Talk:Oxygen toxicity

Oxygen use by scuba divers
The article states that SCUBA divers use up to 100% oxygen. I'd like to see a cite for that; it makes no sense since it would be poison at a fairly low depth.

Learjeff (talk) 16:48, 17 March 2013 (UTC)


 * Hi Learjeff. The two biggest reasons for divers using 100% oxygen at depth are both done at shallow depths.
 * 1. Oxygen rebreathers are used by the military for shallow diving operations where detection needs to be limited. This paper discusses rebreathers and 100% oxygen use in them. (Please excuse the need for citations in the wiki article, I had not seen the requests until now and will address those soon)
 * 2. Divers use 100% oxygen for decompression stops. (Here is one of my abstracts)
 * Hope this helps! --Gene Hobbs (talk) 17:28, 17 March 2013 (UTC)

Consistency in basis of measurement, please!
I understand the distinction between oxygen partial pressure (e.g. 20% af 15 psi is 3 psi O2 partial pressure) and concentration of oxygen (oxygen percentage of inhaled atmosphere), but the article doesn't seem to. It bounces from one to the other as though they were somehow commensurate, which isn't so (e.g., 100% O2 at 5 psi and 25% O2 at 20 psi both produce an O2 partial pressure of 5 psi). If the partial pressure of O2 is relevant in some contexts and its atmospheric concentration is relevant in others, then some indication should be given of which is relevant where. — Preceding unsigned comment added by 199.223.125.164 (talk) 05:32, 13 May 2013 (UTC)
 * Could you be more specific please, and give some indication of where the problematic text is to be found (which section heading, at least, and if there is likely to be any confusion, quote the instance.) &bull; &bull; &bull; Peter (Southwood) (talk): 11:47, 13 May 2013 (UTC)
 * From "Causes", subsection "Central nervous system toxicity": "Exposures, from minutes to a few hours, to partial pressures of oxygen above 1.6 bars (160 kPa)—about eight times the atmospheric concentration." Partial pressure (measured in kPa or bars) is not a concentration. Thank you, anonymous editor. I shall check through the whole article. Axl  ¤  [Talk]  12:23, 13 May 2013 (UTC)
 * A search on "concentration" and "fraction" shows that the use of these terms in the article is widespread, and in a high proportion of the cases they are used where partial pressure is the intended meaning. As there are many references to different ambient pressures in the article one cannot make the assumption of constant ambient pressure which would make the terms effectively equivalent, so they will have to be changed. I will make a start. Good feedback from 199.223.125.164. &bull; &bull; &bull; Peter (Southwood) (talk): 08:59, 14 May 2013 (UTC)
 * I have changed all the instances that I consider ambiguous. Those remaining seem appropriate. The section on Mechanism refers to dissolved oxygen, and I think concentration is appropriate in that context, but will defer to expert opinion. Otherwise most instances are now either referring to gas fraction directly as a percentage, or are in an implied normobaric context. &bull; &bull; &bull; Peter (Southwood) (talk): 09:37, 14 May 2013 (UTC)
 * The only problem is that the sources quite often use the word 'concentration' in an informal sense to mean either partial pressure or volume fraction (which coincide numerically at normobaric pressures). The first one I spot-checked was Bitterman 2009 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688103/) which contained "Resolution of the acute phase of pulmonary oxygen toxicity or prolonged exposures to oxygen at sublethal concentrations such as during prolonged hyperoxic mechanical ventilation ...". Pedantically, there is no such thing as a "[sub]lethal concentration" of oxygen, since any concentration would become toxic at sufficiently high ambient pressure, but we all understand what Bitterman is saying. It may be that we need to consistently use "partial pressure of x bar" when considering exposure, but please remember that it is a cumbersome phrase, and "concentration of x" (implied at normal atmospheric pressure) represents the same condition, so many sources themselves do not distinguish between the two phrases. --RexxS (talk) 16:16, 14 May 2013 (UTC)
 * In "Causes", subsection "Pulmonary toxicity", paragraph 2, it is unclear if the rat experiments are at atmospheric pressure. At first, I assumed that this was the case. However the last sentence of the paragraph implies hyperbaric conditions. Axl  ¤  [Talk]  20:51, 14 May 2013 (UTC)
 * Demchenko et al's 2007 paper was conducted by having rats breathe >98% O2 at 1, 1.5, 2, 2.5, and 3 ATA, so the answer is "both", but it's effectively a hyperbaric trial. The authors are all colleagues of our Gene Hobbs, so we could always get more information almost first-hand if we needed. I've tried to clarify the text. --RexxS (talk) 02:37, 15 May 2013 (UTC)
 * Thanks. The current information is fine. An extended statement about these experiments is beyond the scope of this article, and interested readers should go to the source. Axl  ¤  [Talk]  10:58, 15 May 2013 (UTC)

