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CHEMINFO Record Number: 774
CCOHS Chemical Name: Ozone

Triatomic oxygen

Chemical Name French: Ozone
Chemical Name Spanish: Ozono
CAS Registry Number: 10028-15-6
RTECS Number(s): RS8225000
Chemical Family: Inorganic oxygen compound / elemental oxygen / triatomic oxygen
Molecular Formula: 03
Structural Formula: Triangular molecule of 3 oxygen atoms.


Appearance and Odour:
Colourless gas at low concentrations, which becomes blue as the concentration increases. The characteristic odour is similar to freshly mown hay.(1,7,24,25)

Odour Threshold:
Reported values vary; 0.0076 ppm (minimum perceptible value) (26); 0.005 -2.0 ppm (detection threshold) (1); 0.1 ppm (recognition) (27).

Warning Properties:
NOT RELIABLE - variations in the detection range reported and olfactory fatigue occurs (ability to smell ozone is lost quickly as exposure continues).

Ozone is generated on-site, at its point of use, because of the difficulty, hazards and high cost of transporting ozone and because it is not easily stored.(6) Ozone can be generated by a variety of methods, the most common of which involves the dissociation of molecular oxygen electrically (silent discharge) or photochemically (ultraviolet irradiation).(25) Excess ozone is destroyed on-site. Gaseous ozone can be adsorbed by porous solid substrates, such as silica gel, and is often used in this form in organic synthesis.(25) Trace amounts of oxygen accumulate slowly with ozone decomposition.

Uses and Occurrences:
Ozone is used for the purification and disinfection of drinking water; for high purity water systems (e.g., bottling and canning plants); disinfection and odour control of industrial and municipal wastewater and sewage, swimming pools and spas, and industrial processes; bleaching agent; food preservative; in cold storage rooms, brewery cellars, hotel and hospital air ducts and air conditioning systems; in organic synthesis; medical applications; aquatic oxidant; and production of high purity silver.(25,29)
Ozone is a natural component of the Earth's stratosphere (1-10 ppm). Ozone can be produced from electric arc welding, electroplating, mercury vapour lamps, X-ray generators, photoengraving, photocopying machines, electrostatic air cleaners, high voltage electrical equipment and indoor ultraviolet sources.(6,7,29)


Colourless gas at low concentrations, which becomes blue as the concentration increases. The characteristic odour is similar to freshly mown hay. Will not burn. POWERFUL OXIDIZER. Contact with combustible materials may cause fire or explosion. DANGEROUSLY REACTIVE. Unstable at room temperature at high concentrations. May decompose violently, under conditions of shock or elevated temperatures. Can react violently or explosively with many chemicals. VERY TOXIC. May be fatal if inhaled. Causes lung injury--effects may be delayed. POSSIBLE MUTAGEN - May cause genetic damage, based on animal information.


Effects of Short-Term (Acute) Exposure

Even very low concentrations of ozone can be harmful to the upper respiratory tract and the lungs. The severity of injury depends on both by the concentration of ozone and the duration of exposure. Severe and permanent lung injury or death could result from even a very short-term exposure to relatively low concentrations.
Exposure to extremely low concentrations of ozone initially increases the reactivity of the airways to other inhaled substances (bronchial hyperresponsiveness) and causes an inflammatory response in the respiratory tissue. Exposure to ozone during exercise or work increases susceptibility to this effect.(4,6,12) Increased bronchial responsiveness has been observed following 7-hour exposures to 0.08, 0.1 or 0.12 ppm (with moderate exercise), or a 1-hour exposure to 0.35 ppm.(12) This response occurs almost immediately following exposure to ozone and persists for at least 18 hours.(4,6) Other symptoms observed following acute exposures to 0.25-0.75 ppm include cough, shortness of breath, tightness of the chest, a feeling of an inability to breathe (dyspnea), dry throat, wheezing, headache and nausea.(7,9) More severe symptoms have been seen following exposure to higher concentrations (greater than 1 ppm) and have included reduced lung function, extreme fatigue, dizziness, inability to sleep and to concentrate and a bluish discolouration of the skin (cyanosis).(1,7) Intermittent exposure to 9 ppm for 3-14 days has produced inflammation of the bronchi and lungs.(1) An acute occupational exposure to approximately 11 ppm for 15 minutes caused severe respiratory irritation and almost caused unconsciousness.(14) A 30-minute exposure to 50 ppm is considered potentially lethal.(1) Animal studies indicate that ozone can also cause a potentially fatal accumulation of fluid in the lungs (pulmonaryedema). Symptoms of pulmonary edema, such as shortness of breath, may not appear for 24 hours after exposure and are aggravate d by physical exertion.
The severity respiratory responses to ozone becomes reduced following repeated daily exposures. This "functional adaptation" to the effects of ozone may persist for several days after exposure stops.(12) Decreases in respiratory function do not appear to be more pronounced in cigarette smokers or people with pre-existing lung disorders.(4)

