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OXYGEN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Pure oxygen is an odorless, colorless to light bluish noncombustible gas which accelerates the burning of a fire and is shipped as a non-liquid gas at pressures of 2000 psig or greater and a refrigerated liquid at pressures below 200 psig.

Specific Substances

    1) OXYGEN
    2) OXYGEN, compressed
    3) OXYGEN, refrigerated liquid (cryogenic liquid)
    4) WISWESSER NOTATION: .O2
    5) NIOSH/RTECS RS 2060000
    6) CAS 7782-44-7
    7) Molecular Formula: O2
    8) References: RTECS, 1993
    9) LIQUID OXYGEN
    10) LOX
    11) MOLECULAR OXYGEN
    12) OXYGEN MOLECULE
    13) OXYGEN, LIQUIFIED
    14) OXYGEN-16
    15) PURE OXYGEN
    1.2.1) MOLECULAR FORMULA
    1) O2

Available Forms Sources

    A) FORMS
    1) Oxygen is available as high purity, low purity, and USP grades (Lewis, 1997).
    2) Oxygen is available in a 99.5+% grade of purity. It is stored at -183 degrees C (CHRIS , 1993).
    B) SOURCES
    1) On a large scale, oxygen is produced by liquefaction and fractional distillation of air (ILO, 1983).
    2) It may also be obtained from water by electrolysis, but mainly as a byproduct of hydrogen production (ILO, 1983).
    3) STORAGE -
    a) Oxygen is transported and stored under pressure in cylinders at 150 to 160 ATA; insulated tanks are used for liquid oxygen (ILO, 1983).
    b) In the USA, oxygen is supplied in green cylinders at a pressure of 2000 psi (Hayes & Laws, 1991).
    1) Liquid oxygen is shipped as a refrigerated liquid at pressures below 200 psig (AAR, 1987).
    c) Smaller quantities of liquid oxygen (2 to 50 Liters) can be stored in Dewar flasks (ILO, 1983).
    C) USES
    1) MEDICAL USES: As a supply of respiratory oxygen.
    2) AVIATION/SPACECRAFT/SUBMARINES: As a supply of breathing oxygen.
    3) INDUSTRIAL USES: In gas welding; oxygen cutting of metals, rock, concrete, etc; flame scarfing; metallization; in iron and steel production; for gasification of solid fuel; as a blasting agent; in the production of synthesis gas from coal; and as a rocket engine fuel.
    a) Oxygen is used in welding as oxyhydrogen or oxyacetylene flames; for lighting in calcium lights; by SCUBA and deep-sea divers; as a propellant for rockets; and in human and veterinary medicine as an adjunct to anesthetic agents, in cryotherapy, and for the treatment of carbon monoxide poisoning and hypoxia (Budavari, 1996).
    b) Oxygen is used in blast furnaces, copper smelting, and steel production by the basic oxygen converter process (Lewis, 1997).
    4) It is used in manufacturing the synthesis gas for producing ammonia, methanol, and acetylene (Lewis, 1997).
    5) Oxygen is used as an oxidizer for rocket propellants, in decompression chambers and spacecraft, as a chemical intermediate, as a replacement for air in oxidation of municipal and industrial organic wastes, in coal gasification, and to counteract the effect of eutrophication in reservoirs and lakes (Lewis, 1997).
    6) INCREASED FIRE INTENSITY: Oxygen is noncombustible, but will support the burning of combustible materials and increases the intensity of any fire (AAR, 1987; (CHRIS , 1993; de Richemond & Bruley, 2000).

Overview

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) UNLIKELY ROUTE OF EXPOSURE - Because oxygen is a gas at ambient temperatures, ingestion is an unlikely route of exposure.
    0.4.3) INHALATION EXPOSURE
    A) Oxygen toxicity usually occurs only by the inhalation route.
    1) HYPERBARIC HYPEROXIA - AIR BREAKS - (discontinuing 100% oxygen breathing) may quickly resolve CNS symptoms encountered during hyperbaric oxygen therapy periods.
    2) Treatment for an oxygen toxicity seizure is SUPPORTIVE; anticonvulsants are inefficacious.
    3) Discontinuation of oxygen breathing is generally all that is required.
    4) In hyperbaric oxygen therapy situations, DO NOT CHANGE THE PRESSURE DURING A SEIZURE.
    5) NORMOBARIC HYPEROXIA - PREVENTIVE MEASURES - When possible, keep FiO2 less than 50%.
    a) NEONATES - maintaining arterial pO2 between 55 and 70 mmHg is recommended to minimize the risk of development of retrolental fibroplasia.
    b) When oxygen must be supplied for medicinal purposes for prolonged periods at 100%, it should be interrupted by the use of air or 50% oxygen for 1 hour, 4 times daily.
    c) HUMIDIFICATION - To avoid irritation of the mucous membranes and interference with ciliary action from the dry gas, when possible, oxygen should be humidified.
    0.4.4) EYE EXPOSURE
    A) Eye splashes with liquid oxygen may result in frostbite injury. Early ophthalmologic consultation is advised in such cases.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) FROSTBITE -
    a) Dermal contact with liquid oxygen or escaping compressed gas may cause FROSTBITE INJURY or HYPOTHERMIA.
    b) OTHER - REFER TO MAIN DOCUMENT - under TREATMENT, DERMAL EXPOSURE for MORE INFORMATION.

Range Of Toxicity

    A) TCLo (HUMANS) (INHALATION) - 100 pph for 4 hours
    B) In the dry environment, breathing oxygen at pressures of 2 ATA or greater can result in CNS dysfunction with convulsions, retinal injury, paralysis, and DEATH.
    1) The threshold for this generalized metabolic event is reduced in the diving environment, particularly where high workloads and cold temperatures are encountered.
    a) In these situations the threshold may be as low as 1.6 ATA.
    C) HUMANS - 0.5 ATA - Can probably be tolerated indefinitely without lung damage; SYMPTOMS may appear after 36 hours
    1) 1.0 ATA - Pulmonary irritation and edema can occur after 24 hours; SYMPTOMS may appear after 10 hours
    2) 2.0 ATA - SYMPTOMS may appear after 4 to 6 hours
    3) 3.0 ATA - Probably safe for healthy adults for 1 hour; a 2-hour exposure may be the safe limit at this pressure
    4) 4.0 ATA - Muscular twitching and generalized convulsions may occur within 1 hour (humans and animals)

