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Oxygen toxicity
Oxygen toxicity
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Oxygen toxicity or oxygen toxicity syndrome (also known as the "Paul Bert effect" or the "Lorrain Smith effect") describes harmful effects caused by breathing oxygen at elevated partial pressures.^[1]^[2]^[3] The condition of an excess of oxygen in body tissues is known as hyperoxia. Such above-normal concentrations of oxygen within the body can cause cell damage and death.^[1] Oxidative damage is most often reported in the central nervous system (CNS), lungs (pulmonary) and eye (retinopathic conditions).^[1]^[4]^[5]^[6]^[7] It may also be implicated in red blood cell destruction (erythrocyte hemolysis), liver (hepatic) effects, heart (myocardial) damage, endocrine effects (adrenal, gonads, and thyroid), kidney (renal) damage, and general damage to cells.^[1]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]

The damage is caused by long exposure (days) to lower concentrations of oxygen or by shorter exposure (minutes or hours) to high concentrations. Short exposures to partial pressure of oxygen above 1.6 bar (160 kPa) are usually associated with CNS oxygen toxicity and are most likely to occur among patients undergoing hyperbaric oxygen therapy and divers.^[17]^[18]^[19] Long exposures to partial pressures of oxygen above 0.5 bar (50 kPa) can result in pulmonary oxygen toxicity and are a concern for patients breathing pure oxygen for extended periods.^[20]^[21]^[22]

The serious effect of CNS oxygen toxicity is a seizure, consisting of a brief period of rigidity followed by convulsions and unconsciousness, which is of concern to divers who breathe gases at much greater than atmospheric pressure. Pulmonary oxygen toxicity results in damage to the lungs causing pain and difficulty in breathing, while oxidative damage to the eye may lead to myopia or partial detachment of the retina. These occur when supplemental oxygen is administered as part of a treatment, particularly to newborn infants.

Prevention of oxygen toxicity is an important precaution whenever oxygen is breathed at greater than normal partial pressures and has led to use of protocols for avoidance of hyperoxia in such fields as diving, hyperbaric therapy, neonatal care and human spaceflight. This has lead to oxygen toxicity seizures becoming increasingly rare, with pulmonary and ocular damage being mainly confined to the problems of managing premature infants.

Classification

In humans, a convenient classification is by organ affected. There are three principal types of oxygen toxicity:^[1]^[3]

Central nervous system (CNS), characterised by convulsions followed by unconsciousness, occurring under hyperbaric conditions

Pulmonary, characterised by difficulty in breathing and pain within the chest, occurring when breathing elevated pressures of oxygen for extended periods

Ocular, characterised by alterations to the eye, occurring when breathing elevated pressures of oxygen for extended periods

Oxidative damage may occur in any cell in the body but the effects on the most susceptible organs will be the primary concern. In unusual circumstances, effects on other tissues may be observed: it is suspected that during spaceflight, high oxygen concentrations may contribute to bone damage. Hyperoxia can also indirectly cause carbon dioxide narcosis in patients with chronic obstructive pulmonary disease (COPD).^[23] Oxygen toxicity is not associated with hyperventilation, because it never results from breathing air at atmospheric pressure.

Signs and symptoms

CNS oxygen toxicity manifests as symptoms such as visual changes, ringing in the ears, nausea, twitching (especially on the face), irritability (personality changes, anxiety, confusion, etc.), and dizziness. This may be followed by a tonic-clonic seizure where intense muscle contraction occurs for several seconds followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking, which is followed by a period of unconsciousness (the postictal state).^[1]^[2] The onset depends upon partial pressure of oxygen (ppO₂) in the breathing gas and exposure duration but experiments have shown that there is a wide variation in exposure time before onset amongst individuals and in the same individual from day to day.^[1]^[2]^[4] In addition, many external factors, such as underwater immersion, exposure to cold, and exercise will decrease the time to onset of CNS symptoms.^[17]^[18] Decrease of tolerance has been shown to be closely linked to retention of carbon dioxide.^[24]^[25]^[26] Other factors, such as darkness and caffeine increase tolerance in test animals, but these effects have not been proven in humans.^[27]^[28]

Early symptoms of pulmonary oxygen toxicity are breathing difficulty and pain or discomfort within the chest (substernal pain). The lungs show inflammation and swelling (pulmonary edema).^[1]^[2]. Tests in animals have indicated a similar variation in tolerance as found in CNS toxicity as well as significant variations between species. When the exposure to oxygen above 0.5 bar (50 kPa) is intermittent, it permits the lungs to recover and delays the onset of toxicity.^[29]

Causes

CNS 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 following short exposures to the high pressure oxygen.^[1]^[19]^[30] For the same reason, divers breathing air at depths greater than 60 metres (200 ft) face a risk of an oxygen toxicity "hit" (seizure) as do divers breathing a gas mixture enriched with oxygen (Enriched Air Nitrox).^[24]

Pulmonary toxicity

The lungs have a very large area in contact with the breathing gas and contain thin membranes with limited antioxidant defenses, making them particularly susceptible to damage by oxygen. Pulmonary toxicity occurs with prolonged exposure to elevated concentrations of oxygen. Pulmonary manifestations of oxygen toxicity are not the same for normobaric conditions as they are for hyperbaric conditions.^[31]

The risk of bronchopulmonary dysplasia ("BPD") in infants, or adult respiratory distress syndrome (ARDS) in adults, begins to increase with exposure for over 16 hours to oxygen partial pressures of 0.5 bar (50 kPa) or more.^[20]^[21]^[22] At sea-level, 0.5 bar (50 kPa) is exceeded by gas mixtures having oxygen fractions greater than 50%, while the rate of damage rises non-linearly between the 50% threshold of toxicity and the rate at 100% oxygen. Partial pressures between 0.2 bar (20 kPa) (normal at sea level) and 0.5 bar (50 kPa) are considered non-toxic but intensive care patients breathing more than 60% oxygen, and especially patients at fractions near 100% oxygen, are considered to be at particularly high risk. If the treatment continues for a lengthy period, it may begin to cause lung damage which exacerbates the original problem requiring the high-oxygen mixture. Oxygen toxicity is also a potential complication of mechanical ventilation with pure oxygen, where it is called respiratory lung syndrome.

