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.

 

[Akimbo]

... This type of thing makes evaluation of a rare event quite difficult. If there is a baseline occurrence of an event in a population, independent of the provocative material being studied, and the event is rare even in the presence of the provocative material, ONE baseline occurrence can markedly skew the results.

Well stated. Think of what drug companies go through with stage 3 human trials. At least the vast majority of divers are generally healthy compared to populations that are compromised with the target disease. It is all fantastically difficult even with the purest of scientific and humanitarian motivations.

Sadly, even if somebody came up with a pill to prevent OxTox it would never be released. It is tough to scrape up hundreds of thousands of dollars to study Oxygen Toxicity, let alone half a billion dollars or more to bring the drug to market.

---------- Post added March 18th, 2014 at 10:12 AM ----------

This is about the point where FFMs (Full Face Masks) come up. No doubt they are great assets in a rare OxTox seizure, if you don't barf in it first. Unfortunately, recommending them for the entire population would probably drown more divers on the surface than save others from convulsions.

Gas switching and sharing capability for FFMs still needs work for more advanced dives where convulsion is more likely. Add rebreathers to the mix and the job gets harder (not impossible). All things considered, convulsion is pretty low on the probability list compared to all the other things that conspire to kill us while deep diving -- not to diminish the importance in any way.

 

[diverdoug1]

Dopler, there is a difference in CNS and CNS oxidative toxicity. I am not talking about pulmonary toxicity, only stating that other tissues in the post mortem exam did not speak to high OTU. Time is NOT always of the essence and most certainly is NOT always part of the equation! One time exposure of a high ppO2 can result in an instantaneous seizure. I am a hyperbaric physician, and know this to be true, as does Duke Dive Medicine. Please do not do a disservice to your students, and continue to ignore your misunderstanding.

---------- Post added March 18th, 2014 at 01:20 PM ----------

One of the most frightening things about oxygen toxicity is the extreme variability both between subjects and in the same subject on different days. I think you can only choose a level at which oxygen toxicity is statistically extremely rare; seizures at or below 1.4 are extremely infrequent, .

This is very true, I have had patients seize on a schedule in the chamber, but go on to tolerate the same schedule on subsequent treatments. I have personally never seen a seizure in the chamber (in an adult) lower than 1.8 ATA (2.0 ATA in adult males), unless I count febrile patients or who were debilitated and may have seized for other reasons or had a good reason for having a decreased seizure threshold. During the analysis of a dive accident data set, we have to acknowledge that a finite number of divers may have a seizure while at depth for reasons other than oxygen toxicity. This will confound a meaningful analysis of the data set. Risk / Benefit analysis is always a good thing to look at, and the above comments regarding full face masks have a lot of merit. As Akimbo notes, risk of seizure is not high on the risk stratification given proper instruction.

Akimbo, I am curious, as a saturation diver, what is the highest ppO2 that your protocols currently allow for commercial work?


---------- Post added March 18th, 2014 at 01:21 PM ----------

 

[Doppler]

Dopler, there is a difference in CNS and CNS oxidative toxicity. I am not talking about pulmonary toxicity, only stating that other tissues in the post mortem exam did not speak to high OTU. Time is NOT always of the essence and most certainly is NOT always part of the equation! One time exposure of a high ppO2 can result in an instantaneous seizure. I am a hyperbaric physician, and know this to be true, as does Duke Dive Medicine. Please do not do a disservice to your students, and continue to ignore your misunderstanding.

I use the limits set by NOAA and teach the tables they have published. If that is ill-advised, please explain more fully why.

If time is truly not a contributing factor and should not always be considered when working within the parameters now adopted by the dive community, surely it's not just my misunderstanding but NOAA's too.

Can you explain for us the difference for a diver tracking his/her likelihood of seizure, between CNS oxidative toxicity and CNS toxicity? I am not a physiologist but a physicist. I do however have a card and certificate someplace from Dick Rutkowski telling me I am a very lowly and unpracticed hyperbaric technician. It's my understanding that the potential outcome of ANY form of CNS toxicity is seizure.

I am aware of the vagaries of physiology and the desperate need for us to use a conservative approach when planning dives, especially those that call for staged decompression and gases delivering elevated partial pressures of oxygen. I am painfully aware of the unpredictable nature of oxygen toxicity.

So, diving conservatively, in the broadest possible terms, means knowing limits and staying within them. Teaching, following and promoting NOAA's single dive AND 24-hour CNS limits as a guideline to be used to avoid a tonic-clonic type episode during a dive hardly seems a disservice to my students. But I am open to re-education on this score.

I am not trying to bust balls here. I have not suggested anything you have posted is a disservice to the community. My initial posting was intended to put forward for debate the possibility that when one exceeds the Daily CNS limit, even though one my be conducting a dive that is well within the single dive limit, a CNS episode is possible.

I fail to see what is wrong or unscientific about that suggestion. Please, in all seriousness, explain why this is not the case, in your opinion.

