Why does O2 become toxic?

[junior]

Dr Deco,

I've been reading your postings and getting enlightened all the same. I've been searching for the postings that explain why oxygen is toxic when you are at depth, but I haven't seen any. Why is this? I have seen navy videos about early divers getting O2 toxicity, but that's all that was mentioned - "...pure oxygen is toxic at depth." I've never heard or learned what makes O2 toxic when you are at depth or what it does to your body.

Gene Brotherton
Lake Mary, FL.

 

[sky50960]

Two types of toxicity acute ( for diver breathing Nitrox and hyperbaric centers) and Chronic ( for hospitals and people in intensive care units for example )

About o2 acute toxicity ( for example diving deeper than 6 meters breathing o2 ) :

Administration of hyperbaric oxygen can be followed by a spectrum of neurologic disturbances leading to frank convulsions. The mechanism leading to cerebral seizure activity is not fully understood but is possibly linked to oxygen radical production and the L-Arginine-NO system.
The maximun ppo2( partial pressure of o2 ) is estimated at 1,6 bar before hi probability of seizure.

About o2 chronique toxicity ( long time exposure ) :

Normobaric oxygen toxicity is well described in all animal species. However susceptibility to oxygen exposure is highly variable according to age, species and strains. Similarly in humans, prolonged high oxygen exposure is reported to induce cough, shortness of breath, decrease vital capacity and increase alveolo-capillary permeability
Oxygen free-radicals play a key role in the pathophysiology of oxygen toxicity.

 

[Dr Deco]

Dear junior:

This question is a popular one. Oxygen, even that in the air, is toxic to all organisms and becomes more so at elevated partial pressures. :egrin:

The toxicity in air is controlled by the special anti-oxidant enzymes in the bodies of living organisms. (Some obligate anaerobic bacteria are extremely sensitive to oxygen.) Virtually all of the oxygen we take into our bodies is utilized in the mitochondria of cells for the production of energy.

There are, however, localized accumulations of reactive oxygen intermediates (ROI), for example, hydrogen peroxide, superoxide anion and hydroxyl free radicals. The oxygen scavenging enzymes (e.g., super oxide dismutase, catalase) can eliminate most of these. In addition there are others such as vitamin A (retinol), vitamin C (ascorbic acid) and E (a-tocopherol). All are found in foods. :viking:

In addition to problems for divers, ROI have been linked to oxidative stress and the rate of aging.:doctor:

There are two typtes of toxicity. The most dangerous has rapid onset and is of the central nervous system (Paul Bert Effect). CNS tissue has a high utilization rate of oxygen and thus a good blood supply. It is first affected when the partial pressure of O2 is greater than 2.5 ATA. Grand mal seizures occur, and these can lead to drowning when they occur in the water. Acute O2 toxicity has warning signs: muscular twitching, tunnel vision, hearing difficulties.Convulsion is followed by fatigue, confusion, poor coordination, anxiety. In general it is this form of toxicity that limits the use of oxygen as a gas for diving.

The second type is pulmonary and was first reported by J. Lorrain-Smith (in 1897). The symptoms are, in order of appearance, (a) mild irritation beneath sternum (breastbone) on deep inspiration, (b.) occasional cough. (c.) burning on inspiration, (d.) frequent cough, (e.) intense substernal irritation, and (f.) uncontrollable cough. In general, it is this form of toxicity that limits the long-term use of oxygen at pressure. For example, compressed air cannot be used for underwater habitats that are deeper than fifty feet.

Dr Deco

 

[junior]

So the ROIs build up in our system and cause damage to the nervous system? 2.5 ATA is about 75 feet. Should we start to be more cautious at this depth? How much of a danger is O2 toxicity to recreational divers?

 

[blacknet]

Hello,

From 'mixed gas diving' page 125.

ATA
3.0 50/50 therapy gas
2.8 100% o2 at 60'
2.5 deco for operation diving (max)
2.4 60/40 therapy gas
2.0 USN exceptional exposure to working divers
1.6 USN maximum normal exposure to working divers
.5 max saturation exposure
.35 normal saturation exposure
.21 normal enviroment
.16 begining of hypoxia
.12 serious signs of hypoxia
.10 unconsciousness
<.10 coma/death

Keep in mind this is Po2 (Partial Pressure of o2) in ATA. Most recomend 1.4 Po2 levels. Also note that work levels play a very important factor in your ox tox levels.