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) EFFECTS NOT INCLUDED - The EFFECTS of BREATHING INSUFFICIENT OXYGEN (HYPOXIA) are NOT DISCUSSED in this review.
    B) CIRCUMSTANCES OF OXYGEN TOXICITY -
    1) NORMOBARIC HYPEROXIA -
    a) Prolonged Breathing of Elevated Oxygen Concentrations at Normal Pressure
    b) SUMMARY -
    1) TOXIC EFFECTS involving the EYES, LUNGS, and CNS may develop in persons breathing oxygen at partial pressures greater than those in normal air.
    2) Inhalation of 100% oxygen can result in nausea, dizziness, pulmonary irritation leading to pulmonary edema, and pneumonitis. Intense and potentially fatal pulmonary edema may develop.
    a) Tracheal irritation, fever, nausea, vomiting, acute bronchitis developing several hours later, sinusitis, malaise, transient paresthesias and conjunctivitis may occur.
    c) NEONATAL -
    1) SUMMARY - Premature neonates requiring prolonged normobaric hyperoxygenation may develop RETROLENTAL FIBROPLASIA, BRONCHOPULMONARY DYSPLASIA, myopia, pulmonary air leaks from ALVEOLAR RUPTURE with a variety of complications, and (CONTROVERSIAL if due all or in part to hyperoxia) intracerebral hemorrhage or necrotizing enterocolitis.
    2) HYPERBARIC HYPEROXIA -
    a) CNS TOXICITY - Toxicity of oxygen at elevated concentrations and pressures is usually only seen in divers, personnel and patients in hyperbaric chambers, and in rescue squad members in tunnels and mines. Seizures may be seen in diving or hyperbaric chamber accidents.
    b) PULMONARY TOXICITY - Volunteers breathing oxygen at 3.0 ATA for 3.5 hours experienced chest discomfort, dyspnea, and cough; decreased mean FEV1, FEF(25-75), and vital capacity; and one subject had a seizure.
    c) OCULAR TOXICITY - In normal adult volunteers exposed at 3.0 ATA for 4 hours, a progressive contraction of the visual fields, impaired central vision, and mydriasis developed. These effects were reversible if the exposure was stopped.
    1) Nuclear cataracts have developed during prolonged hyperbaric oxygen therapy.
    d) PRESSURE COMPLICATIONS - Treatment in hyperbaric chambers has been associated with complications of tension pneumothorax, epistaxis, otalgia, and tympanic membrane rupture.
    3) HYPOBARIC HYPEROXIA -
    a) This situation is specific to astronauts during extravehicular activity (EVA) maneuvers when wearing a reduced pressure single-gas space suit.
    4) LIQUID OXYGEN -
    a) FROSTBITE INJURY - Direct contact with the escaping compressed gas or liquid oxygen may cause frostbite injury to the skin and eyes.
    0.2.3) VITAL SIGNS
    A) Significant dermal exposure to the escaping compressed gas or LIQUID OXYGEN may cause hypothermia.
    0.2.4) HEENT
    A) Vision loss, myopia, nuclear cataracts, retrolental fibroplasia, and ocular frostbite injury may occur under various conditions of oxygen exposure.
    B) Sinus mucosal inflammation, and pharyngeal edema may occur with oxygen administration.
    0.2.5) CARDIOVASCULAR
    A) PATENT DUCTUS ARTERIOSUS may be, at least partially, caused by oxygen-generated free radicals.
    0.2.6) RESPIRATORY
    A) Inhalation of elevated concentrations and/or pressures of oxygen may cause respiratory tract irritation with chest tightness, substernal discomfort or chest pain, cough, decrements in measured pulmonary functions, alveolar rupture, and bronchopulmonary dysplasia (neonates).
    B) Pulmonary function testing may reveal a progressive restrictive defect.
    0.2.7) NEUROLOGIC
    A) SEIZURES - Central nervous system involvement in hyperbaric situations may pose a significant threat to safety.
    1) WARNING SYMPTOMS preceding seizures include muscular twitching, nausea, dizziness, abnormalities of vision or hearing, difficulty in breathing, anxiety and confusion, unusual fatigue, and incoordination.
    B) While controversial, there is a possible relationship between inhalation of elevated oxygen concentrations by premature neonates and development of intracerebral hemorrhage.
    0.2.8) GASTROINTESTINAL
    A) NECROTIZING ENTEROCOLITIS in premature neonates may be, at least partially, caused by oxygen-generated free radicals.
    0.2.10) GENITOURINARY
    A) In rats exposed to hyperbaric hyperoxia at 6.8 ATA until seizures developed, renal function alterations (decreased urinary excretion of urea and creatinine; elevated BUN and creatinine; decreased glomerular filtration rate) were seen.
    1) The above alterations returned nearly to normal over the following 24 hours.
    2) Similar findings have not been reported in exposed humans.
    0.2.13) HEMATOLOGIC
    A) Suppression of erythropoiesis and decreased erythrocyte mass may be seen in some conditions of hyperoxia.
    0.2.14) DERMATOLOGIC
    A) Direct contact with the escaping compressed gas or LIQUID OXYGEN may cause frostbite injury to the skin.
    0.2.20) REPRODUCTIVE
    A) One human case each of circulatory system abnormalities and Down's syndrome following maternal exposure to normobaric hyperoxia have been reported.
    1) The relationship between these abnormalities and oxygen exposure is tenuous at best.
    B) Structural abnormalities in the offspring and other adverse effects on reproductive outcomes have been seen in experimental animals exposed to hyperoxic conditions.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    B) Reduced oxygen species may play a role in cancer initiation.

Laboratory Monitoring

    A) BLOOD GASES
    1) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    B) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    C) Pulmonary function testing may be useful in monitoring patients and employees exposed to oxygen in the range of 0.5 ATA to 1.6 ATA.
    D) Obtain baseline chest x-ray and monitor as clinically indicated in patients with severe pulmonary oxygen toxicity.

Clinical Effects

Summary Of Exposure

    A) EFFECTS NOT INCLUDED - The EFFECTS of BREATHING INSUFFICIENT OXYGEN (HYPOXIA) are NOT DISCUSSED in this review.
    B) CIRCUMSTANCES OF OXYGEN TOXICITY -
    1) NORMOBARIC HYPEROXIA -
    a) Prolonged Breathing of Elevated Oxygen Concentrations at Normal Pressure
    b) SUMMARY -
    1) TOXIC EFFECTS involving the EYES, LUNGS, and CNS may develop in persons breathing oxygen at partial pressures greater than those in normal air.
    2) Inhalation of 100% oxygen can result in nausea, dizziness, pulmonary irritation leading to pulmonary edema, and pneumonitis. Intense and potentially fatal pulmonary edema may develop.
    a) Tracheal irritation, fever, nausea, vomiting, acute bronchitis developing several hours later, sinusitis, malaise, transient paresthesias and conjunctivitis may occur.
    c) NEONATAL -
    1) SUMMARY - Premature neonates requiring prolonged normobaric hyperoxygenation may develop RETROLENTAL FIBROPLASIA, BRONCHOPULMONARY DYSPLASIA, myopia, pulmonary air leaks from ALVEOLAR RUPTURE with a variety of complications, and (CONTROVERSIAL if due all or in part to hyperoxia) intracerebral hemorrhage or necrotizing enterocolitis.
    2) HYPERBARIC HYPEROXIA -
    a) CNS TOXICITY - Toxicity of oxygen at elevated concentrations and pressures is usually only seen in divers, personnel and patients in hyperbaric chambers, and in rescue squad members in tunnels and mines. Seizures may be seen in diving or hyperbaric chamber accidents.
    b) PULMONARY TOXICITY - Volunteers breathing oxygen at 3.0 ATA for 3.5 hours experienced chest discomfort, dyspnea, and cough; decreased mean FEV1, FEF(25-75), and vital capacity; and one subject had a seizure.
    c) OCULAR TOXICITY - In normal adult volunteers exposed at 3.0 ATA for 4 hours, a progressive contraction of the visual fields, impaired central vision, and mydriasis developed. These effects were reversible if the exposure was stopped.
    1) Nuclear cataracts have developed during prolonged hyperbaric oxygen therapy.
    d) PRESSURE COMPLICATIONS - Treatment in hyperbaric chambers has been associated with complications of tension pneumothorax, epistaxis, otalgia, and tympanic membrane rupture.
    3) HYPOBARIC HYPEROXIA -
    a) This situation is specific to astronauts during extravehicular activity (EVA) maneuvers when wearing a reduced pressure single-gas space suit.
    4) LIQUID OXYGEN -
    a) FROSTBITE INJURY - Direct contact with the escaping compressed gas or liquid oxygen may cause frostbite injury to the skin and eyes.