Confusion between partial pressures for pulmonary toxicity
Current text reads: The statement about 50% partial pressure reads like an introduction, but the begins with clause in the next sentence contradicts it. These do not seem to be from the same source, suggesting the first statement is without source. Does someone have an unambiguous RS telling at what point pulmonary toxicity begins? Grammar&#39;sLittleHelper (talk) 19:36, 7 April 2016 (UTC)
 * Pulmonary toxicity occurs with exposure to partial pressures of oxygen greater than 0.5 bar (50 kPa), corresponding to 50% oxygen at normal atmospheric pressure. Signs of pulmonary toxicity begins with evidence of tracheobronchitis (inflammation of the upper airways) after an asymptomatic period between 4 and 22 hours at greater than 95% oxygen,[1]
 * Both statements can be true (and probably are) as the time depends on the partial pressure and varies between people. Information is probably available in the US Navy diving manual, freely available on the internet, and there will be lots of reliable references in the Rubicon Research Repository also freely accessible, and definitely in the NOAA diving manual, which is not, as far as I know, freely available. It is more likely that the description needs to be clarified than that there is an error in the facts. &bull; &bull; &bull; Peter (Southwood) (talk): 19:58, 7 April 2016 (UTC)
 * OK, if I close one eye and squint the other, I can see that it might be consistent. But to a prima facie reader, I think it is confusing and contradictory.  I look forward to a clarified text from some editor who has greater certainty of the subject. Grammar&#39;sLittleHelper (talk) 21:06, 7 April 2016 (UTC)
 * This is a fair point. I can see that my small edit may not have been sufficient to provide complete clarity to the layperson. My uncertainty in this case is specific to the numbers, not the concept. &bull; &bull; &bull; Peter (Southwood) (talk): 06:56, 8 April 2016 (UTC)
 * The figure of 0.5 bar was established by Lambertsen et al in 1987:
 * Lambertsen CJ, Clark JM, Gelfand R, et al. Definition of tolerance to continuous hyperoxia in man: an abstract report of predictive studies V. In: Bove AA, Bachrach AJ, Greenbaum LJ, eds. Proc 9th International Symposium on Underwater and Hyperbaric Physiology. Undersea and Hyperbaric Society, Bethesda, MD. 1987: 717-735.
 * The tolerance curves connecting O2 partial pressure and duration of exposure derived experimentally can be seen in the current reference 19:
 * The CNS tolerance curve is asymptotic to about 2.0 bar and the pulmonary toxicity curves asymptotic to 0.5 bar and represent exposures in excess of 30 hours for partial pressures marginally above 0.5 bar. These are typical relationships for normal individuals, not lower limits for the population as a whole. Signs may be observed as early as 4 hours if the partial pressure of O2 is higher. That's exactly what is written in the article.
 * SF: in excess of 30 hours is not in the current text, but is vital to understanding. Please add it.
 * I concur that the time scale is relevant and improves understanding. &bull; &bull; &bull; Peter (Southwood) (talk): 06:56, 8 April 2016 (UTC)
 * The problem is that you're trying to put a number of hours to when a curve reaches an asymptote. It doesn't. You might as well pluck out a figure of 36 hours or 24 hours instead of 30 hours. There's no simple number that does anything but mislead the reader. I've created a graph similar to Bitterman's, but much simpler, to illustrate the decrement in lung vital capacity resulting from pulmonary oxygen toxicity. Does that help? --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * I find it useful information and relevant to the point. Whether it is sufficient for everybody I cannot say.&bull; &bull; &bull; Peter (Southwood) (talk): 10:45, 8 April 2016 (UTC)
 * Now, I'm about to revert your edits because in a search for simpler language you've altered the meaning in several places. I'll give some examples:
 * Oxygen toxicity is managed by reducing the exposure to increased oxygen levels / Oxygen toxicity is managed by reducing the oxygen levels - for individuals undergoing recompression treatment, for example, the risk of pulmonary oxygen toxicity is managed by having a 5 minute "air break" every 30 minutes. Even a brief reduction in exposure allows the lungs to recover significantly. It's not the level of oxygen, it's the length of exposure that is used.
 * SF: The phrase, reducing the exposure to increased oxygen levels is self-contradictory. If you already know what it means, you do not need to read it.  But if you read it as a new person, it is difficult to scan.  How about periodically reducing the oxygen levels. I that is what you are describing?
 * My understanding of air breaks is that they are used to reduce the risk of CNS toxic episodes, and I do not know of them having a significant influence on pulmonary toxicity.&bull; &bull; &bull; Peter (Southwood) (talk): 06:56, 8 April 2016 (UTC)
 * No Peter. CNS seizures are ideally managed in situ, simply by removing the mask or hood from the patient and waiting for the seizure to subside before returning to oxygen breathing. There's nothing periodic about that. Air breaks are specifically designed to reduce pulmonary toxicity because of the effect that the lungs recover much more rapidly than they deteriorate. A 5-minute air break can allow the lungs to recover from 25 minutes of breathing oxygen at any ambient pressure below about 3 bar. @SF: Reducing the exposure to breathing at a given partial pressure means reducing the length of time spent breathing at that pressure. There's nothing self-contradictory about that. Your version implies that lower levels of oxygen may be used to manage risk of toxicity. That's simply untrue: the partial pressures used are decided by the treatment schedule for recompression (which depends on depth and duration of the dive and severity of symptoms). Toxicity is managed by treatment of any seizures (CNS) and air breaks (pulmonary) as I've explained. --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * Interesting. I am surprised that I managed to retain that misapprehension for so long. I will look for further clarification in the literature. If you can direct me to a good reference it may save me time. &bull; &bull; &bull; Peter (Southwood) (talk): 10:45, 8 April 2016 (UTC)
