Oxygen Toxicity aka Oxtox

Under the right circumstance, the very air we breathe can actually kill us. Well, not the air so much as the oxygen component within it. If you're a seasoned diver, particularly if you hold a nitrox certification, you may already know that. But if you're new to diving, the fact that the gas we depend on to sustain life can, under the right conditions, become deadly poisonous may come as a real shocker.

The condition I'm referring to is called oxygen toxicity — oxtox, for short — and is a subject that's all but ignored in many Open Water training courses. Even in some basic nitrox classes, the subject isn't dealt with on the level of detail that may be warranted. So, if you're still new to diving, or it's been a while since your nitrox class, it's not a bad idea to review the downside of our good friend oxygen.

We sometimes forget that supplemental oxygen is considered a drug, and like any drug it can be toxic at high doses. Being a gas, the “dose” of oxygen one receives is based on both the length of time it's breathed and the pressure at which it's delivered. There are actually several types of oxtox, but the two relevant to diving are the chronic form that affects the lungs and the acute form that affects the brain (central nervous system). The two disorders are also sometimes referred to by the names of the persons who first described the problem. In the first case it was James Lorrain Smith, and in the second the eminent French physiologist Paul Bert (he also made significant contributions to our understanding of decompression illness). Thus, pulmonary oxtox is also known as the Lorrain Smith Effect and the CNS form, the Paul Bert Effect. The chronic form of the disorder, sometimes referred to as low-pressure oxtox, requires breathing oxygen for hours. So, except where recompression therapy is involved, it's not something a recreational diver breathing air would encounter (though it can be a concern when using nitrox). The acute form, sometimes referred to as high-pressure or CNS oxtox, is a very different story. While chronic oxtox isn't likely to be more serious than a bad case of the flu for a healthy individual, the end game of acute oxtox is a grand mal-like seizure which, when it occurs underwater to aJt diver, can cause drowning.

The Physics of Oxtox

When we talk about the oxtox problem arising from “too much oxygen,” we don't mean the percentage of oxygen you breathe. At the right depth, any gas mixture containing any percentage of oxygen can become toxic. The critical factor in the acute form of oxtox is the molecular concentration, not the percentage, and that's defined by what's known as the oxygen partial pressure. Unfortunately, it's probably because of the need to delve into this confusing realm of physics that instructors avoid discussing oxtox in entry-level scuba courses. So, as you may have no idea what I'm talking about, here's the CliffsNotes version of the physics involved.

When gases occur in mixtures, they still retain their own identity. This phenomenon was first described back in the early 19th century by the famous English scientist, John Dalton (the first person to propose that matter was composed of atoms). He found that even though a gas mixture was made up of several different constituents, each gas continues to demonstrate its own behavior, as though the other gases didn't exist. For example, if a gas mixture is made up of 80 percent nitrogen and 20 percent oxygen — like air — then 80 percent of the pressure is exerted by the nitrogen and 20 percent by the oxygen. These individual pressures are what he termed “partial pressures,” and the phenomenon that each partial pressure is proportional to the number of molecules of that gas within the mixture is described as Dalton's law.

To understand how oxtox occurs let's look at how Dalton's law works on a diver breathing air. For ease of arithmetic, we'll assume that the gas mixture a diver breathes is 20 percent oxygen and 80 percent nitrogen, and we'll further assume the surface pressure is 15 psi. According to Dalton's law, oxygen exerts 20 percent of the total pressure of the gas, while nitrogen exerts 80 percent. Put another way, of the 15 psi total pressure, the partial pressure of the oxygen exerts 3 psi (20 percent) while nitrogen partial pressure exerts the other 12 psi (80 percent).

Now, if we double the total pressure to 30 psi — as we do when we dive to 33 feet (10 m) — each gas component continues to exert its partial pressure in proportion to the 80/20 mixture. So, of the total 30 psi, nitrogen exerts 80 percent or 24 psi, and oxygen exerts 20 percent or 6 psi. Note that the partial pressure has doubled while the percentage of gases has remained unchanged. Here's why that's important: As the pressure increases with depth, the pressure inside our lungs must increase as well to maintain a full lung volume. Accordingly, a diver must inhale more gas molecules from the tank. So, the gas density is twice that of the surface (15 psi), so twice the number of gas molecules reach the lungs.

Let's illuminate the concept a bit more with an example by assuming a lung volume at the surface contains 100 molecules of air. (An absurdly low number, of course, but easy to understand.) At the surface, if we continue breathing an 80/20 nitrogen-oxygen mixture, then of the 100 molecules, 80 will be nitrogen and 20 oxygen. Now what happens if the diver descends to 132 feet or 5 ATA (atmospheres absolute)? At that depth the ambient pressure is five times what it was at the surface. So, to maintain a normal lung volume, the diver must inhale not 100 but 500 molecules with each breath, or five times the number he breathed at the surface. As this is still an 80/20 gas mixture, nitrogen accounts for 400 molecules or 4 ATA, while the oxygen component is responsible for 100 molecules or 1 ATA. Now for the real take-home message: Notice that breathing this air mixture at 132 feet (40 m) is physiologically equivalent to breathing pure oxygen at the surface — 100 molecules at 1 atmosphere. Yet, the gas mixture within the tanks has in no way changed. What's important is the gas concentration — the number of molecules that actually reach the lungs.