Vital Signs

    3.3.1) SUMMARY
    A) Significant dermal exposure to the escaping compressed gas or LIQUID OXYGEN may cause hypothermia.
    3.3.3) TEMPERATURE
    A) Patients with significant dermal exposure to the escaping compressed gas or LIQUID OXYGEN may develop hypothermia.

Heent

    3.4.1) SUMMARY
    A) Vision loss, myopia, nuclear cataracts, retrolental fibroplasia, and ocular frostbite injury may occur under various conditions of oxygen exposure.
    B) Sinus mucosal inflammation, and pharyngeal edema may occur with oxygen administration.
    3.4.3) EYES
    A) VISION LOSS/NORMOBARIC HYPEROXIA -
    1) ADULT -
    a) CASE REPORT - An adult kept in an 80% oxygen atmosphere for months during treatment for myasthenia gravis developed profound, permanent vision loss in both eyes.
    1) Arrest of retinal circulation and deterioration of visual cells were found on ophthalmoscopic and electroretinographic examinations (Grant & Schuman, 1993).
    2) NEONATAL -
    a) OCULAR TOXICITY - Exposure to high concentrations of normobaric oxygen during the neonatal period has been responsible for numerous cases of RETROLENTAL FIBROPLASIA (retinopathy of prematurity) (Grant & Schuman, 1993; Nichols & Lambertsen, 1969; Saugstad, 1990).
    1) In premature neonates, a satisfactory compromise between oxygen concentrations that are LIFE-SAVING and those that are VISION-SAVING is not easy to achieve (Grant & Schuman, 1993; Halliwell, 1984).
    b) Premature, underweight neonates respond to elevated oxygen concentrations with retinal vascular proliferation, followed by development of vascular proliferation in the peripheral retina with possible cicatrization and retinal detachment upon resumption of ambient air breathing (Grant & Schuman, 1993; Halliwell, 1984).
    c) MYOPIA has also been seen in premature infants treated with high concentrations of normobaric oxygen, and may be related to the degree of cicatricial retinopathy (Grant & Schuman, 1993).
    B) OCULAR INJURY/HYPERBARIC HYPEROXIA - In the dry environment, breathing oxygen at pressures of 2 ATA or greater can result in RETINAL INJURY (Finkel, 1983).
    1) PROGRESSIVE MYOPIA occurs during sequential hyperbaric oxygen therapy treatments, but resolves afterward over 3 to 6 weeks in most cases (Thom, 1990).
    a) A shallow increase in myopia secondary to a change in the refractive properties of the lens during several months of repeated exposure to hyperbaric oxygen has been described in adults (Grant & Schuman, 1993).
    2) DECREASED LIGHT PERCEPTION - CASE (ADULT) - One young man with a history of two episodes of retrobulbar optic neuritis had decreased light perception in that eye when exposed to hyperbaric oxygen (Grant & Schuman, 1993).
    3) NUCLEAR CATARACTS - Patients treated for prolonged periods with hyperbaric oxygen have developed persistent nuclear cataracts (Grant & Schuman, 1993).
    C) LIQUID OXYGEN -
    1) FROSTBITE INJURY - Direct contact with the escaping compressed gas or LIQUID OXYGEN may cause frostbite injury to the eyes (AAR, 1987; (Lewis, 1992; CHRIS , 1993).
    3.4.5) NOSE
    A) NASAL MUCOSA INFLAMMATION - Decreased mucociliary clearance, rhinorrhea and nasal mucosa inflammation with elevated IL-6 and IL-8 concentrations in the nasal lavage fluid has occurred in a group of patients following intranasal administration of oxygen. Because the histology and the behavior of the nasal and bronchial mucosa are similar, it is suspected that high concentrations of inhaled oxygen may also result in the same type of mucosal inflammation (Capellier et al, 1997; Capellier et al, 1999).
    3.4.6) THROAT
    A) PHARYNGEAL ANGIOEDEMA (CASE REPORT) - An aviator developed breathing impairment, difficulty swallowing, discomfort and edema of the soft palate, and hyperemia of the uvula while breathing 100% oxygen at either actual or simulated altitudes of 25,000 feet (Ildiz, 1994).

Cardiovascular

    3.5.1) SUMMARY
    A) PATENT DUCTUS ARTERIOSUS may be, at least partially, caused by oxygen-generated free radicals.
    3.5.2) CLINICAL EFFECTS
    A) PATENT DUCTUS ARTERIOSUS
    1) PATENT DUCTUS ARTERIOSUS may be, at least partially, caused by oxygen-generated free radicals (Saugstad, 1990).
    B) AIR EMBOLISM
    1) GAS EMBOLISM/CASE REPORT - An 80-year-old male receiving oxygen therapy for pulmonary emphysema and pneumonia died, following cardiac arrest, after inadvertently connecting his oxygen tube to his indwelling catheter that had been inserted into the left cephalic vein for an intravenous drip. An autopsy showed that venous gas embolism had occurred, characterized by the petechial hemorrhages of the skin and the numerous gas bubbles found in most of the vessels throughout the body (Bunai et al, 1999).