 * I'm glad you asked, that,, because it forced me to search for sources for something I'd taken for granted for years. Turning to Bennett & Elliott (5th Ed), Moon and Gorman state on page 621 "... implement 100% O2 breathing throughout the entire treatment, with the exception of short 'air beaks', used to minimize pulmonary and CNS toxicity." So they attribute the breaks to both forms of toxicity. However, on pages 391 and 393, Clark and Thom provide graphs showing rates of decrement and recovery of lung vital capacity, where it can be seen that the reduction in VC occurs at rates of 1-2% per hour, depending on pp of O2, whereas recovery of VC initially takes place at rates of between 5-10% per hour or more. As for CNS toxicity, we usually track the CNS loading with the "oxygen clock", and that is normally considered to decay exponentially with a nominal half-time of 90 minutes at the surface. Calculating 2^(-5/90) we get 0.96, which isn't much of reduction in loading for a 5 minutes air break (even it were at 1 bar, which it isn't). The air break is going to give some small protection against CNS toxicity, but nothing like the prophylactic effect against pulmonary toxicity. Sorry about the synthesis and I'll keep looking for a good source that spells out the effect explicitly. Maybe will know? --RexxS (talk) 14:00, 8 April 2016 (UTC)
 * I have managed to find a couple of references that support the use of air breaks to reduce CNS risk - http://ceaccp.oxfordjournals.org/content/1/5/150.full.pdf Hyperbaric oxygen therapy by Andrew David Pitkin MRCP, Nicholas John Hawksley Davies DM MRCP FRCA in British Journal of Anaesthesia CEPD Reviews  Volume 1 Number 5 2001 p155 Oxygen toxicity to the central nervous system, states "The development of oxygen toxicity is dependent on both partial pressure (dose) and the time of exposure. It is found that ‘air breaks’ lasting 5 min, i.e. short periods breathing air that interrupt the periods  breathing  oxygen  at  30  min  intervals,  allow  recovery  of antioxidant  defences.  This  strategy  significantly  extends  the time of HBO before there are any manifestations of oxygen toxicity. It is a much more effective way of preventing seizures that giving  prophylactic  anticonvulsants."  and at http://www.nbdhmt.org/position_statements.asp  National Board of Diving and Hyperbaric Medical Technology Position Statements Intermittent Air Breathing: (2009-04) August 2009 "It is the position of the National Board of Diving & Hyperbaric Medical Technology that every recompression treatment facility and every clinical hyperbaric chamber, regardless of type or class, be equipped to provide intermittent air breathing. Intermittent air breathing, commonly referred to as an ‘air break', serves to prophylax against and lower the incidence of, central nervous system oxygen toxicity. Intermittent air breathing also serves to treat premonitory signs and symptoms of oxygen toxicity, thereby reducing the potential for symptom progression to overt seizure. The application and sequencing of intermittent air breathing will be at the discretion of the hyperbaric physician. However, intermittent air breathing should be immediately instituted (by either the multiplace chamber tender or monoplace chamber operator) whenever an acute change in patient status occurs and is consistent with, or suggestive of, CNS oxygen toxicity. " Rubicon Research Repository has several articles referring to air breaks as protection against pulmonary tox in rats, but after going through about a hundred abstracts I ran out of steam. &bull; &bull; &bull; Peter (Southwood) (talk): 19:52, 8 April 2016 (UTC)
 * The Pitkin paper is published in British Journal of Anaesthesia, so has a good provenance. It also suggests a mechanism, so is convincing. The only problem for me is that Pitkin doesn't say what studies or reports his statement is based on, so I went to his "key references" section to see if I could track down his source. Oddly, the likeliest-looking source is given as a committee report by NP Hampson, UHMS 1999. I say odd because I don't know of NP Hampson, but NB Hampson has 18 publications in the Undersea and Hyperbaric Medicine Journal that are archived at Rubicon. None of those is a 1999 committee report on HBOT, though. Anyway, the article is certainly reliable enough by Wikipedia standards, but personally I tend to be a little wary of articles where I can't find the source for the conclusions. I'll drop Gene a line and see if he can tell me where to find Hampson's report. --RexxS (talk) 22:28, 8 April 2016 (UTC)
 * Would that be NP Hampson, the famous typographical error? &bull; &bull; &bull; Peter (Southwood) (talk): 17:15, 9 April 2016 (UTC)
 * Protocols for avoidance of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial pressures / Protocols have been designed to avoid hyperoxia in the situations where it is a hazard - No. The protocols are specifically for use "where oxygen is breathed at higher-than-normal partial pressures", not some vague "situations where it is a hazard", which presumably might include fire hazard, etc.
 * SF: In the original text, the usage of "hyperoxia" is incorrect. See hyperoxia.  When oxygen is breathed at higher-than-normal partial pressures, hyperoxia is inevitable and cannot be prevented.  What CAN be prevented is oxygen toxicity, which is a hazard.  This statement should be corrected.