 

[diverdoug1]

Dopler, when you say "Also, and I am sounding like a broken record, PO2 is only half the equation. TIME and PO2 = dose." It does not sound like you were teaching the NOAA single dive limits, which clearly do have some limits that are REGARDLESS of time. If you are teaching both and realize that ppO2 certainly is not only half the equation in all circumstances, then BRAVO! To answer your direct question regarding CNS vs CNS oxidative risks, the former is felt to have cumulative risk in by purely an increased time for the event to occur so cumulative in risk by duration of risk event alone, resulting in a linear increase in risk of an occurrence over time and is less predictably anticipated. While the later is a cumulative increase in risk by accumulation of CNS-OTU AND time causing an exponential increase in risk of an occurrence over time and can somewhat reliably be avoided by decreased exposure duration.

 

[danvolker]

Dopler, when you say "Also, and I am sounding like a broken record, PO2 is only half the equation. TIME and PO2 = dose." It does not sound like you were teaching the NOAA single dive limits, which clearly do have some limits that are REGARDLESS of time. If you are teaching both and realize that ppO2 certainly is not only half the equation in all circumstances, then BRAVO! To answer your direct question regarding CNS vs CNS oxidative risks, the former is felt to have cumulative risk in by purely an increased time for the event to occur so cumulative in risk by duration of risk event alone, resulting in a linear increase in risk of an occurrence over time and is less predictably anticipated. While the former is a cumulative increase in risk by accumulation of OTU AND time causing an exponential increase in risk of an occurrence over time and can somewhat reliably be avoided by decreased exposure duration.

Speaking of the oxidative risks you mentioned....Back when I was enjoying all my deep air nonsense, I had a belief that enzyme systems were being compromised at 200 foot plus depths on air, and that the Oxygen Toxicity and seizure could potentially be prevented by powerful free radical scavenging vitamins loaded prior to the dive--days and hours prior.....Back then, I would take a mineral ascorbate of Vitamin C ( super gram II by a lacer), of which I would take 2000 mg every three hours, and could do this all day long with no gastric upset...it was not acidic at all like most Vitamin c....
I believed this was helping.....though I will be the first to admit the research I had read on this was not all that much more credible than reading about BigFoot
But, it made sense to me, and I did it religiously, and always felt better than my buddies after diving. Even better than George
Today, you could use astaxanthin or [FONT=Arial, Helvetica, sans-serif]SUPEROXIDE DISMUTASE...( which would seem more interesting for this). Thoughts? Research on this?[/FONT]

 

[diverdoug1]

Free radical scavenging may very well help with the cumulative cell damaging effects of oxidative toxicity. It is less likely to have an effect on superoxic CNS pathology because of a different onset of action. This is thought to possibly be mediated by impairment of transport proteins across the lipid bilayer of the neural tissues and possibly more sensitively in the reticular activating cortex, and mediated by free radicals. I know of no ongoing research involving this, but it does make sense and would be an interesting study to pursue! Here is the info for a study about free radicals. Stone, W.L.; Henderson, R.A.; Howard, G.H.; Hollis, A.L.; Payne, P.H.; Scott, R.L. (1989). "The role of antioxidant nutrients in preventing hyperbaric oxygen damage to the retina". Free Radical Biology & Medicine

 

[Nirvana]

Dopler, when you say "Also, and I am sounding like a broken record, PO2 is only half the equation. TIME and PO2 = dose." It does not sound like you were teaching the NOAA single dive limits, which clearly do have some limits that are REGARDLESS of time. If you are teaching both and realize that ppO2 certainly is not only half the equation in all circumstances, then BRAVO! To answer your direct question regarding CNS vs CNS oxidative risks, the former is felt to have cumulative risk in by purely an increased time for the event to occur so cumulative in risk by duration of risk event alone, resulting in a linear increase in risk of an occurrence over time and is less predictably anticipated. While the later is a cumulative increase in risk by accumulation of CNS-OTU AND time causing an exponential increase in risk of an occurrence over time and can somewhat reliably be avoided by decreased exposure duration.

diverdoug1, are you saying that, when dealing with single exposure oxygen toxicity, the risk of occurrence of an event is constant with time? If I understand you correctly, for a given PPO2, the diver is at much risk of seizing during his first minute in the water as he is in his 100th. An analogy, then, would be rolling a dice multiple times. The player has as much chance of getting a 6 in his second throw as in his 80th, but he his a bigger chance of getting a 6 at least once by throwing 80 times.

Am I understanding you correctly?

 

[diverdoug1]

Nirvana, all other factors being equal, the answer would be yes, but with caveats. When compared with CNS OTU which greatly increase over time, the risk of a superoxic CNS hit would look linear. To be meticulously honest, things usually do change with time. Divers do tend to slowly drop their core temperature during a dive. Their partial pressure of CO2 will rise slightly even with a good minute ventilation. Kidney function will continue and intravascular volume will decrease over time. So incidence is thought to increase slightly over time. The concern is that the plot of risk increase over time is insidious. Whereas the curve for risk vs time with CNS-OTU injury has a comparatively steep curve. In your dice analogy, with a superoxic CNS event, you are rolling the dice to get a six every minute, to maybe every 50 seconds towards the end of the dive (although the true risk is not that high), whereas the risk with CNS-OTU injury, you start the dive rolling the dice every 15 minutes, and end the dive rolling the dice every 10 seconds. These risk levels are much higher than real life, and are just for illustrative purpose of explaining the linear vs exponential nature of the risks.