Breathing 100% oxygen eventually leads to collapse of the alveoli (atelectasis), while — at same partial pressure of oxygen — the presence of significant partial pressures of inert gases will prevent this effect.^[32] In the treatment of decompression sickness, divers are exposed to long periods of oxygen breathing under hyperbaric conditions. This exposure, coupled with that from the dive preceding the symptoms, can be a significant cumulative oxygen exposure and pulmonary toxicity may occur.^[19]

Ocular toxicity

Prolonged exposure to high inspired fractions of oxygen causes damage to the retina.^[5]^[33]^[34]^[35] Damage to the developing eye of infants exposed to high oxygen fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions.^[36]^[6] Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants.^[5]^[36] In preterm infants, the retina is often not fully vascularised. ROP occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of ROP, and may raise the risk of other hypoxia-related systemic complications.^[36]

Hyperoxic myopia has occurred in closed circuit oxygen rebreather divers with prolonged exposures.^[6]^[33]^[37]^[38] This must be due to an increase in the refractive power of the lens, since axial length and keratometry readings do not reveal a corneal or length basis for a myopic shift.^[6]^[39]

Mechanism

A high concentration of oxygen damages cells.^[4] Not all mechanisms of damage caused by reactive oxygen species (ROS) are known, but the process of lipid peroxidation causes damage to cell membranes.^[40] ROS form as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling. However, during times of environmental stress ROS levels can increase dramatically, which can result in significant damage to cell structures. This cumulates into a situation known as oxidative stress.^[4]^[41] One example is that oxygen has a propensity to react with certain metals to form the ROS superoxide, which attacks double bonds in many organic molecules, including the unsaturated fatty acid residues in cells.^[42]^[43] High concentrations of oxygen are also known to increase the formation of free radicals which harm DNA and other structures (see nitric oxide, peroxynitrite, and trioxidane).^[4]^[44] Normally the body has many defense systems against such injury, such as glutathione, catalase, and superoxide dismutase, but at higher concentrations of free oxygen, these systems are eventually overwhelmed, and the rate of damage to cell membranes exceeds the capacity of the systems which control or repair it.^[45]^[46]^[47] Cell damage and cell death then result.

Diagnosis

Diagnosis of CNS oxygen toxicity in divers prior to seizure is difficult as the symptoms of visual disturbance, ear problems, dizziness, confusion and nausea can be due to many factors common to the underwater environment such as narcosis, congestion and coldness. However, these symptoms may be helpful in diagnosing the first stages of oxygen toxicity in patients undergoing hyperbaric oxygen therapy. In either case, a seizure occurring while breathing oxygen at partial pressures of 1.4 bar (140 kPa) or greater will be diagnosed as oxygen toxicity.

Diagnosis of BPD in new-born infants with breathing difficulties is difficult in the first few weeks. However, if the infant's breathing does not improve during this time, blood tests and x-rays may be used to confirm BPD. In addition, an echocardiogram can help to eliminate other possible causes such as congenital heart defects or pulmonary arterial hypertension.^[48]

The diagnosis of ROP in infants is typically suggested by the clinical setting. Prematurity, low birth weight and a history of oxygen exposure are the principal indicators, while no hereditary factors have been shown to yield a pattern.^[49]

Prevention

A seizure caused by CNS oxygen toxicity is a deadly but entirely avoidable event while diving.^[24] The diver may experience no warning symptoms. The effects are sudden convulsions and unconsciousness, during which victims can lose their regulator and drown.^[1]^[2] There is an increased risk of CNS oxygen toxicity on deep dives, long dives and dives where oxygen-rich breathing gases are used.^[24] Divers are taught to calculate a maximum operating depth for oxygen-rich breathing gases.^[24]^[26] Cylinders containing such mixtures must be clearly marked with that depth.^[24]^[26]

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.^[24] This is a notional alarm clock, which "ticks" more quickly at increased ppO₂ and is set to activate at the maximum single exposure limit recommended in the National Oceanic and Atmospheric Administration (NOAA) Diving Manual.^[24]^[26] For the following partial pressures of oxygen the limit is: 45 minutes at 1.6 bar (160 kPa), 120 minutes at 1.5 bar (150 kPa), 150 minutes at 1.4 bar (140 kPa), 180 minutes at 1.3 bar (130 kPa) and 210 minutes at 1.2 bar (120 kPa), but is impossible to predict with any reliability whether or when CNS symptoms will occur.^[1]^[2]^[50]^[51] Many Nitrox-capable dive computers calculate an "oxygen loading" and can track it across multiple dives. The aim is to avoid activating the alarm by reducing the ppO₂ of the breathing gas or the length of time breathing gas of higher ppO₂. As the ppO₂ depends on the fraction of oxygen in the breathing gas and the depth of the dive, the diver obtains more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas or by shortening the duration of exposure to oxygen-rich gases.

BPD is reversible in the early stages by use of "break periods" on lower oxygen pressures, but it may eventually result in irreversible lung injury if allowed to progress to severe damage. Usually several days of exposure without "oxygen breaks" are needed to cause such damage.

Pulmonary oxygen toxicity is an entirely avoidable event while diving. The limited duration and 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.^[1]^[2]^[52]^[53]^[54]^[55]

In low-pressure environments oxygen toxicity may be avoided since the toxicity is caused by high oxygen partial pressure, not merely by high oxygen fraction. This is illustrated by oxygen use in spacesuits (historically, for example, the Gemini and Apollo spacecraft).^[56] In such applications high-fraction oxygen is non-toxic, even at breathing mixture fractions approaching 100%, because the oxygen partial pressure is not allowed to chronically exceed 0.35 bar (35 kPa).