 * The text should read "for avoidance of the effects of hyperoxia". That's a good catch, but the "hazard" phraseology is very wrong. I'll amend the text. --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * hyperoxia seizures - Please don't make up terms that don't exist in the literature.
 * SF: You are correct -- should have been hyoperoxic seizures].
 * I don't recognise that either. What makes tecvault.t101.ro a reliable source? I'm not aware of Johnny E. Brian's credentials as a published expert in the field. It's better to stick with what we find in the current sources as they have been vetted during the GAN and FAC processes. --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * relative rarity - relative to what?
 * SF: This should be decreased incidence. The phrase "increasing rarity" is awkward and unnatural. The language does not usually increase to zero.
 * I disagree. Google finds plenty of ghits for "increasing rarity". The phrase "decreased incidence" is not a synonym and is less precise. A decrease in incidence from '1 in 2' to '1 in 3' would be "decreased incidence" as would a decrease in incidence from '1 in 20,000' to '1 in 30,000'; but only the latter would be an "increasing rarity". --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * problems of managing premature infants / the problems of neonatal care of premature infants - This is a Featured Article. We don't use three words when one will do.
 * SF: The original text suggests those babies get annual performance reviews.  But since they are confined to incubators, they are easy to manage -- the problem is keeping them alive.
 * No, the main problem is finding a balance between keeping very premature babies alive and allowing their retinas to develop normally, which requires protocols to ensure adequate monitoring of their eyes' development while keeping them on supplemental oxygen. I really don't see where you find anything suggestive of "annual performance reviews" in the article text. --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * the lower limit for toxicity is more than 0.3 bar / the minimum for toxicity is more than 0.3 bar - poor phrasing, begging the question "minimum what"? "lower limit" is clear and precise.
 * SF: "Lower limit" means something can go no lower, or should not be allowed to go lower. It does not mean what is intended here.  Minimum toxicity is meaningful in such contexts as
 * "A preliminary evaluation of efficacy and minimum toxic concentration of AQUI-S";
 * "We also calculated the "minimum toxicity" of the tested chemicals."
 * "predictions of minimum toxicity for nonreactive nonelectrolyte organic compounds"
 * "Limit" is also used as a value which is approached but not crossed by a trend. &bull; &bull; &bull; Peter (Southwood) (talk): 06:56, 8 April 2016 (UTC)
 * SF: Sure. But the dosage of oxygen delivered to the tissues is the subject. Surely we do not "limit" the dosage so that the patient always receives the toxic level, and hopefully nothing else "limits" the dosage in that way either.  Minimum toxicity is the term of art.  Why not use it? Grammar&#39;sLittleHelper (talk) 07:11, 8 April 2016 (UTC)
 * Because there's no source for a "minimum toxicity" for oxygen. There is a lower limit for the value of the inspired partial pressure of oxygen which can produce toxicity, probably somewhere between 0.3 and 0.7 bar, depending on other factors. Both Lambertsen and Bitterman discuss "lower limit" when discussing tolerance curves, but neither refers to a "minimum toxicity". Do you have a source that uses "minimum toxicity" in this context? --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * And so on. If you want to discuss these changes, then I'm happy to do so. --RexxS (talk) 21:11, 7 April 2016 (UTC)
 * Discussion open. Grammar&#39;sLittleHelper (talk) 22:43, 7 April 2016 (UTC)
 * ,, please edit your interleaved comments above do that a third party can follow the discussion. Currently it is very difficult to see who said what, and I would like to add my input. Cheers, &bull; &bull; &bull; Peter (Southwood) (talk): 06:21, 8 April 2016 (UTC)--RexxS (talk) 10:32, 8 April 2016 (UTC)
 * "predictions of minimum toxicity for nonreactive nonelectrolyte organic compounds"
 * "Limit" is also used as a value which is approached but not crossed by a trend. &bull; &bull; &bull; Peter (Southwood) (talk): 06:56, 8 April 2016 (UTC)
 * SF: Sure. But the dosage of oxygen delivered to the tissues is the subject. Surely we do not "limit" the dosage so that the patient always receives the toxic level, and hopefully nothing else "limits" the dosage in that way either.  Minimum toxicity is the term of art.  Why not use it? Grammar&#39;sLittleHelper (talk) 07:11, 8 April 2016 (UTC)
 * Because there's no source for a "minimum toxicity" for oxygen. There is a lower limit for the value of the inspired partial pressure of oxygen which can produce toxicity, probably somewhere between 0.3 and 0.7 bar, depending on other factors. Both Lambertsen and Bitterman discuss "lower limit" when discussing tolerance curves, but neither refers to a "minimum toxicity". Do you have a source that uses "minimum toxicity" in this context? --RexxS (talk) 09:48, 8 April 2016 (UTC)
 * And so on. If you want to discuss these changes, then I'm happy to do so. --RexxS (talk) 21:11, 7 April 2016 (UTC)
 * Discussion open. Grammar&#39;sLittleHelper (talk) 22:43, 7 April 2016 (UTC)
 * ,, please edit your interleaved comments above do that a third party can follow the discussion. Currently it is very difficult to see who said what, and I would like to add my input. Cheers, &bull; &bull; &bull; Peter (Southwood) (talk): 06:21, 8 April 2016 (UTC)--RexxS (talk) 10:32, 8 April 2016 (UTC)
 * ,, please edit your interleaved comments above do that a third party can follow the discussion. Currently it is very difficult to see who said what, and I would like to add my input. Cheers, &bull; &bull; &bull; Peter (Southwood) (talk): 06:21, 8 April 2016 (UTC)--RexxS (talk) 10:32, 8 April 2016 (UTC)

