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PubChem CID: 977
Chemical Names: Oxygen; Molecular oxygen; Oxygen molecule; Dioxygen; 7782-44-7; Pure oxygen More...
Molecular Formula: O2
Molecular Weight: 31.998 g/mol
InChI Key: MYMOFIZGZYHOMD-UHFFFAOYSA-N
Drug Information: Drug Indication Therapeutic Uses Clinical Trials FDA UNII
Safety Summary: Laboratory Chemical Safety Summary (LCSS)
Oxygen is an element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most
abundant element on earth and essential for respiration.
 from MeSH
Oxygen is an element with atomic symbol O, atomic number 8, and atomic weight 16.
 Pharmacology from NCIt
Oxygen is the third most abundant element in the universe after hydrogen and helium and the most abundant element by
mass in the Earth's crust. Diatomic oxygen gas constitutes 20. 9% of the volume of air. All major classes of structural
molecules in living organisms, such as proteins, carbohydrates, and fats, contain oxygen, as do the major inorganic
compounds that comprise animal shells, teeth, and bone. Oxygen in the form of O2 is produced from water by
cyanobacteria, algae and plants during photosynthesis and is used in cellular respiration for all living organisms. Green algae
and cyanobacteria in marine environments provide about 70% of the free oxygen produced on earth and the rest is
produced by terrestrial plants. Oxygen is used in mitochondria to help generate adenosine triphosphate (ATP) during
oxidative phosphorylation. For animals, a constant supply of oxygen is indispensable for cardiac viability and function. To
meet this demand, an adult human, at rest, inhales 1. 8 to 2. 4 grams of oxygen per minute. This amounts to more than 6
billion tonnes of oxygen inhaled by humanity per year. At a resting pulse rate, the heart consumes approximately 8-15 ml
O2/min/100 g tissue. This is significantly more than that consumed by the brain (approximately 3 ml O2/min/100 g tissue)
and can increase to more than 70 ml O2/min/100 g myocardial tissue during vigorous exercise. As a general rule,
mammalian heart muscle cannot produce enough energy under anaerobic conditions to maintain essential cellular
processes; thus, a constant supply of oxygen is indispensable to sustain cardiac function and viability. However, the role of
oxygen and oxygen-associated processes in living systems is complex, and they and can be either beneficial or contribute to
cardiac dysfunction and death (through reactive oxygen species). Reactive oxygen species (ROS) are a family of oxygen-
derived free radicals that are produced in mammalian cells under normal and pathologic conditions. Many ROS, such as the
superoxide anion (O2-)and hydrogen peroxide (H2O2), act within blood vessels, altering mechanisms mediating mechanical
signal transduction and autoregulation of cerebral blood flow. Reactive oxygen species are believed to be involved in cellular
signaling in blood vessels in both normal and pathologic states. The major pathway for the production of ROS is by way of
the one-electron reduction of molecular oxygen to form an oxygen radical, the superoxide anion (O2-). Within the
vasculature there are several enzymatic sources of O2-, including xanthine oxidase, the mitochondrial electron transport
chain, and nitric oxide (NO) synthases. Studies in recent years, however, suggest that the major contributor to O2- levels in
vascular cells is the membrane-bound enzyme NADPH-oxidase. Produced O2- can react with other radicals, such as NO, or
spontaneously dismutate to produce hydrogen peroxide (H2O2). In cells, the latter reaction is an important pathway for
normal O2- breakdown and is usually catalyzed by the enzyme superoxide dismutase (SOD). Once formed, H2O2 can
undergo various reactions, both enzymatic and nonenzymatic. The antioxidant enzymes catalase and glutathione peroxidase
act to limit ROS accumulation within cells by breaking down H2O2 to H2O. Metabolism of H2O2 can also produce other,
more damaging ROS. For example, the endogenous enzyme myeloperoxidase uses H2O2 as a substrate to form the highly
reactive compound hypochlorous acid. Alternatively, H2O2 can undergo Fenton or Haber-Weiss chemistry, reacting with
Fe2+/Fe3+ ions to form toxic hydroxyl radicals (-. OH). (PMID: 17027622, 15765131).
 Metabolite Description from Human Metabolome Database (HMDB)
PUBCHEM  COMPOUND  OXYGEN Modify Date: 2018-10-06; Create Date: 2004-09-16

 Contents
1 2D Structure
2 3D Conformer
3 Names and Identifiers
 4 Chemical and Physical Properties
5 Related Records
6 Chemical Vendors
7 Drug and Medication Information
8 Food Additives and Ingredients
9 Pharmacology and Biochemistry
10 Use and Manufacturing
11 Identification
12 Safety and Hazards
13 Toxicity
14 Literature
15 Patents
16 Biomolecular Interactions and Pathways
17 Biological Test Results
18 Classification
19 Information Sources
1 2D Structure
 Search  Download  Get Image
 Magnify
 from PubChem
2 3D Conformer
 Search  Download  Get Image
 Magnify
 Show Hydrogens  Show Atoms  Animate
 from PubChem
3 Names and Identifiers
3.1 Computed Descriptors
3.1.1 IUPAC Name
molecular oxygen
 from PubChem
3.1.2 InChI
InChI=1S/O2/c1-2
 from PubChem
3.1.3 InChI Key
MYMOFIZGZYHOMD-UHFFFAOYSA-N
 from PubChem
3.1.4 Canonical SMILES
O=O
 from PubChem
3.2 Molecular Formula

O2
 from EU Food Improvement Agents, ILO-ICSC, Wikipedia, PubChem
3.3 Other Identifiers
3.3.1 CAS
7782-44-7
 from CAMEO Chemicals, ChemIDplus, DrugBank, EPA DSStox, European Chemicals Agency (ECHA), Human Met…
3.3.2 EC Number
231-956-9
 from EU Food Improvement Agents
231-956-9
 from European Chemicals Agency (ECHA)
3.3.3 ICSC Number
0138
 from ILO-ICSC
0880
 from ILO-ICSC
3.3.4 RTECS Number
RS2060000
 from The National Institute for Occupational Safety and Health (NIOSH)
3.3.5 UN Number
1072
 from CAMEO Chemicals, DOT Emergency Response Guidebook, ILO-ICSC, NJDOH RTK Hazardous Substance List
1073
 from ILO-ICSC
3.3.6 UNII
S88TT14065
 from FDA/SPL Indexing Data
3.3.7 Wikipedia
Title liquid oxygen
Description one of the physical forms of elemental oxygen
Title dioxygen
 from Wikipedia
3.4 Synonyms
3.4.1 MeSH Entry Terms

1. Dioxygen
2. Oxygen
3. Oxygen 16
4. Oxygen-16
 from MeSH
3.4.2 Depositor-Supplied Synonyms
1. Oxygen 11. Oxygen-16 21. UN1072 31. Com

2. Molecular oxygen 12. Oxygen (liquid) 22. UN1073 32. Oxyg
3. oxygen molecule 13. Oxygen, liquified 23. UNII-S88TT14065 33. Oxyg
4. Dioxygen 14. Oxygenium medicinale 24. EINECS 231-956-9 34. dioxi
5. 7782-44-7 15. oxygene 25. CHEBI:15379 35. dioxy
6. Pure oxygen 16. Oxygene [French] 26. MYMOFIZGZYHOMD-UHFFFAOYSA-N 36. Disau
7. Liquid oxygen 17. Oxigeno [Spanish] 27. S88TT14065 37. oxyg
8. Hyperoxia 18. CCRIS 1228 28. E948 38. Perox
9. Oxygenium 19. HSDB 5054 29. Oxygen, compressed [UN1072] [Nonflammable gas] 39. single
10. Sauerstoff 20. O2 30. OXY 40. triple
 from PubChem
4 Chemical and Physical Properties
4.1 Computed Properties
Property Name Property Value
Molecular Weight 31.998 g/mol
Hydrogen Bond Donor Count 0
Hydrogen Bond Acceptor Count 2
Rotatable Bond Count 0
Complexity 0
AAADcQAAMAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA
AAAAAAAAAAAAAAAAABAAAAAAAAAAAAAAAAAAAAA
CACTVS Substructure Key Fingerprint
AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA
AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA==
Topological Polar Surface Area 34.1 A^2
Monoisotopic Mass 31.99 g/mol
Exact Mass 31.99 g/mol
XLogP3-AA -1.1
Compound Is Canonicalized true
Formal Charge 0
Heavy Atom Count 2
Defined Atom Stereocenter Count 0
Undefined Atom Stereocenter Count 0
Defined Bond Stereocenter Count 0
Undefined Bond Stereocenter Count 0
Isotope Atom Count 0
Covalently-Bonded Unit Count 1
 from PubChem
4.2 Experimental Properties
4.2.1 Physical Description

Physical description in general
Oxygen is a colorless, odorless and tasteless gas. It will support life. It is noncombustible, but will actively support the
burning of combustible materials. Some materials that will not burn in air will burn in oxygen. Materials that burn in air
will burn more vigorously in oxygen. As a non-liquid gas it is shipped at pressures of 2000 psig or above. Pure oxygen is
nonflammable. Under prolonged exposure to fire or intense heat the containers may rupture violently and rocket. Oxygen
is used in the production of synthesis gas from coal, for resuscitation and as an inhalant.
 from CAMEO Chemicals
Colourless, odourless, non-flammable gas

Liquid
 from Human Metabolome Database (HMDB)
ODOURLESS COMPRESSED GAS.

 from ILO-ICSC
LIQUEFIED GAS. COLOURLESS-TO-BLUE EXTREMELY COLD LIQUID.

 from ILO-ICSC
Colorless, odorless and tasteless gas.

 from OSHA Occupational Chemical DB
4.2.2 Color
Colorless gas
Lide, D.R. CRC Handbook of Chemistry and Physics 86TH Edition 2005-2006. CRC Press, Taylor & Francis, Boca Raton, FL 2005, p. 4-76
 from HSDB
Slightly bluish liquid at -183 deg C

Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 13th ed. New York, NY: John Wiley & Sons, Inc. 1997., p. 830
 from HSDB
4.2.3 Odor
Odorless
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck
and Co., Inc., 2001., p. 1246
 from HSDB
4.2.4 Taste
Tasteless
and Co., Inc., 2001., p. 1246
 from HSDB
4.2.5 Boiling Point
-297.3° F at 760 mm Hg (USCG, 1999)

-183
Airgas SDS
 from DrugBank
-182.96 deg C
and Co., Inc., 2001., p. 1246
 from HSDB
-183°C
 from ILO-ICSC
-297.3°F
4.2.6 Melting Point
-361° F (USCG, 1999)

-218.4
Airgas SDS
 from DrugBank
-218.4 deg C
and Co., Inc., 2001., p. 1246
 from HSDB
-218.4 °C
-218.4°C
 from ILO-ICSC
-361°F
4.2.7 Solubility
Water Solubility
39mg/L
Linde SDS
 from DrugBank
1 vol gas dissolves in 32 vol water at 20 deg C, in 7 vol alcohol at 20 deg C; sol in other organic liquids and usually to a
greater extent than in water
and Co., Inc., 2001., p. 1246
 from HSDB
4.89 CU M SOL IN 100 CC WATER @ 0 DEG C; 2.46 CU M SOL IN 100 CC WATER @ 50 DEG C; 2.30 CU M SOL IN 100 CC
WATER @ 100 DEG C; 2.78 G SOL IN 100 CC ALC @ 25 DEG C
Weast, R.C. (ed.). Handbook of Chemistry and Physics. 60th ed. Boca Raton, Florida: CRC Press Inc., 1979., p. B-104
 from HSDB
37.5 mg/mL at 21 °C
Solubility in water, ml/100ml at 20°C: 3.1

 from ILO-ICSC
4.2.8 Density
1.14 at -297.4° F (USCG, 1999)

Gas: 1.429 g/L at 0 deg C; liq: 1.14 g/ml at -183 deg C

and Co., Inc., 2001., p. 1246
 from HSDB
1.14 at -297.4°F
4.2.9 Vapor Density
1.43 (AIR= 1)
International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour
Office, 1983., p. 1578
 from HSDB
Relative vapour density (air = 1): 1.1

 from ILO-ICSC
4.2.10 Vapor Pressure
1 kPa at -211.9 deg C; 10 kPa at -200.5 deg C; 100 kPa at -183.1 deg C
 from HSDB
Vapour Pressure
Vapour pressure, kPa at -118°C: 5080
 from ILO-ICSC
4.2.11 LogP
0.65
SDS
 from DrugBank
log Kow = 0.65

Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - Hydrophobic, Electronic, and Steric Constants. Washington, DC: American Chemical
Society., 1995., p. 3
 from HSDB
0.65
HANSCH,C ET AL. (1995)
0.65
 from ILO-ICSC
4.2.12 Viscosity
Gas: 101.325 kPa at 25 deg C (0.020 75 cP); Liquid: 99.70 K (0.156 cP)
Braker W, Mossman A; Matheson Gas Data Book 6th ED p.562 (1980)
 from HSDB
4.2.13 Heat of Vaporization
50.9 cal/g at -183 deg C

and Co., Inc., 2001., p. 1246
 from HSDB
4.2.14 Surface Tension
Liq: liquid-surface tension: 13.47 dynes/cm= 0.01347 N/m @ -183 deg C

U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Manual Two. Washington, DC: U.S. Government
Printing Office, Oct., 1978.
 from HSDB
4.3 Spectral Properties

Index of refraction: liq: 1.2243 at -181 deg C/D
 from HSDB
4.3.1 Mass Spectrometry
4.3.1.1 GC-MS
GC-MS Spectrum 2742 - GC-MS Ei Predicted by CFMID-EI, energy0

GC-MS: 1 of 1 (GC-MS Fields)
NIST Number 61306
Library Main library
Total Peaks 2
m/z Top Peak 32
m/z 2nd Highest 16
m/z 3rd Highest 0
Thumbnail
 from NIST
4.3.1.2 MS-MS
1. MS-MS Spectrum 27272 - 10V Positive Predicted by CFM-ID

4. MS-MS Spectrum 33830 - 10V Negative Predicted by CFM-ID

5 Related Records
5.1 Related Compounds with Annotation
 Download
Medications (4) Literature (19) 3D Structure (7) Bioactivities (11) Patents (107)
Hydrogen peroxide Nitrogen Sulfanol Heliox
 from PubChem
5.2 Related Compounds
Same Connectivity 10 records
Mixtures, Components, and

153 records
Neutralized Forms
Similar Compounds 17 records
Similar Conformers 145 records
 from PubChem
5.3 Substances
5.3.1 Related Substances
All 700 records
Same 429 records
Mixture 271 records
 from PubChem
5.3.2 Substances by Category
 Download
 Chemical Vendors (14)
 Curation Efforts (15)
 Governmental Organizations (380)
 Journal Publishers (2)
 Research and Development (22)
 Subscription Services (7)
 Legacy Depositors (7)
 from PubChem
5.4 Entrez Crosslinks
PubMed 633 records
Protein Structures 372 records
Taxonomy 29 records
OMIM 19 records
Gene 2856 records
 from PubChem
6 Chemical Vendors
 Refine/Analyze  Download
Vendor/Supplier Purchasable Chemical PubChem SID
00476_SIAL 329747080
295604_ALDRICH 24857799
Sigma-Aldrich 32021_SIAL 329753966
37428_SIAL 329755644
769053_ALDRICH 329767431
Yuhao Chemical XJ3353 347745731
Alfa Chemistry 7782-44-7 347758181
Chembase.cn 136723 162230993
Chemieliva Pharmaceutical Co., Ltd PBCM0830551 349312409
Ambinter Amb22349329 373738934
Aurora Fine Chemicals LLC A17.880.963 310108680
Finetech Industry Limited FT-0603287 164788466
Molepedia M90110616P 252414498
Parchem 42181 354742028
 from PubChem
7 Drug and Medication Information
7.1 Drug Indication

Oxygen therapy in clinical settings is used across diverse specialties, including various types of anoxia, hypoxia or dyspnea
and any other disease states and conditions that reduce the efficiency of gas exchange and oxygen consumption such as
respiratory illnesses, trauma, poisonings and drug overdoses. Oxygen therapy tries to achieve hyperoxia [L745] to reduce
the extent of hypoxia-induced tissue damage and malfunction.
 from DrugBank
For oxygen supplementation and as a carrier gas during inhalation anaesthesia.For oxygen supplementation during
recovery.
 from EU Community Register of Medicinal Products
7.2 Clinical Trials
 Download
1 to 5 of 78 View More
Record ID Title Status Phase
Inhaled Nitric Oxide in Neonates With Elevated A-a DO2 Gradients Not
NCT00041548 Terminated 2
Requiring Mechanical Ventilation
NCT00142051 Inhaled Nitric Oxide for Pediatric Painful Sickle Crisis Terminated 2
Effects of Supplementary Oxygen on Dyspnoea and Exercise Tolerance in COPD

NCT00249093 Completed
Patients Given LTOT
Supplemental Oxygen and Complications After Abdominal Surgery (The PROXI-

NCT00364741 Completed 4
trial)
NCT00394225 Helium-Hyperoxia and 6MWT Distance in COPD Completed
 from ClinicalTrials.gov
7.3 Therapeutic Uses

Supplemental oxygen is indicated when normal oxygenation is impaired because of pulmonarry injury, which may result
from aspiration (chemical pneumonitis) or inhalation of toxic gases. The PO2 shoud be maintained at 70-80 mm Hg or
higher if possible.
Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical Books/McGraw-Hill. New York, N.Y. 2007., p. 490
 from HSDB
Supplemental oxyugen usually is given empirically to patients with altered mental status or suspected hypoxemia.
 from HSDB
Oxygen (100%) is indicated for patients with carbon monoxide poisoning, to increase the conversion of
carboxyhemoglobin and carboxymyoblobin to hemoglobin and myoglobin, and to increase oxygen saturation of the
plasma and subsequent delivery to tissues.
 from HSDB
Hyperbaric oxygen (HBO) (100%) oxygen delivered to the patient in a pressurized chamber at 2-3 atm of pressure) may be
beneficial for patients with severe carbon monoxide (CO) poisoning. It can hasten the reversal of CO binding to
hemoglobin and intracellular myoglobin, can provide oxygen independent of hemoglobin, and may have protective
actions in reducing postischemic brain damage.
 from HSDB
Hyperbaric oxygen may be beneficial for patients with severe carbon monoxide poisoning, although the clinical evidence
is mixed. Potential indications include history of loss of consciousnesss; metabolic acidosis, age over 50 years, pregancy,
carboxyhemoglobin level greater than 25%, and cerbellar dysfunction (e.g., ataxia).
 from HSDB
Hyperbaric oxygen has also been advocated for treatment of poisoning by carbon tettrachlorde, cyanide, and hydrogen
sulfide and for severe methemoglobinemia, but the experimental and clinical evidence is scanty.
 from HSDB
Medicinal gas to relieve hypoxia; at hyperbaric pressures in cardiac or other surgery, anaerobic infections, carbon
monoxide poisoning; in cryotherapy (liq form).
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc.,
2006., p. 6962
 from HSDB
Hyperbaric O2 therapy is a medical treatment in which the entire patient is enclosed in a pressure chamber while
breathing 100% O2 at elevated ambient pressures. Hyperbaric O2 therapy has been effective in treating decompression
sickness and air or gas embolism by mechanically decreasing the size of air bubbles, and increasing dissolved O2 levels in
the blood. It is also a treatment of choice in carbon monoxide poisoning and smoke inhalation. Other approved
indications for adjunctive hyperbaric O2 therapy include acute traumatic ischemia (crush injuries depriving tissues of O2),
large blood loss (anemia), intracranial abscess, osteomyelitis, enhancement of healing in selected problem wounds, gas
gangrene, radiation tissue damage, and thermal burns. This therapy has also been used in preparation and preservation of
skin grafts or flaps in compromised tissue.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:674
 from HSDB
... A hyperbaric chamber is ... the preferred method of treatment in severe carbon monoxide poisoning ... Hyperbaric
chambers may be either of the large walk-in type or small, monoplace chambers that are pressurized with compressed air,
and the patient breathes oxygen by mask for reasons of fire safety ... The rationale for hyperbaric treatment is ... 1. Carbon
monoxide is apparently displaced from cytochrome A3 oxidase by a surfeit of oxygen, and electron transport is restored.
Lipid peroxidation in the brain is halted. 2. If the patient is given oxygen to breathe at 3 ATA, the half-time for carbon
monoxide elimination from the blood is reduced to 23 min. 3. As soon as the patient breathes oxygen at 3 ATA, 6.4 vol%
of completely available oxygen are physically dissolved in the plasma -- enough to support metabolism even in the
complete absence of functioning hemoglobin. The arteriovenous difference in the cerebral blood flow is only 6.1 vol%.
Thus, the patient's problem with oxygenating the brain and other tissues is immediately over reaching 3 ATA. 4.
Intracranial pressure secondary to cerebral edema is reduced to the order of 50% within 1 min of the commencement of
oxygen breathing.
Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 450
 from HSDB
Hypoxemia generally implies a failure of the respiratory system to oxygenate arterial blood ... Low inspired oxygen
fraction (FIO2), is a cause of hypoxemia only at high altitude or in the event of equipment failure, such as a gas blender
malfunction of a mislabeled compressed-gas tank. An increase in the barrier to diffusion of oxygen within the lung is
rarely a cause of hypoxemia in a resting subject, except in end-stage parenchymal lung disease. Both of these problems
may be alleviated with admin of supplemental oxygen, the former by definition and the latter by increasing the gradient
driving diffusion. Hypoventilation causes hypoxemia by reducing the alveolar PO2 in proportion to the build-up of CO2 in
the alveoli. In essence, during hypoventilation there is decreased delivery of oxygen to the alveoli while its removal by the
blood remains the same, causing its alveolar concn to fall. The opposite occurs with carbon dioxide ... This cause of
hypoxemia is readily prevented by admin of even small amt of supplemental oxygen ... Optimal gas exchange occurs
when blood flow (Q) and ventilation (V) are quantitatively matched. However, regional variations in V/Q matching typically
exist within the lung particularly in the presence of lung disease ... High V/Q ratio lung regions have a relatively reduced
blood flow, eventually becoming pure dead space region at the extreme--contributing nothing to the oxygenation of the
blood while decreasing the efficiency of CO2 removal ... At the extreme of low V/Q ratios, there is no ventilation to a
perfused region and pure shunt results, and the blood leaving the region has the same low PO2 and high PCO2 as mixed
venous blood ... Adding supplemental oxygen will generally make up for the fall in PAO2 (alveolar partial pressure of O2)
in low V/Q units and thus improve arterial oxygenation. However, since there is no ventilation of units with pure shunt,
supplemental oxygen will not be effective in reversing the hypoxemia from this cause ... Even moderate amt of pure shunt
will cause significant hypoxemia despite oxygen therapy ...
Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York,
NY: McGraw-Hill, 2001., p. 386
 from HSDB
... Inhaled oxygen tension that exceeds 300 kPa (3 atm) rarely is used /in hyperbaric chambers/ ... Hyperbaric oxygen
therapy has two components: increased hydrostatic pressure and increased oxygen pressure. Both factors are necessary
for the treatment of decompression sickness and air embolism. The hydrostatic pressure reduces bubble volume, and the
absence of inspired nitrogen increases the gradient for elimination of nitrogen and reduces hypoxia in downstream
tissues ... Even a small increase in PO2 in previously ischemic areas may enhance the bactericidal activity of leukocytes and
increase angiogenesis. Thus repetitive, brief exposure to hyperbaric oxygen is a useful adjunct in the treatment of chronic
refractory osteomyelitis, osteoradionecrosis, or crush injury or for the recovery of compromised skin, tissue grafts, or flaps
... Increased oxygen tension can itself be bacteriostatic; the spread of infection with Clostridium perfringens and
production of toxin by the bacteria are slowed when oxygen tensions exceed 33 kPa (250 mm Hg), justifying the early use
of hyperbaric oxygen in clostridial myonecrosis (gas gangrene) ... In carbon monoxide poisoning, hemoglobin and
myoglobin become unavailable for oxygen binding because of the high affinity of CO for these proteins. A high PO2
facilitates competition of oxygen with CO for binding sites ... Hyperbaric oxygen decreases the incidence of neurological
sequelae after CO intoxication; this effect may be independent of the ability of hyperbaric oxygen to speed the
elimination of CO. However, a recent randomized study suggests that hyperbaric oxygen is not beneficial in carbon
monoxide poisoning and may even be harmful. The occasional use of hyperbaric oxygen in cyanide poisoning has a
similar rationale. Hyperbaric oxygen also may be useful in severe, short-term anemia, since sufficient oxygen can be
dissolved in the plasma at 3 atm to meet metabolic needs. However, such treatment must be limited, because oxygen
toxicity is dependent on increased PO2, not on the oxygen content of the blood. Hyperbaric oxygen therapy also has
been used in ... multiple sclerosis, traumatic spinal cord injury, cerebrovascular accidents, bone grafts and fractures, and
leprosy. However, data from well-controlled clinical trials are not sufficient to justify these uses, and the costs of
hyperbaric therapy remain very high.
 from HSDB
In certain situations, such as bowel distension from obstruction or ileus, intravascular air embolism, or pneumothorax, it is
desirable to reduce the volume of ... air-filled spaces. Since nitrogen is relatively insoluble, inhalation of high concn of
oxygen (and thus low concn of nitrogen) rapidly lowers total body partial pressure of nitrogen and provide a substantial
gradient for the removal of nitrogen from gas spaces. Admin of oxygen for air embolism is additionally beneficial,
because it also helps to relieve the localized hypoxia distal to the embolic vascular obstruction. In the case of
decompression sickness or bends, lowering of inert gas tension in blood and tissues by oxygen inhalation prior to or
during a barometric decompression can reduce th degree of supersaturation that occurs after decompression so that
bubbles do not form ...
 from HSDB
In patients with chronic congestive heart failure, increased inspired O2 (30 or 50%) had a beneficial effect on exercise
performance. A significant increase was determined for arterial O2 saturation and significant decreases in minute volume,
cardiac output, and subjective scores for fatigue and breathlessness.
 from HSDB
It is used to oxygenate perfusates for tissues being held in readiness for transplantation & to oxygenate blood during
cardiopulmonary bypass.
American Medical Association, AMA Department of Drugs. AMA Drug Evaluations. 4th ed. Chicago: American Medical Association,
1980., p. 342
 from HSDB
/MEDICATION: Vet/ In hypoxia and in conjunciton with volatile anesthetics.