Vitamin E and selenium were proposed and later rejected as a potential method of protection against pulmonary oxygen toxicity.^[57]^[58]^[59] There is however some experimental evidence in rats that vitamin E and selenium aid in preventing in vivo lipid peroxidation and free radical damage, and therefore prevent retinal changes following repetitive hyperbaric oxygen exposures.^[60]

Management

Treatment of seizures during oxygen therapy consists of removing the patient from oxygen, thereby dropping the partial pressure of oxygen delivered.^[2] A seizure underwater requires that the diver is brought to the surface as soon as practicable. The buddy will ensure that the victim's air supply is established and maintained, then carry out a controlled buoyant lift. The buddy will need to ensure their own safety is not compromised during the convulsive phase, but lifting an unconscious body is taught by most diver training agencies. Upon reaching the surface, emergency services should be contacted as there is a possibility of further complications requiring medical attention.

The occurrence of symptoms of BPD or ARDS is treated by lowering the fraction of oxygen administered, along with a reduction in the periods of exposure and an increase in the break periods where normal air is supplied. Where supplemental oxygen is required for treatment of another disease (particularly in infants), a ventilator may be needed to ensure that the lung tissue remains inflated. Reductions in pressure and exposure will be made progressively and medications such as bronchodilators and pulmonary surfactants may be used.^[61]

ROP may regress spontaneously, but should the disease progress beyond a threshold (defined as five contiguous or eight cumulative hours of stage 3 ROP), both cryosurgery and laser surgery have been shown to reduce the risk of blindness as an outcome. Where the disease has progressed further, techniques such as scleral buckling and vitrectomy surgery may assist in re-attaching the retina.^[49]

Prognosis

Although the convulsions caused by CNS oxygen toxicity may lead to incidental injury to the victim, it remained uncertain for many years whether damage to the nervous system following the seizure could occur and several studies searched for evidence of such damage. An overview of these studies by Bitterman in 2004 concluded that following removal of breathing gas containing high fractions of oxygen, no long-term neurological damage from the seizure remains.^[4]^[62]

The majority of infants who have survived following an incidence of BPD will eventually recover near-normal lung function, since lungs continue to grow during the first 5–7 years and the damage caused by BPD is to some extent reversible (even in adults). However, they are likely be more susceptible to respiratory infections for the rest of their lives and the severity of later infections is often greater than that in their peers.^[63]^[64]

ROP in infants frequently regresses without intervention and eyesight may be normal in later years. Where the disease has progressed to the stages requiring surgery, the outcomes are generally good for the treatment of stage 3 ROP, but are much worse for the later stages. Although surgery is usually successful in restoring the anatomy of the eye, damage to the nervous system by the progression of the disease leads to comparatively poorer results in restoring vision. The presence of other complicating diseases also reduces the likelihood of a favourable outcome.^[49]

Epidemiology

The incidence of CNS toxicity among divers has decreased since the Second World War, as protocols have developed to limit exposure and partial pressure of oxygen inspired. In 1947, Donald recommended limiting the depth breathing pure oxygen to 25 ft (7.6 m), or a ppO₂ of 1.8 bar (180 kPa). This limit has been reduced until today a limit of 1.4 bar (140 kPa) during a dive and 1.6 bar (160 kPa) during shallow decompression stops is accepted: oxygen toxicity has become a rare occurrence other than when caused by equipment malfunction and human error. Historically, the U.S. Navy has refined its Navy Diving Manual Tables to reduce oxygen toxicity incidents. Between 1995 and 1999, reports showed 405 surface-supported dives using the helium-oxygen tables; of these, oxygen toxicity symptoms were observed on 6 dives (1.5%). As a result, the U.S. Navy in 2000 modified the schedules and conducted field tests of 150 dives, none of which produced symptoms of oxygen toxicity. Revised tables were published in 2001.^[65]

The variability in tolerance and other variable factors such as workload have resulted in the U.S. Navy abandoning screening for oxygen tolerance. Of the 6,250 oxygen-tolerance tests performed between 1976 and 1997, only 6 episodes of oxygen toxicity were observed (0.1%).^[66]^[67]

The incidence of CNS oxygen toxicity among patients undergoing hyperbaric oxygen therapy is rare and influenced by a number of a factors: individual sensitivity and treatment protocol; and probably therapy indication and equipment used. A study by Welslau in 1996 reported 16 incidents out of a population of 107,264 patients (0.015%), while Hampson and Atik in 2003 found a rate of 0.03%. Yildiz, Ay and Qyrdedi, in a summary of 36,500 patient treatments between 1996 and 2003, reported only 3 oxygen toxicity incidents, giving a rate of 0.008%.^[68]

BPD is among the most common complications of prematurely born infants and its incidence has grown as the survival of extremely premature infants has increased. Nevertheless, the severity has decreased as better management of supplemental oxygen has resulted in the disease now being related mainly to factors other than hyperoxia.^[20]

In 1997 a summary of studies of neonatal intensive care units in industrialised countries showed that up to 60% of low birth weight babies develop ROP, which rises to 72% in extremely low birth weight babies, i.e. less than 1,000 g (2.2 lb) at birth. However, severe outcomes are much less frequent: for very low birth weight babies (defined as less than 1,500 g (3.3 lb) at birth), the incidence of blindness was found to be no more than 8%.^[69]