Still, even at 132 feet — the limit of recreational scuba diving — oxtox really isn't a concern. As it turns out, acute oxtox doesn't become a factor until the pO: reaches around 1.6 ATA, which doesn't happen when breathing air until a depth of 218 feet (66 m). So, as recreational divers, why should we care about oxtox? The reason can be summed up in one word: nitrox. When breathing gas mixtures enriched with oxygen, because of those pesky partial pressures, the rules change completely. For example, a diver breathing a 40 percent nitrox mixture will reach the 1.6 ATA point at just 99 feet (30 m). This is why it's so critically important for nitrox divers to know for certain the oxygen content of their breathing mixture and adhere to its “Maximum Operating Depth” (something you'll learn about when you take a nitrox class). Another concern is that some divers are now using pure oxygen to acilitate nitrogen elimination during decompression. In this case, the pO: of 1.6 ATA occurs in a mere 20 feet (6 m). Of course, in the technical diving realm, where gas mixtures other than air are used routinely, oxtox is a critical concern that must be taken into account on every dive.

The Mechanism

Exactly why the acute form of oxtox occurs isn't fully understood, but we do know how life-giving oxygen can damage cells and have other harmful biochemical effects. It all starts in structures within every cell of our body called mitochondria. If you remember your high school biology, mitochondria serve as the cell's “power house.” They take oxygen — O2 — from our blood and disassemble it into its two component atoms. In the process, by attaching some hydrogen nuclei, some water is formed. The problem is that during the process other molecules called oxygen radicals are also formed, and these are the culprits. Radicals are molecules that contain one or more unpaired electrons, making them highly reactive. Generated from collisions between oxygen molecules during the metabolic processes, oxygen radicals are formed continuously in all cells. (This is why there's such great interest in the role of antioxidants as in our diet.) One physiologist has described these radicals as acting like “coals in a furnace,” meaning as long as they're contained within the mitochondria, we get lots of safe chemical energy. But if hey get out, they can do some real damage. Of course, some do escape, but we have evolved ways of neutralizing most of these radicals. The problem stems from, when the number of radicals is too high, the cell's defenses are overwhelmed and damage occurs.

There are literally hundreds of ways that oxygen radicals can be harmful, but generally there are three fundamental mechanisms involved. First, oxygen radicals can cause inac-tivation of enzymes — molecules that act as catalysts for chemical reactions — so certain biochemical processes cannot take place. Second, radicals can literally change the shape of some proteins, and the shape of a protein is as important to its proper function as its chemical composition. Lastly, radicals can cause degradation of lipids (fat-based molecules) by stealing electrons in a process called peroxidation. This is bad news because the very membranes of our cells are made up of ipid-based compounds.

While these effects can occur in all cells of the body, at partial pressures below about 1.6 ATA, the damages tend to happen most rapidly in the lungs (chronic oxtox). However, above 1.6 ATA, the toxic effects occur most rapidly in the brain. The exact cause is still uncertain, but one popular theory is that the high pOz halts or slows down the production of a neurotransmitter called Gamma-aminobutyric acid or GABA. This inhibits muscle contraction, so without it, the neurons fire uncontrollably, causing convulsions.

Typically, the seizure starts with an immediate loss of consciousness and a period of about 30 seconds when the muscles are relaxed. Then, all of the muscles of the body contract violently for about one minute. This is followed by rapid breathing and, when consciousness returns, a state of extreme confusion. In hyperbaric chambers, people who succumb to acute oxtox — provided they don't hurt themselves by thrashing about during the seizure event — recover fully once the pOa is reduced. However, it's a whole different matter when this happens to divers; anyone experiencing a seizure underwater, and not wearing the proper equipment, is virtually certain to drown. The reason: The scuba regulator most likely will not remain in place. This is why full-face systems are used more commonly in technical and commercial diving, particularly when the risk of oxtox is high. Another concern is that if a diver in seizure is brought to the surface, and the glottis is closed, a lung expansion injury is likely.

There are factors that are known to increase the risk of acute oxtox. The first is just being underwater. Although we don't know why, it's clear that divers have a much higher risk than those breathing high-pressure oxygen in recompression chambers. In a chamber, some individuals can tolerate a p02 as high as 3 ATA, nearly twice the assumed 1.6 ATA limit.

An even more important factor is the workload one encounters while diving; the higher the workload, the greater the risk of acute oxtox. The reason is the increased carbon dioxide level associated with exercise, along with increased blood flow to the brain. It's also believed that some drugs and hormones like adrenaline, atropine, amphetamine and other stimulants could increase oxtox susceptibility. Even aspirin is suspected.

The Squishy Limits

Another complicating factor in the acute oxtox equation is that the partial pressure at which it occurs isn't definitive. This is illustrated in the wide oxygen tolerance between those in chambers versus divers. Yet even among divers there's huge variation among individuals, and an equal variation within individuals from day to day. This can be insidious because a diver can make numerous dives exposed to a high pCh with no difficulties one day then, for no apparent reason, succumb to oxtox at a lower pOz on another.

Like any “limit,” whatever we consider the maximum tolerance for oxygen exposure is just a commonly agreed-upon guideline because, when it comes to human physiology, few things are rock-solid. The reality is that there are lots of complicating factors that make it a virtual impossibility to predict with certainty at what point someone will experience symptoms of oxtox. So, to be on the safe side, most diving organizations use a lower limit than 1.6 ATA. In recreational diving it's typically 1.4 ATA, while the U.S. Navy uses 1.3 ATA for its closed-circuit rebreathers.

In the final analysis, there simply is no magic, absolute limit beyond which everyone will experience a problem and above which no one will. Human bodies just don't act that way. Our understanding of acute oxtox, and the quirks of individual variance make predicting any hard-and-fast limit very problematic. All we can do is follow the established safe practices and guidelines using a healthy dose of common sense. Just remember what the ancient Greeks told us: Nothing in excess.

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