Respiratory

    3.6.1) SUMMARY
    A) Inhalation of elevated concentrations and/or pressures of oxygen may cause respiratory tract irritation with chest tightness, substernal discomfort or chest pain, cough, decrements in measured pulmonary functions, alveolar rupture, and bronchopulmonary dysplasia (neonates).
    B) Pulmonary function testing may reveal a progressive restrictive defect.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) Inhalation of normobaric oxygen at concentrations of 80% or greater for more than about 12 hours causes respiratory tract irritation (HSDB , 2001).
    a) Tracheitis develops in humans breathing 100% oxygen for 24 to 48 hours (Deneke & Fanburg, 1980).
    b) In normal adults, the first manifestations of normobaric pulmonary oxygen toxicity are development of respiratory tract symptoms (chest tightness, substernal discomfort, coughing, intense burning pain with prolonged exposure) and decreased vital capacity (Beckett & Wong, 1988; Bingham et al, 2001; Bryan & Jenkinson, 1988; Klein, 1990; Capellier et al, 1999).
    1) Reduction in vital capacity is usually the earliest sign detectable in oxygen poisoning (Bingham et al, 2001; Harabin et al, 1987; Dolezal, 1995). A median decrease of 4% in vital capacity may be predicted from a one-hour exposure to an FiO2 of 100% (Harabin et al, 1987).
    c) Symptoms may be more sensitive than signs in detecting early normobaric pulmonary oxygen toxicity.
    1) RETROSTERNAL PAIN (possibly due to tracheal inflammation) occurred before measurable biochemical changes in normal volunteers (Montgomery et al, 1989; Klein, 1990).
    2) NEONATES -
    a) BRONCHOPULMONARY DYSPLASIA -
    1) Premature infants who require significant hyperoxic respiratory support develop acute and chronic lung changes of oxygen toxicity, called bronchopulmonary dysplasia (Frank, 1985; Hansen & Gest, 1984; Saugstad, 1990).
    2) These changes have acute (exudative) and chronic (proliferative) phases (Frank, 1985; Hansen & Gest, 1984). The progression is from an acute edematous to a chronic fibroemphysematous condition (Frank, 1985).
    3) The mechanisms of neonatal pulmonary toxicity are similar to those seen in adults and experimental animals (Frank, 1985). However, mechanical ventilation and pulmonary air leak may also play a role (Hansen & Gest, 1984; Saugstad, 1990).
    4) PREMATURITY is the major risk factor for development of bronchopulmonary dysplasia (Frank, 1985).
    5) The incidence of chronic lung disease following prolonged mechanical ventilation and hyperoxia for the treatment of neonatal persistent pulmonary hypertension may be as great as 25% (Hansen & Gest, 1984). Pulmonary disability tends to improve with increasing age (Hansen & Gest, 1984).
    6) In one study, infants with the lowest administration of colloidal solutions had the lowest rates of bronchopulmonary dysplasia (BPD), suggesting that differences in hydration during the first days of life might account for different rates of BPD (Van Marter et al, 1992).
    b) PULMONARY AIR LEAK -
    1) A further complication of mechanical ventilation in premature neonates is pulmonary air leak (Hansen & Gest, 1984). Manifestations due to ALVEOLAR RUPTURE may include:
    1) Pulmonary Interstitial Emphysema
    2) Pneumomediastinum
    3) Subcutaneous Emphysema
    4) Pneumothorax
    5) Pneumopericardium
    6) Pneumoperitoneum
    7) Intravascular Air
    2) MINIMIZING ALVEOLAR OVER-DISTENSION can prevent alveolar rupture (Hansen & Gest, 1984).
    3) EFFECTS OF NORMOBARIC HYPEROXIA (Lodato, 1990)
    1) Absorption Atelectasis
    2) Acute Tracheobronchitis
    3) ARDS
    4) Bronchopulmonary Dysplasia
    5) Decreased Mucociliary Clearance
    6) Diffuse Alveolar Damage
    7) Hypercapnia
    8) Pulmonary Vasodilatation
    9) Respiratory Drive Depression
    10) Ventilation-Perfusion Mismatch
    4) PULMONARY ATELECTASIS - Inspired oxygen at concentrations of 30% and 80%, administered to patients during and for 2 hours after colon resection, has resulted in similar incidences and severity of pulmonary atelectasis (Akca et al, 1999).
    5) HYPERBARIC HYPEROXIA -
    a) PULMONARY EFFECTS -
    1) EFFECTS ON PULMONARY FUNCTION TESTS - In volunteers breathing oxygen at 1.5 to 3.0 ATA, of all pulmonary functions measured, only airway resistance and closing volumes were not significantly affected (Clark, 1988).
    2) Recovery of mechanical lung function generally occurred over 12 to 24 hours, but required longer than 24 hours in some subjects (Clark, 1988).
    3) PULMONARY TOXICITY - Volunteers breathing oxygen at 3.0 ATA for 3.5 hours experienced chest discomfort, dyspnea, and cough; decreased mean FEV1, FEF(25-75), and vital capacity; and one subject had a seizure (Clark et al, 1991).
    4) In divers intermittently exposed to hyperbaric oxygen, no significant changes occurred in pulmonary ventilation and CO diffusing capacities (HSDB , 1993).
    5) In one volunteer study, the CO diffusing capacity was not changed (Clark et al, 1991).
    6) Diffusing capacity was significantly reduced in divers who had been exposed to 29 days of 4.5-MPa oxygen. Increased ethane in expired air indicated lipid peroxidation; oxygen-derived free radicals may have been involved in the reduction of diffusing capacity (Suzuki, 1994).
    6) PULMONARY INFLAMMATION, ATELECTASIS, pulmonary HEMORRHAGE, and deceleration of metabolic processes may occur during inhalation of oxygen at greater than atmospheric pressure (ILO, 1983).
    a) This effect follows a latent period and, if the partial pressure exceeds 1.6 ATA, it is likely that CNS symptoms will occur before pulmonary symptoms become clinically evident (US Navy Diving Manual, 1980).
    7) PRESSURE EFFECTS -
    a) CASE SERIES (ADULT) - Three patients developed TENSION PNEUMOTHORAX during hyperbaric oxygen treatment for carbon monoxide poisoning. All had been intubated and received closed-chest compression for cardiac arrest prior to the HBO treatment (Murphy et al, 1991).

Neurologic

    3.7.1) SUMMARY
    A) SEIZURES - Central nervous system involvement in hyperbaric situations may pose a significant threat to safety.
    1) WARNING SYMPTOMS preceding seizures include muscular twitching, nausea, dizziness, abnormalities of vision or hearing, difficulty in breathing, anxiety and confusion, unusual fatigue, and incoordination.
    B) While controversial, there is a possible relationship between inhalation of elevated oxygen concentrations by premature neonates and development of intracerebral hemorrhage.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) HYPERBARIC HYPEROXIA -
    a) Toxicity of oxygen at elevated concentrations and pressures is usually only seen in divers, personnel and patients in hyperbaric chambers, and in rescue squad members in tunnels and mines (Finkel, 1983).
    b) CNS toxicity (SEIZURES) may be seen in diving or hyperbaric chamber accidents (Tinits, 1983; Sax & Lewis, 1987).
    c) If the partial pressure exceeds 1.6 ATA, it is likely that CNS symptoms will occur before pulmonary symptoms become clinically evident (US Navy Diving Manual, 1980).
    d) SEIZURES and adverse effects on neuromuscular coordination and attention are symptoms of hyperbaric oxygen toxicity (HSDB , 2001; Plafki et al, 2000).
    1) PRODROME - Symptoms and signs may include muscle twitching, nausea, vertigo, mood disturbances, and paresthesias, leading to loss of consciousness and seizures (HSDB , 2001).
    e) In the dry environment, breathing oxygen at pressures of 2.0 ATA or greater can result in CNS dysfunction with seizures, retinal injury, paralysis, and death (Finkel, 1983).
    1) The threshold for this generalized metabolic event is reduced in the diving environment, particularly where high workloads and cold temperatures are encountered.
    2) In these situations the threshold may be as low as 1.6 ATA (US Navy Diving Manual, 1980).
    f) CASE REPORT - A 47-year-old diver drowned after experiencing a generalized seizure due to breathing a 50% oxygen/nitrogen mixture during a 19 minute "technical" dive to a depth of 47 meters (Lawrence, 1996). During this dive, the diver had been exposed to a partial pressure of 291kPa (2.9 atmospheres). An appropriate oxygen pressure for a 19 minute dive should be below 161 kPa (1.6 atmospheres).
    B) CEREBRAL HEMORRHAGE
    1) NORMOBARIC HYPEROXIA -
    a) In premature babies, the intracerebral blood vessels are quite fragile and rupture easily (Halliwell, 1984).
    b) There may be a relationship between neonatal intracerebral hemorrhage and oxygen radical toxicity in premature infants (Saugstad, 1990).