History

CNS toxicity was first described by Paul Bert in 1878.^[1]^[70]^[71] He showed that oxygen was toxic to insects, arachnids, myriapods, molluscs, earthworms, fungi, germinating seeds, birds, and other animals. 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 0.42 atm (43 kPa) had no effect but 0.74 atm (75 kPa) of oxygen was a pulmonary irritant.^[29] The first recorded human exposure was undertaken in 1910 by Bornstein when two men breathed oxygen at 2.8 atm (280 kPa) for 30 minutes while he went on to 48 minutes with no symptoms.^[72] In 1912, Bornstein developed cramps in his hands and legs while breathing oxygen at 2.8 atm (280 kPa) for 51 minutes.^[73] Smith then went on to show that intermittent exposure to a breathing gas with less oxygen permitted the lungs to recover and delayed the onset of pulmonary toxicity.^[29]

Behnke et al. in 1935 were the first to observe visual field contraction (tunnel vision) on dives between 1.0 atm (100 kPa) and 4.0 atm (410 kPa).^[74]^[75] During World War II, Donald and Yarbrough et al. performed over 2,000 experiments on oxygen toxicity to support the initial use of closed circuit oxygen rebreathers.^[17]^[18]^[76]^[33] Naval divers in the early years of oxygen rebreather diving developed a mythology about a monster called "Oxygen Pete", who lurked in the bottom of the Admiralty Experimental Diving Unit "wet pot" (a water-filled hyperbaric chamber) to catch unwary divers. They called having an oxygen toxicity attack "getting a Pete".^[77]^[78]

In the decade following World War II, Lambertsen et al. made further discoveries on the effects of oxygen at pressure as well as methods of prevention.^[79]^[80] Their work on intermittent exposures for extension of oxygen tolerance and on a model for prediction of pulmonary oxygen toxicity based on pulmonary function are key documents in the development of operational oxygen procedures.^[52]^[81] Lambertsen's work showing the effect of carbon dioxide in decreasing time to onset of CNS symptoms has influenced work from current exposure guidelines to future breathing apparatus design.^[24]^[25]^[26]

ROP was not observed prior to World War II, but with the availability of supplemental oxygen in the decade following, it rapidly became one of the principal causes of infant blindness in developed countries. By 1960 the use of oxygen had become identified as a risk factor and its administration restricted. The resulting fall in ROP was accompanied by a rise in infant mortality and hypoxia-related complications. Since then, more sophisticated monitoring and diagnosis has established protocols for oxygen use which aim to balance between hypoxic conditions and problems of ROP.^[69]

Bitterman et al. in 1986 and 1995 showed that darkness and caffeine will delay the onset of changes to brain electrical activity in rats.^[27]^[28] In the years since, research on CNS toxicity has centered around methods of prevention and safe extension of tolerance.^[82] These include topics such as circadian rhythm, drugs, age, and gender that have been shown to contribute to CNS oxygen toxicity sensitivity.^[83]^[84]^[85]^[86] In 1988, Hamilton et al. wrote procedures for NOAA to establish oxygen exposure limits for habitat operations.^[1]^[53]^[54]^[55] Even today, models for the prediction of pulmonary oxygen toxicity do not explain all the results of exposure to high partial pressures of oxygen.^[87]