I've revisited 's multiple changes and incorporated those that will have consensus to a greater or lesser extent. I find that the remainder remove nuances (such as replacing "is usually associated with" by "causes"; replacing "coldness" with "hypothermia"), or dilute the point of the text (such as removing the statement that CNS toxicity can only occur under hyperbaric conditions), or are tautological (such as "the lungs and respiratory tract"). Please feel free to discuss further disputed changes below. --RexxS (talk) 10:32, 8 April 2016 (UTC)


 * Instead of "sea-level air has a partial pressure of oxygen of 0.21 bar (21 kPa) and the lower limit for toxicity is more than 0.3 bar (30 kPa)", how about "sea-level air has a partial pressure of oxygen of 0.21 bar (21 kPa) but toxicity does not occur below 0.3 bar (30 kPa)." Axl ¤ [Talk] 10:44, 8 April 2016 (UTC)
 * Interestingly, there is a slight contradiction with the phrase "Pulmonary toxicity occurs only with exposure to partial pressures of oxygen greater than 0.5 bar (50 kPa)". The key word here is "only". Can pulmonary toxicity ever occur with pO2 between 30 and 50 kPa? Axl ¤ [Talk] 10:48, 8 April 2016 (UTC)
 * Actually, we don't know. All I can say is that I'm unaware of any reported incidents and that Lambertsen's conclusions settled on 0.5 bar as the lower limit for a normal male. Nevertheless susceptibility to toxicity seems very variable within the population. It seems likely that carbon dioxide retention and maybe the relative abundance of anti-oxidants in the body are also significant contributory factors, so I'd hate to try to quantify the susceptibility. We can be pretty sure the lower limit is at least 0.3 bar and it's probably more than 0.5 bar most of the time, but we misrepresent current knowledge if we try to be more precise. I know that's not much help. Anyway, I'd be perfectly happy with your reformulation of the text and it might meet one of Sfarney's concerns. Would "... toxicity has never been observed below 0.3 bar" be unnecessarily cagey? --RexxS (talk) 11:27, 8 April 2016 (UTC)
 * Has it ever been reported below 0.5 bar? (whether it has been observed doesn't help us if it hasn't been reported, and by reported I imply by a plausible source, but not necessarily WP:MEDREF) &bull; &bull; &bull; Peter (Southwood) (talk): 12:20, 8 April 2016 (UTC)
 * Have a look at JM Clark's 1970 PhD thesis from http://archive.rubicon-foundation.org/xmlui/handle/123456789/3863 pages 157–161 and you'll see that the lower limit for the partial pressure that can be tolerated indefinitely was postulated by Clark to be 0.33 bar for normal men and the upper limit for that value was definitely 0.79 bar. Both Clark and Lambertsen propose 0.5 bar as "the best approximation". It is worthy of note that in relation to very premature infants, Patel at al 2003 states "The cause [of retrolental fibroplasia] is almost always related to the liberal administration of high concentration of oxygen above 40% for a prolonged period (1-2 days) following birth." so there's a suggestion that 0.4 bar may represent the limit for premature infants. --RexxS (talk) 12:57, 8 April 2016 (UTC)
 * I took a look at Clark and Lambertson. I don't see any reason not to go with their best approximation of 0.5bar or their estimated lower limit of 0.33bar for adults until someone with good credentials publishes findings that differ. &bull; &bull; &bull; Peter (Southwood) (talk): 20:19, 8 April 2016 (UTC)