Skin Contact:
There is no information available. Ozone gas can probably cause skin irritation due to its oxidizing ability, but only at concentrations capable of causing severe respiratory injury.

Eye Contact:
Ozone concentrations greater than 2 ppm can be irritating to the eyes within minutes. No definite effects on vision were noted in volunteers exposed for 3 or 6 hours to 0.2-0.5 ppm, although some increase in side vision (peripheral) and a slight reduction in visual sharpness (acuity) was noted during dark adaptation tests.(3)

Ingestion is not an applicable route of exposure for gases.

Effects of Long-Term (Chronic) Exposure

A small number of studies examining the potential effects of long- term occupational exposures to ozone have reported headache, irritation of the nose and throat, chest constriction and lung congestion in exposed workers.(1) Human population studies indicate that people living in communities with high background ozone levels have experienced a greater decrease in lung function over 5 years than people living in communities with lower background levels. These studies suggest that long-term exposures to ozone may result in impaired lung function.(4) These reports are consistent with animal studies which also indicate that long-term exposure to ozone can impair lung function and cause structural changes to the lungs.

Based on animal evidence, exposure to ozone may increase susceptibility to bacterial infections of the respiratory system.


There is no human information available. Animal studies are inconclusive.

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not classifiable as a human carcinogen (A4).

Teratogenicity and Embryotoxicity:
There is no human information available. No conclusions can be drawn from the available animal studies because effects were either seen in the presence of maternal toxicity or maternal toxicity was not evaluated.

Reproductive Toxicity:
There is no human information available. No effects were observed in one animal study.

A number of studies have examined the potential mutagenicity of ozone in humans. Several of these studies have shown negative results and the two positive studies have had weaknesses in their study designs (no statistical analysis of the data was conducted in one study and the other study did not rule out other possible causes, such as smoking). Therefore, it is not possible to draw any conclusions from these studies. Ozone is mutagenic in isolated human cells, animal cells and bacteria. Positive results have also been observed in animal cells (somatic) following inhalation exposure.(18,22)

Toxicologically Synergistic Materials:
Ozone exposures may influence clearance of other hazardous substances from the lung. Individuals with asthma were reported to be sensitized to the effects of other irritants when pre-exposed to 0.12 ppm ozone for 1 hour.(6) Animal studies have shown that rats exposed to ozone prior to an exposure to asbestos had significantly more asbestos in their lungs one month later than animals not exposed to ozone.(7) No synergism has been observed between ozone and either nitrogen dioxide or sulphuric acid in terms of impaired respiratory function.(13)

Potential for Accumulation:
Ozone is absorbed in both the upper and lower respiratory tract. It is a potent oxidant that reacts with protein and lipids, particularly within biological membranes. A small amount of inhaled ozone is absorbed into the blood. The extreme reactivity of ozone limits its ability to accumulate.(5,6)


Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the buddy system). Remove source of contamination or move victim to fresh air. If breathing is difficult, oxygen may be beneficial if administered by a trained person, preferably on a doctor's advice. DO NOT allow the victim to move about unnecessarily. Symptoms of pulmonary edema can be delayed up to 48 hours after exposure. Immediately transport victim to an emergency care facility.

Skin Contact:
If symptoms develop, remove source of contact or have victim move to fresh air.

Eye Contact:
If symptoms develop, remove source of contact or have victim move to fresh air.

Ingestion is not an applicable route of exposure for gases or liquefied gases.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures.
Some recommendations in the above sections may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.