O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc.,
2006., p. 6962
 from HSDB
/MEDICATION: Vet/ Patients with severe left-sided congestive heart failure and pulmonary edema can become hypoxic, in
part as a result of the increased diffusion distance for alveolar oxygen to enter the blood into the pulmonay capillaries. By
administering oxygen to these patients, diffusion into the blood is facilitated. The percent inspired oxygen is generally
icnresed to 40-50% (room air is 21%). In patients with severe congestive heart failure, 100% oxygen may be needed in the
acute treatment phase. Oxygen can be administered via an oxygen cage, tight-fitting maks, or nasal cannula. Stress
should be minimized durign oxygen administration.
Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 89
 from HSDB
7.4 Drug Warning

In paraquat poisoning, oxygen may contribute to lung injury. In fact, slightly hypoxic environments (10-12% oxygen) have
been advocated to reduce the risk of pulmonary fibrosis from paraquat.
 from HSDB
Relative contraindications to hyperbaric oxygen therapy include a history of recent middle ear or thoracic surgery,
untreated pneumothorax, seizure disorder, and severe sinusitis.
 from HSDB
Prolonged high concentrations of oxygen are associated with pulmonary alveolar tissue damage. In general, the fraction
of inspired oxygen (FIO2) shoud not be maintained at greater than 80% for more than 24 hours.
 from HSDB
Oxygen therapy may increase the risk of retrolental fibroplasia in neonates.

 from HSDB
Administration of high oxygen concentrations to patients with severe chronic obstructive pulmonary disease and chronic
carbon dioxide retention who are dependent on hypoxemia to provide a drive to breathe may result in respiratory arrest.
 from HSDB
Hyperbaric oxygen treatment can cause hyperoxic seizures, aural trauma (ruptured tympanic memberane), and acute
anxiety resulting from claustorphobia. Seizure are more likely at higher atmospheric pressures (e.g., 3 atm or greater).
 from HSDB
Oxygen may potentiate toxicity via enhanced generation of free radicals with some chemotherapeutic agents (e.g.,
bleomycin, Adriamycin, and daunorubicin).
 from HSDB
Use in pregnancy - No known adverse effects.

 from HSDB
When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have
normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending
on the severity of the respiratory distress. The majority of patients with exacerbations of chronic obstructive pulmonary
disease who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is
known. When treating patients who have chronic severe hypercapnia, the initial FiO2 should be 24% even though renal
compensation of the respiratory acidosis has occurred.
Tinits P; Oxygen Therapy and Oxygen Toxicity; Ann Emerg Med 12 (5): 321-8 (1983)
 from HSDB
Although high concn of O2 may be necessary in life-threatening situations ... /it/ should not be used for long periods.
When continuous admin is indicated, lowest possible concn should be used. Regardless of concn provided by
oxygenating system, measuring O2 tension of arterial blood is only means of monitoring effectiveness ...
1980., p. 342
 from HSDB
Grand mal convulsions may result from admin of oxygen at greater than 2 1/2 atmospheres; these cease without
permanent sequelae upon resumption of air breathing. When oxygen is required for premature infants, the inspired
oxygen concn should not exceed 40% for any substantial period without measurement of arterial oxygen tension, unless
infant has cyanotic heart disease or the hypoxemia is dangerous. /in premature infants/ arterial oxygen tension above 150
mm hg may cause retrolental fibroplasia; permanent blindess occurs several mo later. Brief periods of admin of 100%
oxygen ... impose little risk of retinal injury. Retinal changes do not occur in full-term infants, although susceptible to
pulmonary complications
1980., p. 343
 from HSDB
... Oxygen toxicity can be extremely serious at pressures of 3 ATA. Within approx 3 hr, even someone quietly at rest will
experience a grand mal seizure ... Exposure time at 3 ATA must be limited to no more than 90 min ... Even at 2 ATA, oxygen
poisoning can take place. This is in the form of the Lorrain Smith effect or oxygen toxicity to the lungs. Within approx 6 hr
of continuous exposure to 2 ATA, the patient will experience substernal pain, decreased vital capacity, and patchy
atelectasis. If exposure is continued chronically, this can give rise to pulmonary microhemorrhage and fibrosis.
 from HSDB
VET: ... uninterrupted use of high concn for more than 3-5 hr can be harmful. Hyperventilation with pure O2 can actually
decrease cerebral O2 tension, decr cerebral blood flow, cause retinal detachment, & other eye problems in dogs.
Hyperbaric O2 may cause fetal damage.
Rossoff, I.S. Handbook of Veterinary Drugs. New York: Springer Publishing Company, 1974., p. 403
 from HSDB
Animals or humans exposed to a 4-ATA (atmosphere absolute) pressure of O2 are likely to show muscular twitching or
general convulsions (like those of epilepsy) within 1 hr. Pure O2, at atmospheric pressure or less, can cause pulmonary
irritation and edema after 24-hr exposures; higher pressures cause damage in a shorter time. Half an atmosphere of pure
O2 can probably be tolerated indefinitely without lung damage; 3 ATA is probably safe for healthy adults for 1 hr.
Intermittent breathing of air or another gas mixture containing O2 at the accustomed 0.2 ATA pressure lessens the risk of
lung injury.
 from HSDB
At a pressure of 3 ATA (66 feet of seawater pressure), a grand mal seizure will result in nearly everyone after approx 3 hr.
This is termed the "Paul Bert effect." ... Oxygen breathing can be tolerated by most people for periods up to 90 min at 3
ATA with little difficulty if they are at rest and recumbent in a dry chamber breathing oxygen by mask. However, actual
tests show that a diver working in water at a depth of 50 feet (2.5 ATA) may suffer convulsions within 10 to 30 min ... 100%
oxygen must never be administered at pressures greater than 3 ATA (29.4 psig) in the dry chamber. Even with the subject
recumbent, comfortably at rest, and well ventilated, exposure time should not exceed 90 min ...
 from HSDB
... CNS toxicity (the "Paul Bert effect") ... may develop within a few to many minutes from exposure to levels of oxygen
above about 1.8 bars and may result in an epileptic-like convulsion which is not dangerous in itself but which will be quite
disruptive in any case, and can result in drowning or physical injury. Susceptibility to CNS toxicity is exacerbated by other
factors, particularly those that cause an increase in internal PCO2 such as exercise and breathing dense gas or breathing
against a resistance ... There may be no warning symptoms before a convulsion, and one may occur several minutes after
the exposure to high oxygen has stopped ... There is an enormous variation /of oxygen toxicity/ among individuals, and a
significant variation in a single individual at different times ...
 from HSDB
... Oxygen's effect on the lung (the "Lorrain Smith effect") ... takes hours or longer to develop from exposure levels that
may be lower than those that cause CNS symptoms; it is seen as chest ("substernal") pain or discomfort, coughing,
inability to take a deep breath without pain or coughing, the development of fluid in the lungs, and a reduction in vital
capacity. This has been called "pulmonary oxygen toxicity" ... The pulmonary oxygen poisoning encountered in diving or
in relation to decompression is, in time, fully reversible and leaves no long-term effects. A different hospital-related
"chronic lung toxicity" may lead to lung fibrosis after very long exposures ...
 from HSDB
... /"Whole body" oxygen toxicity/ develops after hours to days of exposure ... Its effects are a collection of symptoms in
addition to the lung problems ... that include paresthesias (especially numbness in fingertips and toes), headache,
dizziness, nausea, effects on the eyes, and a dramatic reduction of aerobic capacity ... After many days of exposure to
increased oxygen, a reduction of hemoglobin and red blood cells has also been noted in some divers; this is a normal
adaptive response, the converse of the acclimation to high altitude ... All forms of oxygen toxicity show highly variable
effects on different individuals, and even significant differences in the same individual at different times.
 from HSDB
... "Off phenomenon" /was reported/, in which the patient may show only a few mild premonitory sign but as soon as the
oxygen mask is removed, he sustains a grand mal seizure ... /It was/ demonstrated that with a mass spectrograph catheter
placed in muscle tissue, the amt of oxygen measurable increases many-fold as soon as oxygen breathing is discontinued.
This may be due to the fact that when the oxygen-induced vasoconstriction is stopped, the tremendous amt of oxygen
dissolved in the blood and plasma then reach the tissues suddenly.
 from HSDB
When the partial pressure of oxygen is increased, an unphysiologic condition results. Oxygen at partial pressures much
greater than the 160 mm Hg experienced when breathing atmospheric air acts as a poison, and metabolism is actually
slightly slowed. A profound vasoconstriction takes place, with striking blanching of the face and extremities, seen in
experiments carried out with subjects breathing 100% oxygen at 4 ATA.
 from HSDB
Transient impairment of visual fields and visual acuity have been reported in adult humans in association with hyperbaric
O2.
 from HSDB
Although severe retinal damage in adults is rare during hyperoxia, one case was reported concerning an individual
suffering from myasthenia gravis who developed irreversible retinal atrophy after breathing 80% oxygen for 150 days. The
retinal vasculature was markedly constricted with no blood flowing through both eyes. The vascular disorder was limited
only to retinal circulation.
Amdur, M.O., J. Doull, C.D. Klaasen (eds). Casarett and Doull's Toxicology. 4th ed. New York, NY: Pergamon Press, 1991., p. 544
 from HSDB
... Premature infants have organs that are not fully developed at birth, including the lungs and eyes, where growth of new
capillaries is still very active ... /and/ may have difficulty in getting sufficient O2 into their blood, so they are placed in
enclosed incubators or on respirators with an increased PO2. In the early history of this life-saving procedure, high O2
concentrations were used. The immediate benefit of tissue oxygenation was followed by a high incidence of pulmonary
damage. It was soon observed that these babies were blind, the result of hyperoxic damage to the retinal capillaries. This
injury was followed by proliferation of fibrous tissue. Careful adjustment of the O2 pressure to meet the needs of the
infant has been effective in controlling the damage to the eye.
 from HSDB
... Restriction of oxygen significantly reduced the incidence and severity of retinopathy of prematurity without unduly
increasing death rates.
Askie LM, Henderson-Smart DJ; Cochrane Database Syst Rev 4: CD001077 (2001)
 from HSDB
In infants who are given oxygen therapy after birth, a syndrome known as bronchopulmonary dysplasia may develop.
Lung pathology is characterized by necrotizing bronchiolitis, fibroblast proliferation, squamous metaplasia of the
bronchial lining, and destruction of alveolar ducts.
Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 6th ed. New York, NY: McGraw-Hill, 2001., p. 529
 from HSDB
High oxygen concn delivered to poorly ventilated lung regions can promote absorption atelectasis, occasionally resulting
in an increase in shunt and a paradoxical worsening of hypoxemia after a period of oxygen admin.
 from HSDB
... Elevated pulmonary artery pressures in patients living at altitude who have chromic hypoxic pulmonary hypertension
may reverse with oxygen therapy ... In neonates with congenital heart disease and left-to-right shunting of cardiac output,
oxygen supplementation must be carefully regulated because of the risk of further reducing pulmonary vascular
resistance and increasing pulmonary blood flow.
 from HSDB
In addition to the potential to promote absorption atelectasis and depress ventilation ... high flows of dry oxygen can dry
out and irritate mucosal surfaces of the airway and the eyes, as well as decrease mucociliary transport and clearance of
secretions. Humidified oxygen thus should be used when therapy of greater than an hour's duration is required.
 from HSDB
8 Food Additives and Ingredients
8.1 Food Additive Classes
JECFA Functional Classes

Food Additives: PROPELLANT
 from FAO/WHO Food Additive Evaluations (JECFA)
8.2 FDA Indirect Additives used in Food Contact Substances
FDA Indirect Additives used in Food Contact Substances: 1 of 1 (Indirect Additives)
Indirect Additives OXYGEN
Title 21 of the U.S. Code of

176.210; 177.2800
Federal Regulations (21 CFR)
 from FDA Center for Food Safety and Applied Nutrition (CFSAN)
8.3 Evaluations of the Joint FAO/WHO Expert Committee on Food Additives - JECFA
Evaluations of the Joint FAO/WHO Expert Committee on Food Additives - JECFA: 1 of 1 (JECFA Chemical)
Chemical Name OXYGEN

9 Pharmacology and Biochemistry
9.1 Pharmacology
Oxygen therapy improves effective cellular oxygenation, even at a low rate of tissue perfusion. Oxygen molecules adjust
hypoxic ventilatory drive by acting on chemoreceptors on carotid bodies that sequentially relay sensory information to
the higher processing centers in brainstem. It also attenuates hypoxia-induced mitochondrial depolarization that
generates reactive oxygen species and/or apoptosis. Studies investigating on hyperbaric oxygen therapy has shown that
oxygen supplementation can induce neural stem cell proliferation in neonatal rats thus promoting neurological
regeneration after injuries [A19117]. CD34+, CD45-dim leukocytes are also potential targets for hyperbaric oxygen
therapy benefit as their mobilization was increased in vitro which could facilitate the acceleration of recovery at peripheral
sites [A19113].
 from DrugBank
Oxygen is an element with atomic symbol O, atomic number 8, and atomic weight 16.
 from NCIt
9.2 ATC Code

Anatomical main group: QV - Various
|Therapeutic subgroup: QV03 - All other therapeutic products
|Pharmacological subgroup: QV03A - All other therapeutic products
|Chemical subgroup: QV03AN - Medical gases
|Chemical substance: QV03AN01 - oxygen
V - Various
V03 - All other therapeutic products
V03A - All other therapeutic products
V03AN - Medical gases
V03AN01 - Oxygen
 from WHO ATC
9.3 Bionecessity
Man is designed to breathe 20.93% oxygen at atmospheric pressure or 14.7 psi absolute.
 from HSDB
Oxygen ... accounts for approximately 65% by weight of the human body ... Its greatest importance is the dependence of
most life forms on O2 as a source of cellular energy ... On entry into the cells, the mitochondria use the diffused O2 in
chemical reactions that ultimately supply the energy required for cellular functions. Most O2 combines with carbon and
hydrogen atoms from glucose molecules to form cellular energy, known as adenosine triphosphate or ATP, along with
carbon dioxide (CO2) and water. The remaining O2 is combined with various compounds to synthesize cellular structures
or elimination products ... For each liter of O2 used, approximately 5 kcal (~20 J) of energy is liberated ...
 from HSDB
Hypoxia is a life-threatening condition in which oxygen delivery is inadequate to meet the metabolic demands of the
tissues. Since oxygen delivery is the product of blood flow and oxygen content, hypoxia may result from alterations in
tissue perfusion, decreased oxygen tension in the blood, or decreased oxygen carrying capacity. In addition, hypoxia may
result from a problem in oxygen transport from the microvasculature to the cells or in utilization within the cell.
Irrespective of cause, an inadequate supply of oxygen ultimately results in the cessation of aerobic metabolism and
oxidative phosphorylation, depletion of high-energy cmpd, cellular dysfunction, and death.
 from HSDB
Tissue oxygen deficiency (hypoxia) ... may be defined as a decrease in O2 delivery to the cells resulting in an energy
production that is below the cellular requirements ... Hypoxic effects are usually undetectable when PO2 is greater than
120 mm Hg. Interference with the adaptation of the eye to darkness, however, can occur at this pressure.
 from HSDB
Response of Humans to the Inhalation of Atmospheres Deficient in Oxygen: Stage 1 (oxygen vol 12 to 16%) -- Breathing
and pulse rate increased, muscular coordination slightly disturbed; Stage 2 (oxygen vol 10 to 14%) -- Consciousness
continues, emotional upsets, abnormal fatigue upon exertion, disturbed respiration; Stage 3 (oxygen vol 6 to 10%) --
Nnausea and vomiting, inability to move freely, loss of consciousness may occur; may collapse and although aware of
circumstances be unable to move or cry out; Stage 4 (oxygen vol below 6%) -- Convulsive movements, gasping
respiration; respiration stops and a few minutes later heart action ceases. /From table/
 from HSDB
... The time course of cellular demise /from hypoxia/ depend upon the tissue's relative metabolic requirements, oxygen
and energy stores, and anaerobic capacity. Survival times (the time from the onset of circulatory arrest to significant organ
dysfunction) range from 1 min in the cerebral cortex to around 5 min in the heart and 10 min in the kidneys and liver, with
the potential for some degree of recovery if reperfused. Revival times (the duration of hypoxia beyond which recovery is
no longer possible) are approx 4 to 5 times longer. Less severe degrees of hypoxia have progressive physiological effects
on different organ systems.
 from HSDB
... Hypoxia stimulates the carotid and aortic baroreceptors to cause increases in both the rate and depth of ventilation ...
/Dyspnea/ occurs when the respiratory minute volume approaches half the max breathing capacity; this may occur with
minimum exertion in patients in whom max breathing capacity is reduced by lung disease. In general, little warning
proceeds the loss of consciousness resulting from hypoxia ... Hypoxia causes reflex activation of the sympathetic nervous
system via both autonomic and humoral mechanisms, resulting in tachycardia and increased cardiac output. Peripheral
vascular resistance ... decreases primarily via local autoregulatory mechanisms, with the net result that blood pressure is
generally maintained unless hypoxia is prolonged or severe ... Hypoxia causes pulmonary vasoconstriction and
hypertension, an extension of the normal regional vascular response that matches perfusion with ventilation to optimize
gas exchange in the lung (hypoxic pulmonary vasoconstriction ... The CNS is least able to tolerate hypoxia. Hypoxia is
manifest initially by decreased intellectual capacity and impaired judgement an psychomotor ability ... /and/ progresses to
confusion and restlessness and ultimately to stupor, coma, and death as the arterial PO2 decreases below 4 to 5.3 kPa (30
to 40 mm Hg) ... When the mitochondrial PO2 falls below about 0.13 kPa (1 mm Hg), aerobic metabolism stops, and the
less efficient anaerobic pathways of glycolysis become responsible for the production of cellular energy. End-products of
anaerobic metabolism, such as lactic acid, may be released into the circulation in measurable quantities. Energy-
dependent ion pumps slow and transmembrane ion gradients dissipate. Intracellular concn of Na+, Ca2+, and H+
increase, finally leading to cell death ... Restoration of perfusion and oxygenation prior to hypoxic cell death paradoxically
can result in an accelerated form of cell injury (ischemia-reperfusion syndrome), thought to result from the generation of
highly reactive oxygen free radicals.
 from HSDB
Although the percentage of O2 in the inspired air remains constant at different altitudes, the lower atmospheric pressure
at higher altitudes decreases the PO2, and thus the driving force for gas exchange in the lungs. Rapid ascent by humans
to an altitude of 2500 m (8200 ft) causes an illness known as acute mountain sickness (acute benign mountain sickness
(AMS), puna, soroche) in many people. The etiology of AMS is poorly understood, but the likely cause is the hypoxia
brought about by exposure to a PO2 of 119 mm Hg, for periods of time greater than about 4 hr ... During ascent to higher
altitudes, an increased rate and depth of breathing, along with shortness of breath on mild exertion, and an increased
pulse rate may be noticed ... After an interval of about 6 to 12 hr to several days of sustained hypoxia, insomnia,
headache, loss of appetite, impaired mental concentration, nausea, vomiting, muscular weakness and fatigue, cough,
chest pain, and heart palpitation may ensue ... Among apparently healthy people, no one has yet found reliable clues to
identify susceptible individuals. Strength and physical fitness offer no protection ... A life-threatening acute illness that
may be encountered at altitudes over about 3000 m (or 10,000 ft) is high altitude pulmonary edema (HAPE), which may or
may not be preceded by symptoms of AMS ... /and/ is characterized by cough, labored breathing, and collapse. If left
untreated, HAPE can progress rapidly and be fatal ... High altitude cerebral edema (HACE) is ... initially as an exaggeration
of AMS, but progressing to severe headache, muscular incoordination (ataxia), irrationality, drowsiness, confusion, stupor,
and coma. Other signs and symptoms ... include nausea, vomiting, hallucinations, cranial nerve palsies, seizures, and
sometimes visual symptoms. Progression of symptoms also creates the potential for fatal accidents, such as falls.
Neurological symptoms of altitude illness can progress from those of AMS to coma within 12 to 72 hr ... Chronic
mountain sickness (Monge's disease) is a disorder that affects ... residents of high altitude regions (>4000 m). The primary
characteristic is inadequate breathing (hypoventilation), which lowers the already inadequate oxygenation of the blood
and leads to excessive production of red blood cells (polycythemia), with consequent thickening of the blood. Damage to
the lungs and heart may follow, including right ventricular hypertrophy and the corresponding electrocardiogram
alterations ....
 from HSDB
A ... common problem in industry is oxygen deficiency in the atmosphere of a confined space ... The first physical signs of
anoxia are increased rate and depth of breathing. Oxygen concn of less than 16% cause dizziness, rapid heart beat, and
headache. Oxygen-deficient atmospheres may also cause an inability to move and a semiconscious lack of concern about
the imminent loss of consciousness. An individual entering an oxygen-deficient atmosphere usually has no warning
symptoms but immediately loses consciousness ...
 from HSDB
The dependence on a continual source of energy, in the absence of energy reserves, places the neuron in a vulnerable
position. To meet these high energy requirements, the brain utilizes aerobic glycolysis and, therefore, is extremely
sensitive to even brief interruptions in the supply of oxygen or glucose.
 from HSDB
9.4 Absorption, Distribution and Excretion
Route of Elimination
Exhalation
 from DrugBank
During inhalation of normal air the arterial blood leaves lungs about 95% saturated with oxygen, and with a subject
standing at rest, the venous blood returns to lungs about 60 to 70% saturated. During 1 min approx 360 cc of oxygen are
used up. After forced deep inspiration normal lung vol is about 5 to 5.5 L, 1 L which is O2 ...
Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 914
 from HSDB
Arterial blood carries O2 in 2 forms. Most is normally bound to hemoglobin ... A smaller amt is free in soln. The amount of
O2 carried ... depends on partial pressure of oxygen. When fully saturated with O2, each g of hemoglobin binds 1.3 vol %
of O2. At 37 deg C, 0.003 vol % O2 is dissolved in blood/torr of partial pressure of O2.
Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New
York: Macmillan Publishing Co., Inc. 1980., p. 325
 from HSDB
Fetal hemoglobin has more affinity for oxygen than maternal hemoglobin under similar conditions of pH & temp. If
incompletely oxygen-saturated fetal & maternal blood are allowed to equilibrate across a membrane, partial pressure of
O2 will be identical on both sides of membrane, but O2 content of fetal blood ... /will be/ higher ...
LaDu, B.N., H.G. Mandel, and E.L. Way. Fundamentals of Drug Metabolism and Disposition. Baltimore: Williams and Wilkins, 1971., p. 94
 from HSDB
Oxygen enters the body primarily through the lungs, but may also be taken up by mucous membranes of the GI tract, the
middle ear, and the paranasal sinuses. It diffuses from the alveoli into the pulmonary capillaries, dissolves in the blood
plasma, enters the red blood cells, and binds to hemoglobin. The red cells transport bound O2 to tissues throughout the
body via the circulatory system. In tissues where the partial pressure of O2 is lower than that of the blood, the O2 diffuses
out of the red cells, through the capillaries and plasma, and into the cells. As the O2 plasma concentration diminishes, it is
replaced by that contained in the red cells. The red blood cells are then circulated back to the lungs in a continuous
recycling process ...
 from HSDB
9.5 Metabolism/Metabolites
... Most O2 combines with carbon and hydrogen atoms from glucose molecules to form cellular energy, known as
adenosine triphosphate or ATP, along with carbon dioxide (CO2) and water. The remaining O2 is combined with various
compounds to synthesize cellular structures or elimination products. The CO2 generated in the cells then diffuses back to
the red blood cells and returns to the lungs, where it is exhaled. The metabolic water combines with ingested water and
the excess is eliminated by excretion through the kidneys or by evaporation from the lungs and skin.
 from HSDB
In the course of O2 metabolism, several toxic substances are generated, including superoxide anion (O2-), hydrogen
peroxide (H2O2), hydroxyl radical (OH-), lipid peroxides, and others. Without the availability of several enzymes that
destroy these toxic intermediary compounds, cell death quickly occurs. The protective enzymes include superoxide
dismutases (SODs), catalase (CAT), and glutathione peroxidase (GP). Glutathione reductase (GR) participates by re-forming
glutathione, which is preferentially oxidized, thereby sparing sulfhydryl-bearing proteins and cell wall constituents. Other
contributors to the control of oxidant toxicity include vitamin C (ascorbic acid), vitamin E (alpha-tocopherol), vitamin A,
and selenium, a cofactor for GP.
 from HSDB
Oxygen (O2) is reduced by both enzymatic and nonenzymatic processes to the superoxide radical (O2-). This radical
species of oxygen is postulated to be formed in vivo in animals through activity of some iron-sulfur oxidation-reduction
enzymes and certain flavoproteins ...
Doull, J., C.D. Klaassen, and M. D. Amdur (eds.). Casarett and Doull's Toxicology. 2nd ed. New York: Macmillan Publishing Co., 1980., p.
65
 from HSDB
The partial reduction of molecular oxygen in biological systems produces the cytotoxic intermediates superoxide,
hydrogen peroxide, and hydroxyl radical. The superoxide radical is now recognized to play significant roles in a number of
pathophysiologic states including oxygen toxicity, radiation damage, phagocyte-mediated inflammation, and
postischemic injury.
McCord JM; The Superoxide Free Radical; Its Biochemistry and Pathophysiology; Surgery 94 (3): 412-4 (1983)
 from HSDB
Oxygen toxicity is mediated through increased production of partially reduced oxygen products such as superoxide anion,
perhydroperoxy and hydroxyl radicals, peroxynitrite and possibly singlet molecular oxygen.
 from HSDB
9.6 Biological Half-Life