References

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^ Wittner, M. (1966). "Pathophysiology of pulmonary oxygen toxicity". Proceedings of the Third International Conference on Hyperbaric Medicine. NAS/NRC, 1404, Washington DC. pp. 179–188. {{cite conference}}: Unknown parameter |booktitle= ignored (|book-title= suggested) (help); Unknown parameter |coauthors= ignored (|author= suggested) (help) - and others as discussed by Clark, John M. and Lambertsen, Christian J. (1970) Pulmonary oxygen tolerance in man and derivation of pulmonary oxygen tolerance curves pages 256-260.
^ ^a ^b ^c Yarbrough, O.D.; Welham, W.; Brinton, E.S.; Behnke, Alfred R. (1947). "Symptoms of Oxygen Poisoning and Limits of Tolerance at Rest and at Work". U.S. Naval experimental diving unit technical report. NEDU-47-01. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Anderson, B.; Farmer, Joseph C. (1978). "Hyperoxic myopia". Trans Am Ophthalmol Soc. 76: 116–24. PMC 1311617. PMID 754368.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Ricci, B.; Lepore, D.; Iossa, M.; Santo, A.; D'Urso, M.; Maggiano, N. (1990). "Effect of light on oxygen-induced retinopathy in the rat model. Light and OIR in the rat". Documenta ophthalmologica. 74 (4): 287–301. PMID 1701697.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b ^c Drack, A.V. (1998). "Preventing blindness in premature infants". New England Journal of Medicine. 338 (22): 1620–1. PMID 9603802. Retrieved 2008-09-19. {{cite journal}}: Unknown parameter |month= ignored (help)
^ Shykoff, Barbara E. (2005). "Repeated Six-Hour Dives 1.35 ATM Oxygen Partial Pressure". US Naval Experimental Diving Unit Technical Report. NEDU-TR-05-20. Panama City, FL, USA. Retrieved 2008-09-19.
^ Shykoff, Barbara E. (2008). "Pulmonary effects of submerged oxygen breathing in resting divers: repeated exposures to 140 kPa". Undersea and Hyperbaric Medicine. 35 (2): 131–43. PMID 18500077. {{cite journal}}: |access-date= requires |url= (help)
^ Anderson, B.; Shelton, D.L. (1987). "Axial length in hyperoxic myopia". In: Bove, Alfred A.; Bachrach, Arthur J.; Greenbaum, Leon (eds.) Underwater and hyperbaric physiology IX. Ninth international symposium of the Undersea and Hyperbaric Medical Society: 607–611.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Bowen, R. "Free Radicals and Reactive Oxygen". Colorado State University. Retrieved 2008-09-26.
^ Piantadosi, Claude A. (2008). "Carbon monoxide, reactive oxygen signaling, and oxidative stress". Free radical biology and medicine. 45 (5): 562–9. doi:10.1016/j.freeradbiomed.2008.05.013. PMID 18549826. Retrieved 2008-09-26. {{cite journal}}: Unknown parameter |month= ignored (help)
^ Thom, Steven R. (1992). "Inert gas enhancement of superoxide radical production". Archives of biochemistry and biophysics. 295 (2): 391–6. PMID 1316738. {{cite journal}}: Unknown parameter |month= ignored (help)
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^ Oury, T.D.; Ho, Y.S.; Piantadosi, Claude A.; Crapo, J.D.; (1992). "Extracellular superoxide dismutase, nitric oxide, and central nervous system O2 toxicity". Proceedings of the National Academy of Sciences of the United States of America. 89 (20): 9715–9. PMC 50203. PMID 1329105. Retrieved 2008-09-26. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
^ Thom, Steven R.; Marquis, R.E. (1987). "Free radical reactions and the inhibitory and lethal actions of high-pressure gases". Undersea Biomedical Research. 14 (6): 485–501. PMID 2825395. Retrieved 2008-09-26. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Djurhuus, R.; Svardal, A.M.; Thorsen, E. (1999). "Glutathione in the cellular defense of human lung cells exposed to hyperoxia and high pressure". Undersea and Hyperbaric Medicine. 26 (2): 75–85. PMID 10372426. Retrieved 2008-09-26.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Freiberger, John J.; Coulombe, Kathy; Suliman, Hagir; Carraway, Martha-sue; Piantadosi, Claude A. (2004). "Superoxide dismutase responds to hyperoxia in rat hippocampus". Undersea and Hyperbaric Medicine. 31 (2): 227–32. PMID 15485085. Retrieved 2008-09-26.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ "How is bronchopulmonary dysplasia diagnosed?". U.S. Department of Health & Human Services. Retrieved 2008-09-28.
^ ^a ^b ^c Regillo, Carl D. (1998). Vitreoretinal Disease: The Essentials. New York: Thieme, 693 pages. ISBN 0865777616. OCLC 39170393. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Butler, Frank K.; Thalmann, Edward D. (1986). "Central nervous system oxygen toxicity in closed circuit scuba divers II". Undersea Biomedical Research. 13 (2): 193–223. PMID 3727183. Retrieved 2008-04-29. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Butler, Frank K. (2004). "Closed-circuit oxygen diving in the U.S. Navy". Undersea and Hyperbaric Medicine. 31 (1): 3–20. PMID 15233156. Retrieved 2008-04-29.
^ ^a ^b Clark, John M. (2004). "Extension of oxygen tolerance by interrupted exposure". Undersea and Hyperbaric Medicine. 31 (2): 195–8. PMID 15485080. Retrieved 2008-04-29.
^ ^a ^b Hamilton R W., Kenyon David J., Peterson R. E., Butler G. J., Beers D. M. (1988). "Repex habitat diving procedures: Repetitive vertical excursions, oxygen limits, and surfacing techniques". NOAA Office of Undersea Research. Technical Report 88-1A. Rockville, MD. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Hamilton, Robert W.; Kenyon, David J.; Peterson, R.E. (1988). "Repex habitat diving procedures: Repetitive vertical excursions, oxygen limits, and surfacing techniques". NOAA Office of Undersea Research. Technical Report 88-1B. Rockville, MD. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Hamilton, Robert W. (1997). "Tolerating oxygen exposure". South Pacific Underwater Medicine Society journal. 27 (1). ISSN 0813-1988. OCLC 16986801. Retrieved 2008-04-29.
^ Webb, James T.; Olson, R.M.; Krutz, R.W.; Dixon, G.; Barnicott, P.T. (1989). "Human tolerance to 100% oxygen at 9.5 psia during five daily simulated 8-hour EVA exposures". Aviation Space and Environmental Medicine. 60 (5): 415–21. PMID 2730484. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Schatte, C.L. (1977). "Dietary selenium and vitamin E as a possible prophylactic to pulmonary oxygen poisoning". Proceedings of the Sixth International Congress on Hyperbaric Medicine, University of Aberdeen, Aberdeen, Scotland: 84–91. ISBN 0-08-024918-3.
^ Boadi, W.Y.; Thaire, L.; Kerem, D.; Yannai, S. (1991). "Effects of dietary supplementation with vitamin E, riboflavin and selenium on central nervous system oxygen toxicity". Pharmacology & toxicology. 68 (2): 77–82. ISSN 0901-9928. PMID 1852722. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Piantadosi, Claude A. In: The Mysterious Malady: Toward an understanding of decompression injuries (DVD). Global Underwater Explorers. Retrieved 2008-09-19. {{cite AV media}}: Unknown parameter |year2= ignored (help)
^ Stone, W.L.; Henderson, R.A.; Howard, G.H.; Hollis, A.L.; Payne, P.H.; Scott, R.L. (1989). "The role of antioxidant nutrients in preventing hyperbaric oxygen damage to the retina". Free radical biology & medicine. 6 (5): 505–12. PMID 2744583.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ "NIH MedlinePlus: Bronchopulmonary dysplasia". U.S. National Library of Medicine. Retrieved 2008-10-02.
^ Lambertsen, Christian J. (1965). "Effects of oxygen at high partial pressure". In: Fenn, W.O.; Rahn, H. (eds.) Handbook of Physiology: Respiration. Sec.3 Vol.2. American Physiological Society: 1027–46.
^ "National Institutes of Health: What is bronchopulmonary dysplasia?". U.S. Department of Health & Human Services. Retrieved 2008-10-02.
^ Spear, Michael L. - reviewer, (June 2008). "Bronchopulmonary dysplasia (BPD)". Nemours Foundation. Retrieved 2008-10-03.{{cite web}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
^ Gerth, Wayne A. (2006). "Decompression sickness and oxygen toxicity in U.S. Navy surface-supplied He-O2 diving". Proceedings of Advanced Scientific Diving Workshop. Smithsonian Institution. ISBN 20060725. Retrieved 2008-10-02. {{cite journal}}: Check |isbn= value: length (help); Unknown parameter |month= ignored (help)
^ Walters, K.C.; Gould, M.T.; Bachrach, E.A.; Butler, Frank K. (2000). "Screening for oxygen sensitivity in U.S. Navy combat swimmers". Undersea and Hyperbaric Medicine. 27 (1): 21–6. PMID 10813436. Retrieved 2008-10-02.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Butler, Frank K.; Knafelc, M.E. (1986). "Screening for oxygen intolerance in U.S. Navy divers". Undersea Biomedical Research. 13 (1): 91–8. PMID 3705251. Retrieved 2008-10-02. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Yildiz, S,; Ay, H.; Qyrdedi, T. (2004). "Central nervous system oxygen toxicity during routine hyperbaric oxygen therapy". Undersea and Hyperbaric Medicine. 31 (2): 189–90. PMID 15485078. Retrieved 2008-10-03.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Gilbert, Clare (1997). "Retinopathy of prematurity: epidemiology". Journal of Community Eye Health. 10 (22). London: International Centre for Eye Health: 22–24. Retrieved 2008-10-04.
^ Bert, Paul (originally published 1878). "Barometric pressure: Researches in experimental physiology". Translated by: Hitchcock, M.A. and Hitchcock, F.A. College Book Company; 1943. {{cite journal}}: Check date values in: |date= (help)
^ British Sub-aqua Club (1985). Sport diving : the British Sub-Aqua Club diving manual. London: Stanley Paul. p. 110. ISBN 0091638313. OCLC 12807848.
^ Bornstein, A. (1910). "Versuche über die Prophylaxe der Pressluftkrankheit". Pflügers Archiv European Journal of Physiology. 4: 1272–1300.
^ Bornstein, A.; Stroink, M. (1912). "Ueber Sauerstoff vergiftung". Deutsche medizinische Wochenschrift. 38: 1495–1497.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Behnke, Alfred R.; Johnson, F.S.; Poppen, J.R.; Motley, E.P. (1935). "The effect of oxygen on man at pressures from 1 to 4 atmospheres". The American journal of physiology. 110: 565–572. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Behnke, Alfred R.; Forbes, H.S.; Motley, E.P. (1935). "Circulatory and visual effects of oxygen at 3 atmospheres pressure". The American journal of physiology. 114: 436–442. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Donald, Kenneth W. (1992). Oxygen and the diver. UK: Harley Swan. p. 237. ISBN 1854211765.
^ Taylor, Larry "Harris" (1993). "Oxygen Enriched Air: A New Breathing Mix?". IANTD Journal. Retrieved 2008-09-05.
^ Davis, Robert H. (1955). Deep Diving and Submarine Operations (6th ed.). Tolworth, Surbiton, Surrey: Siebe Gorman & Company Ltd, 693 pages. p. 291.
^ Lambertsen, Christian J.; Clark, John M.; Gelfand, R. (2000). "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". Environmental Biomedical Stress Data Center, Institute for Environmental Medicine, University of Pennsylvania Medical Center. EBSDC-IFEM Report No. 3-1-2000. Philadelphia, PA.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Vann, Richard D. (2004). "Lambertsen and O2: Beginnings of operational physiology". Undersea and Hyperbaric Medicine. 31 (1): 21–31. PMID 15233157. Retrieved 2008-04-29.
^ Clark, John M.; Lambertsen, Christian J. (1970). Pulmonary oxygen tolerance in man and derivation of pulmonary oxygen tolerance curves. Vol. IFEM Report No. 1-70. Philadelphia, PA. Retrieved 2008-04-29. {{cite book}}: |journal= ignored (help)CS1 maint: location missing publisher (link) CS1 maint: multiple names: authors list (link)
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^ Shykoff, Barbara E. (2007). "Performance of various models in predicting vital capacity changes caused by breathing high oxygen partial pressures". U.S. Naval Experimental Diving Unit Technical Report. NEDU-TR-07-13. Panama City, FL: Navy Experimental Diving Unit. Retrieved 2008-06-06.