Flash Point:
Non-flammable (does not burn)

Lower Flammable (Explosive) Limit (LFL/LEL):
Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):
Not applicable

Autoignition (Ignition) Temperature:
Not applicable

Sensitivity to Mechanical Impact:
Explosions of gaseous ozone, gaseous ozone-oxygen mixtures, pure liquid ozone, or strong solutions in oxygen can be initiated by mechanical shock.(25,30)

Sensitivity to Static Charge:
Not sensitive

Combustion and Thermal Decomposition Products:
Decomposes to molecular oxygen, especially at elevated temperatures.

Fire Hazard Summary:
Ozone is not combustible (does not burn). However, pure ozone poses a serious fire and explosion risk by reacting with combustible materials, due to its very strong oxidizing ability.

Extinguishing Media:
Use extinguishing media appropriate to surrounding fire conditions. Use water in large quantities for fires involving ozone.

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or a protected location. Do not enter areas with high ozone concentrations, since a serious fire, explosion and health risk exists.
If it can be done safely, shut down the ozone generating equipment. If there is an ozone leak, stop the flow of ozone, if this can be done safely. Otherwise, withdraw from area and let fire burn. For massive fires, use unmanned hose holder or monitor nozzles. If this is not possible, withdraw from area and let fire burn. If possible, isolate materials not involved in the fire and protect personnel. Remove all flammable and combustible materials from the vicinity, especially oil and grease.
Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.


NFPA - Comments:
NFPA has no listing for this chemical in Codes 49 or 325.


Molecular Weight: 48.00

Conversion Factor:
1 ppm = 1.96 mg/m3; 1 mg/m3 = 0.51 ppm at 25 deg C (calculated)

Physical State: Gas
Melting Point: Approximately -192.5 deg C (-314.5 deg F) (25,29)
Boiling Point: -111.9 deg C (-169.4 deg F) (25,29)
Relative Density (Specific Gravity): Not applicable (gas)
Solubility in Water: Slightly soluble (0.11 g/100 mL (25,29) or 49.4% v/v at 0 deg C (28); 0.06 g/100 mL at 20 deg C) (29)
Solubility in Other Liquids: Soluble in a number of organic solvents, such as chlorofluorocarbons, alkaline solvents and oils (1,31); soluble in all proportions in liquid oxygen.(29)
Coefficient of Oil/Water Distribution (Partition Coefficient): Not available.
pH Value: Not applicable.
Vapour Density: 1.66 (air=1) (28)
Vapour Pressure: Not applicable (gas).
Vapour Pressure at 50 deg C: Greater than 7000 kPa (69 atm) (estimated from graph) (28b)
Saturation Vapour Concentration: Not applicable (gas).
Evaporation Rate: Not applicable (gas).
Critical Temperature: -12.1 deg C (10.2 deg F) (25,27,29)
Critical Pressure: 5532.8.63 kPa (54.6 atmospheres) (25,28,29)


Ozone decomposes slowly to oxygen with a half-life of 3 days at 20 deg C and of 3 months at -50 deg C.(1,5) The rate of decomposition is increased by light, trace organic matter, nitrogen oxides, mercury vapour, peroxides, metals (e.g. copper, copper alloys, iron and chromium) and metal oxides.(25)

Hazardous Polymerization:
Does not occur

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

Ozone is a very strong oxidizer capable of reacting dangerously and explosively with many substances. Ozone is strongly endothermic (absorbs heat) and liquid ozone is highly explosive. For a review of the many substances ozone can react with, consult references 30, 31 and 32. These include:
ALKALI METALS, AROMATICS (e.g. benzene, aniline), FLUOROETHYLENE, ALKENES (e.g. ethylene), ISOPROPYLIDENE COMPOUNDS (e.g. citronellic acid) or DIETHYL ETHER - may decompose with explosive violence.(30,32)
ALKYLMETALS (e.g. dimethylzinc or diethylzinc) or DIENES and OXYGEN - immediate ignition and flames.(30)
COMBUSTIBLE GASES (e.g. ammonia, carbon monoxide, nitrogen oxide or phosphine) - immediate explosion on contact at 0 deg C.(30)
COMBUSTIBLE MATERIALS (e.g. oil and grease) - can ignite.(30)
OXIDIZABLE MATERIAL (e.g. hydrides, boranes or hydrazine) - can explode upon contact.(30,32)
BROMINE, NITROGEN, or NITROGEN DIOXIDE - may explode.(30,32)
DIFLUOROETHYLENE or TRIFLUOETHYLENE - form shock-sensitive or temperature sensitive peroxidic species.(30)

Conditions to Avoid:
Electrical sparks, heat, shock wave, intense light flash.