I want to thank you both for your careful attendance to these edits, and your general improvements to the topic. Grammar&#39;sLittleHelper (talk) 22:42, 8 April 2016 (UTC)
 * You are welcome. Attention to detail, adequate coverage, and best reasonably achievable accuracy are what we aim for. Cheers, &bull; &bull; &bull; Peter (Southwood) (talk): 17:10, 9 April 2016 (UTC)
 * In the absence of any objection, I have adjusted the toxicity statement in the article. Axl ¤ [Talk] 09:52, 12 April 2016 (UTC)

Irritability
From "Signs and symptoms", subsection "Central nervous system": "Central nervous system oxygen toxicity manifests as... irritability (personality changes, anxiety, confusion, etc.)." I don't think that confusion is a feature of irritability. Anxiety is borderline too. Axl ¤ [Talk] 10:00, 12 April 2016 (UTC)
 * Good catch,, I've looked again at Bennett & Elliott p376 and at Donald's original reports. They talk about "changes of behaviour" as a sub-category of effects. I've changed our text to:
 * Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness.
 * It doesn't need 'etc' in a list of examples. Does that read better? --RexxS (talk) 14:57, 12 April 2016 (UTC)
 * Yes, thank you! Axl ¤ [Talk] 18:57, 12 April 2016 (UTC)
 * Yes, thank you! Axl</b> ¤ <small style="color:#808000">[Talk] 18:57, 12 April 2016 (UTC)

