Understanding Oxygen Toxicity

Text by Dennis Guichard
It’s an amazing gift to be alive isn’t it. The relative blink of a moment across the eons of time that we get to be here at all. And on top of that that we get gifted the opportunity to scuba dive. Surely nothing could be better.

Our being here at all however is a very fortunate quirk of physics and physiology. Our life systems are immensely fragile and can only survive in a very narrow range of oxygen tolerance pressures. And our atmosphere currently happens to give us exactly what it is that our cells need to survive. Any less oxygen, or too much more, and our atmosphere would kill us.
Oxygen is a critical component in the metabolic processes that give us life. Nearly every cell of our body houses thousands of tiny power structures called mitochondria. The function of which are to convert the nutrients we eat into an energy source called ATP that our cells can further use for energy for all the bodily functions we require. And oxygen is acritical component of that process. But the generation of ATP is a messy process and our cells also generate various forms of reactive oxygen species (ROS) when some oxygen molecules react badly with electrons and spill out from the mitochondria.

But the body is clever because it has some in- built protective defence systems, called antioxidants, who’s function it is to hunt down and clean up these destructive ROS. The most powerful antioxidant called glutathione, one of many in our body, is produced in our liver as long as we provide the essential nutrients to generate it. The problem however occurs when our antioxidant systems are either insufficient, perhaps through poor diet and/or from a poor lifestyle, or when our antioxidant systems are overwhelmed with too much ROS.

A misnomer that we’ve all been lead to believe, or that we’ve all admittedly been teaching as dive instructors for literally decades, is that oxygen toxicity in diving only occurs at certain limits. And this is not strictly true.

A certain amount of ROS are valuable in our bodies because they function as signalling molecules that control many physiological processes. Amongst many benefits of course in hyperbaric medicine, we also specifically administer high partial pressures of oxygen in the chamber to purposefully generate excess ROS. These trigger stem cell release critical for wound healing. So ROS can be a good thing as long as we keep a delicate balance in check.

The extent of oxygen toxicity (excess ROS) is influenced by intensity of exposure (partial pressure of oxygen), the duration of exposure (time), exercise (metabolic rate), immersion (wet vs dry), and also individual susceptibility. Overwhelm our antioxidant defence systems and that good can very quickly become bad.

ROS are generated in our tissue cells endlessly even at the atmospheric pressure at which we’re fortunate enough as a species to survive. The ROS/antioxidant toxicity battle between vital cell signalling and destructive cell damage balance is a delicate and endless process.

Up to about 0.50 bar ppO2 and for relatively short periods of time, our bodies cope well in cleaning out the rampant ROS. At levels of up to about 1.20 bar ppO2 our lungs seem to be one of the primary organs of decay. Beyond a level of about 1.60 ppO2 central nervous system (CNS) decay starts to dominate as the exposure-limiting process.

At low levels of hyperoxia the ROS predominantly damages the alveolar-capillary barrier in our lungs over time. Plasma leaks into our alveoli and our critical gas exchange interface is hindered until we literally drown in our own plasma. Given enough time, even breathing 100% oxygen at surface pressures (1.00 ppO2) would kill us. Reason enough why air breaks are always included in oxygen breathing administration. This process starts as soon as we breathe elevated ppO2 above atmospheric pressure (0.21 ppO2). That alveolar cellular damage also leads to secondary acute inflammation further compounding the injury.

The production of excess ROS ceases as soon as we stop breathing the elevated ppO2 mixture. The cellular alveoli damage will immediately start to recover, although the inflammation process can still continue for many hours.

Various mathematical models have been proposed over the decades to try and help predict the detrimental effects of both pulmonary and CNS oxygen toxicity, all of which have their benefits and shortfalls.

NOTE: In forthcoming editions we will look at oxygen toxicity more closely.