Oxygen toxicity
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2008-07-01T09:51:52Z
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'''Oxygen toxicity''' or '''oxygen toxicity syndrome''' (also known as the "[[Paul Bert]] effect" or the "Lorrain Smith effect") is severe hyperoxia caused by breathing [[oxygen]] at elevated [[partial pressure]]s.<ref name=Brubakk>{{cite book |title=Bennett and Elliott's physiology and medicine of diving, 5th Rev ed. |last=Brubakk |first=A. O. |coauthors=T. S. Neuman |year=2003 |publisher=Saunders Ltd. |location=United States |isbn=0702025712 |pages=800 }}</ref><ref name=usn>{{cite book |title=US Navy Diving Manual, 6th revision |year=[[2006]] |publisher=US Naval Sea Systems Command |location=United States |url=http://www.supsalv.org/00c3_publications.asp?destPage=00c3&pageID=3.9 |accessdate=2008-04-24 }}</ref><ref name=Acott>{{cite journal |last=Acott |first=C. |title=Oxygen toxicity: A brief history of oxygen in diving |journal=South Pacific Underwater Medicine Society journal |volume=29 |issue=3 |date=[[1999]] |issn=0813-1988 |oclc=16986801 |url=http://archive.rubicon-foundation.org/6014 |accessdate=2008-04-29 }}</ref> These above-normal [[concentration]]s of oxygen within the body can cause [[cell (biology)|cell]] damage in two principal regions: the [[central nervous system]] (CNS); and the [[lung]]s (pulmonary).<ref name=Bitterman/> Over time, it can also cause damage to the [[retina]] and may be implicated in some retinopathic conditions.<ref name=Nichols/><ref name=Butler/>
The damage may be caused by long exposure (days) to lower concentrations of oxygen or by shorter exposure (minutes or hours) to high concentrations. Long exposures to partial pressure of oxygen above {{convert|0.5|bar|abbr=on|lk=on}} can result in pulmonary oxygen toxicity and are a concern for patients breathing pure oxygen for extended periods.<ref name=Bancalari/><ref name=Tin/><ref name=Thiel/> Short exposures to partial pressure of oxygen above {{convert|1.6|bar|abbr=on}} are usually associated with CNS oxygen toxicity and are most likely to occur among [[divers]] and those undergoing [[hyperbaric oxygen therapy]].<ref name=Donald1/><ref name=Donald2/><ref name=smerz/>
Prevention of oxygen toxicity is an important precaution whenever oxygen is breathed at greater than normal partial pressures. This has led to protocols for avoidance of hyperoxia being used in such fields as diving, hyperbaric therapy and [[human spaceflight]]. Although it may appear that [[hyperventilation]] might lead to hyperoxia, this does not happen since oxygen toxicity never occurs when breathing air at atmospheric pressure.
== Hyperoxia ==
Hyperoxia is excess oxygen in body tissues or higher than normal partial pressure of oxygen. Hyperoxia is caused by breathing gas at pressures greater than normal [[atmospheric pressure]] or by breathing oxygen-rich gases at normal atmospheric pressure for a prolonged period of time.
== Mechanism ==
The high concentration of oxygen damages cells.<ref name=Bitterman>{{cite journal |author=Bitterman N |title=CNS oxygen toxicity |journal=Undersea Hyperb Med |volume=31 |issue=1 |pages=63–72 |year=2004 |pmid=15233161 |url=http://archive.rubicon-foundation.org/3991 |accessdate=2008-04-29}}</ref> The precise mechanism(s) of the damage caused by these [[reactive oxygen species]] are not known, but oxygen gas has a propensity to react with certain metals to form [[superoxide]] which may attack [[Covalent_bonds#Bond_order|double bonds]] in many organic systems, including the [[Fatty_acid#Unsaturated_fatty_acids|unsaturated fatty acid]] residues in cells. High concentrations of oxygen are known to increase the formation of [[Free radical|free-radicals]] which harm [[DNA]] and other structures (see [[nitric oxide]], [[peroxynitrite]], and [[trioxidane]]). Normally, the body has many defense systems against such damage (see [[glutathione]], [[catalase]], and [[superoxide dismutase]]) but at higher concentrations of free oxygen, these systems are eventually overwhelmed with time, and the rate of damage to [[cell membranes]] exceeds the capacity of systems which control or repair it. Cell damage and cell death then results. Note similarity to [[Reperfusion injury]].