Gastrointestinal

    3.8.1) SUMMARY
    A) NECROTIZING ENTEROCOLITIS in premature neonates may be, at least partially, caused by oxygen-generated free radicals.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting have occurred in volunteers breathing 90% to 100% normobaric oxygen (HSDB , 2001; Bryan & Jenkinson, 1988).
    B) ENTEROCOLITIS
    1) NECROTIZING ENTEROCOLITIS may be, at least partially, caused by oxygen-generated free radicals (Saugstad, 1990).

Genitourinary

    3.10.1) SUMMARY
    A) In rats exposed to hyperbaric hyperoxia at 6.8 ATA until seizures developed, renal function alterations (decreased urinary excretion of urea and creatinine; elevated BUN and creatinine; decreased glomerular filtration rate) were seen.
    1) The above alterations returned nearly to normal over the following 24 hours.
    2) Similar findings have not been reported in exposed humans.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FUNCTION ABNORMAL
    a) EXPERIMENTAL ANIMALS - In rats exposed to hyperbaric hyperoxia at 6.8 ATA until seizures developed, renal function alterations were noted (Chen et al, 1987).
    1) ALTERATIONS SEEN - Decreased urinary excretion of urea and creatinine; elevated BUN and creatinine; decreased glomerular filtration rate.
    2) RECOVERY - The above alterations returned nearly to normal over the following 24 hours.
    b) Similar findings have not been reported in exposed humans.

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) RESPIRATORY ACIDOSIS
    1) Individuals who sustain a SEIZURE during hyperbaric oxygen therapy may have exaggerated post-ictal apnea and develop transient hypercarbia and respiratory acidosis (Thom, 1990).
    a) Resolves quickly when breathing resumes (due to delayed hypoxic drive).

Hematologic

    3.13.1) SUMMARY
    A) Suppression of erythropoiesis and decreased erythrocyte mass may be seen in some conditions of hyperoxia.
    3.13.2) CLINICAL EFFECTS
    A) ANEMIA
    1) NORMOBARIC HYPEROXIA - SUPPRESSION of ERYTHROPOIESIS is seen with exposure to hyperoxia (Lodato, 1990; Furr, 1987).
    2) HYPOBARIC HYPEROXIA - Both MICROGRAVITY ("weightlessness") and HYPEROXIA are associated with a decrease in red blood cell mass (Furr, 1987). The effect of a combination of these conditions is not currently well-defined (Furr, 1987).

Dermatologic

    3.14.1) SUMMARY
    A) Direct contact with the escaping compressed gas or LIQUID OXYGEN may cause frostbite injury to the skin.
    3.14.2) CLINICAL EFFECTS
    A) FROSTBITE
    1) Direct contact with the escaping compressed gas or LIQUID OXYGEN may cause frostbite injury to the skin (AAR, 1987; (Lewis, 1992; CHRIS , 1993).

Reproductive

    3.20.1) SUMMARY
    A) One human case each of circulatory system abnormalities and Down's syndrome following maternal exposure to normobaric hyperoxia have been reported.
    1) The relationship between these abnormalities and oxygen exposure is tenuous at best.
    B) Structural abnormalities in the offspring and other adverse effects on reproductive outcomes have been seen in experimental animals exposed to hyperoxic conditions.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) CASE REPORT - One woman exposed to 12 pph of normobaric oxygen for 10 minutes during the 26th to 39th week of pregnancy delivered a child with abnormalities of the circulatory system (RTECS , 2001).
    2) CASE REPORT - A child with Down's syndrome was born to a mother who had received a gas-oxygen anesthetic in the second trimester (Schardein, 1985).
    3) The relationship between these abnormalities and oxygen exposure is tenuous at best.
    4) Hypoxemia caused changes in both fetal and adult arteries, but changes were more severe in fetuses. This may explain why the fetus is more sensitive to oxygen deprivation than the mother (Longo et al, 1993).
    5) In a study of 94 newborns, there was a significant relationship between newborn hypotension, hypoxemia, or low birth weight and major abnormal neurological outcome; the probability of a major abnormal outcome was 53 percent in children with both hypotension and hypoxemia (Low et al, 1993). Abnormal growth or development can occur as a result of energy conservation measures in response to limitation of oxygen (Richardson, 1993).
    6) Newborn mammals are more resistant to the acute CNS effects of hyperbaric oxygen than adults. However, there is evidence in rats that excess oxygen may induce persistent cerebral vasoconstriction. It is not known if a similar response occurs in humans, but might explain how oxygen therapy in premature infants can cause retinopathy and retarded brain development (Torbati et al, 1993).
    B) ANIMAL STUDIES
    1) Rats exposed to 10 pph of oxygen for 9 or 12 hours on the 22nd day of pregnancy delivered pups with congenital anomalies of the respiratory system (RTECS , 2001).
    2) EYE DEFECTS were seen in the offspring of pregnant rats exposed to oxygen at 360 to 460 mmHg for short periods (Schardein, 1985).
    3) Mice exposed to 10 pph of oxygen for 24 hours on the 8th day of pregnancy delivered offspring with abnormalities of the skin and appendages (RTECS , 2001).
    4) GROSS MALFORMATIONS were noted in the offspring of pregnant mice exposed to hyperbaric oxygen at 3.6 to 4.0 ATA on single days (Schardein, 1985).
    5) RESORPTION and MALFORMATIONS were seen in the offspring of pregnant rabbits exposed to hyperbaric oxygen at 1.5 to 2.0 ATA for 5 hours on a single gestation day (Schardein, 1985).
    a) In rabbits, maternal exposure for 15-minute intervals to normobaric hyperoxia (97% to 100%) over 15 hours resulted in EYE DEFECTS, HIGH MORTALITY, and a low frequency of PREMATURITY (Schardein, 1985).
    6) Pregnant hamsters exposed to 3.0 or 4.0 ATA hyperbaric oxygen for 2 to 3 hours on days 6, 7, or 8 of gestation delivered an increased number of offspring with umbilical hernias, exencephaly, spina bifida, and limb defects (HSDB , 2001).
    7) Hyperbaric oxygen administered to pregnant rats at 324 and 426 kPa for 90 minutes per day during days 8 to 12 of gestation produced lower fetal body weight and increased placental weight. Maternal weight, litter size, and incidence of malformations were not affected. Thickening of the placenta in response to hyperbaric oxygen might explain the lower fetal weights (Sapunar et al, 1993).
    8) HYPOXIA in the absence of chemical asphyxiants was teratogenic in mice (Ingalls, 1950; Ingalls, 1952; Curley & Ingalls, 1957), rabbits (Degenhardt, 1954), and hamsters (Erickson, 1960).
    9) Inhalation of oxygen at 3 to 4 atmospheres caused numerous kinds of birth defects in hamsters, including umbilical hernia, exencephaly, spina bifida, and limb defects (Ferm, 1964). Oxygen at concentrations of 70 to 96 percent was not teratogenic in rabbits, but did cause prematurity and increased mortality (Fujikura, 1964).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no information was available about the possible effects of exposure to elevated concentrations and/or pressures of oxygen during lactation.
    3.20.5) FERTILITY
    A) FERTILITY DECREASED MALE
    1) Long-term oxygen therapy reversed sexual impotence in 42% of men with respiratory failure and hypoxia (Aasebo et al, 1993). Reactive oxygen species may be beneficial or detrimental to human sperm, depending on the concentration. Reactive oxygen is principally generated by hydrogen peroxide in semen. While hydrogen peroxide can cause immobilization at low and cell death at higher concentrations, superoxide ion can induce hyperactivation and capacitation of sperm (Delamirande & Gagnon, 1995).
    B) ANIMAL STUDIES
    1) Female rats exposed to hypobaric oxygen at a simulated altitude of 5,500 meters for 23 weeks had increased ovary weights and increased capacity for estradiol production. Rats exposed to a 4,400 meters simulated altitude had a higher prevalence of estrus, but lower fertility. Polycystic ovaries were seen in both high-altitude groups. These results suggest that normal reproduction in rats involves some oxygen-dependent factor(s) (Martin & Costa, 1992).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7782-44-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    B) Reduced oxygen species may play a role in cancer initiation.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    B) CARCINOMA
    1) Reduced oxygen species may play a role in cancer initiation (Vuillaume, 1987).