Approximately 122.24 seconds
 from DrugBank
9.7 Mechanism of Action

Oxygen therapy increases the arterial pressure of oxygen and is effective in improving gas exchange and oxygen delivery
to tissues, provided that there are functional alveolar units. Oxygen plays a critical role as an electron acceptor during
oxidative phosphorylation in the electron transport chain through activation of cytochrome c oxidase (terminal enzyme of
the electron transport chain). This process achieves successful aerobic respiration in organisms to generate ATP molecules
as an energy source in many tissues. Oxygen supplementation acts to restore normal cellular activity at the mitochondrial
level and reduce metabolic acidosis. There is also evidence that oxygen may interact with O2-sensitive voltage-gated
potassium channels in glomus cells and cause hyperpolarization of mitochondrial membrane [A19120].
 from DrugBank
The exact mechanism whereby hypoxic pulmonary vasoconstriction is elicited is still unsettled. A possible role for toxic
oxygen metabolites was evaluated, employing a set-up of blood-perfused isolated rat lungs. Hypoxic pulmonary
vasoconstriction reflected as pulmonary arterial pressor responses, was evoked by alternately challenging the airways with
a hypoxic- and a normoxic gas mixture, resulting in gradually increasing responses until a maximum was obtained. In a
sequence of responses (mean +/- s.e. mean) increasing from 2.5 +/ - 0.2 kPa to 3.2 +/ - 0.1 kPa, administration to the
perfusate of the inhibitor of xanthine oxidase, allopurinol reduced the subsequent response to 2.5 +/- 0.2 kPa (P < 0.001).
By contrast, allopurinol did not affect vasoconstriction induced by serotonin or bradykinin. In control experiments
responses continued to increase after administration of hypoxanthine (substrate of xanthine oxidase). Neither
pretreatment with daily injections of the antioxidant vitamin E for 3 days in advance, nor addition to the perfusate of the
scavenger enzymes superoxide dismutase and catalase, or dimethylsulfoxide had any impact on hypoxic pulmonary
vasoconstriction; the subsequent responses rose at the same rate and in the same way as before. Thus, the present study
has shown that allopurinol inhibition of xanthine oxidase depresses hypoxic pulmonary vasoconstriction. This could be
due either to reduced production of toxic oxygen metabolites or to accumulation of purine metabolites. The absence of
inhibitory effects of quenchers of toxic oxygen metabolites refutes a role for these metabolites in the elicitation of hypoxic
pulmonary vasoconstriction. More likely, allopurinol inhibits hypoxic pulmonary vasoconstriction by interfering with the
purine metabolism.
Abstract: PubMed
Kjaeve J et al; Acta Anaesthesiol Scand 34 (5): 384-8 (1990)
 from HSDB
Exposure to hyperoxia results in endothelial necrosis followed by type II cell proliferation. This suggests that type II cells
are resistant to hyperoxia. Oxygen-induced lung injury may result from an overproduction of oxygen metabolites
normally scavenged by antioxidants such as superoxide dismutase, glutathione peroxidase, catalase and reduced
glutathione. Therefore, resistance of type II cells to hyperoxia may be linked to high antioxidant activities. To test this
hypothesis /the authors/ compared in vitro the effects of a 24 hr exposure period to 95% O2 on cultured type II cells, lung
fibroblasts and alveolar macrophages isolated from rats. We show that type II cells, when compared with other cell types,
are highly sensitive to hyperoxia as shown by increased lactate dehydrogenase release, decreased deoxyribose nucleic
acid and protein content of Petri dishes and decreased thymidine incorporation into DNA. Synthesis of
dipalmitoylphosphatidylcholine was also significantly reduced. Antioxidant enzyme activities as well as glutathione
content were not higher in type II cells than in other cell types. However, hyperoxia results in a decreased superoxide
dismutase activity and glutathione content in type II cells which was not observed in fibroblasts. /It was concluded/ that
adaptative changes in superoxide dismutase and glutathione metabolism could be important defense mechanisms in cells
exposed to hyperoxia.
Abstract: PubMed
Housset B et al; Eur Respir J 4 (9): 1066-75 (1991)
 from HSDB
Oxygen, essential for mammalian life, is paradoxically harmful. If O2 is given at high enough concentrations for long
enough times, the body's protective mechanisms are overwhelmed, leading to cellular injury and, with continued
exposure, even death. In the course of O2 metabolism, several toxic substances are generated, including superoxide anion
(O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH-), lipid peroxides, and others. Without the availability of several
enzymes that destroy these toxic intermediary compounds, cell death quickly occurs. The protective enzymes include
superoxide dismutases (SODs), catalase (CAT), and glutathione peroxidase (GP). Glutathione reductase (GR) participates by
re-forming glutathione, which is preferentially oxidized, thereby sparing sulfhydryl-bearing proteins and cell wall
constituents. Other contributors to the control of oxidant toxicity include vitamin C (ascorbic acid), vitamin E (alpha-
tocopherol), vitamin A, and selenium, a cofactor for GP. Normally, a balance exists between the production of toxic
oxidants and their destruction by antioxidant mechanisms. Some individuals may lack the ability to produce sufficient
antioxidants and suffer a slow progressive tissue deterioration as a result.
 from HSDB
Protein accumulation in the BAL fluid results from damage to the pavement-like cells that line the alveolar sacs, known as
type I cells, which cover 95% of the alveolar surface. Type I cells are generally incapable of dividing, but when damaged,
can be replaced by the type II alveolar cells interspersed among them. Type II cells are less susceptible to toxic injury, can
proliferate rapidly, and can be transformed into type I cells. Toxic injuries that affect only type I cells can be repaired by
this proliferative process. To the extent that type II cells are also injured, the effects are more severe and may lead to
permanent changes. Other types of cells in the lung are also affected, especially the capillary endothelial cells, leading to
leakage of blood plasma into the interstitial tissue between the alveoli, and ultimately into the alveoli. Blood cells in the
capillaries may also form a clot or may leak into alveolar spaces (hemorrhage). Other cells in the interstitium, such as
fibroblasts, are damaged. An inflammatory response, with infiltration of white blood cells, proliferation of fibroblasts, and
subsequent fibrosis may follow.
 from HSDB
Alveolar epithelial and capillary endothelial cells are the main metabolic contributors of free radicals in response to
hyperoxia. Other cell types are also involved in free-radical generation, including interstitial macrophages, lymphocytes,
and polymorphonuclear neutrophils, which accumulate in response to irritation. Synergistic interactions were reported
between hyperoxia and neutrophils in producing lung injury ... The edema induced by hyperoxia could be reduced by
depleting rabbits of granulocytes ...
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Relatively late in the course of normobaric hyperoxic exposures, the amount of surfactant in the lungs is reduced. This
leads to an increased surface tension, making the alveoli resistant to expansion and more likely to collapse, thereby
reducing the surface available for gas diffusion.
 from HSDB
Respiratory cells engineered to express high levels of the antioxidant heme oxygenase-1or heat-shock protein 70 had
increased protection from O2-induced injury. Similarly, transgenic mice with targeted overexpression of interleukin-11 in
the lung showed markedly diminished hyperoxic lung injury ... Knockout mice with no heme oxygenase-2 expression were
sensitized to hyperoxia-induced lung injury and had shorter survival times, suggesting heme oxygenase-2 has a protective
role in O2-induced lung injury ... Mice lacking Clara cell secretory protein showed increase sensitivity to hyperoxia. Mice
with a mutated plasminogen activating inhibitor-1 gene were also more susceptible to O2 injury ... Gene therapy ...
/transferring/ SOD and CAT activity into lung cells of rats showed an increased survival time ... /and/ heme oxygenase-1 to
rats demonstrated protection from O2 injury.
 from HSDB
Present data indicate that oxygen toxicity occurs at the cellular level by direct poisoning of the enzyme systems involved
in aerobic and anaerobic metabolism and electron transport. Oxygen behaves like a free radical under pressure and
ruptures sulfhydryl bonds. Gamma aminobutyric acid metabolism is also disrupted.
 from HSDB
Oxidases are enzymes utilizing molecular oxygen. The scission of the O2 molecule is an intrinsically hazardous process
wherein directed oxidation is required. The control of O2 utilization is regulated at the catalytic center of these enzymes
which generally contains a metal with plurivalent potential (Fe, Cu, or Mn). However, all oxidases "leak" non specific
reactive oxygen species (ROS) to a certain extent. There is especially efficient control in the mitochondrial respiratory
chain where the uncoupled leakage rate is less than 2%. The presence of both copper and iron within cytochrome oxidase
may allow this tight regulation, and enzymes containing iron alone, such as the mixed function oxidases and monoamine
oxidases, may be less effective in this respect ...
Chang, L.W. (ed.). Toxicology of Metals. Boca Raton, FL: Lewis Publishers, 1996, p. 702
 from HSDB
Tg and Wt mice were exposed to normobaric hyperoxia (>99% oxygen) for 48, 72, and 84 hours. Mice overexpressing
hEC-SOD in the airways attenuated the hyperoxic lung injury response, showed decreased morphologic evidence of lung
damage, had reduced numbers of recruited inflammatory cells, and had a reduced lung wet/dry ratio. ... Both Wt and Tg
neutrophil-depleted (ND) mice have less severe lung injury compared with non-ND animals.[Folz RJ; J Clin Invest 103 (7):
1055-1066 (1999)] Full text: PMC408251
Abstract: PubMed
 from HSDB
Hyperoxia is commonly used in the treatment of newborn respiratory distress. Although essential and life saving, oxygen
therapy can result in the development of lung injury. Oxygen toxicity is associated with the production of reactive oxidant
species. Nitric oxide (NO) is an oxidant formed by the catalysis of L-arginine when acted upon by the enzyme nitric oxide
synthase (NOS). We studied the differential effects of prolonged normobaric hyperoxia (FIO2 = .95, for 3, 4, and 5 days)
on the two major NOS enzymes, constitutive endothelial cell NOS (ecNOS) and inducible NOS (iNOS). Hyperoxia led to a
significant lung injury, as measured by pulmonary compliance studies. Hyperoxia did not increase serum NO production,
measured as the concentration of nitrite and nitrate. However, hyperoxia did result in a small but significant increase in
NO production in the bronchoalveolar lavage fluid, as measured by the products of nitrite and nitrate concentration. This
increase in NO was not associated with an induction of whole lung iNOS, as measured by the conversion of L-[3H]arginine
to L-[3H]citrulline or by Northern blot analysis. Hyperoxia significantly decreased ecNOS activity as measured by the
conversion of L-[3H]arginine to L-[3H]citrulline. In addition, administration of the NOS inhibitor NG-nitro-L-arginine
methyl ester worsened the injury, as measured by lung compliance and survival.
Abstract: PubMed
Arkovitz MS et al; Shock 7 (5): 345-50 (1997)
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9.8 Human Metabolite Information
9.8.1 Metabolite Description
Description
Oxygen is the third most abundant element in the universe after hydrogen and helium and the most abundant element
by mass in the Earth's crust. Diatomic oxygen gas constitutes 20. 9% of the volume of air. All major classes of structural
molecules in living organisms, such as proteins, carbohydrates, and fats, contain oxygen, as do the major inorganic
compounds that comprise animal shells, teeth, and bone. Oxygen in the form of O2 is produced from water by
cyanobacteria, algae and plants during photosynthesis and is used in cellular respiration for all living organisms. Green
algae and cyanobacteria in marine environments provide about 70% of the free oxygen produced on earth and the rest is
produced by terrestrial plants. Oxygen is used in mitochondria to help generate adenosine triphosphate (ATP) during
oxidative phosphorylation. For animals, a constant supply of oxygen is indispensable for cardiac viability and function. To
meet this demand, an adult human, at rest, inhales 1. 8 to 2. 4 grams of oxygen per minute. This amounts to more than 6
billion tonnes of oxygen inhaled by humanity per year. At a resting pulse rate, the heart consumes approximately 8-15 ml
O2/min/100 g tissue. This is significantly more than that consumed by the brain (approximately 3 ml O2/min/100 g tissue)
and can increase to more than 70 ml O2/min/100 g myocardial tissue during vigorous exercise. As a general rule,
mammalian heart muscle cannot produce enough energy under anaerobic conditions to maintain essential cellular
processes; thus, a constant supply of oxygen is indispensable to sustain cardiac function and viability. However, the role of
oxygen and oxygen-associated processes in living systems is complex, and they and can be either beneficial or contribute
to cardiac dysfunction and death (through reactive oxygen species). Reactive oxygen species (ROS) are a family of
oxygen-derived free radicals that are produced in mammalian cells under normal and pathologic conditions. Many ROS,
such as the superoxide anion (O2-)and hydrogen peroxide (H2O2), act within blood vessels, altering mechanisms
mediating mechanical signal transduction and autoregulation of cerebral blood flow. Reactive oxygen species are believed
to be involved in cellular signaling in blood vessels in both normal and pathologic states. The major pathway for the
production of ROS is by way of the one-electron reduction of molecular oxygen to form an oxygen radical, the superoxide
anion (O2-). Within the vasculature there are several enzymatic sources of O2-, including xanthine oxidase, the
mitochondrial electron transport chain, and nitric oxide (NO) synthases. Studies in recent years, however, suggest that the
major contributor to O2- levels in vascular cells is the membrane-bound enzyme NADPH-oxidase. Produced O2- can react
with other radicals, such as NO, or spontaneously dismutate to produce hydrogen peroxide (H2O2). In cells, the latter
reaction is an important pathway for normal O2- breakdown and is usually catalyzed by the enzyme superoxide dismutase
(SOD). Once formed, H2O2 can undergo various reactions, both enzymatic and nonenzymatic. The antioxidant enzymes
catalase and glutathione peroxidase act to limit ROS accumulation within cells by breaking down H2O2 to H2O.
Metabolism of H2O2 can also produce other, more damaging ROS. For example, the endogenous enzyme
myeloperoxidase uses H2O2 as a substrate to form the highly reactive compound hypochlorous acid. Alternatively, H2O2
can undergo Fenton or Haber-Weiss chemistry, reacting with Fe2+/Fe3+ ions to form toxic hydroxyl radicals (-. OH).
(PMID: 17027622, 15765131).
9.8.2 Tissue Locations
All Tissues
9.8.3 Cellular Locations
Endoplasmic reticulumExtracellularMitochondriaNucleusPeroxisome
9.8.4 Metabolite Pathways
1. 11-beta-hydroxylase deficiency (CYP11B1) 11. 3-hydroxyisobutyric aciduria

2. 17-alpha-hydroxylase deficiency (CYP17) 12. 3-Methylcrotonyl Coa Carboxylase Deficiency Type I
3. 17-Beta Hydroxysteroid Dehydrogenase III Deficiency 13. 3-Methylglutaconic Aciduria Type I
4. 2-aminoadipic 2-oxoadipic aciduria 14. 3-Methylglutaconic Aciduria Type III
5. 2-Methyl-3-Hydroxybutryl CoA Dehydrogenase Deficiency 15. 3-Methylglutaconic Aciduria Type IV
6. 21-hydroxylase deficiency (CYP21) 16. 3-Phosphoglycerate dehydrogenase deficiency
7. 27-Hydroxylase Deficiency 17. Acetaminophen Action Pathway
8. 3-Beta-Hydroxysteroid Dehydrogenase Deficiency 18. Acetylsalicylic Acid Action Pathway
9. 3-Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency 19. Acute Intermittent Porphyria
10. 3-hydroxyisobutyric acid dehydrogenase deficiency 20. Adenine phosphoribosyltransferase deficiency (APRT)

10 Use and Manufacturing
10.1 Uses
EU Pharmaceutical Product Classes

Veterinary drug
Food additives
JECFA Functional Classes

Food Additives: PROPELLANT
10.2 Methods of Manufacturing

... Oxygen enrichment from air by pressure-swing adsorption (PSA) ... Compressed air enters the adsorption bed at high
pressure. Typical adsorbents are usually based on zeolites. Because zeolite has a higher selectivity for nitrogen, and
oxygen is at a lower partial pressure, nitrogen is adsorbed to an appreciably greater extent and oxygen-enriched air is
obtained at the outlet. The bed is then blown down to a lower pressure to desorb nitrogen. A purge step may sometimes
be used to sweep nitrogen out of the bed before a new cycle begins.
Ullmann's Encyclopedia of Industrial Chemistry. 6th ed.Vol 1: Federal Republic of Germany: Wiley-VCH Verlag GmbH & Co. 2003 to
Present, p. V24 565 (2003)
 from HSDB
Membrane separation of oxygen is accomplished by a thin polymeric film that allows selective transport of oxygen
through it as a result of a driving force, such as differential partial pressure. ... Oxygen dissolves into the membrane at its
upstream surface and diffuses across the membrane to the downstream surface, where it volatilizes into the adjacent gas
phase. Other gases in air also dissolve into the membrane and diffuse along with oxygen; the most important of these is
nitrogen. ... Selectivity of a membrane material for oxygen becomes an important design parameter. The preferred
membrane material must have both a high permeability and a high selectivity for oxygen.
Present, p. V24 566 (2003)
 from HSDB
Oxygen from cryogenic air separation. .. Cryogenic air separation involves three steps: 1) purification of the incoming air
to remove particles, carbon dioxide, and water, 2) refrigeration and economization of refrigeration values contained in the
product and waste streams, /and/ 3) separation by distillation.
Present, p. V24 564 (2003)
 from HSDB
Obtained on large scale by liquefaction of air

and Co., Inc., 2001., p. 1246
 from HSDB
Liquefaction and subsequent controlled fractionation of air; electrolytic decomposition of water; pressure-swing
adsorption of air.
SRI
 from HSDB
... by heating potassium chlorate with manganese dioxide as a catalyst.

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Molecular sieves are used to produce high purity oxygen from air or oxygen-rich air employing a pressure-swing
absorption process ... absorption of nitrogen from air by molecular sieves and desorption at a lower pressure.
Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 1: 552
(1978)
 from HSDB
Barium oxide is converted to barium peroxide when heated in air or oxygen to 500 deg C. Further heating to 700 C the
peroxide decomposes to barium oxide and pure oxygen (Brin process).
Dibello PM et al; Kirk-Othmer Encyclopedia of Chemical Technology. (2005). NY, NY: John Wiley & Sons; Barium compounds. Online
Posting Date: Jul 18, 2003.
 from HSDB
10.3 Impurities
/Possible impurities:/ Argon; krypton; xenon; methane; ethane; ethylene; acetylene; carbon dioxide; carbon monoxide;
nitrous oxide; halogenated refrigerants; solvents /some impurities may be generated from the production process/
Hansel JG; Kirk-Othmer Encyclopedia of Chemical Technology. (2005). NY, NY: John Wiley & Sons; Oxygen. Online Posting Date: May
12, 2005.
 from HSDB
10.4 Formulations/Preparations
Liq: Purity: 99.5+%.
 from HSDB
Grades: low purity; high purity; USP.

Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 827
 from HSDB
Type I, gas, Grades,O2 min: A, 99.0%; B, 99.5%; C, 99.5%; D, 99.5%; E, 99.6%; F, 99.995%. Type II liquid, grades, O2 min: A,
99.0%; B, 99.5%; C, 99.5%; D, 99.5% /Grades with same min have different allowable impurities/
Hansel JG; Kirk-Othmer Encyclopedia of Chemical Technology. (2005). NY, NY: John Wiley & Sons; Oxygen. Online Posting Date: May
12, 2005.
 from HSDB
... Mixtures of oxygen and nitrogen /used in short-duration diving/ that have a larger fraction of oxygen than the 0.2095
normally found in atmospheric air ... are called by several names, including "nitrox," oxygen-enriched air, and enriched air
nitrox.
 from HSDB
Oxygen is now manufactured in only 2 grades: grade A, aviator's breathing oxygen, and grade B, for industrial or medical
purposes. The only difference ... is the permissible moisture content. In high-altitude flying, there is the risk of freeze-up of
any moisture present in an oxygen system ...
 from HSDB
10.5 Consumption
STEEL INDUSTRY USE, 65.4% (BASIC OXYGEN PROCESS, 39.6%); OPEN HEARTH, 9.3%; ELECTRIC 9.3%; ELECTRIC FURNACE,
1.7%; OTHER, 14.8%); NONFERROUS METAL INDUSTRY, 12.0%; OXIDIZING AGENT IN CHEM SYNTH, 12.0% (ETHYLENE
OXIDE, 4.9%; ACETYLENE, 2.3%; TITANIUM DIOXIDE, 1.7%; PROPYLENE OXIDE, 1.4%; VINYL ACETATE, 1.4%; MISC CHEMS,
0.3%); MISC APPLICATIONS, 10.6% (1977)
SRI
 from HSDB
Steel manufacturing, 65%; chemicals, 20%; metal fabrication, 4%; non-ferrous metals, 3%; waste water treatment, 3%; pulp
and paper, 3%; misc, 2% (1981) pulp and paper, 3%; misc, 2% (1981)
CHEMICAL PRODUCTS SYNOPSIS: Oxygen, 1982
 from HSDB
10.6 U.S. Production

(1977) 1.47X10+13 G-EXCLUDES PRODN FOR AMMONIA
SRI
 from HSDB
(1979) 1.71X10+13 G-EXCLUDES PRODN FOR AMMONIA

SRI
 from HSDB
(1985) 3.79x10+11 cu ft
BUREAU OF THE CENSUS. CURRENT INDUSTRIAL REPORTS: INDUSTRIAL GASES JULY 1986 p.1
 from HSDB
(1990) 40.48 billion lb

Chem & Engineering News 70 (15): 17 (4/13/92)
 from HSDB
(1991) 39.07 billion lb

 from HSDB
(1992) 43.46 billion lb

 from HSDB
(1993) 46.52 billion lb

 from HSDB
Production volumes for non-confidential chemicals reported under the Inventory Update Rule.
Year Production Range (pounds)
1986 No Reports
1990 No Reports
1994 No Reports
1998 No Reports
2002 >100 million-500 million
US EPA; Non-confidential Production Volume Information Submitted by Companies for Chemicals Under the 1986-2002 Inventory
Update Rule (IUR). Oxygen (7782-44-7). Available from, as of November 7, 2006: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html
 from HSDB
10.7 U.S. Imports

(1977) No Data
SRI
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(1979) No Data
SRI
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(1987) No Data
SRI
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10.8 U.S. Exports

(1977) 3.07X10+10 GRAMS
SRI
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(1979) No Data
SRI
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(1987) No Data
SRI
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11 Identification
11.1 Analytic Laboratory Methods

DISSOLVED OXYGEN IN WATER: AZIDE (ALSTERBERG) METHOD IS ORDINARLY USED; IT IS NOT AFFECTED BY MOST
COMMON INTERFERENCE, NITRITE, BUT MOST OTHER OXIDIZING OR REDUCING AGENTS SHOULD BE ABSENT. EFFECT
OF FE+3 IS ELIMINATED WITH F-. PERMANGANATE (RIDEAL-STEWART) METHOD IS USED IN PRESENCE OF FE+2 BUT
NOT ORGANIC MATTER. POMEROY-KIRSHMAN-ALSTERBERG METHOD IS USED FOR WATERS SUPERSATURATED WITH O
OR CONTAINING HIGH ORGANIC MATTER CONTENT.
Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of
Official Analytical Chemists, 1965. New editions through 13th ed. plus supplements, 1982., p. 13/550 33.027
 from HSDB
MICROCHEMICAL DETERMINATION OF OXYGEN USING OXYGEN FLASK COMBUSTION METHOD.

Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of
Official Analytical Chemists, 1965. New editions through 13th ed. plus supplements, 1982., p. 13/858 47.024
 from HSDB
Oxygen detn water spectrophotometry. Spectrophotometric determination of dissolved oxygen in water through the
formation of an argentocyanide complex with silver sol.
Pal T, Das PK; Analyst (London) 113 (10): 1601-3 (1988)
 from HSDB
Besides volumetric, chemical, and gc methods, oxygen (concentration >0.1 vol%) may be determined without significant
interference from other components by using instruments based on the measurement of magnetic susceptibility.
Present, p. V15 457 (2003)
 from HSDB
Method: NIOSH 6601, Issue 2; Procedure: electrochemical sensor; Analyte: oxygen; Matrix: air; Detection Limit: not
provided.
CDC; NIOSH Manual of Analytical Methods, 4th ed. Oxygen (7782-44-7). Available from, as of October 4, 2006:
http://www.cdc.gov/niosh/docs/2003-154/
 from HSDB
11.2 OSHA Chemical Sampling

Oxygen
 from OSHA Chemical Sampling Information
11.3 NIOSH Analytical Methods

OXYGEN 6601
 from NIOSH Manual of Analytical Methods
12 Safety and Hazards
12.1 Hazards Identification
12.1.1 GHS Classification
Signal: Danger
GHS Hazard Statements
Aggregated GHS information provided by 1044 companies from 13 notifications to the ECHA C&L Inventory. Each
notification may be associated with multiple companies.
Reported as not meeting GHS hazard criteria by 2 of 1044 companies. For more detailed information, please visit ECHA
C&L website
Of the 12 notification(s) provided by 1042 of 1044 companies with hazard statement code(s):
H270 (100%): May cause or intensify fire; oxidizer [Danger Oxidizing gases]
H280 (26.39%): Contains gas under pressure; may explode if heated [Warning Gases under pressure]
H281 (11.61%): Contains refrigerated gas; may cause cryogenic burns or injury [Warning Gases under pressure]
Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in
parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with
percentage values above 10% are shown.
Precautionary Statement Codes

P220, P244, P282, P315, P336, P370+P376, P403, P41, and P403
(The corresponding statement to each P-code can be found here.)
 from European Chemicals Agency (ECHA)
View all (5) GHS Classification entries
12.1.2 Health Hazard
Inhalation of 100% oxygen can cause nausea, dizziness, irritation of lungs, pulmonary edema, pneumonia, and collapse.
Liquid may cause frostbite of eyes and skin. (USCG, 1999)
12.1.3 Fire Hazard
Behavior in Fire: Increases intensity of any fire. Mixtures of liquid oxygen and any fuel are highly explosive. (USCG, 1999)
Not combustible but enhances combustion of other substances. Heating will cause rise in pressure with risk of bursting.
 from ILO-ICSC
Not combustible but enhances combustion of other substances. Risk of fire and explosion on contact with combustible
substances or reducing agents.
 from ILO-ICSC
12.1.4 Fire Potential
Gas: moderate fire risk as oxidizing agent.

 from HSDB
Oxygen is noncombustible, but actively supports combustion.

 from HSDB
Strong oxidizer ... May initiate fire/explosion in combustible materials. /Oxygen, liquid/
Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 49-112
 from HSDB
Even a slight increase in the oxygen content of air above its usual 21 vol % will greatly increase the rate of oxidation or
combustion of many substances.
Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 1394
 from HSDB
... Fires at the interface of oxygen regulators and cylinder valves because of incorrect use of /the plastic (usually Nylon)
crush gasket of/ CGA 870 seals /was alerted/ ... 12 reports /had been received/ in which regulators used with oxygen
cylinders have burned or exploded, in some cases injuring personnel. Some of the incidents occurred during emergency
medical use or during routine equipment checks.
US FDA; FDA AND NIOSH Public Health Notification: Oxygen Regulator Fires Resulting from Incorrect Use of CGA 870 Seals (Updated:
June 19, 2006). Available from, as of August 29, 2006: http://www.fda.gov/cdrh/safety/042406-o2fires.html
 from HSDB
... 16 reports of aluminum regulators used with oxygen cylinders burning or exploding /had been received/. These
incidents caused severe burns to 11 health care workers and patients. Many of the incidents occurred during emergency
medical use or during routine equipment checkout. FDA and The National Institute for Occupational Safety and Health
(NIOSH) believe that the aluminum in these regulators was a major factor in both the ignition and severity of the fires ...
US FDA; FDA And NIOSH Public Health Advisory: Explosions and Fires in Aluminum Oxygen Regulators (February 1999). Available from,
as of August 30, 2006: http://www.fda.gov/cdrh/oxyreg.html
 from HSDB
12.1.5 Skin, Eye, and Respiratory Irritations
Liq: Irritant to skin & tissues.

 from HSDB
The inhalation, at 1 atm, of 80% O2 for more than about 12 hr /causes/ ... Irritation of resp tract ...
 from HSDB
Contact with liquid will cause frostbite.

 from HSDB
... Short-term /oxygen/ exposure ... at very high concentrations is irritating to the respiratory tract /and/ may cause effects
on ... lungs and eyes.
IPCS, CEC; International Chemical Safety Card on Oxyge. (October 1999). Available from, as of August 29, 2006:
http://www.inchem.org/documents/icsc/icsc/eics0138.htm
 from HSDB
12.2 Safety and Hazard Properties
12.2.1 Flammability
Not flammable in air. /Liquid oxygen/

 from HSDB
12.2.2 Critical Temperature
Critical temperature: -118.95 deg C; critical pressure: 50.14 atm

and Co., Inc., 2001., p. 1246
 from HSDB
12.2.3 Critical Pressure
Critical temperature: -118.95 deg C; critical pressure: 50.14 atm

and Co., Inc., 2001., p. 1246
 from HSDB
12.2.4 NFPA Hazard Classification
Health 3. 3 = Materials extremely hazardous to health, but areas may be entered with extreme care. Full protective
clothing, including self-contained breathing apparatus, rubber gloves, boots and bands around legs, arms and waist
should be provided. No skin surface should be exposed.
National Fire Protection Association. Fire Protection Guide on Hazardous Materials. 7th ed. Boston, Mass.: National Fire Protection
Association, 1978., p. 49-225
 from HSDB
Flammability 0. 0 = Materials that will not burn.
 from HSDB
Reactivity 0. 0 = Materials which are normally stable even under fire exposure conditions and which are not reactive with
water. Normal fire fighting procedures may be used.
 from HSDB
12.2.5 NFPA Health Rating
3
12.2.6 Physical Dangers
The gas is heavier than air.

 from ILO-ICSC
12.2.7 Chemical Dangers
The substance is a strong oxidant. It reacts with combustible and reducing materials. This generates fire and explosion
hazard.
 from ILO-ICSC
12.2.8 Explosive Limits and Potential
The substance is a strong oxidant and reacts with combustible and reducing materials, causing fire and explosion hazard.
 from HSDB
Strong oxidizer ... May initiate fire/explosion in combustible materials ... A leak of liquid oxygen onto combustible material
represents a severe explosion potential ... /Oxygen, liquid/
 from HSDB
12.3 First Aid Measures
12.3.1 First Aid