 

[Doppler]

Dopler, when you say "Also, and I am sounding like a broken record, PO2 is only half the equation. TIME and PO2 = dose." It does not sound like you were teaching the NOAA single dive limits, which clearly do have some limits that are REGARDLESS of time. If you are teaching both and realize that ppO2 certainly is not only half the equation in all circumstances, then BRAVO! To answer your direct question regarding CNS vs CNS oxidative risks, the former is felt to have cumulative risk in by purely an increased time for the event to occur so cumulative in risk by duration of risk event alone, resulting in a linear increase in risk of an occurrence over time and is less predictably anticipated. While the later is a cumulative increase in risk by accumulation of CNS-OTU AND time causing an exponential increase in risk of an occurrence over time and can somewhat reliably be avoided by decreased exposure duration.

Perhaps I am misinterpreting this, but you seem a little snippy. Not to worry, but I am wondering if I've pissed in your cornflakes without realizing it. If you believe I have, then I apologize.

Anyhow, to the real issue, and since this is a public forum being mulled over by people with varying degrees of interest, experience and reading comprehension, let's quote some passages from the NOAA manual, which may help to make the CNS limit issue somewhat clearer, and will certainly clarify what I teach, since you seem intent on issuing me with a grade.

3.3.3.3.5 Concepts of Oxygen Exposure Management
The traditional method used for prevention of CNS oxygen toxicity is to stay within exposure durations that are based on the oxygen level, or PO2, to which the diver is exposed (U.S.Navy Diving Manual 1999). These limits allow a certain time at each PO2 range. Such an approach has been practiced by the U.S. Navy and by NOAA for many years in their procedures for mixed gas and oxygen diving.

As with decompression, a limit appears to be implemented as if it were a solid line dividing “no problems” from “guaranteed problems.” Actually, a limit is a solid line drawn through a wide gray area of gradually increasing risk. The limits given here and in other limit-based algorithms (such as a decompression table) are recommended guidelines for use under normal conditions.

They have been proven in practice. They work for most people most of the time, but they are not guaranteed to work for all people all of the time under all circumstances. They may need to be more conservative when conditions are more stressful.

Diving with procedures described in this chapter imposes a relatively low risk of oxygen toxicity. The exposures are short and outside the limits that are expected to cause problems.

3.3.3.3.6 Prevention of CNS Poisoning
With the help of experts, NOAA developed estimated oxygen exposure limits that were published in the 1991 version of the NOAA Diving Manual. These limits are shown in Table 3.4. [a version of which I included in my earlier post] They are intended for a diver doing dives for research, sampling, inspection, observation, and light to moderate work at the higher PO2 levels. The lower levels can be used for heavier and more stressful types of work.

For each level of oxygen, the chart shows an allowable time for a single exposure and also an accumulated time at that level over a full day.

If more than one dive is made to the maximum exposure of a PO2 of 1.6 ata, a suggested surface interval of at least 90 minutes is advised between dives (three dives of 45 minutes each would theoretically be possible within the 150-minutes daily total allowed at 1.6 ata PO2). This helps lower the accumulated oxygen dose. This only applies to the exposure at 1.6 ata, because only one maximal dive can be done in a single day with lower oxygen exposure levels.

If, however, one or more dives in a 24-hour period have reached or exceeded the limits for a normal single exposure, the diver should spend a minimum of two hours at a normoxic PO2 (such as on the surface breathing air) before resuming diving. If diving in a 24-hour period reaches the Maximum 24-hour Limit, the diver must spend a minimum of 12 hours at normoxic PO2 before diving again.





There is conspicuous by its absence perhaps, no distinction made between CNS toxicity and CNS oxidative toxicity, since the risk from both include the same dire potential for tonic-clonic type seizure... Rereading your answer above (you have used the phrase "the former" in both sides of your comparison which is confusing), it seems both are influenced primarily by exposure... which within the confines of NOAA's limits is "reliably predictable."


AND FINALLY... I'll ask once again:

Is there a possibility that, in the incident which you mentioned, a contributing factor to the episode could be the influence of exceeding NOAA's 24-hour accumulated time limit?

 

[diverdoug1]

You obviously quoted before I had a chance to correct the former/later. I have no interest in grading you or seeming snippy, only in avoiding having to participate in a post-mortem for someone if they were instructed by someone that told them that ppO2 was only half of the equation. This would imply that a very high ppO2 might be permissible for a very short period of time. As I said before, if you do in-fact have an appreciation of the fact that very high ppO2 is not permissible for even very short periods of time, I once again applaud you! BRAVO SIR