Review continued
From "Signs and symptoms", subsection "Central nervous system": "In addition, many external factors, such as underwater immersion... will decrease the time to onset of central nervous system symptoms." Is that really true? (I can see that temperature and exertion could have a bearing.) <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 11:00, 13 April 2016 (UTC)
 * Looks very familiar, but I can't quote a source offhand. A citation would be worth finding. &bull; &bull; &bull; Peter (Southwood) (talk): 13:46, 13 April 2016 (UTC)
 * An article at http://www.alertdiver.com/oxygen_toxicity mentions the effect. The article is written for divers (non-subject matter specialists) by a well known diving medicine researcher, i.e. probably reliable. Would you consider this sufficient? &bull; &bull; &bull; Peter (Southwood) (talk): 14:02, 13 April 2016 (UTC)
 * That source states "Cold, exercise, some drugs and increased partial pressure of carbon dioxide increase susceptibility to oxygen toxicity." There is no mention of immersion itself as a predisposing factor. <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 14:37, 13 April 2016 (UTC)
 * It also states In general, oxygen is better tolerated in dry, resting conditions than in wet conditions and while exercising as in diving.. (last paragraph of section "Who is Exposed to the Risk of Oxygen Toxicity?") Cheers, &bull; &bull; &bull; Peter (Southwood) (talk): 08:17, 14 April 2016 (UTC)
 * Ref for impact of immersion and exercise is here. Enjoy! --Gene Hobbs (talk) 18:08, 13 April 2016 (UTC)
 * Thank you, Gene! <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 19:00, 13 April 2016 (UTC)
 * Professor Donald was aware of the effect as long ago as 1947. "Oxygen Poisoning in Man: Part I" (No.4 in the Sources section) contains a diagram showing his apparatus for testing divers "in the wet" and a description of his experiments - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2053251/?page=3 . He concluded "... it was strongly suggested that there was a marked decrease of average tolerance compared with that obtaining in the experiments in compressed air." I have no idea of the mechanism, but the effect is well-known. --RexxS (talk) 20:49, 13 April 2016 (UTC)

From "Signs and symptoms", subsection "Lungs": "The radiological finding from the lungs shows inflammation and swelling (pulmonary oedema)." Pulmonary oedema is not inflammation and swelling. <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 11:11, 13 April 2016 (UTC)
 * I don't know exactly what the source said as I can't find the full text for . Bennett & Elliott (Clark & Thom) page 383 is much less specific about the radiological data, stating "Chest roentgengrams ... have not revealed significant differences. However, much longer exposures to O2 at 101 kPa ... have been associated with characteristic radiological changes ... These lesions first appeared as diffuse, bilateral pulmonary densities which then extended and coalesced to involve almost the entire lung with dense, bilateral opacification in the most severe cases." I think it's probably best to just use what I can be sure of as a basis, so I'll amend the text. If anybody has access to the 1971 Pharmacological Reviews 23 (2): pages 37–133, and it gives more specific information, it can always be added. Do you think:
 * Radiological findings from the lungs show little change in the short term, but extended exposure leads to increasing density of lesions extending throughout both lungs.
 * is a reasonable reflection of the source? --RexxS (talk) 20:49, 13 April 2016 (UTC)
 * How about: "X-rays of the lungs show little change in the short term, but extended exposure leads to increasing diffuse opacification throughout both lungs." <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 09:47, 15 April 2016 (UTC)
 * That looks good, apart from "opacification" - is there a synonym that's a real word? --RexxS (talk) 12:41, 15 April 2016 (UTC)
 * Hmm, how about "shadowing"? <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 10:26, 16 April 2016 (UTC)
 * Works for me - thank you, that section reads much better now. --RexxS (talk) 12:05, 16 April 2016 (UTC)

Research in animals
Although there is some interest in research into possible means of delaying the onset of oxygen toxicity, there are no secondary sources indicating any significant results in humans. The small amount of research in mice and rats does show promise, but primary sources are insufficient to support biomedical claims as outlined in WP:MEDRS. We should be waiting for secondary sources to assess primary sources and draw conclusions that would then be suitable for inclusion in an article.