INHALATION: in all but the most severe cases (pneumonia), recovery is rapid after reduction of oxygen pressure;
supportive treatment should include immediate sedation, anticonvulsive therapy if needed, and rest. EYES: treat frostbite
burns. SKIN: treat frostbite; soak in lukewarm water. (USCG, 1999)
12.3.2 Inhalation First Aid
Refer for medical attention.

 from ILO-ICSC
Fresh air, rest. Refer for medical attention.

 from ILO-ICSC
12.3.3 Skin First Aid
ON FROSTBITE: rinse with plenty of water, do NOT remove clothes. Refer for medical attention .
 from ILO-ICSC
12.3.4 Eye First Aid
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical
attention.
 from ILO-ICSC
12.4 Fire Fighting Measures

LIQ: When fire results from a leak or flow of liq oxygen onto wood, paper, waste or another similar material, the first thing
to do is stop flow if possible. For small spills, or after leak or flow of liq oxygen has been stopped, use enough water to
put out fire quickly. When fire involves liq oxygen and liq fuels, control it as follows: (a) When liq oxygen leaks or flows
into large quantities of fuel, shut off flow of liq oxygen, and put remaining fuel fire out with extinguishing agents suitable
for use on class B fires. When fuel leaks or flows into large quantities of liq oxygen, shut off flow of fuel. (b) When fuel and
liq oxygen are mixed or mixing but are not yet burning, isolate area from sources of ignition and get out quickly, allowing
oxygen to evaporate. When large pools of water-soluble fuel are present, use water to dilute fuel and reduce intensity of
fire. This method cannot be used with fuels which do not mix with water. Appropriate extinguishing agents may be used
to put out fuel fires after the oxygen has evaporated.
 from HSDB
If material involved in fire: Dangerously explosive. Cool all affected containers with flooding quantities or water. Do not
use water on material itself. Apply water from as far a distance as possible. /Oxygen, refrigerated liquid/
Association of American Railroads; Bureau of Explosives. Emergency Handling of Hazardous Materials in Surface Transportation.
Association of American Railroads, Pueblo, CO. 2005, p. 686
 from HSDB
If material involved in fire: Dangerously explosive. Cool all affected containers with flooding quantities of water. Apply
water from as far as distance as possible. /Oxygen, compressed/
 from HSDB
Evacuation: If fire becomes uncontrollable or container is exposed to direct flame: consider evacuation of one-third (1/3)
mile radius. /Oxygen, compressed; Oxygen, refrigerated liquid/
Association of American Railroads, Pueblo, CO. 2005, p. 685-6
 from HSDB
12.4.1 Fire Fighting
Excerpt from ERG Guide 122 [Gases - Oxidizing (Including Refrigerated Liquids)]: Use extinguishing agent suitable for type
of surrounding fire. SMALL FIRE: Dry chemical or CO2. LARGE FIRE: Water spray, fog or regular foam. Move containers
from fire area if you can do it without risk. Damaged cylinders should be handled only by specialists. FIRE INVOLVING
TANKS: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with
flooding quantities of water until well after fire is out. Do not direct water at source of leak or safety devices; icing may
occur. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay
away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible,
withdraw from area and let fire burn. (ERG, 2016)
In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep cylinder cool by spraying
with water. Combat fire from a sheltered position.
 from ILO-ICSC
In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep drums, etc., cool by spraying
with water. NO direct contact with water. Combat fire from a sheltered position.
 from ILO-ICSC
12.4.2 Other Fire Fighting Hazards
If oxygen-enriched clothing catches fire, extinguish under safety shower; fire blanket may not be effective. Use continuous
water spray to soak clothing of a rescuer who must operate in oxygen-enriched fire area.
General Electric Co; Material Safety Data Sheet #62 (1980)
 from HSDB
Most fibrous fabrics will absorb oxygen when exposed to concn greater than the normal 21% in air, and this is retained
for a long time after excess oxygen is no longer present, greatly increasing the possibility of ignition.
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Heating will cause rise in pressure with risk of bursting ... The gas is heavier than air.
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12.5 Accidental Release Measures

12.5.1 Isolation and Evacuation
Excerpt from ERG Guide 122 [Gases - Oxidizing (Including Refrigerated Liquids)]: As an immediate precautionary measure,
isolate spill or leak area for at least 100 meters (330 feet) in all directions. LARGE SPILL: Consider initial downwind
evacuation for at least 500 meters (1/3 mile). FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters
(1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)
12.5.2 Spillage Disposal
Ventilation.
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Ventilation. Remove all ignition sources. Do NOT absorb in saw-dust or other combustible absorbents. NEVER direct water
jet on liquid.
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12.5.3 Cleanup Methods
Notify safety personnel of significant leaks or spills. ... Shut off oxygen source if possible.
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To increase the rate of controlled evaporation, spray with large amounts of water (fog may be generated and reduce
visibility). /Liquid oxygen/
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Eliminate all ignition sources. Stop or control the leak, if this can be done without undue risk. USe water spray to disperse
vapors and protect personnel.
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Ventilation. Remove all ignition sources. Do NOT absorb in saw-dust or other combustible absorbents. NEVER direct water
jet on liquid. /Oxygen, liquefied/
IPCS, CEC; International Chemical Safety Card on Oxygen (liquified). (April 2000). Available from, as of August 29, 2006:
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12.5.4 Disposal Methods
SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for
occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use
or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air
quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental
and public health regulations.
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Remove waste containers or leaking cylinders to exhaust hood or outdoors away from combustibles and allow to
discharge at moderate rate. Tag cylinder to indicate defect, close valve and return to supplier. /Liquid and compressed
oxygen/
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Evaporation: Remove waste containers or leaking cylinders to exhaust hoods or outdoors away from combustibles and
allow to discharge @ a moderate rate. Tag cylinder to indicate defect, close valve and return to supplier.
United Nations. Treatment and Disposal Methods for Waste Chemicals (IRPTC File). Data Profile Series No. 5. Geneva, Switzerland:
United Nations Environmental Programme, Dec. 1985., p. 219
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12.5.5 Other Preventative Measures
FDA and NIOSH recommend that plastic crush gaskets /on oxygen cylinders/ never be reused, as they may require
additional torque to obtain the necessary seal with each subsequent use. This can deform the gasket, increasing the
likelihood that oxygen will leak around the seal and ignite. The following general safety precautions should also be taken
to avoid explosions, tank ruptures and fires from oxygen regulators. Always "crack" cylinder valves (open the valve just
enough to allow gas to escape for a very short time) before attaching regulators in order to expel foreign matter from the
outlet port of the valve. Always follow the regulator manufacturer's instructions for attaching the regulator to an oxygen
cylinder. Always use the sealing gasket specified by the regulator manufacturer. Always inspect the regulator and CGA 870
seal before attaching it to the valve to ensure that the regulator is equipped with only one clean, sealing- type washer
(reusable metal-bound rubber seal) or a new crush-type gasket (single use, not reusable, typically Nylon) that is in good
condition. Always be certain the valve, regulator and gasket are free from oil or grease. Oil or grease contamination is
widely known to contribute to ignition in oxygen systems. Tighten the T-handle firmly by hand, but do not use wrenches
or other hand tools that may over-torque the handle. Open the post valve slowly. If gas escapes at the juncture of the
regulator and valve, quickly close the valve. Verify the regulator is properly attached and the gasket is properly placed and
in good condition. If you have any questions or concerns contact your supplier.
FDA Center for Devices and Radiological Health; FDA AND NIOSH Public Health Notification: Oxygen Regulator Fires Resulting from
Incorrect Use of CGA 870 Seals. June 19, 2006. Available from, as of November 22, 2006: http://www.fda.gov/cdrh/safety/042406-
o2fires.html
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... Do not use oil or grease to lubricate valves on oxygen cylinders. /Liquid oxygen/
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If material not involved in fire: Keep sparks, flames, and other sources of ignition away. Attempt to stop leak if without
undue personnel hazard. Do not use water on material itself. /Oxygen, refrigerated liquid/
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If material is not involved in fire: Keep sparks, flames and other sources of ignition away. Attempt to stop leak if without
hazard. /Oxygen, compressed/
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Personnel protection: ... Do not handle broken packages unless wearing appropriate personal protective equipment.
Approach fire with caution. /Oxygen, compressed; Oxygen, refrigerated liquid/
Association of American Railroads, Pueblo, CO. 2005, p. 685-6
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CAUTION: AVOID SMOKING, FLAMES, ELECTRIC SPARKS- EXPLOSION HAZARD.

The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983., p. 999
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... Equipment which may emit or leak oxygen should be used sparingly, and never stored in confined spaces ... /Oxygen
enrichment/
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NO open flames, NO sparks, and NO smoking. NO contact with flammable substances. NO contact with reducing agents
... Do not eat, drink, or smoke during work. /Oxygen, liquefied/
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FDA and NIOSH recommend that plastic crush gaskets /of oxygen cylinders/ never be reused, as they may require
additional torque to obtain the necessary seal with each subsequent use. This can deform the gasket, increasing the
likelihood that oxygen will leak around the seal and ignite ... To avoid explosions, tank ruptures and fires from oxygen
regulators: Always "crack" cylinder valves (open the valve just enough to allow gas to escape for a very short time) before
attaching regulators in order to expel foreign matter from the outlet port of the valve. Always follow the regulator
manufacturer's instructions for attaching the regulator to an oxygen cylinder. Always use the sealing gasket specified by
the regulator manufacturer. Always inspect the regulator and CGA 870 seal before attaching it to the valve to ensure that
the regulator is equipped with only one clean, sealing-type washer (reusable metal-bound rubber seal) or a new crush-
type gasket (single use, not reusable, typically Nylon) that is in good condition. Always be certain the valve, regulator and
gasket are free from oil or grease. Oil or grease contamination is widely known to contribute to ignition in oxygen
systems. Tighten the T-handle firmly by hand, but do not use wrenches or other hand tools that may over-torque the
handle. Open the post valve slowly. If gas escapes at the juncture of the regulator and valve, quickly close the valve. Verify
the regulator is properly attached and the gasket is properly placed and in good condition ...
US FDA; FDA AND NIOSH Public Health Notification: Oxygen Regulator Fires Resulting from Incorrect Use of CGA 870 Seals (Updated:
June 19, 2006). Available from, as of August 29, 2006: http://www.fda.gov/cdrh/safety/042406-o2fires.html
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... FDA and NIOSH advise that the following precautions be taken to avoid explosions and fires from oxygen regulators
containing aluminum: ... /Replace/ high pressure oxygen regulators which contain any aluminum exposed to high-
pressure oxygen ... with regulators made of brass. Consult the manufacturer if ... material /not known/ ... If non-aluminum
oxygen regulators are not available /follow guideline of Safe Practices for Handling and Operating Oxygen Equipment/ ...
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Safe Practices for Handling and Operating Oxygen Equipment: Storage, Maintenance and Handling--Do not allow
smoking around oxygen. Store oxygen in clean, dry locations away from direct sunlight. Do not allow post valves,
regulators, gauges, and fittings to come into contact with oils, greases, organic lubricants, rubber or any other
combustible substance. Make sure that any cleaning, repair or transfilling of oxygen equipment is performed by qualified,
properly trained staff. Do not work on oxygen equipment with ordinary tools. Designate special tools, clean them and
store them for Use With Oxygen Equipment Only. Ensure that any components added to the regulator, eg, gauge guards,
are installed so that they do not block the regulator vent holes. Use plugs, caps and plastic bags to protect "off duty"
equipment from dust and dirt. Particulate migration from the cylinder can be minimized by the installation of a standoff
tube (bayonette) at the inlet of the post valve.
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Safe Practices for Handling and Operating Oxygen Equipment: Use--Make sure that staff using oxygen equipment are
adequately trained in its operation and in oxygen safety and have knowledge of manufacturers instructions for using the
equipment. Visually inspect the post valve gasket and regulator inlet prior to installation. If they are not visually clean they
should not be used. Momentarily open and close ("Crack") the post valve to blow out debris prior to installing a regulator.
Ensure that the regulator is set with the flow knob in the off position before attaching it to the cylinder. Position the
equipment so that valve is pointed away from the user and any other persons. Open the cylinder valve slowly and
completely to minimize the heat produced and achieve the desired flow conditions within the equipment. Do not look at
the regulator pressure gauge until the cylinder valve is fully opened.
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12.6 Handling and Storage
12.6.1 Nonfire Spill Response
Excerpt from ERG Guide 122 [Gases - Oxidizing (Including Refrigerated Liquids)]: Keep combustibles (wood, paper, oil,
etc.) away from spilled material. Do not touch or walk through spilled material. Stop leak if you can do it without risk. If
possible, turn leaking containers so that gas escapes rather than liquid. Do not direct water at spill or source of leak. Use
water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Prevent
entry into waterways, sewers, basements or confined areas. Allow substance to evaporate. Isolate area until gas has
dispersed. CAUTION: When in contact with refrigerated/cryogenic liquids, many materials become brittle and are likely to
break without warning. (ERG, 2016)
12.6.2 Safe Storage
Fireproof. Separated from combustible substances and reducing agents. Cool.

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12.6.3 Storage Conditions
GAS & LIQ: GASEOUS OXYGEN IS STORED ... IN CYLINDERS AT A PRESSURE OF 150-160 ATM, & INSULATED TANKS ARE
USED FOR LIQUID OXYGEN; SMALL QUANTITIES OF LIQUID OXYGEN (2-50 L) CAN BE STORED IN DEWAR FLASKS.
Office, 1983., p. 1578
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Oxygen should be stored in an area that is at least 20 ft away from any flammable or combustible materials (especially oil
& grease) or separated from them by a noncombustible barrier at least 5 ft high & having a fire-resistant rating of at least
1/2 hr.
National Research Council. Prudent Practices for Handling Hazardous Chemicals in Laboratories. Washington, DC: National Academy
Press, 1981., p. 222
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LIQ: Protect against physical damage. Isolate from combustible gas installations and combustible materials by adequate
distance or by gas-tight fire-resistive barriers. Protect against overheating. Outside storage of liq oxygen tanks is
recommended.
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Where oxygen may be released, provide adequate ventilation to prevent excessive oxygen-enrichment of the workplace
atmosphere (holding at < 23 Vol % O2 is recommended for fire safety).
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Store oxygen containers in a clean, cool, dry, well-ventilated, low-fire risk area ... Never expose any part of a cylinder to
temperature above 125 deg F. Ground equipment to eliminate build-up of static charge. Ensure that containers of liquid
oxygen are properly vented to prevent pressure build-up and that suitable materials are used to contact liquid oxygen
and high purity oxygen. /Liquid and compressed oxygen/
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12.7 Exposure Control and Personal Protection
12.7.1 Other Occupational Permissible Levels
In the water, the US Navy permits oxygen breathing up to 10 min at a max depth of 50 feet (2.5 ATA) in decompressing
resting divers in a closed, dry, diving suit. In active swimmers, oxygen breathing is only permitted to a max depth of 25
feet. Other navies specify an 18-feet max depth for long underwater swims by attack divers breathing 100% oxygen ...
Scuba divers must never charge their tanks with 100% oxygen. Even when oxygen is diluted, current US Navy regulations
stipulate that the partial pressure of oxygen at any depth in any mixture must not exceed 1.6 ATA effective for more than
30 min.
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Techniques for avoiding CNS toxicity are straightforward in most commercial and military diving: the oxygen level low
enough to prevent any reasonable possibility of having a convulsion or "CNS hit" (called a "fit" in British parlance). In
general practice, this is below a level of about 1.4 bars pO2 ... The exposure guidelines technical divers use to manage
oxygen toxicity are derived from those published in the NOAA Diving Manual. The upper range of these limits (eg, an
"allowed" exposure of 45 min at 1.6 bars pO2) is appropriate for the tethered and helmeted diver or the diver doing very
light work ...
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It is commonly accepted in the commercial world that no more than 0.6 ATA oxygen partial pressure should be
maintained in the saturation complex and in the bell so that metabolic demands are net, but toxic levels are not
exceeded. This equivalent to breathing 60% oxygen on the surface. These exposures have proven safe for up to 2 weeks
with regard to pulmonary oxygen toxicity, both in the North Sea and in air saturation in the Hydrolab habitat. /Saturation
diving/
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12.7.2 Effects of Short Term Exposure
The substance at very high concentrations is irritating to the respiratory tract. The substance may cause effects on the
central nervous system, lungs and eyes.
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Rapid evaporation of the liquid may cause frostbite. The substance at very high concentrations is irritating to the
respiratory tract. The substance may cause effects on the central nervous system.
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12.7.3 Effects of Long Term Exposure
Repeated or prolonged inhalation of high concentrations may cause effects on the lungs.
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12.7.4 Fire Prevention
NO open flames, NO sparks and NO smoking. NO contact with flammables.

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NO open flames, NO sparks and NO smoking. NO contact with flammables. NO contact with reducing agents.
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12.7.5 Skin Prevention
Cold-insulating gloves. Protective clothing.

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12.7.6 Eye Prevention
Wear safety goggles.

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Wear safety goggles or face shield.

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12.7.7 Ingestion Prevention
Do not eat, drink, or smoke during work.

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12.7.8 Protective Equipment and Clothing

Safety goggles or face shield; insulated gloves; long sleeves; trousers worn outside boots or over high-top shoes to shed
spilled liquid. (USCG, 1999)
Liq: Safety goggles or face shield; insulated gloves; long sleeves; trousers worn outside boots or over high-top shoes to
shed spilled liquid.
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LIQ: Wear special protective clothing that will not ignite on contact with liq oxygen and that is designed to prevent liq ...
from coming in contact with skin.
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Wear ... positive pressure self-contained breathing apparatus.

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12.8 Stability and Reactivity
12.8.1 Air and Water Reactions
No rapid reaction with air. No rapid reaction with water.

12.8.2 Reactive Group
Oxidizing Agents, Strong

12.8.3 Reactivity Alerts
Strong Oxidizing Agent

12.8.3.1 Pistoia Alliance CSL Reactivity Alerts
Pistoia Alliance CSL Reactivity Alerts: 1 of 1 (Pistoia Alliance CSL Reaction Information)
CSL No CSL00134
OXYGEN; COPPER(II) CHLORIDE DIHYDRATE; 2,6-DIBROMOPYRIDINE; N-

Reactants/Reagents
BUTYLLITHIUM; DIETHYL ETHER
Pistoia Alliance CSL Reactivity Alerts: 1 of 1 (Pistoia Alliance CSL Reaction Information)
Reaction Class Ullmann coupling
GHS Category Explosive
O2 reacted with the organocopper (or remaining organolithium) reagent to form

Warning Message
some peroxides which exploded
Source Reference ACS Safety Letters
CSL Status Approved
Modified Date 8/7/2018
 from Pistoia Alliance Chemical Safety Library
12.8.4 Reactivity Profile
Propellant; ignites upon contact with alcohols, alkali metals, amines, ammonia, beryllium alkyls, boranes, dicyanogen,
hydrazines, hydrocarbons, hydrogen, nitroalkanes, powdered metals, silanes, or thiols [Bretherick 1979. p.174]. Heat of
water will vigorously vaporize liquid oxygen, pressures may build to dangerous levels if this occurs in a closed container.
Liquid oxygen gives a detonable mixture when combined with powdered aluminum [NFPA 491M. 1991].
12.8.5 Reactivities and Incompatibilities
Liq: Heat of water will vigorously vaporize liquid oxygen.

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Oxygen leaked into the free space in an acetaldehyde storage tank normally purged with nitrogen. Accelerating
exothermic oxidation led to detonation. The self-ignition temperature of acetaldehyde-oxygen mixtures depends on
dimensions of the reactor and the partial pressure of peracetic acid accumulated on the walls. Spontaneous ignition
temperatures of 71 to 73 deg C were observed.
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Oxygen reacts explosively with phosphine, hydrazine, hydrogen sulfide ...

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Synthesis gas (CO + H2) at 40 bar containing a low level of hydrogen sulfide was to be freed of the latter impurity by
adding the theoretical quantity of oxygen and passing the mixture over a catalyst. Introducing of oxygen (from a supply at
60 bar) via a simple T-piece (instead of through the recommended small bore coaxial injection nozzle to ensure thorough
mixing with the gas stream) caused development of an intense inverse flame in the locally very high oxygen concn which
burned through the reactor side wall opposite the oxygen inlet and ejected a meter-long flame-jet.
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Addition of powdered copper to a 1:2 mixture of hydrogen sulfide and oxygen causes the metal to become incandescent
and ignite the explosive mixture ... During an investigation of the spontaneously explosive oxidation of near-
stoichiometric gas mixtures /of hydrogen sulfide and oxygen/ in the range /of/ 280 to 360 deg C, extensive self-heating
was observed before ignition occurred ...
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Interaction /between dimethyl sulfide and oxygen/ is explosive at 210 deg C or above ...
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Calcium and other alkaline-earth phosphides incandesce in oxygen at about 300 deg C.
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An explosive reaction of ... /oxygen and tetrafluorohydrazine/ is likely in the presence of organic matter ... Spontaneous
ignition occurs when ... /hydrazine and liquid oxygen/ are mixed.
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Secondary alcohols are readily autoxidized in contact with oxygen or air, forming ketones and hydrogen peroxide. A
partly full bottle of 2-propanol exposed to sunlight for a long period became 0.36 M in peroxide and potentially
explosive.
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Reactivity towards air or oxygen increases from lithium to cesium, and the intensity depends on state of subdivision and
on presence or absence of moisture. Lithium normally ignites in air above its mp, while potassium may ignite after
exposure to atmosphere, unless it is unusually dry. Rubidium and cesium ignite immediately on exposure. It is reported
that sodium and potassium may be distilled unchanged under perfectly dried oxygen ... Finely divided calcium may ignite
in air, and the massive metal ignites on heating in air, and burns vigorously at 300 deg C in oxygen. Strontium and barium
behave similarly.
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Solid calcium ignites spontaneously in moist oxygen.

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Nickel carbonyl vapor explodes in air or oxygen at 20 deg C and a partial pressure of 15 mm ...
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A mixture of the dry /tetracarbonylnickel/ ... and oxygen will explode on vigorous shaking with mercury (presumably
catalysed by mercury or its oxide) ... The /tetracarbonylnickel/ ... on exposure to atmospheric oxygen produces a deposit
which becomes peroxidized and may ignite. Mixtures with air or oxygen at low partial and total pressures explode after a
variable induction period. Addition of the /tetracarbonylnickel/ ... to a butane-oxygen mixture at 20 to 40 deg C caused
explosive reactions in some cases.
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Sodium hydride ignites in oxygen at 230 deg C, and finely divided uranium hydride ignites on contact. Lithium hydride,
sodium hydride and potassium hydrides react slowly in dry air, while rubidium and cesium hydrides ignite. Reaction is
accelerated in moist air, and even finely divided lithium hydride ignites then. Finely divided magnesium hydride, prepared
by pyrolysis, ignites immediately in air ... Ignition of diborane and tetraborane(10) in contact with air or oxygen is due to
the presence of traces of silicon hydrides. The lower members of the latter class ignite or explode in air or oxygen,
especially at reduced pressure. phosphine is also sensitive.
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Mixtures of lithium hydride powder and liquid oxygen are detonable explosives of greater power than trinitrotoluene
(TNT). /Oxygen, liquid/
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Even small amount of oxygen present in phosphine give an explosive mixture, in which autoignition occurs at low
pressures.
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... /Rhenium/ ignites in oxygen at 300 deg C.

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During preparation of perrhenyl chloride by combustion of rhenium nonachloride in an oxygen stream, a violent
explosion, possibly involving chlorine oxides, occurred on heating the chloride to 250 deg C. A safe procedure involving
heating the chloride to 250 deg C under nitrogen, and then introducing oxygen, is proposed.
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Mixtures /of 1,3,5-trioxane/ with liquid oxygen are highly explosive. /Oxygen, liquid/
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Many ethers, either of open chain (diethyl or diisopropyl ether) or cyclic type (tetrahydrofuran, dioxane), are readily
autoxidized on exposure to air or oxygen in presence of light. The hydroperoxides formed are less volatile than the parent
ether and may be concn to a dangerous extent if distillation of peroxidized material is attempted.
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In the presence of oxygen or air, ethers form peroxides which may explode spontaneously or when heated ... Ethyl ether
forms peroxides which may explode when heated to about 100 deg C ... Isopropyl ether, which had stood on the shelf a
long time, exploded when the stuck cap on the bottle was freed ... Isopropyl ether tends to react with oxygen from the air
to form unstable peroxides which may detonate with extreme violence. Several incidents are cited.
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Autoxidation of dimethylketene with oxygen in ether at -20 deg C gives the poly(peroxylactone) which as a dry solid is
liable to undergo unpredictable and violent detonation.
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Biological material in a polythene bag filled with oxygen and being prepared for analytical combustion exploded. Diethyl
ether used to anaesthetize the experimental animal from which the sample was derived may have still been present, and
ignition from static charge on the plastics bag may have been involved.
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The transition of deflagration to detonation in mixtures /of propylene oxide (methyloxirane) and oxygen/ was studied
with respect to mixing ratio, pressure and spark energy.
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Liquid phase oxidation of 4-methoxytoluene to anisaldehyde at 60 bar/115 deg C in acetic acid containing heavy metal
salts is violent, and must be controlled by the rate of addition of oxygen gas.
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Flash bulbs containing aluminum foil plus oxygen, when ignited, cause similar bulbs up to 8 inches away to be ignited by
radiated heat ... Liquid oxygen gives a detonable mixture when combined with powdered aluminum ... A lecturer was
demonstrating the ignition of powdered aluminum mixed with liquid oxygen when the mixture exploded. Seventeen
persons were injured. This experiment, which is described in several places as a lecture demonstration, has been carried
out successfully hundreds of times but there have been a few explosions when the conditions were just right.
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A demonstration of combustion of aluminium powder in oxygen exploded violently, probably owing to presence of
unevaporated liquid at ignition. Stoichiometric mixtures of the two are explosives much more powerful than
trinitrotoluene (TNT) ... An aluminium filter in a high-capacity liquid oxygen transfer line exploded violently, possibly
owing to friction or impact ignition of an aluminium component in contact with an abrasive particle, which would
penetrate the protective oxide layer ... Mixtures of liquid oxygen with 48 to 64 wt% of fine aluminium powder are
detonable ... A ... liquid oxygen road tanker constructed of aluminium ruptured violently during manoeuvring operations
after a delivery, when the contents had been pressured up with gaseous oxygen (evaporated from the liquid) to expel the
liquid. The rupture was traced to erosion and thinning of the tank wall adjacent to an internal baffle joint, where
aluminium particles, oil and a halocarbon degreasing solvent were trapped in a cavity in the weld. These had reacted with
the pressurizing oxygen atmosphere, raising the wall temperature in the vapor space to that where direct reaction of the
aluminium container with gaseous oxygen was possible. Some 70 kg of metal was missing in all ... /Oxygen, liquid/
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/Aluminium-titanium/ alloys ranging from Al3Ti2 to Al4Ti ... ignite or incandesce on heating in ... oxygen.
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Explosive reaction /between aluminum borohydride and oxygen/ occurs at temperatures as low as 20 deg C. Explosive
range: 5% to 90% ... Aluminum hydride is spontaneously flammable in oxygen or air.
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... Powdered magnesium, titanium or zirconium mixed with liquid oxygen are detonable. A nitrogen-pressurized liquid
oxygen dispenser made of titanium alloy failed during nitrogen pressurizing. The vessel failed because of reaction of the
titanium alloy with liquid oxygen. Titanium is more reactive towards oxygen than either stainless steel or aluminium, and
should therefore not be used for oxygen service, either gas or liquid ... Detonation of mixtures with powdered aluminum,
iron, titanium and chromium-nickel alloy powders was studied ... /Oxygen, liquid/
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Passage of oxygen through a titanium feed pipe into a titanium autoclave caused a titanium-oxygen fire and explosion at
44 bar. When the surface oxide film is damaged, titanium can ignite at 24 bar under static conditions and at 3.4 bar under
dynamic conditions, with oxygen at ambient temperature ... The Drager oxygen-measuring tube contains titanium
trichloride as the indicating substance, and a possible hazard in using these tubes to measure oxygen contents above 25
vol% in gas mixtures has been noted. The temperature in the tube can reach 120 deg C during oxidation of titanium
trichloride to titanium dichloride oxide, so the test should not be used if cmpd with ignition point below 135 deg C (eg
carbon disulfide) are present.
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A titanium alloy tank containing liquid oxygen exploded during a laboratory experiment. Contamination might have
triggered the reaction. An explosion hazard may exist in the use of titanium with either gaseous or liquid oxygen.
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Mixtures /of liquid oxygen with/ liquid carbon monoxide, cyanogen (solidified) and methane are highly explosive.
Autoignition in liquid oxygen-hydrogen propellant system has been reviewed. /Liquid oxygen/
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The thermal homogeneous chain reaction /among hexafluoropropene, oxygen difluoride and oxygen/ to give mainly
octafluoropropane and hexafluoropropylene oxide becomes explosive above a minimum oxygen pressure of 26 mbar.
/Oxygen, liquid/
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1,1,1-Trichloroethane exploded after heating under oxygen at 54 bar and 100 deg C for 3 hr. Trichloroethylene, remaining
in a pipe after cleaning operations, exploded under 27 bar pressure of oxygen at ambient temperature. It was later found
possible to explode stoichiometric mixtures. Chlorotrifluoroethylene and bromotrifluoroethylene each react explosively
with oxygen at ambient temperature, but controlled oxidation of the former produces an explosive cyclic peroxide, 4,5-
dichloro-3,3,4,5,6,6-hexafluoro-1,2-dioxane.
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Mixtures of liquid oxygen with dichloromethane, 1,1,1-trichloroethane, trichloroethylene and 'chlorinated dye penetrants
1 and 2' exploded violently when initiated with a blasting cap. Carbon tetrachloride exploded only mildly, and a partly
fluorinated chloroalkane not at all. Trichloroethylene has been used for degreasing metallic parts before use with liquid
oxygen, but is not safe. /Oxygen, liquid/
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Addition of bromine to a mixture of chlorotrifluoroethylene and oxygen causes an explosion. One of the products of the
reaction is chlorotrifluoroethylene peroxide, which explodes when heated.
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Second stage ignition during oxidation/combustion of iodomethane in oxygen at 300 to 500 deg C was particularly
violent, occasionally causing fracture of the apparatus, and was attributed to formation and decomposition of a periodic
species.
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Oxidation of ... /phosphorous tribromide/ with gaseous oxygen is not easily controlled and become explosive.
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Phosphorus trifluoride does not burn in air, but if it is mixed with oxygen, the gases explode.
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/Tetraphosphorus hexaoxide (phosphorus(III) oxide) Interact/ with air or oxygen /rapidly/ and, at slightly elevated
temperatures in air or at high concn of oxygen, ignition is very probable, particularly if the oxide is molten (above 33 deg
C) or distributed as a thin layer. The solid in contact with oxygen at 50 to 60 deg C ignites and burns very brilliantly.
During distillation of phosphorus(III) oxide, air must be rigorously excluded to avoid the possibility of explosion. The later
reference states that the carefully purified oxide does not ignite in oxygen, and that the earlier observations were on
material containing traces of white phosphorus.
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Phosphorus and oxygen ... undergo a vigorous reaction at room temperature.

