This is an excellent resource and good information to share.

There are several studies underway currently trying to extend our understanding of the triggers for CNS toxicity, and while the jury may be out on single-dive limits published by NOAA, I remain a strong advocate for teaching and following NOAA's 24-hour limits when planning multiple dives over several days.

 

[TSandM]

Good resource. The bottom line is that decompression chamber treatment is given to people who ALREADY have minor or major symptoms of DCS, so the risk of CNS or pulmonary toxicity is incurred in order to relieve the symptoms (and hopefully limit the damage) that has already occurred. When you combine that with the fact that a seizure on land is an unpleasant nuisance but VERY rarely more than that, it's clear that high ppO2s make sense on land.

They do not make sense underwater in a person who does not yet have any illness that's being treated, and where the outcome of a seizure is highly likely to be fatal.

 

[Akimbo]

... When you combine that with the fact that a seizure on land is an unpleasant nuisance but VERY rarely more than that, it's clear that high ppO2s make sense on land.

They do not make sense underwater in a person who does not yet have any illness that's being treated, and where the outcome of a seizure is highly likely to be fatal.

The problem is that divers on Nitrox or rebreathers set to 1.4 PPO2 are about as far above recommended limits as chamber occupants at 2.8 ATA.

9.2.2 Central Nervous System (CNS) Oxygen Toxicity. Central nervous system (CNS) oxygen toxicity, sometimes called high pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 1.3 ATA in a wet diver or 2.4 ATA in a dry diver

I don't know if data supports that CNS OxTox probability for a wet diver at 1.4 is lower than a dry diver at 2.82 (where the most data points are). It would be interesting to know.

I have read that the need for lower oxygen levels for divers and combat swimmers wasn't discovered until WWII. Initial limits were determined in animal and dry human chamber tests. That research was driven more by the needs of caisson workers than divers. Several combat swimmers blacked out within the "established limits" before anyone thought to actually test divers underwater (chamber "wet pot"). Those studies set the limit in the UK for pure oxygen in the water at 33'/10 Meters (1940s). It was 25'/7.6 M in the USN by the 1960s.

Wikipedia has a short reference to it:
Oxygen toxicity - Wikipedia, the free encyclopedia

This quote from that link is entertaining.

Naval divers in the early years of oxygen rebreather diving developed a mythology about a monster called "Oxygen Pete", who lurked in the bottom of the Admiralty Experimental Diving Unit "wet pot" (a water-filled hyperbaric chamber) to catch unwary divers. They called having an oxygen toxicity attack "getting a Pete".

 

[Akimbo]

The following articles on DAN's Web site may be of interest:

Understanding Oxygen Toxicity By Petar J. Denoble, M.D., D.Sc.. Published in Winter 2013 Alert Diver Magazine.

OXTOX: If You Dive Nitrox You Should Know About OXTOX By Dr. E.D. Thalmann, DAN Assistant Medical Director; Captain, Medical Corps, U.S. Navy (retired)

 

[Gene_Hobbs]

Wikipedia has a short reference to it:
Oxygen toxicity - Wikipedia, the free encyclopedia

Great to see that article getting some use. We worked hard to get it referenced and re-written to be useful. The wet vs dry work was done by Donald if you are just looking for the references in the list.

 

[danvolker]

The problem is that divers on Nitrox or rebreathers set to 1.4 PPO2 are about as far above recommended limits as chamber occupants at 2.8 ATA.



I don’t know if data supports that CNS OxTox probability for a wet diver at 1.4 is lower than a dry diver at 2.82 (where the most data points are). It would be interesting to know.

I have read that the need for lower oxygen levels for divers and combat swimmers wasn’t discovered until WWII. Initial limits were determined in animal and dry human chamber tests. That research was driven more by the needs of caisson workers than divers. Several combat swimmers blacked out within the “established limits” before anyone thought to actually test divers underwater (chamber “wet pot&#8221. Those studies set the limit in the UK for pure oxygen in the water at 33'/10 Meters (1940s). It was 25'/7.6 M in the USN by the 1960s.