Genotoxicity

    A) Singlet oxygen can generate modified guanine residues, as well as strand breaks and AP sites. It can act as an ultimate DNA modifying intracellular chemical species.
    B) MOLECULAR OXYGEN is a POTENT GENOTOXICANT.
    1) The action of a number of genotoxic agents is thought to be mediated by oxygen toxicity.
    a) Reactive intermediates generated under oxidative stress conditions include free radicals which can directly damage DNA.
    b) It can induce chromosomal aberrations, mutations, and sister chromatid exchanges in various cell types.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) BLOOD GASES
    1) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    B) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    C) Pulmonary function testing may be useful in monitoring patients and employees exposed to oxygen in the range of 0.5 ATA to 1.6 ATA.
    D) Obtain baseline chest x-ray and monitor as clinically indicated in patients with severe pulmonary oxygen toxicity.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) BLOOD GASES
    a) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    B) HEMATOLOGIC
    1) Monitoring red cell mass may be appropriate in astronauts exposed to both microgravity and hyperoxia.
    2) This agent may produce abnormalities of the hematopoietic system. Monitor the complete blood count in patients with significant exposure.
    C) BLOOD/SERUM CHEMISTRY
    1) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) Pulmonary function testing may be useful in monitoring patients and employees exposed to oxygen in the range of 0.5 ATA to 1.6 ATA.
    1) The appearance of a mild restrictive change (drop in the FVC and increase in the FEV1/FVC ratio) usually accompanies the appearance of mild substernal irritation (Thom, 1990).
    2) Periodic PFT screening is a sensitive early indicator of pulmonary oxygen toxicity (Thom, 1990).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain baseline chest x-ray and monitor as clinically indicated in patients with severe pulmonary oxygen toxicity.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) NIOSH ANALYTICAL METHODS - see OXYGEN (field-readable) 6601 (RTECS , 2001)
    2) A variety of direct reading instruments are available for measuring oxygen (Clayton & Clayton, 1982).
    3) Methods to measure the partial pressure of oxygen (pO2) and percent oxygen saturation (% O2 sat) in blood are readily available clinically.
    4) When abnormal hemoglobins (such as carboxyhemoglobin, methemoglobin, or sulfhemoglobin) are absent, pulse oximetry can be used to determine a patient's state of oxygenation.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) PULMONARY OXYGEN TOXICITY - Hospitalization criteria parallel those for chemically-induced noncardiogenic pulmonary edema.
    B) CNS OXYGEN TOXICITY - Individuals who sustain a seizure or CNS manifestations involving a change in the level of consciousness should be admitted for a 24 hour period of observation.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) PULMONARY OXYGEN TOXICITY - Individuals should be monitored with symptom documentation, vital signs, and PFTs.

Monitoring

    A) BLOOD GASES
    1) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    B) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    C) Pulmonary function testing may be useful in monitoring patients and employees exposed to oxygen in the range of 0.5 ATA to 1.6 ATA.
    D) Obtain baseline chest x-ray and monitor as clinically indicated in patients with severe pulmonary oxygen toxicity.