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Liq: may explode on contact with heat or oxidizable materials ...

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Liquid oxygen plus ordinary fuels, hydrocarbons, and many other organic cmpd are powerful explosives. /Oxygen, liquid/
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Serious explosions have resulted from contact between oil & high-pressure oxygen.
Press, 1981., p. 70
 from HSDB
Traces of oil on the ball bearing of a centrifugal pump reacted with liquid oxygen being transferred by the pump. The heat
of reaction vaporized the oxygen and the pump burst from pressurization.
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Oxygen-saturated wood & asphalt have been known to ... explode when subjected to shock.
Press, 1981., p. 85
 from HSDB
During transfer of liquid oxygen from a factory reservoir to a tanker truck, some of the liquid leaked from a coupling to
the asphalt surface below. When the trucker dropped a hammer on this surface, a violent explosion formed a crater 20
inches square by 4 inches deep in the asphalt and broke windows nearby. /Oxygen, liquid/
 from HSDB
... Mixtures of asphalt and liquid oxygen were shown to be impact-sensitive on the small scale, but on the larger scale a
detonator was necessary to initiate mild explosion of liquid oxygen on a layer of asphalt. Oil, rubber or other impurities
may have been present on the road surface in the first incident. /Oxygen, liquid/
 from HSDB
In a plant manufacturing liquid and gaseous oxygen, spruce wood flooring encased in iron sheeting was charred by an
undetected, smoldering fire started by a welding spark. Subsequent leakage of liquid oxygen saturated the charred wood
and a violent explosion resulted. /Oxygen, liquid/
 from HSDB
In 2 test methods (IP40, IP38) for the oxidative stability of hydrocarbons, samples are heated in a valve-sealed stainless
bomb under an oxygen atmosphere, On several occasions minor explosions occurred when valves with Teflon sealing
discs (rather than the older metal needle closures) were operated during oxygen purging or venting operations. (This was
associated with presence of metal particles and traces of grease being embedded in the Teflon discs). Only stainless
needle valves, and a controlled rate of pressure release, are recommended for these tests.
 from HSDB
Teflon (polytetrafluoroethylene) ignited at 1,300 deg F in a 5 psia pure oxygen atmosphere, when used as a 20 AWG wire
insulation. Polyolefin insulation ignites at about 1,100 deg F under the same conditions ... The combustion of Teflon in
oxygen to give carbonyl fluoride is highly exothermic but a large ignition source is required. The minimum ignition
temperature is 465 deg C even under 7500 psi of oxygen gas. The ignition of Teflon tubing at -60 deg C in supercritical
oxygen at 900 psi required a hot nickel-chromium wire as an initiator.
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Accidental admixture of oxygen gas with unstabilized liquid tetrafluoroethylene produced a polymeric peroxide which was
powerfully explosive, and sensitive to heat, impact or friction. Removal of oxygen by treatment with pyrophoric copper to
prevent explosion of tetrafluoroethylene has been claimed.
 from HSDB
Mixtures /of diborane(6) and oxygen/ at 105 to 165 deg C exploded spontaneously after an induction period dependent
on temperature and composition.
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Reation of pentaborane/(9)/ with oxygen is often violently explosive ... Pentaborane(11) ignites in air.
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Decaborane is spontaneously flammable in oxygen ...

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The vapor /of aluminium tetrahydroborate/ is spontaneously flammable in air, and explodes in oxygen, but only in
presence of traces of moisture ... The /aluminium/ tetrahydroborate reacts with alkenes and, in presence of oxygen,
combustion is initiated even in absence of moisture. Butene explodes after an induction period, while butadiene explodes
immediately.
 from HSDB
Beryllium borohydride reacts explosively with oxygen or water ... In contact with air or oxygen ... /boron arsenotribromide/
is readily oxidized, and in most cases ignites spontaneously ... Boron decahydride ignites spontaneously when exposed to
air or oxygen ... Oxygen and boron trichloride react vigorously on sparking.
 from HSDB
/Diboron tetrafluoride/ gas is extremely explosive in presence of oxygen.

 from HSDB
... The complex /of arsine-boron tribromide/ ignites on exposure to air or oxygen, even at below 0 deg C. It is violently
oxidaized by nitric acid.
 from HSDB
Most fibrous fabrics will absorb oxygen when exposed to concn greater than the normal 21% in air, and this is retained
for a long time after excess oxygen is no longer present, greatly increasing the possibility of ignition. Hose leakage led to
oxygen enrichment inside a vessel in which welding was taking place. A welder lit a cigarette but did not appreciate the
significance of its rapid combustion and the unusually long lighter flame. Sparks from welding later ignited clothing,
leading to fatal burns. Accidental connection of a pneumatic grinder to an oxygen line instead of a compressed air line led
to ignition of the apprentices' clothing when the grinder was started. Accidental connection of a breathing set to an
oxygen cylinder rather than to a medical air cylinder caused ignition of the facepiece.
 from HSDB
Most materials, especially clothing, burn fiercely in an atmosphere containing more than the usual 21 vol% of oxygen. In
presence of petroleum products, fire and explosion can be spontaneous ... The flammability of textiles and other solids
was studied under the unusual conditions which occur in deep diving operations. The greatest effect on ease of ignition
and linear burning rate was caused by oxygen enrichment; increase in pressure had a similar effect. Ignition and flame
spread of fabrics and paper were measured at pressures from 21 bar down to the limiting pressure for ignition to occur.
Increase in oxygen concn above 21% in mixtures with nitrogen caused rapid decrease of minimum pressure for ignition. In
general, but not invariably, materials ignite less readily but burn faster in helium mixtures on the effect of variables on the
rate of burning. At oxygen concn of 41% all materials examined would burn except for glass and polytetrafluoroethylene,
which resisted ignition attempts in pure oxygen. Flame retardants become ineffective on cotton in atmospheres
containing above 32% oxygen ... /Oxygen enrichment/
 from HSDB
Disilane, trisilane, or tetrasilane, when mixed with oxygen or air at ordinary temperatures, ignites or explodes.
 from HSDB
Germanium burns with incandescence when heated in oxygen.

 from HSDB
Finely divided platinum and some other metals will cause a mixture of hydrogen and oxygen to explode at ordinary
temperatures ...
 from HSDB
Lithium will burn in air, oxygen, nitrogen, and carbon dioxide. The susceptibility of molten lithium surfaces to spontaneous
ignition is increased by the presence of lithium oxides or nitrides. These reactions ... are extremely violent at higher
temperatures ...
 from HSDB
Violent explosions resulted when a spark was discharged in a mixture containing 25 to 70% oxygen difluoride in oxygen
over water.
Milne, G.W.A. (ed.). Ashgate Handbook of Pesticides and Agricultural Chemicals. Ashgate Publishing Co. Burlington, VT. 2000., p. 491-
137
 from HSDB
In the form of foam, polyurethane, and also polyvinyl chloride, have exploded when saturated with liquid oxygen.
 from HSDB
The reaction of potassium and carbon monoxide forms an explosive carbonyl cmpd, potassium carbonyl, which reacts
violently with oxygen.
 from HSDB
The reaction fo oxygen and potassium peroxide is violent at pressures of oxygen as low as 10 mm.
 from HSDB
Burning selenium in oxygen has resulted in explosion, probably due to the presence of organic matter.
 from HSDB
To 'ensure proper ignition' during oxygen-flask analysis, a technician put a single drop of acetone onto the filter paper
enclosing the sample, before igniting the tail and insertion into the oxygen-filled flask. An explosion followed which
shattered the flask, fortunately enclosed in a mesh screen which retained the fragments. It was calculated that 0.07 mL of
acetone would have formed an explosive vapor-air mixture in the flask above the lower explosive limit, so considerably
less acetone would have given an explosive mixture in the oxygen atmosphere.
 from HSDB
Accidental addition of liquid oxygen to vacuum jars containing acetone residues from trap-cooling use caused a violent
explosion ... /Oxygen, liquid/
 from HSDB
A combination of faulty equipment and careless working led to an extremely violent explosion during oxy-acetylene
cutting work. The oxygen cylinder was nearly empty and the regulator had a cracked diaphragm. The acetylene cylinder
was lying on its side and was feeding a mixture of liquid acetone and acetylene gas to the burner head. When the oxygen
ran out, the excess pressure line and into the cylinder via the cracked diaphragm. The explosion destroyed the whole
plant ... A safe method for demonstrating explosive combustion of acetylene-oxygen mixtures in bubbles is described
 from HSDB
The detonation capacity of mixtures of acetylene and liquid oxygen is increased by the presence of organic material (oils)
in the oxygen. Hazards of accumulation of oil in air-liquefaction and -fractionation plants are emphasised. /Oxygen,
liquid/
 from HSDB
Accidental connection of an oxygen cylinder to top-up an ammonia-containing refrigeration system led to explosive
destruction of the compressor ... In school demonstrations of the oxidation of ammonia to nitric acid over platinum
catalysts, substitution of oxygen for air causes fairly vigorous explosions to occur ...
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During the synthesis of (15)N-labelled urea by interaction of labelled ammonium nitrate, liquid ammonia and diphenyl
carbonate in presence of copper powder, a series of explosions of the refrigerated sealed tubes was encountered. This
was almost certainly caused by condensation of traces of oxygen in the tubes cooled to -196 deg C during condensation
of ammonia before sealing the tubes. Cooling to -80 deg C would have been adequate and have avoided the hazard.
/Oxygen, liquid/
 from HSDB
The solid inclusion (clathrate) complex of oxygen with hydroquinone had been prepared twice previously by a published
method which involved saturating a solution of hydroquinone in propanol in an autoclave at 70 deg C with oxygen at 20
to 150 bar, followed by slow cooling under oxygen pressure (and most probably without stirring to allow large crystals of
the inclusion complex to form). In a third attempt, (to produce smaller crystals free of the 'quinhydrone complex' impurity)
a solution was prepared and saturated with oxygen at 80 bar, then heated to 90 deg C (when the partial pressure of
oxygen would increased to around 100 bar), then allowed to cool with agitation. After 20 min the bursting disk failed at
450 bar and an explosion damaged the autoclave and premises. Without agitation, the rate of oxidation of the solvent
and hydroquinone would be controlled by diffusion of oxygen through the (small) gas liquid interface. With agitation, the
rate of oxidation would be expected to increase greatly, and lead to runaway oxidation with very fast increase in
temperature and pressure and explosive combustion when the autoignition temperature (371 deg C for propanol in air at
1 bar, less in oxygen) were attained.
 from HSDB
The lower limit for spontaneous ignition of mixtures /of carbon disulfide/ with oxygen has been studied ... Shortly after
mercury was accidentally introduced into a system containing a soln of anthracene in carbon disulfide under an
atmosphere of oxygen, an explosion occurred. Presence of mercury may have catalyzed rapid oxidation of carbon
disulfide ...
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Mixtures of carbon and liquid oxygen have been used as blasting explosives for some time. Mixtures with carbon black
appear unusually sensitive to impact, and a blasting cartridge exploded when dropped ... Carbon containing 3.5% of ...
/iron(II)/ oxide explodes on contact with liquid oxygen. /Oxygen, liquid/
 from HSDB
Interaction of hydrocarbons with gaseous oxygen may be slow or fast, depending on conditions and substrate, but
peroxidic products are always involved, and the rate of formation is highest at a C-H link adjacent to an aromatic ring or a
double bond. Predictable conditions for explosion are those relevant to the internal combustion engine (Otto or Diesel
types). Unpredicted conditions include the following cases. During studies on autoxidation of 1,1,-diphenylethylene with
oxygen at high pressure and low temperature an explosion occurred. Partial oxidation of a gasoline fraction in an
autoclave under oxygen, initially at 22 bar and 100 deg C, ran wild and exploded; several smaller reactions had proceeded
uneventfully. Previously oxidation reactions of gasoline at 20 bar/105 deg C had exploded, and a severe explosion
occurred while admitting oxygen, virtually at 1 bar pressure, to an autoclave containing a glass bottle of gasoline ... An
attempt to decarbonize a gasoline motor cycle engine by inserting a lighted match through the spark plug hole into the
cylinder, and then blowing in oxygen caused a violent explosion to occur ... Use of oxygen instead fo compressed air to
start a diesel engine, or to clear a blocked petrol pipe, led to violent explosions ... Among other cmpd, methyl nitrate,
nitromethane, ethyl nitrate and tetrafluorohydrazine function as promoters of spontaneous ignition of mixtures of
methane or propane with oxygen and argon.
 from HSDB
Mixtures of hydrocarbons with liquid oxygen are highly dangerous explosives, not always requiring external initiation ...
/Early examples included lighted candles being/ accidentally knocked ... into a bucket of liquid oxygen in 1903 /and a/
violent explosion /ensued/. Mixtures with liquid methane or benzene are specifically described as explosive ... Mixtures
with petroleum and absorbent charcoal have been used experimentally as blasting explosives. Addition of a little
aluminium powder to liquid methane-oxygen mixtures increase the explosive power. An explosion in a liquid oxygen
evaporator was attributed to the presence of acetylene, arising from unusual plant conditions and higher than usual
hydrocarbon concentrations in the atmospheric air taken in for liquefaction ... Experimental work appeared to implicate
ozone as a major contributory factor ... During investigation of an explosion in a portable air liquefaction-separation plant,
hydrocarbon oil was found in a silica filtration bed. The mechanism of slow heterogeneous accumulation of hydrocarbons
dissolved in trace amount in liquid oxygen on the liquid evaporator surfaces is discussed. It was concluded that months of
continuous evaporation would be required to attain explosion-hazardous levels in real evaporators. /Oxygen, liquid/
 from HSDB
When oxygen was passed through a drying tower containing activated alumina previously used to dry hydrogen,
explosions occurred. Nitrogen purging between changing gases would prevent this. During preparation of stoichiometric
mixtures in a steel mixing tank (at 17 to 82 bar, with or without 15% argon), several spontaneous explosions occurred
during valve manipulation at 30 min after mixing, but not 10 min after mixing. A possible catalytic effect of the surface of
the steel tank was eliminated by coating it thinly with silcone grease. There is a marrow range of concn in which the
mixture is supersensitive to initiation ...
 from HSDB
The hazards arising from presence of oil films in oxygen-handling systems are reviewed, with consideration of cleanliness
specifications, film flammability, film migration and hazard mechanisms.
 from HSDB
The rate of absorption of oxygen by liquid butenyne increased with time, and eventually a yellow liquid phase separated.
After evaporation of excess hydrocarbon, the yellow peroxidic liquid was explosive. Presence of 5% of chloroprene
increased the rate of absorption 5 to 6-fold, and of 2% of water decreased the rate by 50%, but residue were explosive in
each case ...
 from HSDB
Benzoic acid is burned in oxygen as a primary thermochemical standard to calibrate oxygen bomb calorimeters used in
the IP12/ASTM D240 standard tests for determination of calorific value of liquid hydrocarbon fuels. If the benzoic acid is
powdered (rather than pelleted as IP12 recommends), very rapid combustion occurs and the flame front may burn
through the non-metallic (Teflon) seals on valve seats and the bomb may be destroyed. Ignition of a pelleted sample in a
bomb with a faulty closure valve led to sudden venting of combustion gases which blew off the insulating cover and
thermometer ...
 from HSDB
Oxygenation of lithiated dialkylnitrosamines in tetrahydrofuran (THF) at -78 deg C is fast and gives good yields of the N-
alkyl-N-(1-hydroperoxyalkyl)nitrosamines. If oxygenation is too prolonged, poor yields and explosive by-products result.
 from HSDB
Hazards /of organic analytical samples/ involved in the use of the oxygen flask combustion technique are discussed ...
Some explosions occurred after completion of combustion, when the oxygen concn in the flask is still some 75%.
Shielding of the flask, minimally with wire gauze seems advisable. Explosion during a blank combustion (of a folded filter
paper) was attributed possibly to thermal strains. Similar occurrences had been noted previously. Fitting a simple pressure
relief (Bunsen) valve to the flask improves safety aspects, and the oxygen flask method is also to be preferred (for
qualitative work) to the more hazardous sodium fusion method.
 from HSDB
Many common polymers, polymeric additives and lubricants oxidize so rapidly after impact in liquid oxygen that they are
hazardous. Of those tested, only acrylonitrile-butadiene, poly(cyanoethylsiloxane), poly(dimethylsiloxane) and polystyrene
exploded after impact of 6.8 to 95 J intensity (5 to 70 ft.lbf). All plasticizers (except dibutyl sebacate) and antioxidants
examined were very reactive ... /Oxygen, liquid/
 from HSDB
A form rubber sample, being tested for oxidation resistance under oxygen at 34 bar at 90 deg C exploded with extreme
violence after 4 days. Use of a Neoprenelined hose in a high-pressure oxygen manifold caused failure and ignition of the
burst hose. Possible ignition sources include adiabatic compressive heating, and friction from vibration of metal
reinforcing fibers in the high velocity stream of escaping oxygen. Polytetrafluoroethylene (Teflon) ignited at 705 deg C in
oxygen at 0.34 bar pressure when used as wire insulation, while polyolefine insulation ignited at 593 deg C under the
same conditions.
 from HSDB
In an attempt to introduce carboxyl group to improve the adhesive properties of rubber, 6 L of powdered rubber (0.1 to
0.5 mm particle size) in an 8 L flask was treated with ozonized oxygen. The gas stream, containing 5% of ozone was led to
the bottom of the flask via a dip tube at the rate of 4 L/min for 2 min, when treatment was discontinued and the flask
closed. After 5 min a violent explosion occurred. This was attributed to formation of ozonides, but exothermic interaction
of the high surface area rubber with almost pure oxygen under virtually adiabatic conditions may also have been involved.
 from HSDB
... Fires /occurred/ in which endotracheal /plastic/ tubes became ignited by surgical lasers or electrocautery in
atmospheres enriched by oxygen ...
 from HSDB
The plastic caps (or tape) which cover the outlets on refilled oxygen cylinders will burn readily in oxygen and must be
completely removed and no bits trapped in the fittings attached to the cylinder outlet.
 from HSDB
A 4.9 g sample of the liquid siloxane in a glass dish was put into a bomb calorimeter (on an open bench) containing 5 mL
of sodium hydroxide soln to absorb combustion gases. The electric igniter system consisted of a metal wire in contact
with a cotton-wool wick which dipped into the siloxane sample. The bomb was sealed, pressured up to 39 to 44 bar with
oxygen, and the igniter was fired. A violent explosion blew the lid off the bomb (rated at 190 bar working, 250 bar test),
and examination of the deformed bomb indicated that a maximum detonation pressure of around 900 bar had been
attained. Detailed examination of the reaction showed a 2 stage mechanism. Hydrolysis of the volatile partially methylated
siloxane by the alkaline soln liberated hydrogen which formed an explosive mixture with oxygen. When the igniter was
fired, the hydrogen-oxygen explosion atomized the remaining liquid siloxane leading to a very violent secondary
explosion. The wick also played a decisive separate role, as the siloxane-soaked cotton also underwent extremely rapid
detonative decomposition on ignition. The rate of pressure rise was measured as 10 kbar/sec, with a maximum pressure
calculated for a 4.9 g sample of 800 bar. Hexamethyldisiloxane (which can't produce hydrogen by hydrolysis) burned
smoothly under the same conditions. It is recommended that no more than 0.5 g samples should be used, with oxygen
pressure limited to 20 bar and protective enclosure of the bomb equipment. A more detailed investigation of the
combustion of tetramethyldisiloxane in oxygen showed that, even in the absence of hydrogen, combustion was still
extremely violent, the rate of pressure increase being inversely proportional to the pressure of oxygen, as expected for a
homogeneous gas-phase combustion reaction. The unusually high rate of pressure rise (256 kbar/sec, to max 113 bar for
10 bar oxygen pressure) is indicative of detonation. Under heterogeneous conditions, liquid tetramethyldisiloxane gave a
maximum rate of pressure rise of 90 kbar/sec to max 160 kbar with 30 bar oxygen pressure. Pentamethyldisiloxane
showed generally similar behavior (maximum rate 38 kbar/sec to max 205 bar for 30 bar oxygen pressure), with an abrupt
increase between 25 and 30 bar pressure of oxygen.
 from HSDB
Autoxidation of the hydrazone (O2/C6H6/UV) gives the explosive isomeric 1,2-dihydroperoxy-1,2-

bis(benzeneazo)cyclohexane, and the same is true for cyclooctatetraene (COT) derivatives ... In a procedure to oxygenate
photochemically COT to the 1,4-endoperoxide, highly explosive undefined polymeric peroxides are formed as by-
products.
 from HSDB
The evaporated residue from sensitized photochemical oxidation of ... /methoxy-1,3,5,7-cyclooctatetraene/ ignited
spontaneously, on several occasions explosions ocurring.
 from HSDB
The nature of the reaction and the products in methylal-oxygen mixtures /of dimethoxymethane/ during cool flame or
explosive oxidation were studied.
 from HSDB
Glycerol is oxidized at an appreciable rate by high-pressure oxygen in the presence of copper alloys to give glyceric acid,
oxalic acid and formic acid, which lead to severe corrosion of the alloy. Malfunction of aircraft oxygen gauges operating at
125 bar was attributed to blockage of the brass Bourdon tubes by copper salts of the acids produced by long-term
oxidation of residual traces of glycerol-water solutions used for gauge testing.
 from HSDB
12.9 Transport Information

12.9.1 DOT Emergency Guidelines
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Fire or Explosion: Substance does not burn but
will support combustion. Some may react explosively with fuels. May ignite combustibles (wood, paper, oil, clothing, etc.).
Vapors from liquefied gas are initially heavier than air and spread along ground. Runoff may create fire or explosion
hazard. Containers may explode when heated. Ruptured cylinders may rocket. /Oxygen; Oxygen, compressed; Oxygen,
refrigerated liquid (cryogenic liquid)/
U.S. Department of Transportation. 2004 Emergency Response Guidebook. A Guide book for First Responders During the Initial Phase of
a Dangerous Goods/Hazardous Materials Incident. Washington, D.C. 2004
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Health: Vapors may cause dizziness or
asphyxiation without warning. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Fire may
produce irritating and/or toxic gases. /Oxygen; Oxygen, compressed; Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Public Safety: CALL Emergency Response
Telephone Number ... . As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet)
in all directions. Keep unauthorized personnel away. Stay upwind. Many gases are heavier than air and will spread along
ground and collect in low or confined areas (sewers, basements, tanks). Keep out of low areas. Ventilate closed spaces
before entering. /Oxygen; Oxygen, compressed; Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Protective Clothing: Wear positive pressure self-
contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the
manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited
protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
Always wear thermal protective clothing when handling refrigerated/cryogenic liquids. /Oxygen; Oxygen, compressed;
Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Evacuation: Large spill: Consider initial downwind
evacuation for at least 500 meters (1/3 mile). Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters
(1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. /Oxygen; Oxygen,
compressed; Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Fire: Use extinguishing agent suitable for type of
surrounding fire. Small fires: Dry chemical or CO2. Large fires: Water spray, fog or regular foam. Move containers from fire
area if you can do it without risk. Damaged cylinders should be handled only by specialists. Fire involving tanks: Fight fire
from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of
water until well after fire is out. Do not direct water at source of leak or safety devices; icing may occur. Withdraw
immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks
engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area
and let fire burn. /Oxygen; Oxygen, compressed; Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ Spill or Leak: Keep combustibles (wood, paper,
oil, etc.) away from spilled material. Do not touch or walk through spilled material. Stop leak if you can do it without risk. If
possible, turn leaking containers so that gas escapes rather than liquid. Do not direct water at spill or source of leak. Use
water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Prevent
entry into waterways, sewers, basements or confined areas. Allow substance to evaporate. Isolate area until gas has
dispersed. CAUTION: When in contact with refrigerated/cryogenic liquids, many materials become brittle and are likely to
break without warning. /Oxygen; Oxygen, compressed; Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
/GUIDE 122: GASES - OXIDIZING (INCLUDING REFRIGERATED LIQUIDS)/ First Aid: Move victim to fresh air. Call 911 or
emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes. Clothing frozen to the skin should be thawed before being
removed. In case of contact with liquefied gas, thaw frosted parts with lukewarm water. Keep victim warm and quiet.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves. /Oxygen;
Oxygen, compressed; Oxygen, refrigerated liquid (cryogenic liquid)/
 from HSDB
12.9.2 Shipment Methods and Regulations
No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in
condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
49 CFR 171.2 (7/1/96)
 from HSDB
The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous
Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be
followed by all IATA Member airlines when transporting hazardous materials.
International Air Transport Association. Dangerous Goods Regulations. 47th Edition. Montreal, Quebec Canada. 2006., p. 232
 from HSDB
The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals.
Detailed recommendations for individual substances and a number of recommendations for good practice are included in
the classes dealing with such substances. A general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or
article.
International Maritime Organization. International Maritime Dangerous Goods Code. London, UK. 2004., p. 44
 from HSDB
12.9.3 DOT ID and Guide
1072 122
 from DOT Emergency Response Guidebook
12.9.4 DOT Label
Non-Flammable Gas Oxidizer