Corrosivity to Metals:
Attacks most metals including iron and mild steel.

Stability and Reactivity Comments:
Evaporation of a solution of ozone in liquid oxygen causes ozone enrichment and ultimate explosion.(30) Ozone attacks rubber. It can be used with glass, stainless steel, aluminum, Teflon, Tygon, Hypalon, polyvinyl chloride and polyethylene.(1,28)


LC5O (rat): 7.4-8.2 ppm (4-hour exposure) (1)
LC50 (mouse): 5.9-6.8 ppm (4-hour exposure) (1)
LC50 (hamster): 16.2 ppm (4-hour exposure) (1)

Eye Irritation:

Eye irritation or damage was not observed in dogs exposed to approximately 1 ppm for one year (concentration not specified).(2,3) Corneal damage was not observed in rabbits exposed to 2-2.8 ppm (4 hours/day) for up to 25 days.(3)

Effects of Short-Term (Acute) Exposure:

Studies using a variety of animal species, with ozone concentrations up to 1.0 ppm, show that short-term exposure damages cells and tissues of the upper and lower respiratory tracts. In general, this injury appears to be reversible when exposure stops. However, repeated or higher short-term exposures can lead to progressive and irreversible respiratory tract damage, including effects on pulmonary function. In LC50 studies, animals have died from pulmonary edema (accumulation of fluid in the lungs) and bleeding of the lungs.(4,6-8) There is some evidence that adaptation or tolerance to ozone exposure may occur. Rats exposed to 0.35-1 ppm (2.25 hours/day for 5 days) had decreased lung function at all concentrations on the first two days but adapted to these effects at the low dose only by the fifth day.(4) Exposures of several hours to 0.08 to 1.2 ppm has harmed the natural defence mechanisms of the respiratory system (protective responses to foreign materials). Decreased resistance to bacterial infections and reduced clearance of foreign material from the respiratory tract have been observed.(1,4,5) Female rats exposed to 1 ppm ozone for 6 hours during or just following pregnancy had an increased inflammatory response in the lungs compared to non-pregnant rats.(10)

Effects of Long-Term (Chronic) Exposure:

Harmful effects to the upper and lower respiratory tracts, including inflammation, bronchitis, emphysema, reduced lung function and non-carcinogenic lesions, have been observed in rats, mice and guinea pigs exposed to 1 ppm and lower. In studies with rats and guinea pigs, a significant number of deaths have occurred during the studies.(7,11-13,18) In a series of well-conducted studies, mice and rats exposed to 0.5 or 1.0 ppm for 105 to 130 weeks had an increased incidence of non-carcinogenic lesions of the nose and lungs.(18) Several studies have also examined the effects of long-term ozone exposure on monkeys. Exposures ranging from 0.15-0.64 ppm for 3-18 months consistently showed significant structural alterations to the lungs, abnormal lung growth, and deposition of increased amounts of structurally altered collagen (protein). Many of the structural alterations appeared to be irreversible 6 months after exposure stopped.(7,12,13)

In a comprehensive study, rats and mice were exposed to 0.12, 0.5 or 1.0 ppm ozone for 105 to 130 weeks. There was no evidence of carcinogenicity in male or female rats, inconclusive evidence in male mice, and some evidence in female mice. Ozone did not have tumour promoting properties.(18) Two other studies have reported slight increases in lung tumours in type of mouse known to be particularly susceptible to tumour development.(19,20) Both positive and negative results were reported in another, less susceptible, type of mouse.(20,21)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
No animal studies have assessed the potential developmental effects of ozone in the absence of maternal toxicity. One study reported that offspring of rats continuously exposed to 1.0 or 1.5 ppm for 4 days during middle or late pregnancy had reduced growth rates after birth and delayed behavioral development, when exposed during the late exposure period only. Maternal toxicity was not reported.(15) Fetal body weight gain was reduced in the offspring of mice exposed to 1.2 ppm, but not 0.4 or 0.8 ppm, on days 7-17 of pregnancy. Signs of maternal toxicity were observed.(16) Embryotoxicity (increased resorptions) was observed in rats exposed to 1.5 and 2.0 ppm ozone, but not 0.64-1.26 ppm. Maternal toxicity was not reported.(17) Continuous exposure of mice from 6 days prior to mating to postnatal day 22 resulted in reduced body weight and slight effects in neurobehaviour development of the offspring. Maternal toxicity was not evaluated.(23)