Oral Exposure

    6.5.3) TREATMENT
    A) PROCEDURE EDUCATION
    1) UNLIKELY EXPOSURE ROUTE - Because oxygen is a GAS at ambient temperature and as LIQUID OXYGEN is unlikely to be swallowed, ingestion in a HIGHLY UNLIKELY EXPOSURE ROUTE.
    2) FROSTBITE INJURY - of the GI tract would be theoretically possible if LIQUID OXYGEN were to be ingested.
    B) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Individuals accidently exposed acutely to high concentrations of oxygen should be removed from further overexposure and kept in a well-ventilated or outdoor area for at least 15 minutes (HSDB , 1993).
    6.7.2) TREATMENT
    A) SUPPORT
    1) When possible, keep FiO2 less than 50%.
    a) NEONATES - maintaining arterial pO2 between 55 and 70 mmHg is recommended to minimize the risk of development of retrolental fibroplasia (Behrman et al, 1992).
    2) PULMONARY OXYGEN TOXICITY - AIR BREAKS - When oxygen must be supplied for medicinal purposes for prolonged periods at 100%, it should be interrupted by the use of air or 50% oxygen for 1 hour, 4 times daily (Hayes & Laws, 1991).
    a) HUMIDIFICATION - To avoid irritation of the mucous membranes and interference with ciliary action from the dry gas, when possible oxygen should be humidified before being inhaled by patients (Hayes & Laws, 1991).
    3) CNS OXYGEN TOXICITY - AIR BREAKS - Diving and hyperbaric oxygen therapy may require periods of air breathing to prevent CNS oxygen toxicity. Air breathing at the ambient depth usually is enough to avert progressive CNS involvement leading to seizure.
    4) Oxygen diving is limited in depth and duration with the physiologic constraint of interest being SEIZURE.
    a) Isobaric return to air breathing may be associated with occurrence of seizure - "the off phenomenon" (US Navy Diving Manual, 1980).
    1) Return to the surface prior to return to air breathing seems to decrease the incidence rate for seizure.
    2) AIR BREAKS - are designed into hyperbaric oxygen therapy treatment protocols. These should be extended if there are symptoms of CNS toxicity.
    3) Supportive measures and return to normobaric air breathing are the treatments of choice for generalized seizures that occur with CNS oxygen toxicity (US Navy Diving Medical Officers Manual, 1990).
    4) It is important to maintain a dry airway in a diver and to NOT MOVE THE DIVER VERTICALLY IN THE WATER COLUMN until the seizure runs its course and respiration returns.
    5) In hyperbaric oxygen therapy situations, DO NOT CHANGE THE PRESSURE DURING A SEIZURE.
    6) The individual in a hyperoxic environment may have significant quantities of dissolved oxygen available in the plasma portion of the blood for metabolism; following a seizure, it may be several minutes before respiration begins.
    7) PHENYTOIN INEFFICACIOUS - In experimental animals, phenytoin did NOT suppress seizures due to CNS oxygen toxicity, although blood levels were in the therapeutic range (Bitterman & Katz, 1987).
    B) EXPERIMENTAL THERAPY
    1) The following treatment modalities for oxygen toxicity have been investigated in experimental animals (HSDB , 1993; Bertelli et al, 1990; Bertelli et al, 1990a; Smith, 1988; Frank, 1988; Jacobson et al, 1990; Lin & Jamieson, 1992; Lodato, 1990). They are NOT RECOMMENDED FOR TREATING OXYGEN-POISONED HUMANS.
    2) Reduction in death rates and percentages of animals having seizures have generally been efficacy end-points.
    a) Intravenous administration of liposomes containing catalase and superoxide dismutase
    1) However, intratracheal administration of polyethylene glycol- conjugated catalase plus superoxide dismutase did NOT protect rats against oxygen toxicity (Frank, 1991).
    b) Niacin -
    c) Indomethacin -
    d) Coenzyme Q10 + Carnitine -
    e) Bacterial Endotoxin -
    1) Diphosphoryl lipid A is the minimal essential compound necessary for the protective effect of bacterial endotoxin against pulmonary oxygen toxicity in rats (Smith, 1988).
    f) Propionyl-L-carnitine -
    g) Vitamin E -
    h) Butylated Hydroxyanisole (BHA) -
    i) Dimethylthiourea -
    j) Dimethylsulfoxide -
    k) Deferoxamine -
    l) Butylated Hydroxytoluene -
    m) In experimental animals, prolonged dietary supplementation with free radical scavengers -- vitamin E, riboflavin, and selenium -- did NOT increase resistance to CNS oxygen toxicity (Boadi et al, 1991). Caffeine prolonged the latent period for onset of seizures by hyperoxia in rats (Bitterman & Schaal, 1995). Bacterial polysaccharide, or endotoxin, has prevented hyperoxic lung injury in experimental animals, even when injected 36 hours after beginning exposure to oxygen (Clayton & Clayton, 1994).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) AT RISK - FINDING
    1) Unlikely Exposure Route - As oxygen is a non-irritating GAS at ambient temperatures, eye exposures are unlikely to occur.
    B) FROSTBITE
    1) Direct eye splashes with LIQUID OXYGEN could result in FROSTBITE INJURY.
    2) Early ophthalmologic consultation would be indicated in such a clinical setting.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) If direct skin contact with liquid oxygen occurs, remove the victim from further exposure and flush exposed areas with large volumes of tepid water.
    6.9.2) TREATMENT
    A) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) HYPOTHERMIA
    1) HYPOTHERMIA - may occur following dermal exposure to liquid oxygen (HSDB , 1993).
    2) In addition to indicated SUPPORTIVE MEASURES, REWARMING is essential in the treatment of significant HYPOTHERMIA.
    a) OPTIONS FOR REWARMING - (Scott & Marx, 1991; Klainer, 1991; Bessen, 1992)
    1) PASSIVE EXTERNAL REWARMING - Evacuation to a warm environment; Insulation (blankets, etc)
    2) ACTIVE EXTERNAL REWARMING - Heating pads; Hot water bottles; Electric blankets; Heat lamps; Hot water baths
    3) ACTIVE CORE REWARMING -
    a) Heated humidified oxygen inhalation or ventilation; gastric or colonic irrigation with heated fluids; Thoracotomy and mediastinal irrigation with heated fluids; Closed-chest thoracostomy irrigation with heated fluids
    b) Peritoneal irrigation with heated fluids; Hemodialysis with an in-line heat exchanger; Diathermy; Extracorporeal blood rewarming
    4) SUGGESTED REWARMING PROTOCOL - (Scott & Marx, 1991; Klainer, 1991; Bessen, 1992)
    a) CORE TEMPERATURE 32 DEGREES C OR GREATER AND CARDIOVASCULAR
    1) STABILITY - Passive external rewarming measures are usually sufficient
    b) CORE TEMPERATURE LESS THAN 32 DEGREES C AND CARDIOVASCULAR
    1) STABILITY - Active core rewarming alone; OR Active external rewarming to the TRUNK ONLY PLUS active core rewarming
    c) Active external rewarming ALONE of THE EXTREMITIES is NOT RECOMMENDED because of possible development of afterdrop in core temperature, rewarming shock, and increased RISK OF DEATH.
    d) CORE TEMPERATURE LESS THAN 32 DEGREES C AND CARDIOVASCULAR
    1) INSTABILITY - Active core rewarming by CARDIOVASCULAR BYPASS is the METHOD OF CHOICE; if bypass cannot be done (trauma, unavailability of equipment, etc), then cardiopulmonary resuscitation with ACTIVE CORE REWARMING techniques either ALONE OR combined with active external rewarming involving the TRUNK ONLY should be done (see cautions above).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) TCLo (HUMANS) (INHALATION) - 100 pph for 4 hours
    B) In the dry environment, breathing oxygen at pressures of 2 ATA or greater can result in CNS dysfunction with convulsions, retinal injury, paralysis, and DEATH.
    1) The threshold for this generalized metabolic event is reduced in the diving environment, particularly where high workloads and cold temperatures are encountered.
    a) In these situations the threshold may be as low as 1.6 ATA.
    C) HUMANS - 0.5 ATA - Can probably be tolerated indefinitely without lung damage; SYMPTOMS may appear after 36 hours
    1) 1.0 ATA - Pulmonary irritation and edema can occur after 24 hours; SYMPTOMS may appear after 10 hours
    2) 2.0 ATA - SYMPTOMS may appear after 4 to 6 hours
    3) 3.0 ATA - Probably safe for healthy adults for 1 hour; a 2-hour exposure may be the safe limit at this pressure
    4) 4.0 ATA - Muscular twitching and generalized convulsions may occur within 1 hour (humans and animals)

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) In the dry environment, breathing oxygen at pressures of 2.0 ATA or greater can result in CNS dysfunction with convulsions, retinal injury, paralysis, and DEATH (Finkel, 1983).
    2) The threshold for this generalized metabolic event is reduced in the diving environment, particularly where high workloads and cold temperatures are encountered.
    3) In these situations the threshold may be as low as 1.6 ATA (US Navy Diving Manual, 1980).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) HUMANS (Clayton & Clayton, 1982) -
    a) 0.5 ATA - Can probably be tolerated indefinitely without lung damage; SYMPTOMS may appear after 36 hours
    b) 1.0 ATA - Pulmonary irritation and edema can occur after 24 hours; SYMPTOMS may appear after 10 hours
    c) 2.0 ATA - SYMPTOMS may appear after 4 to 6 hours
    d) 3.0 ATA - Probably safe for healthy adults for 1 hour; a 2-hour exposure may be the safe limit at this pressure
    e) 4.0 ATA - Muscular twitching and generalized convulsions may occur within 1 hour (humans and animals)
    2) SAFE DIVING WITH 100% OXYGEN (US NAVY GUIDELINES) (Clayton & Clayton, 1982) -
    DEPTH (meters)TIME (minutes)
    3240
    6105
    945
    1210