Bibliography

Brubakk, Alf O. (2003). Bennett and Elliott's physiology and medicine of diving, 5th Rev ed. Edinburgh; New York: Saunders, 800 pages. ISBN 0702025712. OCLC 51607923. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
Donald, Kenneth W. (1992). Oxygen and the diver. UK: Harley Swan, 237 pages. ISBN 1854211765. OCLC 26894235.
Lippmann, John; Bugg, Stan (1993). The Diving Emergency Handbook. Teddington, UK: Underwater World Publications. ISBN 0-946020-18-3. OCLC 52056845.{{cite book}}: CS1 maint: multiple names: authors list (link)
Regillo, Carl D. (1998). Vitreoretinal Disease: The Essentials. New York: Thieme, 693 pages. ISBN 0865777616. OCLC 39170393. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

External links

Scubadoc's Diving Medicine Online
Baker, EC. "Oxygen toxicity calculations" (pdf). decompression.org. Retrieved 2008-09-18. {{cite journal}}: Cite journal requires |journal= (help)
Rubicon Research Repository - Online collection of the oxygen toxicity research
Toxing diver rescue on YouTube - one method of diver rescue from oxygen toxicity
2008 Divers Alert Network Technical Diving Conference - Free download of "Oxygen Toxicity" lecture by Dr. Richard Vann
Template:GeorgiaPhysiology

[Brubakk-1] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ Brubakk, Alf O. (2003). Bennett and Elliott's physiology and medicine of diving, 5th Rev ed. Edinburgh; New York: Saunders, 800 pages. ISBN 0702025712. OCLC 51607923. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

[usn-2] ^ ^a ^b ^c ^d ^e ^f ^g ^h US Navy Diving Manual, 6th revision. United States: US Naval Sea Systems Command. 2006. Retrieved 2008-04-24.