12.9.5 Packaging and Labelling
Special insulated container.

 from ILO-ICSC
12.9.6 EC Classification
Symbol: O; R: 8; S: (2)-17
 from ILO-ICSC
12.9.7 UN Classification
UN Hazard Class: 2.2; UN Subsidiary Risks: 5.1

 from ILO-ICSC
13 Toxicity
13.1 Toxicological Information
13.1.1 NIOSH Toxicity Data
 Download
Measurement System Route/Organism Dose Effect Date
July
Mutation Data Cytogenetic Analysis lymphocyte/human 40 pph/4D
2014
20 pph/3D- July
Mutation Data Cytogenetic Analysis ovary/hamster
continuous 2014
July
Mutation Data Cytogenetic Analysis lung/hamster 80 pph
2014
July
Mutation Data Cytogenetic Analysis embryo/chicken 80 pph
2014
mutation in mammalian somatic July

Mutation Data lung/hamster 95 pph/24H
cells 2014
 from The National Institute for Occupational Safety and Health (NIOSH)
13.1.2 Exposure Routes
The substance can be absorbed into the body by inhalation.

 from ILO-ICSC
13.1.3 Symptoms
Cough; dizziness; sore throat; visual disturbances at very high concentrations. At 100% oxygen for more than 24 hours:
symptoms above plus weakness, fatigue, pain in joints and muscles, numbness and tingling in arms and legs, palpitations,
headache, nasal congestion, ear disturbances, nausea, vomiting, loss of appetite, fever and swelling of mucous
membranes. On contact with liquid: freezing burns
13.1.4 Inhalation Symptoms
Cough. Dizziness. Sore throat. Visual disturbances. See Notes.

 from ILO-ICSC
Cough. Dizziness. Sore throat. See Notes.

 from ILO-ICSC
13.1.5 Skin Symptoms
ON CONTACT WITH LIQUID: FROSTBITE.

 from ILO-ICSC
13.1.6 Eye Symptoms
See Skin.
 from ILO-ICSC
13.1.7 Target Organs
Respiratory system, CNS