This is a featured article and additional sections need to comply with FA criteria, particularly compliance with MOS - in this case, WP:MEDMOS, as well as norms of writing style, such as avoidance of single sentence paragraphs. As a result, I've decided to restore the prior version before the animal studies were added. Here is the text and sources that I've removed:

{{talkquote |1=

Research
A study in rats concluded that ketosis delays central nervous system oxygen toxicity.

Some antiepileptic drugs are also hypothesised to delay onset of oxygen-induced seizures in mice.

A study in mice found that biologically produced nitric oxide is part of the mechanism that causes oxygen toxicity, and that superoxide ions inhibit the oxygen-toxicity-causing role of nitric oxide.

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If wishes to reinstate the text, then that should be discussed here first. I'll ask if he thinks any part of the text or sources might be usable. --RexxS (talk) 11:29, 11 April 2017 (UTC)
 * I did a quick PubMed search to look for any new developments. I did not find any suitable review papers. <b style="color:#808000">Axl</b> ¤ <small style="color:#808000">[Talk] 12:00, 11 April 2017 (UTC)
 * Agree better to stick with reviews and other secondary sources.
 * We have reviews such as this one  Doc James  (talk · contribs · email) 15:10, 11 April 2017 (UTC)

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External links modified
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Column widths of references
I made the positive decision to use a minimum column width of 30em as I feel that is the best compromise between whitespace and line-wrapping for this article. That's not to say that I intended the column widths to be set to the default value for Reflist, which is subject to change of course. If there is an rationale to use a different minimum column width, then I'm happy to discus it here. --RexxS (talk) 11:54, 25 March 2018 (UTC)
 * For what page widths did you make this analysis? How is it affected by different skins? &middot; &middot; &middot; Peter Southwood (talk): 03:43, 26 December 2022 (UTC)

Updates, clarification and expansion
There are a few items I have identified as incomplete or requiring some clarification. This is normal, and does not mean the article needs to be delisted as a featured article as they are minor matters, but it is necessary to do some research to find suitable sources before making the changes. &middot; &middot; &middot; Peter Southwood (talk): 06:01, 23 December 2022 (UTC)

Additional medical specialties involved in dealing with oxygen toxicity
Diving Medicine, Hyperbaric Medicine and Neonatal Medicine all have to deal with oxygen toxicity even more than Emergency Medicine. 2605:59C8:11CF:DF10:BCCB:C9FF:FE2A:B121 (talk) 04:38, 14 June 2023 (UTC)


 * As talk pages request (top of this page), state the specific proposed change to the article and supply a WP:MEDRS source. Zefr (talk) 05:11, 14 June 2023 (UTC)
 * Actually, where is emergency medicine cited? The IP is quite correct, and I have no idea why emergency medicine would be considered the relevant specialty. Also have no idea how the specialty is decided. &middot; &middot; &middot; Peter Southwood (talk): 18:45, 11 August 2023 (UTC)
 * Perhaps the thinking is that if you have this problem, it's probably a medical emergency, and not the sort of thing you should wait however long is necessary to get an appointment for?
 * I agree that it would be better to have the obviously relevant specialties added. As for sources, diving appears 63 times on the page,  hyperbaric 61 times, and infant 24 times.  Emergency, by contrast, only appears five times plus in the infobox.  Anyone who genuinely wonders whether these specialties are involved can start by checking the sources for those 148 existing mentions.  We do not need WP:POINTY-headed behavior over obviously correct information in an infobox.  Even the FA standards say that a given fact need only be cited a single time in an entire article. WhatamIdoing (talk) 23:31, 12 August 2023 (UTC)
 * While I agree in principle, in practice the reader may not be sufficiently familiar with the topic to recognise if, and where, the given fact has been cited elsewhere in the article, and finding it can be a lot of work even when one is very familiar with the topic. Cheers, &middot; &middot; &middot; Peter Southwood (talk): 11:49, 22 December 2023 (UTC)
 * I have changed the infobox according to the IP's suggestion, as those specialties definitely do have to deal with oxtox on a fairly routine basis, while emergency medicine is unlikely to have much exposure to acute oxtox which can only happen under pressure, or pulmonary or ocular oxtox which develop very gradually in almost all cases, and can be dealt with by the relevant specialist, or nurse, before they become emergencies. Cheers, &middot; &middot; &middot; Peter Southwood (talk): 12:06, 22 December 2023 (UTC)