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]

... As far as I know the 1.3 ATA number came out of a general statement in the DAN Technical Diving conference proceedings, which BTW make excellent reading for anyone seeking additional knowledge on this and other subjects.

Technical Diving Conference Proceedings....

Central Nervous System Oxygen Toxicity starts on Acrobat page 39, highly recommended.

 

[diverdoug1]

Good question. I seem to recall that is the lowest PPO2 a convulsion has ever been observed. Maybe some of the hyperbaric docs on the board can chime in?

I agree with Dan though. The Navy standard was 2.0 or higher most of my life. Human variability can sure make a mess of research data.

I was consulted on a post mortem examination of a female cave diver who had an oxygen toxicity induced seizure at 1.3 ATA O2.

 

[danvolker]

I was consulted on a post mortem examination of a female cave diver who had an oxygen toxicity induced seizure at 1.3 ATA O2.

Wow. Did she also have extreme acidity /high CO2 levels--wondering if she was either skip breathing and built high CO2 which induced Ox Tox, or maybe was using a rebreather and had the CO2 scrubber failing????

Hearing that a diver toxed at 1.3 is troubling, aside from the death we are all sorry to hear about--troubling because there is no way we are going to be using 1.2 or below as a new max exposure setting, and because in the large number of accidents where a tox event was involved, there have typically been mitigating factors....which is why I am hoping you were aware of whether she was tested for CO2 level?

 

[diverdoug1]

No evidence of exertion prior to seizure. The decedent signaled distress to her two dive buddies shortly prior to having a witnessed seizure at depth. Deco obligation precluded emrgent ascent of the victim. When you are asking if she was tested for CO2 level are you asking as to analysis of her tanks? This was OK, as was the functioning of her regulators. The amount of gas consumed by the decedent prior to seizure was consitent with her previously documented baseline SAC / gas consumption during previous dives. The decedent did not have an arterial blood gas analysis during her short hospital course prior to determination of death. Post mortem measurement of CO2 in a cadaver is of little use. Post mortem examination was in excess of 20 hours post mortem. The only risk factor the decedent had was being female. She was in peak physical condition in her late 20's. There was no evidence of pathology noted on examination of the tracheobronchial tree, airway, or on gross and microscopic examination of the neural tissues. No indication of AGE was noted. Examination of the heart showed no patency between to left and right circulatory systems. She also had multiple previous exposures to much higher ppO2 with no evidence of problems and no prior history af any medical problems. I really don't want to give any more specifics regarding the decedent other than there was no determination as to why she would have an oxygen toxicity seizure at such a low ppO2.

 

[danvolker]

No evidence of exertion prior to seizure. The decedent signaled distress to her two dive buddies shortly prior to having a witnessed seizure at depth. Deco obligation precluded emrgent ascent of the victim. When you are asking if she was tested for CO2 level are you asking as to analysis of her tanks? .

My question was to her blood CO2.....many divers that are concerned with bottom time ( as in being in a overhead cave environment), can slip into skip breathing if they get nervous about their amount of gas and whether it will be enough for them. Skip breathing, with a high O2 mix, would be considered dangerous with the potential to cause oxygen toxicity at a lower ppO2 than would normally be considered....At least this is my thinking on it ..my 2 cents....

 

[diverdoug1]

Her blood CO2 was not measured as I said. Skip breathing was ruled out because of adequate measured gas consumption, as well as witnessed behaviour in the hour precedent to death. Also, bottom time not at issue, experienced cave divers on exit with surplus gas. Also, victim was on open circuit (did not see your question re: CO2 scrubber).

 

[Doppler]

I was consulted on a post mortem examination of a female cave diver who had an oxygen toxicity induced seizure at 1.3 ATA O2.

But what had been her exposure over the previous 24-hours. NOAA was and is very specific on this score otherwise would never have bothered developing and publishing a 24-hour CNS table in addition to a single dive table.

Also, and I am sounding like a broken record, PO2 is only half the equation. TIME and PO2 = dose.

I'll say it again: Watch the 24-hour limits!

 

[diverdoug1]

Doppler, do not confuse CNS and a CNS oxidative oxygen toxicity. NOAA established the 24-hours CNS table for prevention of oxidative oxygen toxicty. This is why there also is a NOAA single exposure limit. To answer your question, the diver was well within the 24-hour oxygen exposure limits, and displayed no tracheobronchial, myocardial, ocular, hepatic or renal patholgy which would be indicative of oxidative oxygen toxicity. Alveolar damage was present secondary to fresh water aspiration.

When instructing your students it is imperative that you understand the differences between these types of oxygen toxicity and their ramifications Your misunderstanding that time is always a critical factor in an oxygen toxicity event can lead to a fatal misadventure secondary to a poor understanding of the mechanism of risk.

There is a very strong urge to explain an accident within the technical diving community, when an incident occurs when no "rule" has been violated. This is also seen in the cave diving community. For an incident to occur in the absence of a "broken rule" it forces acceptance of the fact that not all accidents and incidents can be avoided with proper preparation. Human variation and luck can be unfortunate confounders of our diving adventures.

 

[Doppler]

Doppler, do not confuse CNS and oxidative oxygen toxicity. NOAA established the 24-hours CNS table for prevention of oxidative oxygen toxicty.

I disagree. The 24-hour limit was developed to manage Central Nervous System involvement and has nothing at all to do with Whole Body or Pulmonary Toxicity. This is managed through a completely different set of guidelines.

Allow me to quote from a paper I keep at hand "Dr. Christian J. Lambertsen and colleagues at the Institute for Environmental Medicine, University of Pennsylvania, developed the current “tracking” method for pulmonary oxygen toxicity in the form of the unit pulmonary toxic dose (UPTD) and the cumulative pulmonary toxic dose (CPTD). The UPTD is more commonly referred to in the diving community as the oxygen toxicity unit (OTU). One UPTD (or OTU) is the degree of pulmonary oxygen toxicity produced by breathing 100% O2 continuously at a pressure of 1 atmosphere absolute (ATA) for 1 minute. The CPTD calculation (see Equation 1 below) converts any continuous oxygen exposure (PO2 above 0.5) and time combination to be expressed as UPTD’s (or OTU’s). The CPTD calculation is carried out for each segment of the dive profile and the results (expressed as OTU’s) are summed up to produce the total number of OTU’s for the dive. This number can then be compared against the daily and multi-day limits established by Dr. Bill Hamilton and colleagues in the NOAA Repetitive Excursions (REPEX) Procedures Report. These published limits have been widely adopted by the technical diving community."

The same paper (Oxygen Toxicity Calculations by Erik C. Baker, P.E.), does a pretty good job of explaining the differences between CNS and Pulmonary Toxicity.

The table below is a little small but is reproduced from the original published by NOAA and in general circulation. It includes in one table single dive and 24-hour or Daily Limits for CNS tracking. And as an aside, the open quoted 90-minute half-time decay for CNS toxicity loading was originally only suggested for PO2 of 1.6 bar by NOAA. Hamilton was empathic that there was no science to back-up its application across all partial pressures. He stated that had this been the case, there would have been no need to publish a 24-hour table.

 

[TSandM]

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, judging from the widespread adoption of Nitrox for recreational diving, and the almost total lack of reported seizures in that population. It is likely, however, that there may be no 100% safe level -- and there is also the possibility that some "ox-tox" seizures are not. I see people several times a year who have apparently seized, with a good observer history of what sounds like seizure activity and lab work to correlate, but who have neither any prior history of seizure nor any identifiable predisposing factors. Some of those people never seize again. 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.