13.1.8 Interactions
... Toxicity of oxygen to dogs' eyes could be enhanced ... by promazine ... chlorpromazine, thioridazine, & chloroquine.
Grant, W. M. Toxicology of the Eye. 2nd ed. Springfield, Illinois: Charles C. Thomas, 1974., p. 777
 from HSDB
... Some anticancer drugs, for example, bleomycin and cyclophosphamide, show increased acute lung damage in animals
in combination with hyperoxia. Whether this is also true in humans is uncertain. It appears that direct interaction between
O2 and the anticancer drugs occurs, rather than interference by O2 with the repair of damage done by the drugs.
 from HSDB
Hyperoxia and nitric oxide act synergistically in their cytotoxicity to A549 cells (human alveolar epithelial cells). This
interaction is of human relevance because nitric oxide is being tested clinically for infants and children with pulmonary
hypertension, and these patients are also frequently receiving simultaneous O2 therapy.
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... Carefully maintained, anesthetized, intubated, and mechanically ventilated baboons /were exposed/ for 11 days to 40%
O2, 80% O2, 100% O2 ... or 80% O2 followed by inoculation with Pseudomonas aeruginosa bacteria. The groups exposed
to 100% O2 or 80% O2 plus bacterial inoculation showed mixed exudative-reparative diffuse alveolar lesions, altered
morphology of type II cells, increased numbers of type II cells and interstitial cells, and decreased numbers of type I and
endothelial cells. The animals exposed to 40% O2 or 80% O2 showed increased numbers of alveolar macrophages and
focal widening of alveolar walls. The most striking finding was that 80% O2 plus infection caused responses as severe as
100% O2. It was suggested that the combination with infection reflects the evolution of adult respiratory distress
syndrome that occurs in some human patients in intensive medical care units (and other situations involving lung injury).
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... Pretreatment of mice with repetitive sublethal intraperitoneal doses of recombinant human tumor necrosis factor for 3
days or a single iv dose followed by exposure to high-dose oxygen afforded a significant survival advantage compared
with high-dose oxygen-exposed mice pretreated with vehicle or interleukin-1. The repetitive intraperitoneal tumor
necrosis factor pretreatment reduced the development of interstitial pneumonitis, pulmonary edema, and lung weight
gain associated with oxygen toxicity and enhanced expression of the gene for the free radical protective enzyme
manganous superoxide dismutase in lung tissue, a gene that is augmented as mice are exposed to high-dose oxygen.
Furthermore a single intravenous dose of tumor necrosis factor 24 hr after oxygen exposure was still protective ...
Abstract: PubMed
Jensen JC et al; J Appl Physiol 72 (5): 1902-7 (1992)
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Agents that increase oxygen toxicity /include/ catecholamines (eg, epinephrine, norepinephrine), corticosteroids (eg,
dexamethasone methylprednisolone), hormones (eg, testosterone, thyroxine), chemotherapeutics (bleomycin,
cyclophosphamide, 1,3-bis(2-chloroethyl)-1-nitrosourea) and antibiotics (eg, nitrofurantoin). /From table/
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... Drugs /and chemicals/ affect O2 tolerance ... unfavorably ... include /those/ that increase tissue O2 consumption, agents
that themselves produce free radicals, or those that interfere with the activity of antioxidant enzymes.
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Species differences are also important in the investigation of interactions of agents with hyperoxia. Whereas bleomycin
potentiated lung disease in the rat, it did not alter toxicity of O2 in rabbits. A difference in drug administration (sc vs iv)
could explain all or part of this differential response.
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... injection of 7-nitroindazole (7-NI) (30 mg/kg) significantly prolonged the latency to observable tonic-clonic convulsions
/in male Sprague Dawley rats/. The 7-NI group also showed a significant decrease in motor activity compared with the
control group. ... injection of 7-NI led to a significant dose-dependent reduction in horizontal and vertical activities.
Abstract: PubMed
Jellestad FK, Gundersen H; Physiol Behav 76 (4-5): 611-6 (2002)
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... Conscious, unrestrained rats implanted with cortical electroencephalogram electrodes were exposed to 0.5 MPa (gauge
pressure) O2 until seizures were observed. Fasting for 24 hr significantly (P < 0.01) decreased blood glucose (from 8.6 +/-
0.9 in fed to 6.9 +/- 0.7 mM in the fasted group), increased blood BHB (0.07 +/- 0.02 mM to 0.38 +/- 0.10 mM,
respectively), and prolonged the latency to seizures compared with normally fed animals (21.0 +/- 9.8 vs. 34.6 +/- 17.7
min, P < 0.05). Injection of the ketone precursor 1,3-butanediol (BD) to the fed animals increased blood BHB level to 0.72
+/- 0.32; however, seizure latency remained the same as in fed animals. Restoration of blood glucose in fasted animals to
the same level as in the fed group did not reverse the protection achieved by fast; instead it increased the latency to
seizures.
Abstract: PubMed
Chavko M et al; Undersea Hyperb Med 26 (2): 99-103 (1999)
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... Forty rats with chronic cortical electrodes were injected i.p. with one of three doses of flumazenil (0.2, 2, and 20 mg/kg)
or their vehicle, before exposure to 0.5 MPa oxygen. ... Significant prolongation of the latent period preceding oxygen
seizures was noted in the group of rats treated with 0.2 mg/kg flumazenil (p < 0.05 in Tukey test). However, when the
dose of flumazenil was increased, the duration of the latent period returned to control values.
Abstract: PubMed
Bitterman N, Halpern P; Methods Find Exp Clin Pharmacol 17 (3): 169-74 (1995)
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... Twenty-six male... Sprague-Dawley rats were exposed to high O2 pressures (507 and 608 kPa) before and after
cinnarizine ingestion (3.3 mg/kg), until the appearance of the first electrical discharge (FED) in the electroencephalogram
(EEG) which precedes the clinical convulsions. Each rat was tested on five exposure protocols (control and cinnarizine at
507 kPa O2, control, cinnarizine, and 15 hr starvation as a control for cinnarizine at 608 kPa O2) at intervals of at least 2
days or until the EEG connector became detached (a mean of 3.1 exposures per rat). Latency to the FED increased after
cinnarizine ingestion in 16 of the 17 pairs of measurements at 507 kPa O2 (by more than 61%, P < 0.002) and in 17 of the
19 pairs of measurements at 608 kPa O2 (by 36%, P < 0.002). There was no significant effect of 15 hr starvation.
Abstract: PubMed
Arieli R et al; Undersea Hyperb Med 6 (2): 105-9 (1999)
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Bacterial lipopolysaccharide (LPS), or endotoxin, a constituent of the cell wall of Gram-negative pathogenic bacteria, has
been one of the most effective agents against hyperoxic lung injury in experimental animals. Even when injected 36 hr
after the beginning of exposure to 95% O2, it has provided 95% protection against death in rats, which otherwise showed
only 76% survival after 72 hr ... Endotoxin has also been found to extend the survival time of adult mice in hyperoxia ... /It
was/ reported that diphosphoryl lipid A extracted from the endotoxin produced by Salmonella minnesota protected rats
from hyperoxic toxicity as effectively as did the parent endotoxin, and was less acutely toxic. Nontoxic lipid fractions from
the endotoxin potentiated the hyperoxic injury ... The monophosphoryl lipid A component was shown not to have O2
protective properties ... Marked prolongation of survival time and partial prevention of increased lung vascular
permeability in sheep given endotoxin just prior to 100% O2 exposure /was reported/. However, impairment of gas
exchange, loss of hypoxic pulmonary vasoconstriction (normally seen with low O2 concentrations), and ultimate
respiratory failure were not prevented.
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... A twofold increase in survival time of rabbits from hyperoxic exposure following the iv injection of ... oleic acid /was
reported/ ... /It was/ suggested that a variety of lung injuries can increase production of antioxidants.
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... Effective protection /from hyperoxia/ by the intratracheal instillation in rats of washed human or rat erythrocytes /was
reported/ ... The erythrocytes /were characterized/ as "biologic packets of encapsulated antioxidants" .
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N-acetylcysteine /was given/ iv to anesthetized, mechanically ventilated dogs, just before and during 100% O2 exposure
for 54 hr. Using both functional and structural criteria, the treated dogs showed significant protection compared to
controls. N-acetylcysteine functions as a surfactant when administered by inhalation, but it is not clear whether such
action affected this experiment. N-acetylcysteine also protected guinea pigs from hyperoxia-induced lung injury but did
not protect rats from lung injury induced by hyperoxia.
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/It was/ found that intratracheal instillation of a calf lung surfactant extract to rabbits during exposure to 100% O2
lessened the progression of hyperoxic injury... A synthetic surfactant (Exosurf), and its non-surface-active components
tyloxapol and cetyl alcohol, can function as antioxidants, and their in vivo instillation is associated with decreased
hyperoxic injury in rats ...
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Pretreatment of rats with recombinant tumor necrosis factor plus interleukin 1 (IL-1) decreased mortality to hyperoxia ...
Mice treated iv, and rats treated intratracheally with recombinant human keratinocyte growth factors had improved lung
protection against O2 injury and decreased mortality. Aerosol administration of manganese-superoxide dismutase (SOD)
to the lungs of primates decreased hyperoxia-induced lung injury (targeted gene overexpression studies have been
performed in cultured cells and animals).
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Diets rich in polyunsaturated fatty acids fed to female rats before and throughout pregnancy and lactation gave their
newborn offspring a measure of protection from the effects of continuous exposure to 95% O2. Survival was improved by
12 to 42%. Use of a diet low in polyunsaturated fatty acids increased susceptibility to hyperoxia. This could be countered,
in part, by having the infants nursed by foster mothers who were receiving the enriched diet.
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Because the sympathetic nervous system had been implicated in O2 toxicity ... guinea pigs /were given/ the
catecholamine inhibitors reserpine or phenoxybenzamine ... The animals /were exposed/ to O2 at 500 mm Hg partial
pressure (equivalent to 66% O2) for 6 days. Scanning and transmission electron microscopy showed extensive changes in
the control animals, including alveoli clogged by proliferation of alveolar type II epithelial cells and macrophages, and
thickening of the air-blood barrier. Animals pretreated with reserpine showed little change from normal after 6 days,
supporting the hypothesis of neural participation in hyperoxic toxicity. Phenoxybenzamine was less effective.
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... Evidence exists that food and/or water deprivation before exposure to hyperbaric O2 may postpone the hyperoxia-
induced seizures ... Use of a cytochrome P450 2E1 enzyme inhibitor (diethyldithiocarbamate), 21-aminosteroid, and
propranolol have been shown to produce significant delays in the onset of seizures by CNS O2 toxicity.
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... Cimetidine, cyclosporin A, dopamine, isoproterenol, lisofylline, pentoxifylline, and the lazaroid U-74389G ... show
protective actions against hyperoxia-induced injury ... Low-level carbon monoxide may protect against oxygen-induced
lung injury ...
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Survival of rats exposed to 100% oxygen was increased from 69.5 +/- 1.5 to 118.1 +/- 9.9 hr (mean +/- SEM, P< 0.05)
when liposomes containing catalase and superoxide dismutase were injected iv before and during exposure. The
increased survival time in 100% oxygen was also associated with significantly less fluid in the pleural cavity.
Turrens JF et al; Protection Against Oxygen Toxicity by Intravenous Injection of Liposome-Entrapped Catalase and Superoxide
Dismutase; J Clin Invest 73 (1): 87-95 (1984)
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Niacin at a concentration of 0.1-10 mM resulted in a dose-dependent reduction of oxygen toxicity in a mouse alveolar
macrophage model. These concentrations of niacin did not affect alveolar macrophage function under normoxic
conditions. The mechanism by which niacin reduces oxygen toxicity may involve the ability of niacin to function as an
alternate substrate for nicotinamide-adenine dinucleotide synthesis...
Pearl RG, Raffin TA; Niacin Reduces Oxygen Toxicity in Mouse Alveolar Macrophages; Pharmacology 27 (4): 219-22 (1983)
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The anti-hypoxic effect of indomethacin (1-10 mg/kg) was studied using the following experimental methods: asphyxic
anoxia in cats, hypobaric and anoxic hypoxia in mice, incomplete ischemia by bilateral carotid occlusion and hemic
hypoxia in rats. Indomethacin showed an anti-hypoxic effect in all the methods used; it significantly increased survival of
rats and mice subjected to experimental hypoxia. Indomethacin potentiated the effect of PG12, shifting and anti-hypoxic
dose-response curve of PG12 to the left.
Nikolov R et al; Anti-Hypoxic Effect of Indomethacin and its Interaction with Prostacyclin; Methods Find Exp Clin Pharmacol 5 (10): 719-
26 (1983)
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13.1.9 Toxicity Summary
Toxicity
May cause burns or frostbites in case of eye or skin contact with rapidly expanding gas. Oxygen therapy can induce
hypercapnic respiratory failure in patients with respiratory diseases and musculoskeletal diseases in upper airways.
Sudden cessation of oxygen supplementation in these patients can further lead to rebound hypoxaemia. In patients with
mild or moderate strokes, hyperoxaemia may cause absorption atelectasis or myocardial infarction. Oxygen content
should be monitored following the administration to verify therapeutic benefit.
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13.1.10 Antidote and Emergency Treatment
Some protection against oxygen toxicity syndrome is offered by admin of gamma-aminobutyric acid, succinate, chelating
agents, certain anesthetics, and trimethamine (tris-(hydroxymethyl)aminomethane).
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Contact with liquid oxygen: Remove victim from source of contact. Flush affected areas with lots of tepid water (Do not
apply directly to affected area). Loosely apply dry sterile, bulky dressings to protect area from infection/injury. Get medical
attention. /Liquid oxygen/
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Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary.
Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask
at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For
eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during
transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if
the patient can swallow, has a strong gag reflex, and does not drool ... . Do not attempt to neutralize because of
exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Oxidizers/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St.
Louis, MO 2005, p. 153
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Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious,
has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway
obstruction, may be necessary. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial.
Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV
administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of
hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid
overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Oxidizers/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St.
Louis, MO 2005, p. 153
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ON FROSTBITE: rinse with plenty of water, do NOT remove clothes. Refer for medical attention ... Eye exposure: First rinse
with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor. /Oxygen,
liquefied/
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13.1.11 Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ "Hyperbaric" is an atmospheric pressure greater than that at sea level. This increase in
pressure, often associated with diving, is opposite of the decrease in atmospheric pressure associated with aviation and
mountain climbing (hypobaric). Partial pressures of O2 are higher in hyperbaric, and lower in hypobaric, atmospheres.
Increased O2 pressures result in hyperoxygenation of the blood (increased dissolved O2) and allows for improved O2
delivery to tissues. Hyperbaric O2 has a number of important uses in medicine. However, the toxicity of increased O2
pressures are also evident in human and animal studies.
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/HUMAN EXPOSURE STUDIES/ As part of a comprehensive study of specific organ oxygen tolerance, oxygen effects on
pulmonary function were measured in normal, resting men who breathed oxygen continuously at 3.0, 2.5, 2.0, and 1.5
atmospheres absolute for average durations of 3.4, 5.7, 9.0, and 17.7 hr, respectively. Rates of development of effects of
pulmonary oxygen toxicity were monitored during oxygen exposure at 2.5, 2.0, and 1.5 atmospheres absolute with
repeated flow-volume loops, spirometry, and symptom assessment. Additional pulmonary measurements before and after
exposure included lung compliance, airway resistance, density dependence of flow, nitrogen closing volumes, carbon
monoxide diffusing capacity, and alveolar-arterial oxygen differences. Of these measurements only airway resistance and
closing volumes were not significantly affected at any pressure, but patterns and magnitudes of effects varied at different
pressures. Overall, the data indicate that continuous oxygen exposure at 3.0 to 1.5 atmospheres absolute affects
pulmonary mechanical function earlier and more prominently than carbon monoxide diffusing capacity. Recovery of lung
mechanical function usually occurred within 12-24 hr after exposure, but required more than 24 hr in some individuals.
No individual measure of pulmonary function was found to be uniquely satisfactory for monitoring rates of development
or reversal of pulmonary oxygen poisoning. The existence of multiple pulmonary effects of oxygen toxicity and the
complexity of their interactions require selective applications of individual toxicity indices to specific conditions of
exposure and recovery.
Abstract: PubMed
Clark JM; Exp Lung Res 14: 897-910 (1988)
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/HUMAN EXPOSURE STUDIES/ ... Direct visual observations /were made/ of the interior of the trachea and ... rate of
mucus transport /measured/ in 10 human volunteers who breathed oxygen through a face mask for 6 hr. The oxygen
concn was 90 to 95%. Observations were made after 3 and 6 hr. Tracheal mucous velocity was decreased after 3 hr and all
subjects showed visual evidence of tracheal irritation after 6 hr. ... Three subjects had fever and two had symptoms of
acute bronchitis several hours after the study was completed; one had sinusitis and conjunctivitis. These phenomena
might be related to the procedure of passing a fiberoptic bronchoscope into the trachea. Two others became nauseated
and vomited during the evening of the study. All were extremely fatigued. None complained of substernal pain or other
symptoms of tracheal or bronchial irritation during the oxygen exposure.
Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John
Wiley Sons, 1981-1982., p. 4064
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/HUMAN EXPOSURE STUDIES/ To study the early changes in the lower respiratory tract in persons exposed to periods of
hyperoxia usually considered safe, 14 normal subjects were evaluated by bronchoalveolar lavage before and immediately
after 16.7 +/ - 1.1 hours of breathing more than 95% oxygen. Hyperoxia caused a significant alveolar-capillary "leak" as
detected by the presence of increased plasma albumin and transferrin in lavage fluid. Although some of the effects of
exposure to 17 hr of more than 95% oxygen are reversible, hyperoxia for even this short period lowers the structural or
functional barriers that normally prevent alveolar-capillary "leak" and induces processes that can culminate in fibrosis of
the alveolar wall.
Davis WB et al; Pulmonary Oxygen Toxicity. Early Reversible Changes in Human Alveolar Structures Induced by Hyperoxia; N Engl J Med
309 (15): 878-83 (1983)
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/HUMAN EXPOSURE STUDIES/ To test the vulnerability of airway epithelial cells to O2-induced injury, antioxidant mRNA
levels (superoxide dismutases (SODs) and catalase (CAT)) were measured in bronchial cells retrieved from normal human
volunteers at baseline and after nearly 15 hr of 100% O2 exposure. CAT activity did not change after hyperoxia, and total
SOD increase could not protect the epithelium from damage. In a follow-up study, human bronchial epithelial cells were
tested in culture for their ability to up-regulate CAT activity after hyperoxia. Constitutive expression of CAT in these cells
was low, and hyperoxia did not induce increased expression ... /It was/ concluded that this inability to up-regulate
antioxidants may play a role in the sensitivity of the human airway epithelium to hyperoxia ...
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/HUMAN EXPOSURE STUDIES/ Although ... all living cells can be damaged by O2, the respiratory system and ... CNS are
most affected by its toxic actions. Whereas the respiratory system is more susceptible to injury, the effects on the CNS are
more dramatic. Animals or humans exposed to a 4-ATA (atmosphere absolute) pressure of O2 are likely to show muscular
twitching or general convulsions (like those of epilepsy) within 1 hr. Pure O2, at atmospheric pressure or less, can cause
pulmonary irritation and edema after 24-hr exposures; higher pressures cause damage in a shorter time. Half an
atmosphere of pure O2 can probably be tolerated indefinitely without lung damage; 3 ATA is probably safe for healthy
adults for 1 hr. Intermittent breathing of air or another gas mixture containing O2 at the accustomed 0.2 ATA pressure
lessens the risk of lung injury.
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/HUMAN EXPOSURE STUDIES/ ... The effects of O2 exposures at pressures ranging from 3.0 ATA (atmosphere absolute)
for 3.4 hr to 1.5 ATA for 17.7 hr continuously /were reported/ in healthy, resting men ... Flow in peripheral airways was
impeded more than diffusion was impaired. No single measure of function was satisfactory for comparing response rates.
There was marked variation among individual subjects. Most showed complete recovery of mechanical functions within 24
hr, but some took longer.
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/HUMAN EXPOSURE STUDIES/ ... 21 men and women, aged 19 to 37 years, /were exposed/ to 100% O2 at an atmospheric
pressure of 9.5 lb/sq in ("equivalent to 11,500 ft, 491 mm Hg or 65.7 kPa"), 8 hr/day for 5 consecutive days, while they
performed moderate exercise. No decompression sickness, symptoms of O2 toxicity, changes in pulmonary function,
blood oxygenation, or other manifestations of injury were observed.
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/HUMAN EXPOSURE STUDIES/ At a pressure of 3 ATA (66 feet of seawater pressure), a grand mal seizure will result in
nearly everyone after approx 3 hr. This is termed the "Paul Bert effect." ... Oxygen breathing can be tolerated by most
people for periods up to 90 min at 3 ATA with little difficulty if they are at rest and recumbent in a dry chamber breathing
oxygen by mask. However, actual tests show that a diver working in water at a depth of 50 feet (2.5 ATA) may suffer
convulsions within 10 to 30 min ... 100% oxygen must never be administered at pressures greater than 3 ATA (29.4 psig) in
the dry chamber. Even with the subject recumbent, comfortably at rest, and well ventilated, exposure time should not
exceed 90 min ...
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/SIGNS AND SYMPTOMS/ The increase of O2 partial pressure in the blood associated with hyperoxia leads to slower,
shallower breathing. This, in turn, leads to accumulation of CO2 in the tissues and the blood, with the further effect of
increasing acidity. The decreased respiration rate in combination with the increased PO2 can also cause some alveoli to
collapse completely, a condition called absorption atelectasis. With this, the adjustment of the flow of blood through the
lung to match the air supply is upset, producing a ventilation/perfusion mismatch. The pulmonary arterioles dilate, the
heart rate is slowed, and the rate of blood flow from the heart decreases ...
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/SIGNS AND SYMPTOMS/ Microscopic injury to the epithelial cells lining the trachea and bronchi occurs early in the
sequence of O2 damage and response. Oxygen exposure depresses mucus secretion and the "upstream" movement of
mucus (mucociliary transport) to the throat; such decreases have been observed after only 3 hr of exposure to 90 to 95%
O2. Other early manifestations of O2-induced lung injury include leakage of proteins from the blood into the air spaces
and increased permeability of the lung epithelium. These have been demonstrated by studies on bronchoalveolar lavage
(BAL) fluid retrieved from humans ... Increases in the blood derivatives albumin and transferrin /were detected in exposed
healthy subjects to >95% O2 for 17 hr/, although the recovered lung cells appeared normal ... Dose-related increases in
albumin in BAL fluids and increased epithelial permeability after 45-hr exposures to 30 to 50% O2 /was reported/.
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/SIGNS AND SYMPTOMS/ In healthy men, the earliest indicators of O2 toxicity are substernal pain and cough after a 4 hr
exposure to > 95% O2. Inflammatory changes in the respiratory mucous membranes appear within 6 hr and, after a 12 hr
exposure, the forced vital capacity (FVC), the amount of air that can be forcibly exhaled after taking a deep breath, is
reduced. At an early stage, water begins to accumulate in the interstices of lung tissue and within the pulmonary cells.
This accumulated water causes a thickening of the alveolar-capillary membrane, impairment of gaseous diffusion, and
interference with the elasticity of the organ. The combined effect is to diminish the FVC.
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/SIGNS AND SYMPTOMS/ Subtle changes in pulmonary function can occur after as little as 8 to 12 hr of exposure to 100%
oxygen. Increases in capillary permeability, which will increase the alveolar/arterial O2 gradient and ultimately lead to
further hypoxemia, and decreased pulmonary function can be seen after only 18 hr of exposure. Serious injury and death
... require much longer exposures.
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/SIGNS AND SYMPTOMS/ The inhalation, at 1 atm, of 80% O2 for more than about 12 hr /causes/ ... irritation of the
respiratory tract ..., progressive decr in vital capacity, coughing, nasal stuffiness, sore throat, and substernal distress,
followed by tracheobronchitits and later by ... pulmonary congestion, transudation, exudation, or atelectasis ...
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/SIGNS AND SYMPTOMS/ Oxygen toxicity with damage to the respiratory system can occur at atmospheric pressure if the
subject is permitted to breathe 100% oxygen for longer than about 24 hr. After approx this period of time, the first
symptoms of respiratory difficulty appear, known as the "Lorraine-Smith effect." These consist of dry cough, substernal
pain, diminished vital capacity, and patchy atelectasis. A chest radiograph film might show findings typical of early
pneumonia. If the pressure is raised from 1 to 2 ATA (equivalent to breathing oxygen at a depth of 33 feet of seawater
(FSW)), these same symptoms will appear within approx 6 hr. With continued exposure, the edematous first stage
proceeds to a microhemorrhagic second stage, with pulmonary fibrosis as the final phase. Pulmonary fibrosis secondary
to oxygen toxicity is irreversible.
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/SIGNS AND SYMPTOMS/ When the partial pressure of oxygen is increased, an unphysiologic condition results. Oxygen at
partial pressures much greater than the 160 mm Hg experienced when breathing atmospheric air acts as a poison, and
metabolism is actually slightly slowed. A profound vasoconstriction takes place, with striking blanching of the face and
extremities, seen in experiments carried out with subjects breathing 100% oxygen at 4 ATA.
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/SIGNS AND SYMPTOMS/ When pure oxygen is inhaled at pressures greater than 2 atmospheres, a characteristic
syndrome is observed. Signs and symptoms incl muscular twitching, nausea, vertigo, mood changes, paresthesias, and ...
loss of consciousness and generalized convulsions.
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/SIGNS AND SYMPTOMS/ ... CNS shows a high tolerance for increased PO2. In healthy men at rest, CNS effects usually
appear only after exposures to 3 ATA (atmosphere absolute) of pressure ... The most prominent effects were convulsive
seizures ... /which are/ closely resemble those of grand mal epilepsy, and show similar electroencephalogram (EEG)
patterns. If the excess PO2 exposure is not quickly ended, severe convulsions can lead to death. As little as 20 min O2
exposure at < 4 ATA can cause convulsions, and the time required is less for higher pressures. The convulsions are
preceded by uncontrollable twitching and various other psychomotor signs and symptoms that are not immediately
relieved by a return to a normal atmosphere ... The CNS effects of O2 ... appear more quickly than the pulmonary
symptoms, but only under higher O2 pressure ... The human infant may ... be more susceptible to hyperbaric O2 than the
adult ...
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/SIGNS AND SYMPTOMS/ ... CNS toxicity (the "Paul Bert effect") ... may develop within a few to many minutes from
exposure to levels of oxygen above about 1.8 bars and may result in an epileptic-like convulsion which is not dangerous
in itself but which will be quite disruptive in any case, and can result in drowning or physical injury. Susceptibility to CNS
toxicity is exacerbated by other factors, particularly those that cause an increase in internal PCO2 such as exercise and
breathing dense gas or breathing against a resistance ... There may be no warning symptoms before a convulsion, and
one may occur several minutes after the exposure to high oxygen has stopped ... There is an enormous variation /of
oxygen toxicity/ among individuals, and a significant variation in a single individual at different times ...
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/SIGNS AND SYMPTOMS/ ... Oxygen's effect on the lung (the "Lorrain Smith effect") ... takes hours or longer to develop
from exposure levels that may be lower than those that cause CNS symptoms; it is seen as chest ("substernal") pain or
discomfort, coughing, inability to take a deep breath without pain or coughing, the development of fluid in the lungs, and
a reduction in vital capacity. This has been called "pulmonary oxygen toxicity" ... The pulmonary oxygen poisoning
encountered in diving or in relation to decompression is, in time, fully reversible and leaves no long-term effects. A
different hospital-related "chronic lung toxicity" may lead to lung fibrosis after very long exposures ...
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/SIGNS AND SYMPTOMS/ ... /"Whole body" oxygen toxicity/ develops after hours to days of exposure ... Its effects are a
collection of symptoms in addition to the lung problems ... that include paresthesias (especially numbness in fingertips
and toes), headache, dizziness, nausea, effects on the eyes, and a dramatic reduction of aerobic capacity ... After many
days of exposure to increased oxygen, a reduction of hemoglobin and red blood cells has also been noted in some divers;
this is a normal adaptive response, the converse of the acclimation to high altitude ... All forms of oxygen toxicity show
highly variable effects on different individuals, and even significant differences in the same individual at different times.
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/SIGNS AND SYMPTOMS/ ... Premature infants ... placed in incubators ... breathe oxygen in concentrations greater than in
air. On removal from hyperoxia, they develop irreversible bilateral ocular disease known as retrolental fibroplasia ... Only
the incompletely developed retinal circulation is susceptible to toxic levels of oxygen, whereas a mature retinal vascular
system and other incompletely formed circulations are not sensitive to oxygen toxicity. Within 6 hr after an infant is
placed in a high oxygen containing atmosphere, vasoconstriction of the immature vessels occurs, which is reversible if the
child is immediately returned to air but is irreversible if hyperoxia therapy is continued.
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/SIGNS AND SYMPTOMS/ ... Premature infants have organs that are not fully developed at birth, including the lungs and
eyes, where growth of new capillaries is still very active ... /and/ may have difficulty in getting sufficient O2 into their
blood, so they are placed in enclosed incubators or on respirators with an increased PO2. In the early history of this life-
saving procedure, high O2 concentrations were used. The immediate benefit of tissue oxygenation was followed by a high
incidence of pulmonary damage. It was soon observed that these babies were blind, the result of hyperoxic damage to
the retinal capillaries. This injury was followed by proliferation of fibrous tissue. Careful adjustment of the O2 pressure to
meet the needs of the infant has been effective in controlling the damage to the eye.
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/SIGNS AND SYMPTOMS/ Transient impairment of visual fields and visual acuity have been reported in adult humans in
association with hyperbaric O2.
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/SIGNS AND SYMPTOMS/ In infants who are given oxygen therapy after birth, a syndrome known as bronchopulmonary
dysplasia may develop. Lung pathology is characterized by necrotizing bronchiolitis, fibroblast proliferation, squamous
metaplasia of the bronchial lining, and destruction of alveolar ducts.
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/SIGNS AND SYMPTOMS/ Rapid evaporation of the liquid may cause frostbite. The substance at very high concentrations
is irritating to the respiratory tract. The substance may cause effects on the central nervous system. /Oxygen, liquefied/
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/CASE REPORTS/ Although severe retinal damage in adults is rare during hyperoxia, one case was reported concerning an
individual suffering from myasthenia gravis who developed irreversible retinal atrophy after breathing 80% oxygen for
150 days. The retinal vasculature was markedly constricted with no blood flowing through both eyes. The vascular
disorder was limited only to retinal circulation.
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/CASE REPORTS/ ... additional oxygen tolerance tests did not produce any signs or symptoms of oxygen toxicity in ...
already proven susceptible divers. ... 9 episodes of nonconvulsive oxygen toxicity were seen in mixed gas diving and 3
episodes of nonconvulsive oxygen toxicity were noted in closed circuit oxygen diving.
Abstract: PubMed
Butler FK Jr, Knafelc ME; Undersea Biomed Res 13 (1): 91-8 (1986)
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/CASE REPORTS/ ... Detailed examinations of the lungs of six persons who died after 14 hr to 13 days of mechanical
ventilation with 60 to 100% O2 /were reported/. After 14 hr, swelling of type I alveolar epithelial cells was most obvious,
accompanied by bronchial hyperemia. After 3 days, endothelial and type I cell damage, interstitial edema, thickened and
ruptured septa, perivascular hemorrhage, and alveolar hemorrhage were present. After 6 days, capillary destruction and
interstitial hemorrhage were noted and after 13 days marked septal fibrosis, proliferation of type II cells, distorted alveoli,
and arteriolar clots were present.
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/EPIDEMIOLOGY STUDIES/ A study was made to determine the type, incidence, and timing of complications that occur in
patients who have a carbon monoxide (CO) exposure serious enough to require hyperbaric oxygen therapy. Complication
data were retrospectively collected for a ten year period for 297 consecutive CO poisoned emergency department
patients who received hyperbaric oxygen therapy. Hyperbaric oxygen therapy was indicated for 41% of the patients
because of an elevated carboxyhemoglobin level alone. Central nervous system dysfunction, including loss of
consciousness and/or cardiovascular dysfunction, was the criteria for hyperbaric oxygen therapy in 59% of patients
regardless of their carboxyhemoglobin level. The mean peak carboxyhemoglobin level was 38 mg%, with 88% of patients
having a peak carboxyhemoglobin level greater than 25 mg%. The mortality rate was 6% in this case series. ... Several
complications ... occurred for the first time or as a recurrent event during hyperbaric oxygen therapy. These included
emesis (6%), seizures (5%), agitation requiring restraints or sedation, (2%) cardiac dysrhythmias or arrests (2%), and
arterial hypotension (2%). No patient's level of consciousness deteriorated subsequent to the initial resuscitation except
for those who later had a generalized seizure. The most significant complication attributable to hyperbaric oxygen therapy
was tension pneumothorax, noted in three patients (1%). Epistaxis of tympanic membrane rupture occurred in 1%. In 3%,
hyperbaric oxygen therapy was terminated prematurely, in half the cases because of complications that required
management outside of the chamber, and in half because of persistent otalgia after complete clinical recovery.
Abstract: PubMed
Sloan EP et al; Ann Emerg Med 18 (6): 629-34 (1989)
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/SURVEILLANCE/ ... Among 20,328 total patient treatments performed from 1992 to 2001, 6 patients experienced an
oxygen-toxic seizure for an overall incidence of 1 in 3,388 treatments (0.03%). No difference in seizure incidence was seen
between the two brands of oxygen hoods utilized.
Abstract: PubMed
Hampson N, Atik D; Undersea Hyperb Med 30 (2): 147-53 (2003)
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/ALTERNATIVE and IN VITRO TESTS/ The activity of intracellular antioxidant enzymes is quickly increased in response to
hyperoxia exposure ... /and is/ associated with increases in the messenger ribonucleic acids (mRNAs), leading to the
production of superoxide dismutases (SOD), catalase (CAT), and glutathione peroxidase (GP) proteins. This was shown by
in vitro cultures of human endothelial cells exposed to 95 percent O2 for 3 or 5 days. The mRNA changes were
accompanied by complex changes in enzyme protein concentrations and activities, generally in the direction of protective
reactions to hyperoxia.
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/OTHER TOXICITY INFORMATION/ Effect of intermittent exposure to hyperbaric oxygen over a long period of time was
evaluated in 65 men. Pulmonary ventilation and diffusion capacities were measured. No significant difference was found
in any of measured respiratory parameters between divers and controls.
MOSELHI H; PULMONARY FUNCTION IN MEN WITH INTERMITTENT LONG-TERM EXPOSURE TO HYPERBARIC OXYGEN; UNDERSEA
BIOMED RES 7 (2): 149-57 (1980)
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13.1.12 Non-Human Toxicity Excerpts
/LABORATORY ANIMALS: Acute Exposure/ ... One-day-old rats were exposed to 2 to 4 days of /normobaric hyperoxia/
(NH) (Fio2>0.98) or normoxia (Fio2=0.21), with or without weaning. Pups were then euthanized and 100 uL of blood was
collected (cardiac puncture) for differential white blood cells analysis (n=12 per group). The lungs, a piece of distal ileum,
and the left kidney were removed for histologic evaluation. Both NH and weaning /(return to air breathing)/ generated
significant increases in blood neutrophil count, whereas lymphocyte population was significantly increased only after
weaning (P<0.05; analysis of variance with Bonferroni correction for multiple comparisons). Normobaric hyperoxia created
mild increases in the renal tubular necrosis, dilation, regeneration, and interstitial inflammation. A significant increase in
the intestinal serosal and submucosal vasodialation and vascularization occurred 1 day after weaning from 4 days of NH
(P<0.001).
Torbati D et al; J of Crit Care 21 (1): 85-93 (2006)
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/LABORATORY ANIMALS: Acute Exposure/ /Dogs inhaling pure O2 at atmospheric pressure/ ... poisoning begins after 36
hr, causes distress within 48 hr, and death in 60 hr. Ninety per cent O2 in air requires double exposure period for similar
results; in 80% oxygen in air the animals did not die but were ill at the end of a continuous exposure of 1 wk. A decline in
O2 saturation of blood, rise in hemoglobin, lung congestion and edema, right-heart failure, and liver congestion were
frequent findings in oxygen poisoning.
Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 913
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/LABORATORY ANIMALS: Acute Exposure/ The role of neutrophils in the mediation of severe normobaric hyperoxic lung
injury was studied by monitoring the effects of neutrophil depletion on a rat model of pulmonary oxygen toxicity.
Pulmonary capillary permeability, assessed using an radioactive iodine labeled albumin lung permeability index,
progressively increased with an increased duration of hyperoxic exposure in normal animals (lung permeability index of
0.43 +/ - 0.09 at 2 hr; 0.95 +/ - 0.17 at 48 hr; 1.56 +/ - 0.21 at 60 hr) despite the absence of any significant tissue or
bronchoalveolar lavage evidence of neutrophil infiltration until 60 hr of hyperoxia exposure. Neutrophil depletion with
cyclophosphamide blocked this late neutrophil infiltrate but failed to attenuate lung injury.
Abstract: PubMed
Boyce NW et al; Exp Lung Res 15 (3): 491-8 (1989)
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/LABORATORY ANIMALS: Acute Exposure/ One litter of term newborn New Zealand albino rabbits (n= 9) and 15 adult
rabbits were exposed to 65 hr of > 95% oxygen (O2). ... Sixty-five hr of oxygen exposure in newborn rabbits produced no
evidence of lung injury on light microscopy, 97% of bronchoalveolar lavage white cells were alveolar macrophages and
bronchoalveolar lavage protein was low. No differences were found in the percentage of alveolar macrophages, and the
proportion of PMN was low in both hyperoxic (n=9) and normoxic (n=7) newborn groups. Mortality was comparable, 14%
and 11% in normoxic and hyperoxic newborn groups, respectively. An equal period of oxygen exposure produced
significant lung injury in adult rabbits, and a mortality of 27% (not significant). Adults appeared dyspneic and frequently
had grossly visible subpleural hemorrhages. Microscopic analysis revealed an intense inflammatory cell infiltrate, an
exudate in the air spaces and areas of intra-alveolar hemorrhage. Bronchoalveolar lavage fluid from oxygen injured adults
contained a 17-fold greater percentage of PMN and 16-fold higher protein than oxygen exposed newborns. Newborns
under normoxic conditions had very high levels of 6-keto-PGF1a and low quantities of TXB2. Hyperoxic newborns had
lower 6-keto-PGF1a and significantly higher TXB2. Hyperoxic adults had significantly lower 6-keto-PGF1a, and significantly
higher LTB4 and LTC4 in bronchoalveolar lavage compared to hyperoxic newborns. Leukotriene D4 values, although 25%
higher on average in the adult rabbits, were not statistically different.
Abstract: PubMed
Holtzman RB et al; Prostaglandins 37 (4): 481-91 (1989)
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/LABORATORY ANIMALS: Acute Exposure/ Oxygen (O2) toxicity was assessed in Balb/C mice exposed to 5 ATA of O2 for
30 min at 5, 15, 25, and 35 deg C. CNS toxicity was measured as the latent period before convulsions, and lung damage
was estimated by wet and dry wt measurements. Mice exposed to 5 ATA of O2 at ambient temp of 15 deg C had a
precompression rectal temp of 36.9 deg C and a postcompression temp of 24.9 deg C. At 5 deg C the precompression
and postcompression temp were 37.6 and 16.1 deg C, respectively. All groups differed from one another statistically. Even
marked hypothermia, however, had very little effect on the latent times to convulsions in mice; time to initial convulsions
ranged from 3.7 to 5.5 min, and sustained convulsions ranged from 17.9 to 23.7 min. There were significant incr in the wet
wt of lungs of mice exposed at 35 deg C and 25 deg C compared to control nonpressurized mice, of 20% and 26%,
respectively. With hyperbaric O2 and at 15 deg C, incr in lung wet wt were 62% compared to controls), and 196% incr at 5
deg C. The lungs in this last group were frankly edematous and hemorrhagic. Incr above control lung dry wt were about
18% in the 15, 25 and 35 deg C groups and 104% in the 5 deg C group. Histology confirmed a great degree of edema
and hemorrhage into alveolar spaces in the 5 deg C group. Falls in body temp of mice exposed to 5 deg C at atmospheric
pressure were minor (3.4 deg C after 40 min). Mice were also exposed to 12% O2/88% N2 at 5 ATA and 5 deg C for 40 to
50 min. The avg rectal temp was 37.9 deg C before compression and dropped by 2.9 deg C to 35.0 deg C after 30 min.
There was some gain in both wet and dry lung wt, but this was much less than in mice exposed to 100% O2.
Abstract: PubMed
Jamieson D, Carmody J; Aviat Space Environ Med 60 (7,1): 639-43 (1989)
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/LABORATORY ANIMALS: Acute Exposure/ A selective effect of hyperoxia on mature visual cells is exemplified by exposing
adult rabbits to 100% oxygen for 48 hours. The result is loss of the ERG and visual cell death. Further experimentation with
rabbits indicated that the centrally located rods, characterized by a low glycogen content and rich choroidal blood supply
and therefore analogous to the human macula, are the most sensitive cells to oxygen toxicity. Peripheral rods and cones
are less sensitive and spared from the toxic effects, whereas other retinal layers--the inner nuclear layer, the ganglion cell
layer, and the pigmented epithelial layer--appear normal. Rods containing a single synaptic ribbon appear to be more
sensitive than rods with multisynaptic ribbons.
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/LABORATORY ANIMALS: Acute Exposure/ ...Exposure of pregnant rats to low concentrations of oxygen resulted in a
marked depression in oxygen consumption and partial oxygen pressure on the skin (tcPo2) during the exposure time. A
significant increase in the lipid peroxide level in serum was observed in the mother rat after birth and in the newborn
offspring of pregnant rats exposed to 16% oxygen for 3 hr.
Abstract: PubMed
Yoshimura Y et al; J Toxicol Sci 13 (3): 141-9 (1988)
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/LABORATORY ANIMALS: Acute Exposure/ ... Increases in systemic arterial oxygen ... resulted in significant increases in
oxygen tension in the choroid and in ... in the avascular area of the rabbit retina ... exposed to high oxygen levels during
systemic hyperoxia. The magnitude of the oxygen changes in all retinal layers was consistent with that in the preretinal
vitreous.
Cringle SJ, Yu DY; Invest Ophthalmol Vis Sci 45 (9); 3223-8 (2004)
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/LABORATORY ANIMALS: Acute Exposure/ ... Preretinal neovascularization subsequently occurred in 66% (63/96) of all rats
exposed to cyclic oxygen followed by a room air period but in no rats (0/50) exposed to constant oxygen followed by
room air. Preretinal vascular proliferation consisted of glomerular tufts of endothelial cells, or mature, lumenized vessels
containing red blood cells.
Abstract: PubMed
Penn JS et al; Invest Ophthalmol Vis Sci 34 (3): 576-85 (1993)
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/LABORATORY ANIMALS: Acute Exposure/ Pulmonary oxygen toxicity is a dose-dependent effect on alveolar epithelial
and endothelial cells resulting in pulmonary oedema. Any concomitant effects on systemic capillary endothelium would
be expected to result in capillary leakage and an increase in the tissues' water content. Total tissue water (TTW) in
different organs was therefore studied in freely moving rats exposed to 100% O2 at normobaric pressure for 24 or 48 h,
and compared to air-breathing control rats. The TTW for the following tissues was measured: Trachea, left bronchus, left
lung, left and right ventricle, left kidney, skin (left paw-hindlimb), skin (back of the rat), left brain, left eye and thigh muscle
left side. There was a significant increase in TTW of the lung accompanied by pleural effusion after 48 h of oxygen
exposure as expected in all exposed animals. There was a small increase in TTW of the paw only, and a small decrease or
no change in other tissues after 24 and 48 h of exposure.
Abstract: PubMed
Stuhr LE et al; Acta Physiol Scand 176 (1): 13-6 (2002)
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/LABORATORY ANIMALS: Acute Exposure/ The most prominent adverse respiratory consequences of O2 exposures with
partial pressures of <3 ATA (atmosphere absolute) include epithelial swelling and breakdown, blood vessel congestion,
interstitial edema and alveolar exudate. These changes, known as the Lorain Smith effect, were first described in mice in
1899 ...
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/LABORATORY ANIMALS: Acute Exposure/ ... Rabbits /exposed to 100% O2 developed/ pathological changes after 24 hr.
A progressive increase in pulmonary capillary permeability was seen by 48 hr, and after 64 hr, decreased phospholipids
(surfactant), decreased lung capacity, pulmonary edema, and high surface tension in lung fluids were noted. Instillation of
calf lung surfactant into the rabbit lungs during the O2 exposure diminished the injury ...
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/LABORATORY ANIMALS: Acute Exposure/ ... /Comparative studies of pre- and postexposure lung biopsies from rats and
baboons /were reported/, using 40 to 60% O2 for periods of 80 hr. Changes were hard to detect in the animals exposed
to 40% O2, but injuries became evident when the animals were subsequently exposed to a different form of lung stress. It
was concluded that the basic reaction pattern was the same for both species, but the primate response was slower ... Rats
/initially/ exposed to 40 or 60% O2 died sooner than did control animals when they were /subsequently/ exposed to
100% O2.
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/LABORATORY ANIMALS: Acute Exposure/ In squirrel monkeys, exposure to 100% oxygen for 50 to 117 hr increases
vascular permeability, with leakage and edema of the retina, but these effects are largely reversible.
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... In baboons, alveolar type I epithelium was almost
completely destroyed after 4 days in 100% O2, and after 7 days, type II cells had almost completely replaced the alveolar
lining.
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Several days exposure of ... rabbits to abnormally high
concn of oxygen ... /produced/ irreversible degeneration of rods in retina, changes in electroretinogram and edema of
ciliary body and iris, with incr permeability of blood-aq barrier. ... With 60% oxygen at 1 ATM toxic effects appeared in 7
days ...
Grant, W. M. Toxicology of the Eye. 2nd ed. Springfield, Illinois: Charles C. Thomas, 1974., p. 778
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Newborn and adult animals of five species /were
exposed/ to >95% O2 for 7 days. Measurements of antioxidant enzymatic activity in the lungs (superoxide dismutases
(SOD), catalase (CAT), glutathione peroxidase (GP)) showed no significant responses in adult animals to a 24-hr exposure,
nor were these enzymes increased in newborn guinea pigs or hamsters. Newborn mice, rabbits, and rats showed
significant increases in all the enzymes ranging from 12 to 36% (except that mice showed only a 5% increase in CAT). The
exposure time to cause 50% mortality was much greater for the newborn mice, rats, and rabbits than for the adults, but
the newborn guinea pigs and hamsters only lived as long as the adults of the same species.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... Umbilical hernias, exencephaly, spina bifida and limb
defects /were produced/ in a small but significant number of hamster fetuses by exposing the mother to 3.0 or 4.0 ATM of
oxygen for periods of 2 to 3 hr on the 6th, 7th, or 8th day of gestation.
Shepard, T. H. Catalog of Teratogenic Agents. 3rd ed. Baltimore, MD.: Johns Hopkins University Press, 1980., p. 554
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ /When dams were/ exposed for 5 hr to 260 to 280 mm
Hg of oxygen on the 9, 10 or 15 gestational day /mouse fetuses had/ hemivertebra, fused ribs, cleft palate and
cranioschisis.
Shepard, T.H. Catalog of Teratogenic Agents. 4th ed. Baltimore, MD: Johns Hopkins University Press, 1983., p. 236
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Freshly laid eggs of White Leghorn chickens were
exposed to one of four oxygen (O2) environments. Hypoxic embryos (10% O2, days 14 through 18, n = 85) were smaller
than controls incubated in normoxia (n = 125), with higher hematocrit values and larger lung wt/body wt ratios (both wet
and dry). Dry lung wt/body wt ratios for hypoxic embryos were 22% higher than those of hyperoxic embryos. Hyperoxic
embryos (50% O2, days 7 through 18 (n = 30) or days 14 through 18 (n = 91)) had lower hematocrit values and smaller
dry lung wt/body wt ratios than controls, with similar DNA concn. In general, the differences from controls were more
apparent in these embryos hyperoxic from day 14 through 18 of incubation than from day 7 to 18.
Abstract: PubMed
Xu L, Mortola JP; Can J Physiol Pharmacol 67 (5): 515-9 (1989)
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/LABORATORY ANIMALS: Neurotoxicity/ ... The effects of O2 inhaled under higher-than-atmospheric pressures on birds
and dogs was described ... using 5 to 10 times normal ATA (atmosphere absolute) containing 73 to 81% O2. The most
prominent effects were convulsive seizures. This CNS response has been called the Paul Bert effect ... CNS effects are
uncommon even after several hours of exposure with PO2 < 3 ATA, and susceptibility is species-dependent ... Although
the CNS of animals is resistant at birth to the Paul Bert effect and to neurological degeneration caused by hyperbaric O2,
it soon becomes susceptible. Exposure to even 1 ATA of pure O2 causes destruction of brain cells.
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/LABORATORY ANIMALS: Neurotoxicity/ Extensive structural damage to the CNS has been described in rats and cats after
high pressure O2 exposures, with lesions in both the spinal cord and the brain. Microscopic evidence suggested that CNS
lesions can be induced by tissue PO2 levels similar to those affecting lung cells ...
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 672
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/ALTERNATIVE and IN VITRO TESTS/ In the first of three experiments, mouse zygotes were cultured in an atmosphere
containing either 5% or 20% oxygen. There was no significant difference in the frequency of the first cleavage in two the
groups during the first 24 hour of culture. However, after 48 hours of culture, 77.6% of the 5% group had reached the 3 to
4 cell stage; 41.1% of the 20% group had progressed to that stage. At 72 hours of culture, >70% of the 5% group had
reached the morula stage; <4% of the 20% group had reached this stage. By 96 hours >57% of the 5% group had reached
the blastula stage; <4% of the 20% group had reached this stage. At the end of the culture period (120 hr), the 5% group
had blastulated at a rate of 66%; <6% of the 20% group, with most having degenerated by this time. In the second
experiment mouse zygotes were cultured in an atmosphere containing 5% oxygen either continuously or after an initial 2
hours in an atmosphere containing 20% oxygen. There was no difference in the development rates of these two groups
through the first 72 hours and 50% reached the morula stage. Differences became apparent at 96 hours of culture. At this
time >51% of the 5% continuously exposed group had blastulated, while only 27% of the embryos exposed to 2 hr of
atmospheric oxygen had blastulated. At the end of the 120 hour culture period >57% of the continuously exposed group
had blastulated; 30% of the 2 hr atmospheric group had blastulated. In the third experiment mouse zygotes were cultured
in an atmosphere containing 5% oxygen either continuously or after an initial 1 hour in an atmosphere containing 20%
oxygen. At 48 hours there was no significant difference in the number of preembryos reaching the 3 to 4 cell stage in
both groups (about 90%). By 72 hours 80% of the continuous group had reached the morula stage; <58% of the group
exposed for 1 hour at 20% oxygen had reached the morula stage. By 96 hours >55% of the continuous group had
blastulated; <37% of those exposed for 1 hour at 20% oxygen had blastulated. By 120 hours >70% of the continuous
group had blastulated; <46% of the other group had reached this stage.
Abstract: PubMed
Pabon JE et al; Fertil Steril 51 (5): 896-900 (1989)
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/ALTERNATIVE and IN VITRO TESTS/ Cultures of animal eye tissues, especially the lens and the retina, are susceptible to
hyperoxic injury at normal pressure.
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/OTHER TOXICITY INFORMATION/ The mortality induced /in rodents/ by exposure to ... 100% oxygen ... /is/ strongly
circadian rhythmic.
Cralley, L.J., L.V. Cralley (eds.). Patty's Industrial Hygiene and Toxicology. Volume III: Theory and Rationale of Industrial Hygiene Practice.
2nd ed., 3A: The Work Environment. New York, NY: John Wiley Sons, 1985., p. 247
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/OTHER TOXICITY INFORMATION/ Marked differences in susceptibility to O2 poisoning have been reported between mice
and rats ... Larger animals, such as dogs and monkeys, are less susceptible to hyperoxic injury than smaller ones, especially
rodents. Older rats ... and heavier rats are more sensitive than /younger ones and/ lighter ones ... Interstrain variations in
hyperoxic injury have been reported in mice and rats ... Significant differences in survival time ... in hyperbaric oxygen
conditions /and/ in ... susceptibility to an inflammatory response to hyperoxic injury /among common inbred mouse
strains were observed/. Protein in BAL was 10-fold higher in the most susceptible mouse strain compared to the most
resistant ...
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/OTHER TOXICITY INFORMATION/ When the overexpression of extracellular copper/zinc-superoxide dismutase (SOD) was
specifically targeted to alveolar type II cells and nonciliated bronchial, epithelial cells, mice showed reduced inflammation
and lung toxicity after hyperoxia. Correlating with a protective role for this enzyme, knockout mice lacking extracellular
copper/zinc-SOD were more sensitive to hyperoxia.
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/OTHER TOXICITY INFORMATION/ ... Preexposure of rats to hypoxia (10% O2) for 3 to 5 days stimulated increases in lung
superoxide dimutases (SOD), catalase (CAT), glutathione peroxidase (GP), and glucose-6-phosphate dehydrogenase
activities and was strongly protective against lung damage by hyperoxia. Mice and hamsters similarly treated, however,
showed no increases in enzyme activities, nor were they protected from injury ... Evidence for the production of
superoxide anion and peroxide as a response to hypoxia /was cited/; this would be a stimulus for the production of
antioxidant enzymes.
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/OTHER TOXICITY INFORMATION/ ... Mice responsive to hepatic microsomal enzyme induction by aromatic hydrocarbons
[C3H/HeJ, C3H/HeN, C3H/HeJ X DBA/2J (designated C3D2F1/J), C3H/HeN X DBA/2J (designated C3D2F1/N)] were more
sensitive to the toxic effects of 100% oxygen exposure than were genetically unresponsive mice (DBA/2J). DBA/2J mice
survived significantly longer exposure periods with less lung damage. Lung and liver cytochrome P-450 levels increased 2-
to 3-fold in C3H and F1 mice during 100% oxygen exposure (maximum levels at 72-96 hr) and subsequently fell prior to
death. No increases were seen in cytochrome P-450 levels in DBA/2J mice.[Gonder JC et al; Proc Natl Acad Sci USA 82
918): 6315-19 (1985)] Full text: PMC391044
Abstract: PubMed
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13.1.13 Populations at Special Risk
Ventilating patients with elevated oxygen tensions alters normal respiratory physiology and may damage lung tissue,
depending on coexisting host and iatrogenic factors. ... Supplemental oxygen should be prescribed at the lowest
concentration possible that will still allow adequate tissue oxygenation...
Abstract: PubMed
Bryan CL, Jenkinson SG; Clin Chest Med 9 (1): 141-52 (1988)
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In a small number of patients whose respiratory center is depressed by long-term retention of carbon dioxide, injury, or
drugs, ventilation is maintained largely by stimulation of carotid and aortic chemoreceptors, commonly referred to as the
hypoxic drive. The provision of too much oxygen can depress this drive, resulting in respiratory acidosis. In these cases,
supplemental oxygen should be titrated carefully to ensure adequate arterial saturation. If hypoventilation results, then
mechanical ventilatory support with or without tracheal intubation should be provided.
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... Premature infants have organs that are not fully developed at birth, including the lungs and eyes ... so they are placed in
enclosed incubators or on respirators with an increased PO2. In the early history of this life-saving procedure, high O2
concentrations were used. The immediate benefit of tissue oxygenation was followed by a high incidence of pulmonary
damage. It was soon observed that these babies were blind, the result of hyperoxic damage to the retinal capillaries. This
injury was followed by proliferation of fibrous tissue. Careful adjustment of the O2 pressure to meet the needs of the
infant has been effective in controlling the damage to the eye.
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... Premature infants ... placed in incubators ... breathe oxygen in concentrations greater than in air. On removal from
hyperoxia, they develop irreversible bilateral ocular disease known as retrolental fibroplasia ... . Only the incompletely
developed retinal circulation is susceptible to toxic levels of oxygen, whereas a mature retinal vascular system and other
incompletely formed circulations are not sensitive to oxygen toxicity. Within 6 hr after an infant is placed in a high oxygen
containing atmosphere, vasoconstriction of the immature vessels occurs, which is reversible if the child is immediately
returned to air but is irreversible if hyperoxia therapy is continued.
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In infants who are given oxygen therapy after birth, a syndrome known as bronchopulmonary dysplasia may develop.
Lung pathology is characterized by necrotizing bronchiolitis, fibroblast proliferation, squamous metaplasia of the
bronchial lining, and destruction of alveolar ducts.
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... In neonates with congenital heart disease and left-to-right shunting of cardiac output, oxygen supplementation must
be carefully regulated because of the risk of further reducing pulmonary vascular resistance and increasing pulmonary
blood flow.
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... Actual tests show that a diver working in water at a depth of 50 feet (2.5 ATA) may suffer convulsions within 10 to 30
min ...
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13.1.14 Protein Binding
Oxygen binds to oxygen-carrying protein in red blood cells called hemoglobin with high affinity. The amount of oxygen
molecules bound to the fixed amount of circulating hemoglobin in the blood determines the overall oxygen saturation
level and this oxygen-delivering capacity is regulated by Bohr effect.
 from DrugBank
13.2 Ecological Information
13.2.1 Natural Occurring Sources
... oxygen, as a gaseous element, forms 21% of atmosphere by volume.