== Types ==
In humans, there are several types of oxygen toxicity:<ref name=Brubakk/><ref name=Acott/>
* Central nervous system (CNS) oxygen toxicity
* Pulmonary oxygen toxicity
* Retinopathic oxygen toxicity
== Central nervous system (CNS) oxygen toxicity ==
CNS oxygen toxicity manifests as symptoms such as [[Tunnel vision|visual changes]], [[Tinnitus|ringing in the ears]], [[nausea]], twitching (especially on the face), irritability (personality changes, anxiety, confusion, etc.), [[Vertigo (medical)|dizziness]], and [[seizure|convulsions]].<ref name=Brubakk/><ref name=usn/> The onset depends upon partial pressure of oxygen (ppO<sub>2</sub>) in the [[breathing gas]] and exposure duration.
=== Background to CNS oxygen toxicity ===
CNS Toxicity was first described by Paul Bert in [[1878]].<ref name=Brubakk/><ref name=Bert>{{cite journal |last=Bert |first=P. |title=Barometric Pressure: researches in experimental physiology |journal=Translated by: Hitchcock MA and Hitchcock FA. College Book Company; 1943 |date= originally published [[1878]] }}</ref><ref>Sport Diving, British Sub Aqua Club, ISBN0091638313, page 110</ref> He showed that oxygen was toxic to [[insects]], [[arachnids]], [[Myriapoda|myriapods]], [[Mollusca|molluscs]], [[earthworm]]s, [[fungi]], [[Germination|germinating seeds]], [[Bird|birds]], and other animals. The first recorded human exposure was recorded in [[1910]] by Bornstein when two men breathed oxygen at {{convert|2.8|atm|abbr=on|lk=on}} for 30 minutes while he went on to 48 minutes with no symptoms.<ref>{{cite journal |author=Bornstein, A. |title=Versuche uber die Prophylaxe der Pressluftkrankheit |journal=Pflug Arch |volume=4 |pages=1272–1300 |date=[[1910]] }}</ref> In [[1912]], Bornstein developed cramps in his hands and legs while breathing oxygen at {{convert|2.8|atm|abbr=on}} for 51 minutes.<ref>{{cite journal |author=Bornstein, A. and Stroink M. |title=Ueber Sauerstoff vergiftung |journal=Dtsch med Wschr |volume=38 |pages=1495–1497 |date=[[1912]] }}</ref> Behnke et. al. were the first to observe [[visual field]] contraction ([[tunnel vision]]) on dives between {{convert|1.0|atm|abbr=on}} and {{convert|4.0|atm|abbr=on}}.<ref>{{cite journal |author=Behnke A. R., Johnson F. S., Poppen J. R., and Motley E. P. |title=The effect of oxygen on man ar pressures from 1 to 4 atmospheres |journal=Am J Physiol |volume=110 |pages=565–572 |date=[[1935]] |url=http://ajplegacy.physiology.org/cgi/reprint/110/3/565 |accessdate=2008-04-29 }}</ref><ref>{{cite journal |author=Behnke A. R., Forbes H. S., and Motley E. P. |title=Circulatory and visual effects of oxygen at 3 atmospheres pressure |journal=Am J Physiol |volume=114 |pages=436–442 |date=[[1935]] |url=http://ajplegacy.physiology.org/cgi/reprint/114/2/436 |accessdate=2008-04-29 }}</ref> During World War II, Donald and Yarbrough et. al. performed many studies on oxygen toxicity to support the initial use of closed circuit oxygen [[rebreather|rebreathers]].<ref name=Donald1>{{cite journal |author=Donald K. W. |title=Oxygen and the diver: Part I |journal=Br Med J |volume=1(4506) |pages=667–672 |date=[[1947]] |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2053251 |accessdate=2008-04-29 }}</ref><ref name=Donald2>{{cite journal |author=Donald K. W. |title=Oxygen and the diver: Part II |journal=Br Med J |volume=1(4506) |pages=712–717 |date=[[1947]] |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2053400 |accessdate=2008-04-29 }}</ref><ref>{{cite book |title=Oxygen and the diver. |last=Donald |first=K. W. |year=1992 |publisher=Harley Swan |location=UK |isbn=1854211765 |pages=237 }}</ref><ref>{{cite journal |author=Yarbrough, O. D., Welham W., Brinton E.S. and Behnke, A. R. |title=Symptoms of Oxygen Poisoning and Limits of Tolerance at Rest and at Work |journal=US Naval Experimental Diving Unit Technical Report |volume=NEDU-47-01 |date=[[1947]] |url=http://archive.rubicon-foundation.org/3316 |accessdate=2008-04-29 }}</ref> They discovered the effects of underwater immersion and exercise. In the decade following World War II, [[Christian J. Lambertsen|Lambertsen]] et. al. made further discoveries on the effects of oxygen at pressure as well as methods of prevention.<ref name=Penn>{{cite journal |author=Lambertsen, C. J., J. M. Clark, R. Gelfand |title=The Oxygen Research Program, University of Pennsylvania: Physiologic Interactions of Oxygen and Carbon Dioxide Effects and Relations to Hyperoxic Toxicity, Therapy, and Decompression. Summation: 1940 to 1999 |journal=Environmental Biomedical Stress Data Center, Institute for Environmental Medicine, University of Pennsylvania Medical Center |volume=EBSDC-IFEM Report No. 3-1-2000 |date=[[2000]] |location=Philadelphia, PA }}</ref><ref>{{cite journal |author=Vann RD |title=Lambertsen and O2: beginnings of operational physiology |journal=Undersea Hyperb Med |volume=31 |issue=1 |pages=21–31 |year=2004 |pmid=15233157 |url=http://archive.rubicon-foundation.org/3987 |accessdate=2008-04-29 }}</ref> In the years since, research on CNS toxicity has centered around methods of prevention and safe extension of tolerance.<ref>{{cite book |title=Factors Affecting CNS Oxygen Toxicity in Humans |author=Natoli, M. J. and Vann R. D. |year=[[1996]] |volume=Report to the US Office of Naval Research |publisher=Duke University |location=Durham, NC |url=http://archive.rubicon-foundation.org/21 |accessdate=2008-04-29 }}</ref>
=== Clinical relevance of CNS oxygen toxicity ===
As CNS toxicity is caused by breathing oxygen at elevated ambient pressures, patients undergoing hyperbaric oxygen therapy are at risk of suffering hyperoxic seizures.<ref name=Brubakk/><ref name=smerz>{{cite journal |author=Smerz RW |title=Incidence of oxygen toxicity during the treatment of dysbarism |journal=Undersea Hyperb Med |volume=31 |issue=2 |pages=199–202 |year=2004 |pmid=15485081 |url=http://archive.rubicon-foundation.org/4010 |accessdate=2008-04-30}}</ref><ref>{{cite journal |author=Hampson NB, Simonson SG, Kramer CC, and Piantadosi CA |title=Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning |journal=Undersea Hyperb Med |volume=23 |issue=4 |pages=215–9 |year=1996 |month=December |pmid=8989851 |url=http://archive.rubicon-foundation.org/2232 |accessdate=2008-04-29}}</ref> Treatment of seizures during treatment consists of removing the patient from oxygen, thereby dropping the partial pressure of oxygen delivered.<ref name=usn/>
=== Diving relevance of CNS oxygen toxicity ===
[[Image:Cylinder mod.jpg|thumb|The diving cylinder contains oxygen-rich gas (36%) and is marked with maximum operating depth of 28 metres.]]
CNS oxygen toxicity is a deadly but entirely avoidable event while diving. The diver generally experiences no warning signs because the brain primarily monitors carbon dioxide levels. The symptoms are sudden convulsions and unconsciousness,<ref name=Brubakk/><ref name=usn/> during which the victim can lose his/her [[Diving regulator|regulator]] and drown. There is an increased risk of CNS oxygen toxicity on deep dives, long dives or dives where oxygen-rich breathing gases are used. Divers are taught to calculate a [[maximum operating depth]] for oxygen-rich [[Breathing gas|breathing gases]]. Cylinders containing such mixtures must be clearly marked with that depth.