[Acott-3] Acott, C. (1999). "Oxygen toxicity: A brief history of oxygen in diving". South Pacific Underwater Medicine Society journal. 29 (3). ISSN 0813-1988. OCLC 16986801. Retrieved 2008-04-29.

[Bitterman-4] ^ ^a ^b ^c ^d ^e ^f Bitterman, N. (2004). "CNS oxygen toxicity". Undersea and Hyperbaric Medicine. 31 (1): 63–72. PMID 15233161. Retrieved 2008-04-29.

[Nichols-5] Nichols, C.W.; Lambertsen Christian (1969). "Effects of high oxygen pressures on the eye". New England Journal of Medicine. 281 (1): 25–30. PMID 4891642. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[Butler-6] Butler, Frank K.; White, E.; Twa, M. (1999). "Hyperoxic myopia in a closed-circuit mixed-gas scuba diver". Undersea and Hyperbaric Medicine. 26 (1): 41–5. PMID 10353183. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid14232720-7] Beehler, C.C. (1964). "Oxygen and the eye". Survey of ophthalmology. 45: 549–60. PMID 14232720. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)

[pmid4613232-8] Clark, J.M. (1974). "The toxicity of oxygen". The American review of respiratory disease. 110 (6 Pt 2): 40–50. PMID 4613232. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)

[pmid5782651-9] Goldstein, J.R.; Mengel, C.E. (1969). "Hemolysis in mice exposed to varying levels of hyperoxia". Aerospace medicine. 40 (1): 12–3. PMID 5782651. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid4403030-10] Larkin, E.C.; Adams. J.D.; Williams, W.T.; Duncan, D.M. (1972). "Hematologic responses to hypobaric hyperoxia". The American journal of physiology. 223 (2): 431–7. PMID 4403030. Retrieved 2008-09-28. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid5885427-11] Schaffner, Fenton; Felig, Philip (1965). "Changes in hepatic structure in rats produced by breathing pure oxygen". The Journal of cell biology. 27 (3): 505–17. PMC 2106769. PMID 5885427. Retrieved 2008-09-28. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid5046798-12] Caulfield, J.B.; Shelton, R.W.; Burke, J.F. (1972). "Cytotoxic effects of oxygen on striated muscle". Archives of pathology. 94 (2): 127–32. PMID 5046798. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid13228600-13] Bean, J.W.; Johnson, P.C. (1954). "Adrenocortical response to single and repeated exposure to oxygen at high pressure". The American journal of physiology. 179 (3): 410–4. PMID 13228600. Retrieved 2008-09-28. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid13889254-14] Edstrom, J.E.; Rockert, H. (1962). "The effect of oxygen at high pressure on the histology of the central nervous system and sympathetic and endocrine cells". Acta physiologica Scandinavica. 55: 255–63. PMID 13889254. {{cite journal}}: |access-date= requires |url= (help)CS1 maint: multiple names: authors list (link)

[Gersh-15] Gersh, I.; Wagner, C.E. (1945). "Metabolic factors in oxygen posoning". The American journal of physiology. 144: 270–277. Retrieved 2008-10-08.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid5155150-16] Hess, R.T.; Menzel, D.B. (1971). "Effect of dietary antioxidant level and oxygen exposure on the fine structure of the proximal convoluted tubules". Aerospace medicine. 42 (6): 646–9. PMID 5155150. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[Donald1-17] Donald, Kenneth W. (1947). "Oxygen and the diver: Part I". British medical journal. 1(4506): 667–672. PMC 2053251. {{cite journal}}: |access-date= requires |url= (help)

[Donald2-18] Donald, Kenneth W. (1947). "Oxygen and the diver: Part II". British medical journal. 1(4506): 712–717. PMC 2053400. {{cite journal}}: |access-date= requires |url= (help)

[smerz-19] Smerz, R.W. (2004). "Incidence of oxygen toxicity during the treatment of dysbarism". Undersea and Hyperbaric Medicine. 31 (2): 199–202. PMID 15485081. Retrieved 2008-04-30.

[Bancalari-20] Bancalari, Eduardo; Claure, Nelson; Sosenko, Ilene R.S. (2003). "Bronchopulmonary dysplasia: changes in pathogenesis, epidemiology and definition". Seminars in Neonatology. 8 (1). London: Elsevier Science: 63–71. doi:10.1016/S1084-2756(02)00192-6. ISSN 1084-2756. PMID 12667831. Retrieved 2008-04-30. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[Tin-21] Tin, W.; Gupta, S. (2007). "Optimum oxygen therapy in preterm babies". Archives of disease in childhood. Fetal and neonatal edition. 92 (2): F143–7. doi:10.1136/adc.2005.092726. PMID 17337663. Retrieved 2008-04-30. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[Thiel-22] Thiel, Manfred; Chouker, Alexander; Ohta, Akio; et al. (2005). "Oxygenation inhibits the physiological tissue-protecting mechanism and thereby exacerbates acute inflammatory lung injury". PLoS biology. 3 (6): e174. doi:10.1371/journal.pbio.0030174. PMID 15857155. Retrieved 2008-04-30. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)

[Patel-23] Patel, Dharmeshkumar N; Goel, Ashish; Agarwal, S.B.; Garg, Praveenkumar; Lakhani, Krishna K. (July 2003). "Oxygen toxicity" (PDF). Journal, Indian Academy of Clinical Medicine. 4 (3): 234–7. Retrieved 2008-09-28.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[dan-24] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ Lang, Michael A. (ed.) (2001). DAN nitrox workshop proceedings. Durham, NC: Divers Alert Network. p. 197. Retrieved 2008-09-20. {{cite book}}: |author= has generic name (help)