Reproductive Toxicity:
No effects on reproductive performance (proportion of successful pregnancies, litter size, offspring viability and sex ratio) were noted in mice exposed for 6 days prior to mating to postnatal day 22.(23)

Studies of mutagenicity in animals following inhalation exposure have produced conflicting results. However, small differences in ozone concentration, exposure duration and air flow may have been sufficient to produce these conflicting results. Positive results (cytogenetic aberrations) were observed in the lymphocytes of hamsters exposed to 0.24-0.43 ppm for 5 hours and in the lung macrophages of female rats exposed to 0.12-0.8 ppm for 6 hours. Cytogenetic aberrations were not observed in the lymphocytes of mice, the bone marrow cells of hamsters or male rats, or the spermatocytes of male mice.(18,22)
Several studies have shown that ozone is mutagenic in bacteria and in mammalian and human cells in vitro.(18,22)


Selected Bibliography:
(1) Hughes, D. The Toxicity of Ozone. Occupational hygiene monograph, no. 3. Science Reviews Ltd., 1979.
(2) Melton, C.E. Effects of long-term exposure to low levels of ozone: a review. Aviation, Space and Environmental Medicine. Vol. 53, no. 2 (February, 1982). p. 105-111
(3) Grant, M. W., et al. Toxicology of the eye. 4th edition. Charles C. Thomas, 1993. p. 1097-1098
(4) Lipman, M. Ozone. In: Environmental and occupational disease. 2nd edition. Edited by W.N. Rom. Little, Brown and Company, 1992. p. 489-501
(5) Dutch expert committee for occupational standards. Health-based recommended occupational exposure limit for ozone. RA 4/92. Ministry of Social Affairs and Labour Employment, Labour Inspectorate, September, 1992.
(6) Lipsett, M. Ozone. In: Hazardous materials toxicology: clinical principles of environmental health. Edited by J.B. Sullivan, et al. Williams and Wilkins, 1992. p. 958-963
(7) Lipsett, M.J., et al. Inorganic compounds of carbon, nitrogen, and oxygen: ozone. In: Patty's industrial hygiene and toxicology. 4th edition. Volume II. Toxicology. Part F. Edited by G.D. Clayton, et al. John Wiley and Sons, 1991. p. 4621-4643
(8) Menzel, D.B. Ozone: An overview of its toxicity in man and animals. Journal of Toxicology and Environmental Health. Vol. 13 (1984). p. 183-204
(9) Folinsbee, L.J. Effects of ozone exposure on lung function in man: a review. Reviews on Environmental Health. Vol. 111, no. 3 (1981). p. 211-240
(10) Gunnison, A.F., et al. Enhanced inflammatory response to acute ozone exposure in rats during pregnancy and lactation. Fundamental and Applied Toxicology. Vol. 19, no. 4 (November, 1992). p. 607-612
(11) Stockinger, H.E., et al. Ozone toxicity studies. III. Chronic injury to lungs of animals following exposure at a low level. American Medical Association Archives of Industrial Health. Vol. 16 (1957). p. 514-522
(12) Lippmann, M. Health effects of ozone: a critical review. Journal of the Air Pollution Control Association. Vol. 39, no. 5 (May, 1989). p. 672-695
(13) Lippmann, M. Ozone. In: Environmental toxicants: human exposures and their health effects. Edited by M. Lippmann. Van Nostrand Reinhold, 1992. p. 465-519
(14) Kelly, F.J., et al. Ozone poisoning: serious human intoxication. Archives of Environmental Health. Vol. 10 (March, 1965). p. 517-519
(15) Kavlock, R.J., et al. Studies on the development of toxicity of ozone: postnatal effects. Toxicology Letters. Vol. 5 (1980). p. 3-9