In some [[diver training]] courses for these types of diving, divers are taught to plan and monitor what is called the "oxygen clock" of their dives. This clock is a notional alarm clock, which "ticks" more quickly at increased ppO<sub>2</sub> and is set to activate at the maximum single exposure limits recommended in the [[NOAA]] Diving Manual. The maximum single exposure limits recommended in the [[NOAA]] Diving Manual are 45 minutes at {{convert|1.6|bar|abbr=on}}, 120 minutes at {{convert|1.5|bar|abbr=on}}, 150 minutes at {{convert|1.4|bar|abbr=on}}, 180 minutes at {{convert|1.3|bar|abbr=on}} and 210 minutes at {{convert|1.2|bar|abbr=on}}, but is impossible to predict with any reliability whether or when CNS symptoms will occur.<ref name=Brubakk/><ref name=usn/><ref>{{cite journal |author=Butler FK, Thalmann ED |title=Central nervous system oxygen toxicity in closed circuit scuba divers II |journal=Undersea Biomed Res |volume=13 |issue=2 |pages=193–223 |year=1986 |month=June |pmid=3727183 |url=http://archive.rubicon-foundation.org/3045 |accessdate=2008-04-29}}</ref><ref>{{cite journal |author=Butler FK |title=Closed-circuit oxygen diving in the U.S. Navy |journal=Undersea Hyperb Med |volume=31 |issue=1 |pages=3–20 |year=2004 |pmid=15233156 |url=http://archive.rubicon-foundation.org/3986 |accessdate=2008-04-29}}</ref> Many Nitrox-capable dive computers also calculate this "Oxygen Loading".
The aim is to avoid activating the alarm by reducing the ppO<sub>2</sub> of the breathing gas or the length of time breathing gas of higher ppO<sub>2</sub>. As the ppO<sub>2</sub> depends on the fraction of oxygen in the breathing gas and the depth of the dive, the diver can obtain more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas or by shortening the exposure to oxygen-rich gases.
== Pulmonary oxygen toxicity ==
Experimentally, early symptoms of breathing 100% oxygen are breathing difficulty and [[Sternum|substernal]] pain or discomfort. The lungs show [[inflammation]] and [[pulmonary edema]].<ref name=Brubakk/><ref name=usn/>
=== Background to pulmonary oxygen toxicity===
Pulmonary oxygen toxicity was first described by Lorrain Smith in [[1899]] when he noted CNS toxicity and discovered in experiments in mice and birds that {{convert|0.42|atm|abbr=on}} had no effect but {{convert|0.74|atm|abbr=on}} of oxygen was a pulmonary irritant.<ref name=Smith>{{cite journal |author=Smith JL |title=The pathological effects due to increase of oxygen tension in the air breathed |journal=J. Physiol. (Lond.) |volume=24 |issue=1 |pages=19–35 |year=1899 |month=March |pmid=16992479 |url=http://www.jphysiol.org/cgi/pmidlookup?view=long&pmid=16992479}}</ref> He then went on to show that intermittent exposure permitted the lungs to recover and delayed the onset of toxicity.<ref name=Smith/> [[Christian J. Lambertsen|Lambertsen]] et. al. made further discoveries on the effects of oxygen effects at pressure as well as methods of prediction and prevention.<ref name=Brubakk/><ref name=usn/><ref name=Penn/> Their work on intermittent exposures for extension of oxygen tolerance<ref name=clark>{{cite journal |author=Clark JM |title=Extension of oxygen tolerance by interrupted exposure |journal=Undersea Hyperb Med |volume=31 |issue=2 |pages=195–8 |year=2004 |pmid=15485080 |url=http://archive.rubicon-foundation.org/4009 |accessdate=2008-04-29}}</ref> and model for prediction of pulmonary oxygen toxicity based on pulmonary function<ref>{{cite book |title=Pulmonary Oxygen Tolerance in Man and Derivation of Pulmonary Oxygen Tolerance Curves |author=Clark, J. M. and Lambertsen, C. J. |year=[[1970]] |journal=Environmental Biomedical Stress Data Center, Institute for Environmental Medicine, University of Pennsylvania Medical Center |volume=IFEM Report No. 1-70 |location=Philadelphia, PA |url=http://archive.rubicon-foundation.org/3863 |accessdate=2008-04-29 }}</ref> are key documents in the development of operational oxygen procedures. In [[1988]], Hamilton et. al. wrote procedures for [[NOAA]] to establish oxygen exposure limits for [[Underwater habitat|habitat]] operations.