    3) Diving to 200 feet depth or more may produce oxygen toxicity, even when air is breathed (Wood et al, 1970).
    4) While 0.5 ATA oxygen is generally harmless in healthy adults, inhalation of 0.9 ATA or greater can cause abnormalities in less than 24 hours (Bostek, 1989).
    a) Impairment of ciliary action and tracheal mucous velocity may be seen, which may cause increased susceptibility to infection (Bostek, 1989).
    5) PREDISPOSING FACTORS
    a) PRE-EXISTING PULMONARY DISEASE does NOT predispose patients to increased susceptibility to the toxic effects of hyperoxia (Bostek, 1989).
    b) However, VENTILATOR-DEPENDENT PATIENTS may be MORE SUSCEPTIBLE to oxygen toxicity than normal volunteers (Bryan & Jenkinson, 1988).
    c) SPECIES - There is wide variation amongst different animal species in susceptibility to oxygen toxicity (Deneke & Fanburg, 1980).
    d) AGE - In general, oxygen toxicity occurs less in immature than mature experimental animals (Deneke & Fanburg, 1980; Frank, 1991).
    e) METABOLIC AND NUTRITIONAL ALTERATIONS - Conditions that may alter susceptibility to oxygen toxicity include thyroid or adrenal abnormalities, hypothermia, altitude acclimatization, protein deprivation, vitamin deficiencies, essential mineral deficiencies, and changes in dietary fatty acid consumption (Deneke & Fanburg, 1980).
    f) OXYGEN PRETREATMENT (EXPERIMENTAL) - In some experimental animal species, pretreatment with inhalation of oxygen concentrations less than 100% provides some protection against later 100% oxygen inhalation by stimulating protective enzymes (Deneke & Fanburg, 1980).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) PREVENTION - It is generally suggested that keeping the inspired Fi02 at 50% may prevent development of normobaric oxygen toxicity (Bostek, 1989).

Workplace Standards

    A) ACGIH TLV Values for CAS7782-44-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7782-44-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7782-44-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7782-44-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) (Das & Stickle, 1993; Lewis, 1992 Marshall & Mcquaid, 1993 RTECS, 1993
    1) TCLo- (INHALATION)HUMAN:
    a) Female 26-39W preg, 12 pph for 10M -- TER
    b) 100 pph for 14H -- PUL

Pharmacology Toxicology

Toxicologic Mechanism

    A) NORMOBARIC HYPEROXIA -
    1) After several days of breathing 100% oxygen at 1 ATA pressure, a disruption of capillary endothelium and type I alveolar cells, interstitial lung edema, fibrin deposition over the alveolar lining, proliferation of interstitial fibers, and proliferation of alveolar type II cells develops (Finkel, 1983; Jackson, 1985).
    a) The pathology of oxygen toxicity is nonspecific, consisting of atelectasis, fibrin deposition, edema, alveolar hemorrhage, inflammation, and thickening and hyalinization of the alveolar membranes (Deneke & Fanburg, 1980; Jackson, 1985).
    b) Ciliated tracheal and bronchial cells can be damaged by inhalation of 80% to 100% normobaric oxygen (Deneke & Fanburg, 1980).
    c) The capillary endothelium is damaged early, allowing plasma leakage into interstitial and alveolar spaces (Deneke & Fanburg, 1980).
    2) Increased plasma albumin and transferrin levels have been found in bronchoalveolar lavage fluid in volunteers breathing 95% normobaric oxygen for about 17 hours, indicating an increased alveolar-capillary "leak" induced by hyperoxia (HSDB , 2001).
    3) Normobaric hyperoxia is toxic to cultured human pulmonary endothelial cells (HSDB , 2001).
    4) High oxygen concentrations inhibit a variety of enzymes, including those for respiration, electron transport, ATP synthesis, glycolysis, and a number of enzymes and coenzymes which require free sulfhydryl groups for normal functioning (HSDB , 2001).
    5) Oxygen toxicity is mediated by production of the superoxide radical and other free radicals (ie, hydroxyl and hydrogen peroxide) which can attack and disrupt virtually all organic molecules (Clayton & Clayton, 1982; Bostek, 1989; Bryan & Jenkinson, 1988; Deneke & Fanburg, 1980; Halliwell, 1984; Jackson, 1985; Lodato, 1990; Saugstad, 1990; Tinits, 1983).
    a) Such free radicals initiate the chain reactions of lipid peroxidation which leads to cell rupture and destruction (Bostek, 1989; Halliwell, 1984).
    6) A fibrotic reaction involving the lung interstitium is seen in patients with prolonged exposure to hyperoxia; increased pulmonary levels of hydroxyproline and collagen have been documented (Crapo, 1986).
    7) In sheep exposed to 100% normobaric oxygen, decreased dynamic compliance with increased lung stiffness precedes the development of pulmonary edema (Fukushima et al, 1990).
    8) If successful weaning to room air can be accomplished, some recovery from hyperoxia-induced diffuse lung injury may be seen (Jackson, 1985).
    B) HYPERBARIC HYPEROXIA -
    1) DIVERS -
    a) In divers exercising at 25 fsw (1.76 ATA) for 80 to 271 minutes, CNS oxygen toxicity was not observed, although 2/6 subjects developed clinical and spirometric evidence of early pulmonary oxygen toxicity (Piantadosi et al, 1979).
    1) Low resistance and minimalization of dead space resulting in a low inspired pCO2 may have contributed to the absence of CNS oxygen toxicity (Piantadosi et al, 1979).
    2) EXPERIMENTAL ANIMALS - Increased collagen production consistent with the development of pulmonary fibrosis has been seen in experimental animals exposed to hyperbaric oxygen (Clayton & Clayton, 1982).
    3) CNS TOXICITY MECHANISM - The mechanism of the CNS toxicity is unclear, but may involve destruction of neurotransmitters (eg, GABA) in hyperoxic conditions (Clayton & Clayton, 1982).

Physicochemical

Physical Characteristics

    A) Oxygen is a colorless, odorless, tasteless gas (AAR, 1987; (Budavari, 1996; Lewis, 1997; Bingham et al, 2001).
    1) At -183 degrees C, oxygen is liquefiable to a slightly bluish liquid (Lewis, 1997).
    B) Liquid oxygen is an odorless, colorless to slightly bluish liquid which readily vaporizes to the gaseous state (AAR, 1987).
    C) It is shipped as a refrigerated liquid at pressures < 200 psig (AAR, 1987).
    D) Solidifiable at -218 degrees C (Lewis, 1997).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) ATOMIC WEIGHT (O): 15.9994 (Budavari, 1996)
    B) MOLECULAR WEIGHT (O2): 32.00 (RTECS , 2001)

Other

    A) ODOR THRESHOLD
    1) Odorless (CHRIS , 2002)

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