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EVEN THOUGH LARGE QUANTITIES OF ATMOSPHERIC O2 ARE CONSTANTLY BEING CONSUMED IN RESPIRATION,
COMBUSTION & OTHER OXIDATION PROCESSES, THE CONCN OF O2 IS KEPT @ VIRTUALLY CONSTANT LEVEL, PRIMARILY
AS A RESULT OF O2 LIBERATED IN THE PROCESS OF PHOTOSYNTHESIS IN GREEN PLANTS.
Office, 1983., p. 1578
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13.2.2 Bioconcentration
None /Liquid oxygen/

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13.2.3 Atmospheric Concentrations
Normal air consists of 20.94% oxygen.

Waldbott GL; Health Eff Environ Pollut p.14 (1973)
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13.2.4 Probable Routes of Human Exposure
Industrial exposures to high oxygen pressure are uncommon. Sea diving is probably the most frequent. ... Caison workers
& tunnel makers may also be exposed to pressures that are high enough to cause lung damage.
Leikauf GD, Prows DR; Patty's Toxicology. (2005) NY, NY: John Wiley & Sons, Inc. Inorganic Compounds of Carbon, Nitrogen, and
Oxygen. 7.0. Oxygen, 7.4. Toxic Effects. Apr 16, 2001.
 from HSDB
Some potential risks for intoxication with oxygen also exist for drivers and persons living or working in closed
compartments, where the air is reconditioned by the addition of pure oxygen (eg, submarines and spacecraft), should the
regulation system malfunction.
Seiler, H.G., H. Sigel and A. Sigel (eds.). Handbook on the Toxicity of Inorganic Compounds. New York, NY: Marcel Dekker, Inc. 1988., p.
508
 from HSDB
14 Literature
14.1 Depositor Provided PubMed Citations
CLICK TO LOAD...
 from PubChem
14.2 NLM Curated PubMed Citations
CLICK TO LOAD...
 from PubChem
14.3 Synthesis References

Wynn, Richard L. Production of hydrogen and oxygen by thermal disassociation of water. U.S. Pat. Appl. Publ. (2007),
26pp.
14.4 General References
General Reference
Heyboer M 3rd, Milovanova TN, Wojcik S, Grant W, Chin M, Hardy KR, Lambert DS, Logue C, Thom SR: CD34+/CD45-dim
stem cell mobilization by hyperbaric oxygen - changes with oxygen dosage. Stem Cell Res. 2014 May;12(3):638-45. doi:
10.1016/j.scr.2014.02.005. Epub 2014 Feb 28.
Abstract: PubMed
 from DrugBank
General Reference
Prabhakar NR: Oxygen sensing by the carotid body chemoreceptors. J Appl Physiol (1985). 2000 Jun;88(6):2287-95.
Abstract: PubMed
 from DrugBank
General Reference
Feng Z, Liu J, Ju R: Hyperbaric oxygen treatment promotes neural stem cell proliferation in the subventricular zone of
neonatal rats with hypoxic-ischemic brain damage. Neural Regen Res. 2013 May 5;8(13):1220-7. doi: 10.3969/j.issn.1673-
5374.2013.13.007.
Abstract: PubMed
 from DrugBank
General Reference
Lopez-Barneo J, Gonzalez-Rodriguez P, Gao L, Fernandez-Aguera MC, Pardal R, Ortega-Saenz P: Oxygen sensing by the
carotid body: mechanisms and role in adaptation to hypoxia. Am J Physiol Cell Physiol. 2016 Apr 15;310(8):C629-42. doi:
10.1152/ajpcell.00265.2015. Epub 2016 Jan 13.
Abstract: PubMed
 from DrugBank
General Reference
Liu W, Khatibi N, Sridharan A, Zhang JH: Application of medical gases in the field of neurobiology. Med Gas Res. 2011 Jun
27;1(1):13. doi: 10.1186/2045-9912-1-13.
Abstract: PubMed
 from DrugBank
General Reference
British Thoracic Society: Guideline for emergency oxygen use in adult patients
 from DrugBank
General Reference
Airgas SDS
 from DrugBank
General Reference
Linde SDS
 from DrugBank
14.5 Metabolite References
 Download
PMID Reference
PMID Reference
Carrier M, Denault A, Lavoie J, Perrault LP: Randomized controlled trial of pericardial blood processing with
16798186 a cell-saving device on neurologic markers in elderly patients undergoing coronary artery bypass graft
surgery. Ann Thorac Surg. 2006 Jul;82(1):51-5.
Valadka AB, Furuya Y, Hlatky R, Robertson CS: Global and regional techniques for monitoring cerebral
16821755
oxidative metabolism after severe traumatic brain injury. Neurosurg Focus. 2000 Nov 15;9(5):e3.
Armonda RA, Vo AH, Bell R, Neal C, Campbell WW: Multimodal monitoring during emergency
16757831
hemicraniectomy for vein of Labbe thrombosis. Neurocrit Care. 2006;4(3):241-4.
Sassaroli A, deB Frederick B, Tong Y, Renshaw PF, Fantini S: Spatially weighted BOLD signal for comparison
16945553 of functional magnetic resonance imaging and near-infrared imaging of the brain. Neuroimage. 2006 Nov
1;33(2):505-14. Epub 2006 Aug 30.
Zhang YT, Geng ZJ, Zhang Q, Li W, Zhang J: Auditory cortical responses evoked by pure tones in healthy
16996009 and sensorineural hearing loss subjects: functional MRI and magnetoencephalography. Chin Med J (Engl).
2006 Sep 20;119(18):1548-54.
14.6 Chemical Co-Occurrences in Literature
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 from PubChem
14.7 Chemical-Disease Co-Occurrences in Literature
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View More Chemical-Disease Co-Occurrences and Evidence for Oxygen
 from PubChem
14.8 Chemical-Gene Co-Occurrences in Literature
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View More Chemical-Gene Co-Occurrences and Evidence for Oxygen
 from PubChem
15 Patents
15.1 Depositor-Supplied Patent Identifiers
CLICK TO LOAD...
 from PubChem
16 Biomolecular Interactions and Pathways
16.1 Protein Bound 3-D Structures
CLICK TO LOAD...
 from PDB
View 372 proteins in NCBI Structure

 from PubChem
16.2 Biosystems and Pathways
CLICK TO LOAD...
 from PubChem
16.3 DrugBank Interactions
Target NADPH oxidase 1
Action agonist
Action activator
PubChem
Protein Q9Y5S8
Target
PubChem
Gene NOX1
Target
General Voltage-gated proton channel activity
Function
NOH-1S is a voltage-gated proton channel that mediates the H(+) currents of resting phagocytes and
Specific other tissues. It participates in the regulation of cellular pH and is blocked by zinc. NOH-1L is a pyridine
Function nucleotide-dependent oxidoreductase that generates superoxide and might conduct H(+) ions as part of
its electron transport mechanism, whereas NOH-1S does not contain an electron transport chain.
Smith RG: An appraisal of potential drug interactions regarding hyperbaric oxygen therapy and frequently
Reference prescribed medications. Wounds. 2011 Jun;23(6):147-59.
Abstract: PubMed
Prabhakar NR: Oxygen sensing by the carotid body chemoreceptors. J Appl Physiol (1985). 2000
Reference Jun;88(6):2287-95.
Abstract: PubMed
 from DrugBank
Target Hemoglobin subunit alpha
PubChem
Protein P69905
Target
PubChem
Gene HBA1
Target
General
Oxygen transporter activity
Function
Specific
Involved in oxygen transport from the lung to the various peripheral tissues.
Function
Miyashita H, Hashimoto K, Mohri H, Ohokubo T, Harano T, Harano K, Imai K: Hb Kanagawa [alpha

40(C5)Lys----Met]: a new alpha chain variant with an increased oxygen affinity. Hemoglobin. 1992;16(1-
Reference
2):1-10.
Abstract: PubMed
 from DrugBank
Target Hemoglobin subunit beta
PubChem
Protein P68871
Target
PubChem
Gene HBB
Target
General
Oxygen transporter activity
Function
Involved in oxygen transport from the lung to the various peripheral tissues.LVV-hemorphin-7 potentiates
the activity of bradykinin, causing a decrease in blood pressure.Spinorphin: functions as an endogenous
Specific
inhibitor of enkephalin-degrading enzymes such as DPP3, and as a selective antagonist of the P2RX3
Function
receptor which is involved in pain signaling, these properties implicate it as a regulator of pain and
inflammation.
Reference Hamilton HB, Iuchi I, Miyaji T, Shibata S: Hemoglobin Hiroshima (beta-143 histidine--aspartic acid): a newly
identified fast moving beta chain variant associated with increased oxygen affinity and compensatory
erythremia. J Clin Invest. 1969 Mar;48(3):525-35.
Abstract: PubMed
 from DrugBank
View all (4) DrugBank Interactions entries
17 Biological Test Results
17.1 BioAssay Results
CLICK TO LOAD...
 from PubChem
18 Classification
18.1 Ontologies
18.1.1 MeSH Tree
CLICK TO LOAD...
 from MeSH
18.1.2 ChEBI Ontology
CLICK TO LOAD...
 from ChEBI
18.1.3 KEGG: Drug
CLICK TO LOAD...
 from KEGG
18.1.4 KEGG: ATC
CLICK TO LOAD...
 from KEGG
18.1.5 KEGG: JP15
CLICK TO LOAD...
 from KEGG
18.1.6 WHO ATC Classification System
CLICK TO LOAD...
 from WHO ATC

18.1.7 WIPO IPC
CLICK TO LOAD...
 from WIPO
18.1.8 ChemIDplus
CLICK TO LOAD...
 from ChemIDplus
18.1.9 CAMEO Chemicals
CLICK TO LOAD...
18.1.10 ChEMBL Target Tree

CLICK TO LOAD...
 from ChEMBL
19 Information Sources
1. CAMEO Chemicals /source/CAMEO Chemicals
OXYGEN
https://cameochemicals.noaa.gov/chemical/8967 https://cameochemicals.noaa.gov/chemical/8967
CAMEO Chemical Reactivity Classification
https://cameochemicals.noaa.gov/browse/react https://cameochemicals.noaa.gov/browse/react
2. ChemIDplus /source/ChemIDplus
Oxygen [USP]
https://chem.nlm.nih.gov/chemidplus/sid/0007782447 https://chem.nlm.nih.gov/chemidplus/sid/0007782447
ChemIDplus Chemical Information Classification
https://chem.sis.nlm.nih.gov/chemidplus/chemidheavy.jsp https://chem.sis.nlm.nih.gov/chemidplus/chemidheavy.jsp
3. DrugBank /source/DrugBank
Oxygen
http://www.drugbank.ca/drugs/DB09140 http://www.drugbank.ca/drugs/DB09140
http://www.drugbank.ca/drugs/DB09140#targets http://www.drugbank.ca/drugs/DB09140#targets
4. EPA DSStox /source/EPA DSStox

Oxygen
https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID2037681 https://comptox.epa.gov/dashboard/dsstoxdb/results?
search=DTXSID2037681
5. European Chemicals Agency (ECHA) /source/European Chemicals Agency (ECHA)

oxygen
https://echa.europa.eu/substance-information/-/substanceinfo/100.029.051 https://echa.europa.eu/substance-
information/-/substanceinfo/100.029.051
Oxygen
https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/130251 https://echa.europa.eu/information-
on-chemicals/cl-inventory-database/-/discli/details/130251
6. Human Metabolome Database (HMDB) /source/Human Metabolome Database (HMDB)

Oxygen
http://www.hmdb.ca/metabolites/HMDB0001377 http://www.hmdb.ca/metabolites/HMDB0001377
7. ILO-ICSC /source/ILO-ICSC
OXYGEN
http://www.ilo.org/dyn/icsc/showcard.display?p_version=2&p_card_id=0138 http://www.ilo.org/dyn/icsc/showcard.display?
p_version=2&p_card_id=0138
OXYGEN (LIQUEFIED)
http://www.ilo.org/dyn/icsc/showcard.display?p_version=2&p_card_id=0880 http://www.ilo.org/dyn/icsc/showcard.display?
p_version=2&p_card_id=0880
8. OSHA Occupational Chemical DB /source/OSHA Occupational Chemical DB

OXYGEN
http://www.osha.gov/chemicaldata/chemResult.html?RecNo=920 http://www.osha.gov/chemicaldata/chemResult.html?RecNo=920
9. The National Institute for Occupational Safety and Health (NIOSH) /source/The National Institute
for Occupational Safety and Health (NIOSH)
Oxygen
https://www.cdc.gov/niosh-rtecs/RS1F6EE0.html https://www.cdc.gov/niosh-rtecs/RS1F6EE0.html
10. DOT Emergency Response Guidebook /source/DOT Emergency Response Guidebook

oxygen
http://phmsa.dot.gov/hazmat/outreach-training/erg http://phmsa.dot.gov/hazmat/outreach-training/erg
11. NJDOH RTK Hazardous Substance List /source/NJDOH RTK Hazardous Substance List
oxygen
http://nj.gov/health/eoh/rtkweb/documents/fs/1448.pdf http://nj.gov/health/eoh/rtkweb/documents/fs/1448.pdf
12. EU Food Improvement Agents /source/EU Food Improvement Agents

OXYGEN
http://eur-lex.europa.eu/legal-content/EN/ALL/?uri=CELEX%3A32012R0231 http://eur-lex.europa.eu/legal-content/EN/ALL/?
uri=CELEX%3A32012R0231
13. ChEBI /source/ChEBI

Dioxygen
http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:15379 http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:15379
ChEBI Ontology
http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology
http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology
14. NCIt /source/NCIt

Oxygen
https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C722
https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C722
15. HSDB /source/HSDB

OXYGEN
https://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+7782-44-7 https://toxnet.nlm.nih.gov/cgi-
bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+7782-44-7
16. ClinicalTrials.gov /source/ClinicalTrials.gov

Oxygen
https://clinicaltrials.gov/ https://clinicaltrials.gov/
17. EU Community Register of Medicinal Products /source/EU Community Register of Medicinal

Products
Oxygen
https://ec.europa.eu/health/documents/community-register/html/v067.htm https://ec.europa.eu/health/documents/community-
register/html/v067.htm
18. FAO/WHO Food Additive Evaluations (JECFA) /source/FAO/WHO Food Additive Evaluations
(JECFA)
OXYGEN
http://apps.who.int/food-additives-contaminants-jecfa-database/chemical.aspx?chemID=2739 http://apps.who.int/food-additives-
contaminants-jecfa-database/chemical.aspx?chemID=2739
19. WHO ATC /source/WHO ATC

https://www.whocc.no/atc/ https://www.whocc.no/atc/
ATC Code
https://www.whocc.no/atc_ddd_index/ https://www.whocc.no/atc_ddd_index/
20. Wikipedia /source/Wikipedia

dioxygen
https://en.wikipedia.org/wiki/Dioxygen https://en.wikipedia.org/wiki/Dioxygen
liquid oxygen
https://en.wikipedia.org/wiki/Liquid_oxygen https://en.wikipedia.org/wiki/Liquid_oxygen
21. EU REGULATION (EC) No 1272/2008 /source/EU REGULATION (EC) No 1272/2008

oxygen
http://ec.europa.eu/growth/sectors/chemicals/classification-labelling/index_en.htm
http://ec.europa.eu/growth/sectors/chemicals/classification-labelling/index_en.htm
22. Hazardous Chemical Information System (HCIS), Safe Work Australia /source/Hazardous Chemical
Information System (HCIS), Safe Work Australia
oxygen
http://hcis.safeworkaustralia.gov.au/HazardousChemical/Details?chemicalID=3353
23. NITE-CMC /source/NITE-CMC

Oxygen
http://www.safe.nite.go.jp/english/ghs/09-mhlw-2105e.html http://www.safe.nite.go.jp/english/ghs/09-mhlw-2105e.html
24. Safe Work Australia - HCIS /source/Safe Work Australia - HCIS

oxygen
25. FDA Center for Food Safety and Applied Nutrition (CFSAN) /source/FDA Center for Food Safety
and Applied Nutrition (CFSAN)
OXYGEN
https://www.accessdata.fda.gov/scripts/fdcc/index.cfm?set=IndirectAdditives&id=OXYGEN
https://www.accessdata.fda.gov/scripts/fdcc/index.cfm?set=IndirectAdditives&id=OXYGEN
26. FDA/SPL Indexing Data /source/FDA/SPL Indexing Data

S88TT14065
https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/
https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/
27. NIOSH Manual of Analytical Methods /source/NIOSH Manual of Analytical Methods

7782-44-7
https://www.cdc.gov/niosh/docs/2003-154/pdfs/6601.pdf https://www.cdc.gov/niosh/docs/2003-154/pdfs/6601.pdf
28. NIST /source/NIST

Oxygen
http://www.nist.gov/srd/nist1a.cfm http://www.nist.gov/srd/nist1a.cfm
29. OSHA Chemical Sampling Information /source/OSHA Chemical Sampling Information

Oxygen
https://www.osha.gov/dts/chemicalsampling/data/CH_259105.html
https://www.osha.gov/dts/chemicalsampling/data/CH_259105.html
30. PDB /source/PDB

The Protein Data Bank (PDB) is a crystallographic database for the three-dimensional structural data of large biological molecules,
such as proteins and nucleic acids
http://www.rcsb.org/ligand/OXY http://www.rcsb.org/ligand/OXY
31. Pistoia Alliance Chemical Safety Library /source/Pistoia Alliance Chemical Safety Library
OXYGEN; COPPER(II) CHLORIDE DIHYDRATE; 2,6-DIBROMOPYRIDINE; N-BUTYLLITHIUM; DIETHYL ETHER
http://www.pistoiaalliance.org/projects/chemical-safety-library/ http://www.pistoiaalliance.org/projects/chemical-safety-library/
32. PubChem
Data deposited in or computed by PubChem
https://pubchem.ncbi.nlm.nih.gov https://pubchem.ncbi.nlm.nih.gov
33. MeSH /source/MeSH

Oxygen
https://www.ncbi.nlm.nih.gov/mesh/68010100 https://www.ncbi.nlm.nih.gov/mesh/68010100
MeSH Tree
http://www.nlm.nih.gov/mesh/meshhome.html http://www.nlm.nih.gov/mesh/meshhome.html
34. KEGG /source/KEGG

Therapeutic category of drugs in Japan
http://www.genome.jp/kegg-bin/get_htext?br08301.keg http://www.genome.jp/kegg-bin/get_htext?br08301.keg
Anatomical Therapeutic Chemical (ATC) classification
Drugs listed in the Japanese Pharmacopoeia
35. WIPO /source/WIPO

International Patent Classification
http://www.wipo.int/classifications/ipc/ http://www.wipo.int/classifications/ipc/
36. ChEMBL /source/ChEMBL

Target Tree
https://www.ebi.ac.uk/chembl/target/browser https://www.ebi.ac.uk/chembl/target/browser

Oxygen PubChem

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National Library of Medicine National Center for Biotechnology Information

Oxygen  Cite this Record

PubChem CID: 977

Safety Summary: Laboratory Chemical Safety Summary (LCSS)

PUBCHEM  COMPOUND  OXYGEN Modify Date: 2018-10-06; Create Date: 2004-09-16

3 Names and Identifiers

 4 Chemical and Physical Properties

7 Drug and Medication Information

8 Food Additives and Ingredients

9 Pharmacology and Biochemistry

10 Use and Manufacturing

12 Safety and Hazards

16 Biomolecular Interactions and Pathways

17 Biological Test Results

 Show Hydrogens  Show Atoms  Animate

3.1 Computed Descriptors

3.1.1 IUPAC Name

3.1.3 InChI Key

3.1.4 Canonical SMILES

3.2 Molecular Formula

3.3 Other Identifiers

3.3.3 ICSC Number

3.3.4 RTECS Number

Title liquid oxygen

Description one of the physical forms of elemental oxygen

3.4.1 MeSH Entry Terms

3.4.2 Depositor-Supplied Synonyms

1. Oxygen 11. Oxygen-16 21. UN1072 31. Com

4.1 Computed Properties

Property Name Property Value

Molecular Weight 31.998 g/mol

Hydrogen Bond Donor Count 0

Hydrogen Bond Acceptor Count 2

Rotatable Bond Count 0

Topological Polar Surface Area 34.1 A^2

Monoisotopic Mass 31.99 g/mol

Exact Mass 31.99 g/mol

Compound Is Canonicalized true

Heavy Atom Count 2

Defined Atom Stereocenter Count 0

Undefined Atom Stereocenter Count 0

Defined Bond Stereocenter Count 0

Undefined Bond Stereocenter Count 0

Isotope Atom Count 0

Covalently-Bonded Unit Count 1

4.2 Experimental Properties

4.2.1 Physical Description

Colourless, odourless, non-flammable gas

ODOURLESS COMPRESSED GAS.

LIQUEFIED GAS. COLOURLESS-TO-BLUE EXTREMELY COLD LIQUID.

Colorless, odorless and tasteless gas.

Slightly bluish liquid at -183 deg C

4.2.5 Boiling Point

-297.3° F at 760 mm Hg (USCG, 1999)

4.2.6 Melting Point

-361° F (USCG, 1999)

Solubility in water, ml/100ml at 20°C: 3.1

1.14 at -297.4° F (USCG, 1999)

Gas: 1.429 g/L at 0 deg C; liq: 1.14 g/ml at -183 deg C

4.2.9 Vapor Density

Relative vapour density (air = 1): 1.1