<ref name=Brubakk/><ref name=repex1>{{cite book |title=Repex habitat diving procedures: Repetitive vertical excursions, oxygen limits, and surfacing techniques. |author=Hamilton R. W., Kenyon D. J., Peterson R. E., Butler G. J., Beers D. M. |year=[[1988]] |journal=NOAA Office of Undersea Research |volume=Technical Report 88-1A |location=Rockville, MD |url=http://archive.rubicon-foundation.org/4865 |accessdate=2008-04-29 }}</ref><ref name=repex2>{{cite book |title=Repex habitat diving procedures: Repetitive vertical excursions, oxygen limits, and surfacing techniques. |author=Hamilton R. W., Kenyon D. J., Peterson R. E. |year=[[1988]] |journal=NOAA Office of Undersea Research |volume=Technical Report 88-1B |location=Rockville, MD |url=http://archive.rubicon-foundation.org/4866 |accessdate=2008-04-29 }}</ref><ref name=spums>{{cite journal |author=Hamilton R. W. |title=Tolerating oxygen exposure |journal=South Pacific Underwater Medicine Society journal |volume=27 |issue=1 |date=[[1997]] |issn=0813-1988 |oclc=16986801 |url=http://archive.rubicon-foundation.org/6038 |accessdate=2008-04-29 }}</ref> Models for the prediction of pulmonary oxygen toxicity do not explain the results of all exposures to high partial pressures of oxygen.<ref>{{cite book |title=Performance of Various Models in Predicting Vital Capacity Changes Caused by Breathing High Oxygen Partial Pressures. |author=Shykoff, B |year=[[2007]] |journal=US Naval Experimental Diving Unit Technical Report |volume=NEDU-TR-07-13 |location=Panama City, FL, USA |url=http://archive.rubicon-foundation.org/6867 |accessdate=2008-06-06 }}</ref>
=== Clinical relevance of pulmonary oxygen toxicity ===
The risk of [[bronchopulmonary dysplasia]] ("BPD") in infants,<ref name=Bancalari>{{cite journal |author=Bancalari E, Claure N, Sosenko IR |title=Bronchopulmonary dysplasia: changes in pathogenesis, epidemiology and definition |journal=Semin Neonatol |volume=8 |issue=1 |pages=63–71 |year=2003 |month=February |pmid=12667831 |url=http://linkinghub.elsevier.com/retrieve/pii/S1084275602001926 |accessdate=2008-04-30 |doi=10.1016/S1084-2756(02)00192-6}}</ref><ref name=Tin>{{cite journal |author=Tin W, Gupta S |title=Optimum oxygen therapy in preterm babies |journal=Arch. Dis. Child. Fetal Neonatal Ed. |volume=92 |issue=2 |pages=F143–7 |year=2007 |month=March |pmid=17337663 |doi=10.1136/adc.2005.092726 |url=http://fn.bmj.com/cgi/pmidlookup?view=long&pmid=17337663 |accessdate=2008-04-30}}</ref> or [[adult respiratory distress syndrome]] in adults,<ref name=Thiel>{{cite journal |author=Thiel M, Chouker A, Ohta A, ''et al'' |title=Oxygenation inhibits the physiological tissue-protecting mechanism and thereby exacerbates acute inflammatory lung injury |journal=PLoS Biol. |volume=3 |issue=6 |pages=e174 |year=2005 |month=June |pmid=15857155 |doi=10.1371/journal.pbio.0030174 |url=http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0030174 |accessdate=2008-04-30}}</ref> begins to increase with exposure for over 16 hours to oxygen partial pressures of {{convert|0.5|bar|abbr=on}} or more. At sea-level, {{convert|0.5|bar|abbr=on}} is exceeded by gas mixtures having oxygen fractions greater than 50%. Lung oxygen toxicity damage-rates at sea-level pressure rise non-linearly between the 50% threshold of toxicity, and the rate of damage on 100% oxygen. For this reason, [[intensive care]] patients requiring more than 60% oxygen, and especially patients at fractions near 100% oxygen, are considered to be at especially high risk. If the situation is not corrected, the treatment may begin to cause lung damage which exacerbates the original problem requiring the high-oxygen mixture. Care must be used in distinguishing oxygen mole fraction from oxygen partial pressure. Partial pressures between {{convert|0.2|bar|abbr=on}} (normal at sea level) and {{convert|0.5|bar|abbr=on}} usually are considered non-toxic. BPD is reversible in the early stages during "break" periods on lower oxygen pressures, but it may eventually result in irreversible lung damage, if allowed to progress to severe damage. Usually several days of exposure without "oxygen breaks" are needed to cause severe lung damage.