(16) Bignami, G., et al. Limited effects of ozone exposure during pregnancy on physical and neurobehavioral development of CD-1 mice. Toxicology and Applied Pharmacology. Vol. 129, no. 2 (December, 1994). p. 264-271
(17) Kavlock, R., et al. Studies on the developmental toxicity of ozone. I. prenatal effects. Toxicology and Applied Pharmacology. Vol. 48 (1979). p. 19-28
(18) Boorman, G.A. NTP technical report on the toxicology and carcinogenesis studies of ozone (Cas no. 10028-15-6) and ozone/NNK (Cas no. 10028-15-6/64091-91-4) in F344/N rats and B6C3F1 mice: inhalation studies. Technical report series no. 440. National Toxicology Program, U.S. Department of Health and Human Services, October, 1994
(19) Hasset, C., et al. Murine lung carcinogenesis following exposure to ambient ozone concentrations. Journal of the National Cancer Institute. Vol. 75, no. 4 (October, 1985). p. 771-777
(20) Last, J.A., et al. Modification by ozone of lung tumor development in mice. Journal of the National Cancer Institute. Vol. 78, no. 1 (January, 1987). p. 149-153
(21) Mustafa, M. G., et al. Pulmonary carcinogenic effects of ozone. Annals of the New York Academy of Sciences. Vol. 534 (June 30, 1988). p. 714-723
(22) Victorin, K. Review of the genotoxicity of ozone. Mutation Research. Vol. 277, no. 3 (September, 1992). p. 221-238
(23) Dell'Omo, G., et al. Neurobehavioural development of CD-1 mice after combined gestational and postnatal exposure to ozone. Archives of Toxicology. Vol. 69 (1995). p. 608-616.
(24) NIOSH pocket guide to chemical hazards. National Institute for Occupational Safety and Health, June 1994. p. 238
(25) Wojtowicz, J.A. Ozone. In: Kirk-Othmer encyclopedia of chemical technology. 4th edition. Volume 17. John Wiley and Sons, 1996. p. 953-994
(26) Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, 1989. p. 72
(27) Ozone. In: Cloyd, D.R., et al. Handling hazardous materials. Report no. NASA SP-5032. National Aeronautics and Space Administration, September, 1965. p. 63-71
(28a) Ozone. In: Matheson gas book. Edited by W. Braker et al. 6th edition. Matheson, 1980. p. 574-577
(28b) Yaws, C.L. Matheson gas data book. 7th ed. McGraw-Hill, 2001. p. 659
(29) Kirschner, W.J. Ozone. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised edition. Volume A 18. VCH Verlagsgesellschaft, 1991. p. 349-357
(30) Urben, P.G., ed. Bretherick's handbook of reactive chemical hazards. 5th edition. Volume 1. Butterworth-Heinemann Ltd., 1995. p. 1764-1770
(31) HSDB record for ozone. Last revision date: 96/06/11
(32) Fire protection guide on hazardous materials. 11th edition. National Fire Protection Association, 1994. NFPA 491
(33) Thiele, J.J., et al. Ozone depletes tocopherols and tocotrienols topically applied to murine skin. Federation of European Biochemical Societies Letters. Vol. 401 (1997). p. 167-170

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

Review/Preparation Date: 1997-02-25

Revision Indicators:
TLV-C 1997-10-01
Clean-up 1998-01-01
Skin (Health) 1998-01-01
Resistance of materials 1998-01-01
Eye/Face Protection 1998-01-01
Skin Protection 1998-01-01
TLV-TWA 1999-03-01
TLV comments 1999-03-01
PEL-TWA final 2003-12-04
PEL-STEL final 2003-12-04
PEL transitional comments 2003-12-04
TLV basis 2004-01-04
WHMIS proposed classification 2005-01-05
Emergency overview 2005-01-05
Handling 2005-01-05
Bibliography 2006-01-18
Vapour pressure at 50 deg C 2006-01-18
Bibliography 2006-04-27
Relative density 2006-09-28

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