Wikipedia has a short reference to it:
Oxygen toxicity - Wikipedia, the free encyclopedia

This quote from that link is entertaining.

Back when we were doing 280 foot deep air dives in the early and mid 90's, we KNEW that it was critical that we did practically no exertion, as your body does not rid itself of CO2 effectively at depth....and high CO2 levels will trigger an Ox Tox event. I actually had the beginning of this happen to me around '95 on a 240 foot deep spearfishing dive......I shot a 40 pound grouper with a free shaft, had to swim fast to the fish 8 feet away to grab the spear and fish....and then it started kicking the h*ll out of me as I held it close so it could not get away....after about 20 seconds of this, I began feeling a malaise that was terrible, and rapidly worsening....I had never stopped being aware that exertion at depth would build CO2, and that I should not do this....S0, figuring Ox tox was starting to trigger, I fully inflated my BC, and rocketed from 240 to 100---still holding the fish tight of course
The fish stopped fighting, and the combination of no exertion and shallower depth, allowed the CO2 buildup to pass....and the enzyme shutdown reversed....and I stopped feeling so bad....

My thought on this mention of combat swimmers, etc., is that with the exertions involved, CO2 was the X-Factor that made the high oxygen concentration far more dangerous.

 

[Akimbo]

...
I shot a 40 pound grouper with a free shaft, had to swim fast to the fish 8 feet away to grab the spear and fish....and then it started kicking the h*ll out of me as I held it close so it could not get away....after about 20 seconds of this, I began feeling a malaise that was terrible, and rapidly worsening....I had never stopped being aware that exertion at depth would build CO2, and that I should not do this....S0, figuring Ox tox was starting to trigger, I fully inflated my BC, and rocketed from 240 to 100---still holding the fish tight of course ...

The trouble is that OxTox may or may not have been a factor at all. I have experienced similar symptoms when the PPO2 was 0.3. Let's not forget that the actual mechanism of Oxygen Toxicity is still being debated and there are several theories floating around.

There just isn't that much motivation to do the very expensive studies to actually figure it out since we can pretty reliably avoid it.

 

[danvolker]

The trouble is that OxTox may or may not have been a factor at all. I have experienced similar symptoms when the PPO2 was 0.3. Let’s not forget that the actual mechanism of Oxygen Toxicity is still being debated and there are several theories floating around.

There just isn’t that much motivation to do the very expensive studies to actually figure it out since we can pretty reliably avoid it.

True, there is no proof it was an Ox Tox issue.....On the other hand, there is a 99.9% chance I had built up a ridiculously high level of CO2 from the sprint to the fish, and then the fight with the very powerful fish....Most of us have done 80 or 100 foot deep dives where we have decided to sprint to something some distance away--and on getting there, we found the CO2 levels were not clearing, breathing was insufficient no matter how hard we breathed, our head was hurting, and this could never have happened with the same exertion in 10 feet of water....

So what I do know is that I was at a very high physical output ( wattage), and this was much worse for clearing CO2 at 240 feet, than it would be at 100 feet.....and I also know that high CO2 levels will trigger Ox Tox.

Not trying to be argumentative...I just want to be sure that rebreather divers and other out there, that run high PO2's, are carefull at depth NOT to exert. Maybe it is some form of depth related CO2 poisening.....and not even PO2 related...in any event, it is a very bad thing you want to avoid

 

[Akimbo]

...I just want to be sure that rebreather divers and other out there, that run high PO2's, are carefull at depth NOT to exert. Maybe it is some form of depth related CO2 poisening.....and not even PO2 related...in any event, it is a very bad thing you want to avoid

Couldn't agree more. Unfortunately we also don't know that much about CO2 poisoning in the hyperbaric environment. Both are not good and could be collaborating against us.

The increase in dead air space on rebreathers, especially when coupled with a FFM and BOV (open circuit second stage for bail-out), is pretty significant. I suspect this works against open-circuit divers that switch to rebreathers who have spent years learning to minimize their RMV. Commercial divers are encouraged to breathe deep to reduce CO2 in hats and masks, but they aren't dealing with such finite gas supplies or paying for it.