Oxygen toxicity is a potential complication of [[mechanical ventilation]] with pure oxygen, where it is called the respiratory lung syndrome.
=== Diving relevance of pulmonary oxygen toxicity ===
Pulmonary oxygen toxicity is entirely avoidable event while diving. The time-factor and the naturally intermittent nature of most diving makes this a relatively rare (and even then, reversible) complication for divers. Guidelines have been established that allow divers to calculate when they are at risk of pulmonary toxicity.<ref name=Brubakk/><ref name=usn/><ref name=clark/><ref name=repex1/><ref name=repex2/><ref name=spums/>
In the treatment of [[Decompression Sickness]], divers are exposed to long periods of oxygen breathing under [[Hyperbaric medicine|hyperbaric]] conditions. This exposure coupled with that from the dive that preceded the symptoms can be a significant cumulative oxygen exposure and pulmonary toxicity may occur.<ref name=smerz/>
=== Space relevance of pulmonary oxygen toxicity ===
As noted earlier in this article, the toxicity is from high partial pressure. This is illustrated by oxygen use in spacesuits and other low-pressure applications (historically, for example, the [[Project Gemini|Gemini]] spacecraft and [[Apollo spacecraft]]). High fraction oxygen is non-toxic even at breathing mixture oxygen fractions approaching 100%, because the oxygen partial pressure is not allowed to [[Chronic toxicity|chronically]] exceed {{convert|0.35|bar|abbr=on}} in these applications.
== Retinopathic oxygen toxicity ==
Prolonged exposure to high inspired fractions of oxygen causes damage to the [[retina]]. Oxygen may be a contributing factor for the disorder called [[retinopathy of prematurity|retrolental fibroplasia]].<ref name=Nichols>{{cite journal |author=Nichols CW, Lambertsen C |title=Effects of high oxygen pressures on the eye |journal=N. Engl. J. Med. |volume=281 |issue=1 |pages=25–30 |year=1969 |month=July |pmid=4891642 }}</ref> Hyperoxic [[myopia]] has occurred in closed circuit oxygen rebreather divers with prolonged exposures.<ref name=Butler>{{cite journal |author=Butler FK, White E, Twa M |title=Hyperoxic myopia in a closed-circuit mixed-gas scuba diver |journal=Undersea Hyperb Med |volume=26 |issue=1 |pages=41–5 |year=1999 |pmid=10353183 |url=http://archive.rubicon-foundation.org/2312 |accessdate=2008-04-29}}</ref>
== Hyperventilation ==
Oxygen toxicity is not a major factor in [[hyperventilating]], as some people believe. The problems caused by hyperventilating are due to decreased [[carbon dioxide]] within the blood. With or without hyperventilating, it is impossible to develop oxygen toxicity breathing [[air]] at typical surface [[atmospheric pressure]].
== References ==
{{Reflist|2}}
== Further reading ==
* Scubadoc's Diving Medicine Online[http://www.scuba-doc.com/oxygentox.html]
* The Diving Emergency Handbook, John Lippmann and Stan Bugg, ISBN 0-946020-18-3
== External links ==
* [http://www.uhms.org Undersea and Hyperbaric Medical Society] Scientific body, publications about Oxygen Toxicity
* [http://archive.rubicon-foundation.org Rubicon Research Repository] Online collection of the UHMS published journal articles, free content
* {{GeorgiaPhysiology|4/4ch7/s4ch7_7}}
{{Respiratory physiology}}
[[Category:Pulmonology]]
[[Category:Diving medicine]]
[[Category:Intensive care medicine]]
[[Category:Oxygen]]
[[Category:Element toxicology]]
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