Ed

 

[Dr Deco]

Dear blacknet:

That is a very nice summary. You are correct in stating that carbon dioxide is thought to play a role in the partial pressures at which oxygen manifests signs and symptoms of central nervous system (CNS) toxicity. The general thought is that elevated arterial levels, usually derived from exercise, cause the prearteriolar capillaries of the brain circulatory system to open. When this occurs, more blood flows and more oxygen can diffuse into brain tissue. The cells of the CNS are thus exposed to even greater elevations of oxygen than in the resting individual.

Therefore, people in a hyperbaric chamber undergoing treatment can be exposed to greater oxygen partial pressures than those in the water. This is because patients in a chamber are resting while divers in the water are often swimming and/or undergoing some physical activity.

Dr Deco

 

[blacknet]

hello,

Yup i've been reading up on co2 alot lately and ran into that little tidbit about co2 and o2 tox. Guess this would be the correct thread to bring it up in. In light of the recent discussion on o2 tox and water vs chamber dives how do you feel about use of 100% o2 while diving? (in water doing deco) Also you know how use of higher Po2 levels affects flying after diving?

Ed

 

[Dr Deco]

Dear Ed:

The use of oxygen in water has gained interest in the past decade by technical divers who are using it to increase the rate of inert gas washout during the final stage of in-water decompression. These individuals are trained in its use and follow rules of dose (that is, depth at which it is breathed). An import distinction to make, here, is that decompression is different that oxygen as a diving gas. In the later case, the individual is active and swimming, while in the former the diver is relatively quiet.

It is the relative quite that is important when we are discussing the build up of carbon dioxide and its contribution of central nervous system oxygen toxicity. As mention in the past in this forum, some physical activity (bicycle motions of the legs and movements of the arms) is good to promote an increase in peripheral blood flow. This must not be exaggerated, however.

Physical activity is a powerful modifier of gas exchange, both uptake during the dive portion, and off gassing during the ascent and while on the surface. Those of you who have followed the recent space walk by the NASA astronauts on Friday night will have noted that vigorous activity on the bicycle ergometer was a part of the new prebreathe procedure. The off gassing aspects of this maneuver were investigated by scientists at Duke University, the US Air Force altitude laboratory, and at the Johnson Space Center at NASA. It is the last group with which I am associated. I developed an algorithm that relates the effective half-time of a tissue to the oxygen consumption (workload). This enabled us to calculate the mix of very active and moderately active exercise that would go into the reduced duration prebreathe.

This activity is closely monitored (and all at surface pressure) to prevent any untoward effects. Naturally, such close observation is precluded by recreational divers without the close support that is possible at NASA. Thus vigorous exercise in water with oxygen to promote off gassing would not be recommended.

The risk of DCS when flying after diving is certainly reduced by oxygen breathing. There are so many dive scenarios however, that a simple rule of the length of the surface interval is not really possible.

Dr Deco

For those of you who are interested, this is a reminder of the Decompression Physiology class I have at the Catalina Island station. For more information, connect on:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

 

[blacknet]

Hello,

OK how about this one

When talking about ox tox and why it happens I started reading up on it. Found that that epilepesy and ox tox happens in the same manner, with the GABA thing. Seems that GABA levels are responsible for seizures. Would it be safe to assume we should be taking GABA supplments before doing 'hot' o2 mixes to reduce our risks?

Ed

 

[Dr Deco]

Dear Ed and Readers:

There have never been any sure fire preventatives for oxygen toxicity. It is also good to remember that oxygen affects all of the organs of the body. It is a general poison.

In higher concentrations (partial pressures), it will damage the central nervous system (CNS). This can be prevented by the administration of a general anesthetic (to a laboratory animal, for example). However, when the pressure is released and the oxygen removed, the animal will not awaken. It has been poisoned.

Thus, prevention of the CNS effects of oxygen toxicity will not necessarily protect the lungs, kidneys or liver. It might be possible to completely block the effects of oxygen on several systems of the body, but other are also being affected. The only truly safe way is to prevent problems in the most sensitive organ system (the CNS). Then the others, in their turn, will be free from harm.

Some ameliorating agents have also been found but are useable only in injectable forms. One must bear in mind that administration of enzymes by the oral routes is generally not possible, since they are digested.

Dr Deco