Info Oxygen Toxicity Limits & Symptoms

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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.

full.jpg

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.


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



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.

Akimbo:
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


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.

Akimbo:
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.

Akimbo:
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.

Akimbo:
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.​
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.​
N: Nausea or spasmodic vomiting. These symptoms may be intermittent.​
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.​
I: Irritability. Any change in the diver’s mental status including confusion, agitation, and anxiety.​
D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.​
C: Convulsions. The first sign of CNS oxygen toxicity may be convulsions that occur with little or no warning.​

Akimbo:
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.
 
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. :wink:


And of course, you know how beautifully this dovetails into my personal rants against the high drag and extra exertion caused by Dry suits.....:D
That a slick wetsuit ( which for very cold water can be a semi-dry with thermalution heated undergarment) and slick bp/wing set up, and fins that optimally propel the diver ( DiveR' Freediving fins with the custom stifness/softness chosen) , or Extra Force Fins, or other optimal propulsion technology...which can also obviously be a scooter where this is called for.... :)
 
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

I'm confused by the mention of 1.3 ATA wet. Can someone explain why we set our computers to 1.4 and some to 1.6, yet 1.3 doesn't sound safe according to this quote.
 
I'm confused by the mention of 1.3 ATA wet. Can someone explain why we set our computers to 1.4 and some to 1.6, yet 1.3 doesn't sound safe according to this quote.
Not really something to concern yourself with for 60 foot dives in recreational profiles and open circuit.
Very high exertion dives...or, really long, or really deep, or in a rebreather, and a whole new world of worries will welcome you :)
 
I'm confused by the mention of 1.3 ATA wet. Can someone explain why we set our computers to 1.4 and some to 1.6, yet 1.3 doesn't sound safe according to this quote.

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. :wink:
 
I'm confused by the mention of 1.3 ATA wet. Can someone explain why we set our computers to 1.4 and some to 1.6, yet 1.3 doesn't sound safe according to this quote.

That's assigning a hard and fast number to a phenomenon that is not hard and fast. Seizures can happen at 1.6 ATA, 1.4 ATA, and 1.3 ATA. The only magic number is 1.0 ATA, below which CNS O2 toxicity is theoretically impossible. The overall risk is lower with decreased inspired pO2, but work level and arterial pCO2 play a significant role as well. What's safe for one diver on one dive may not be safe for another, and what's safe for one individual on one day may not be safe the next. I was talking to one of our visiting scientists, Dr. (LT) Heath Gaiser today about this and he put it very succinctly: the risk is predictable but the occurrence is not.

Best regards,
DDM
 
That's assigning a hard and fast number to a phenomenon that is not hard and fast. Seizures can happen at 1.6 ATA, 1.4 ATA, and 1.3 ATA. The only magic number is 1.0 ATA, below which CNS O2 toxicity is theoretically impossible. The overall risk is lower with decreased inspired pO2, but work level and arterial pCO2 play a significant role as well. What's safe for one diver on one dive may not be safe for another, and what's safe for one individual on one day may not be safe the next. I was talking to one of our visiting scientists, Dr. (LT) Heath Gaiser today about this and he put it very succinctly: the risk is predictable but the occurrence is not.

Best regards,
DDM

I guess that answers it :)

But why still use 1.3 ATA and not 1.4 or 1.6? If anything over 1.0 ATA has predictable risk, then they could have used 1.1. So I get it, I'm at risk using Nitrox, but the way I understand it, the risk is very low at 1.4 and only begins to get dangerous at 1.6.

---------- Post added March 13th, 2014 at 11:36 AM ----------

And for that matter, I know some people that appear Narced on the Surface :)

I've yet to get Narced, but I average around 75-85 ft (deepest being 97, depth of reef) on the Jupiter/WPB drift dives and haven't been on many dives in comparison to those with years of experience (should surpass 50 next month). But with that said, my buddy got narced at 80-85 ft last week. I looked to my left and he wasn't there. I looked right, nope, not there... I stopped, turned around, gone... Seriously? Where did he go, he was JUST beside me, we had been doing a great job of staying side by side, and he couldn't be below me. Up?? Sure enough, 5 ft above me... wth??? After the dive, he said he started feeling really weird, drunk like, so he went up and it cleared. After a bit, he was able to come back down, no problems.
 
I guess that answers it :)

But why still use 1.3 ATA and not 1.4 or 1.6? If anything over 1.0 ATA has predictable risk, then they could have used 1.1. So I get it, I'm at risk using Nitrox, but the way I understand it, the risk is very low at 1.4 and only begins to get dangerous at 1.6.


It's a matter of maximizing the decompression advantage of a hyperoxic mix while minimizing the risk of CNS O2 toxicity. I think people are looking for a "sweet spot", so to speak, and I don't know if you can pin down one single number. 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.

Best regards,
DDM
 
...But why still use 1.3 ATA and not 1.4 or 1.6? If anything over 1.0 ATA has predictable risk, then they could have used 1.1. ...

I personally set my computer to complain at 1.6 and 2.0 instead of 1.4 and 1.6. You can set yours to 1.0 and 1.3 if that makes you comfortable, and I encourage you to do so. We are diving for fun and don't need to be distracted by anxiety.

As with most things in life, there are compromises. I feel more secure running a high PPO2 to reduce DCS risk. The standard was 2.0 though most of my career, which surely affects my emotional comfort zone.

Note that the possibility of OxTox is predictable based on current theory, but nobody can calculate the probability (occurrence). We know that a Scuba tank can blow up on our back or space junk can fall from the sky and pound us into the dirt, but the probability is low enough that we don't let it change our actions. We still drive which is statistically and intellectually accepted to be one of the most dangerous human activities.
 
https://www.shearwater.com/products/teric/

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