[rebreather2.0-25] Richardson, Drew; Menduno, Michael; Shreeves, Karl (eds) (1996). "Proceedings of rebreather forum 2.0". Diving Science and Technology Workshop.: 286. Retrieved 2008-09-20. {{cite journal}}: |author= has generic name (help)CS1 maint: multiple names: authors list (link)

[padi-26] Richardson, D.; Shreeves, K. (1996). "The PADI enriched air diver course and DSAT oxygen exposure limits". South Pacific Underwater Medicine Society journal. 26 (3). ISSN 0813-1988. OCLC 16986801. Retrieved 2008-05-02.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid3705247-27] Bitterman, N.; Melamed, Y.; Perlman, I.; (1986). "CNS oxygen toxicity in the rat: role of ambient illumination". Undersea Biomedical Research. 13 (1): 19–25. PMID 3705247. Retrieved 2008-09-20. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)

[pmid8574677-28] Bitterman, N.; Schaal, S.; (1995). "Caffeine attenuates CNS oxygen toxicity in rats". Brain Research. 696 (1–2): 250–3. PMID 8574677. Retrieved 2008-09-20. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)

[Smith-29] Smith, J.Lorrain (1899). "The pathological effects due to increase of oxygen tension in the air breathed". Journal of Physiology. 24 (1). London: The Physiological Society and Blackwell Publishing: 19–35. PMID 16992479. {{cite journal}}: Unknown parameter |month= ignored (help)

[30] Hampson, Neal B.; Simonson, Steven G.; Kramer, C.C.; Piantadosi, Claude A. (1996). "Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning". Undersea and Hyperbaric Medicine. 23 (4): 215–9. PMID 8989851. Retrieved 2008-04-29. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[pmid17416738-31] Demchenko, Ivan T.; Welty-Wolf, Karen E.; Allen, Barry W.; Piantadosi, Claude A. (2007). "Similar but not the same: normobaric and hyperbaric pulmonary oxygen toxicity, the role of nitric oxide". The American journal of physiology Lung Cell Mol. Physiol. 293 (1): L229–38. doi:10.1152/ajplung.00450.2006. PMID 17416738. Retrieved 2008-09-18. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[32] Wittner, M. (1966). "Pathophysiology of pulmonary oxygen toxicity". Proceedings of the Third International Conference on Hyperbaric Medicine. NAS/NRC, 1404, Washington DC. pp. 179–188. {{cite conference}}: Unknown parameter |booktitle= ignored (|book-title= suggested) (help); Unknown parameter |coauthors= ignored (|author= suggested) (help) - and others as discussed by Clark, John M. and Lambertsen, Christian J. (1970) Pulmonary oxygen tolerance in man and derivation of pulmonary oxygen tolerance curves pages 256-260.

[NEDU47-33] Yarbrough, O.D.; Welham, W.; Brinton, E.S.; Behnke, Alfred R. (1947). "Symptoms of Oxygen Poisoning and Limits of Tolerance at Rest and at Work". U.S. Naval experimental diving unit technical report. NEDU-47-01. Retrieved 2008-04-29.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid754368-34] Anderson, B.; Farmer, Joseph C. (1978). "Hyperoxic myopia". Trans Am Ophthalmol Soc. 76: 116–24. PMC 1311617. PMID 754368.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid1701697-35] Ricci, B.; Lepore, D.; Iossa, M.; Santo, A.; D'Urso, M.; Maggiano, N. (1990). "Effect of light on oxygen-induced retinopathy in the rat model. Light and OIR in the rat". Documenta ophthalmologica. 74 (4): 287–301. PMID 1701697.{{cite journal}}: CS1 maint: multiple names: authors list (link)

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v t e Toxicology
Fields	Aquatic toxicology Ecotoxicology Occupational toxicology Entomotoxicology Environmental toxicology Forensic toxicology Medical toxicology In vitro toxicology Toxicogenomics
Concepts	Acceptable daily intake Acute toxicity Bioaccumulation Biomagnification Fixed-dose procedure Lethal dose Poison Toxic capacity Toxicity class Toxin Venom
Treatments	Activated carbon Antidote Cathartic Chelation therapy Gastric lavage Hemodialysis Hemoperfusion Whole bowel irrigation
Incidents	1858 Bradford sweets poisoning 2007 pet food recalls Bhopal disaster Minamata disease Niigata Minamata disease Poisoning of Alexander Litvinenko Seveso disaster Consumption of Tide Pods Visakhapatnam gas leak 2022 Aqaba toxic gas leak List of poisonings
Related topics	Biological warfare Carcinogen Food safety Hazard symbol List of extremely hazardous substances Mutagen Occupational safety and health
Category Commons WikiProject

v t e Respiratory physiology
Respiration	breath inhalation exhalation obligate nasal breathing respiratory rate respirometer pulmonary surfactant compliance elastic recoil hysteresivity airway resistance bronchial hyperresponsiveness constriction dilatation mechanical ventilation
Control	pons pneumotaxic center apneustic center medulla dorsal respiratory group ventral respiratory group chemoreceptors central peripheral pulmonary stretch receptors Hering–Breuer reflex
Lung volumes	VC FRC Vt dead space CC PEF calculations respiratory minute volume FEV1/FVC ratio Lung function tests spirometry body plethysmography peak flow meter nitrogen washout
Circulation	pulmonary circulation hypoxic pulmonary vasoconstriction pulmonary shunt
Interactions	ventilation (V) Perfusion (Q) Ventilation/perfusion ratio V/Q scan zones of the lung gas exchange pulmonary gas pressures alveolar gas equation alveolar–arterial gradient hemoglobin oxygen–hemoglobin dissociation curve (Oxygen saturation 2,3-BPG Bohr effect Haldane effect) carbonic anhydrase (chloride shift) oxyhemoglobin respiratory quotient arterial blood gas diffusion capacity (DLCO)
Insufficiency	high altitude death zone oxygen toxicity hypoxia