OZONE

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.

MOLECULAR FORMULA

ERG GUIDE NUMBER

123-GASES - TOXIC and/or CORROSIVE

SYNONYM REFERENCE

(EPA, 1985)RTECS, 1996;(HSDB , 1996)

USES/FORMS/SOURCES

USES

Ozone is used as a disinfectant and bleaching agent, in the manufacture of ink, as a catalyst, in water treatment, and as an inhibitor of mold and bacteria (EPA, 1985).
Ozone is used as a disinfectant for air and water by virtue of its oxidizing power; for bleaching waxes, textiles, and oils; and in organic syntheses. It forms ozonides which are sometimes useful oxidizing compounds (Budavari, 1989; Lewis, 1993).
OZONE THERAPY: Medical ozone (O3) gas is used to disinfect and treat diseases (eg, infected wounds, circulatory disorders, macular degeneration, rheumatism/arthritis) by inactivating bacteria, viruses, fungi, yeast and protozoa, and stimulating oxygen metabolism, and activating the immune system (Elvis & Ekta, 2011). Intraarticular ozone infiltrations in 2 patients resulted in cortical blindness and seizures (Rolan et al, 2012). In dental medicine, the ozonized water is used as a spray or compress (Elvis & Ekta, 2011).
WATER TREATMENT

Ozone has been used for more than 80 years, primarily for disinfection of municipal drinking water (Freeman, 1989).
The first water treatment plants using ozone were installed in the US in the 1940s. The first wastewater plant to use ozone for disinfection was operated in 1973 (Freeman, 1989).
Ozone treatment at more than 1.0 mg of TROs per L for several minutes efficiently disinfects seawater for mariculture applications (Sugita et al, 1992).
A continuous flow laboratory reactor was constructed to investigate the decomposition of ozone to produce hydroxyl radicals that oxidize micropollutants in water. The reactor had a flow rate of 34 mL/min and the residence time could be varied between 1.4 to 27 seconds so that relatively short term effects could be monitored. Radical formation was found to be a function of the chemical composition of the water in natural systems (Guittonneau et al, 1992).
In a study of the design of a new ozone contactor (the deep U tube), laboratory and modeling data were compared to experimental data from a full-scale plant and a pilot plant. The results showed the deep U tube reactor to be more efficient than the stirred tank reactor design and close to the plug flow reactor in performance (Roustan et al, 1992).
A study was done to evaluate the kinetic parameters for the ozonation of wastewaters from a distillery and a tomato processing plant (Beltran et al, 1992).
The evolution of organic and inorganic matter, as a function of ozonation time, was followed by monitoring the chemical oxygen demand.
The early (faster rate) stage was dominated by gas-liquid reaction and the later stages by bulk solution reactions, particularly for the tomato wastewaters.

FORMS

Under ambient conditions ozone is a colorless to bluish gas with a characteristic, pleasant odor in concentrations of less than 2 ppm (Budavari, 1989; Lewis, 1993).
Between minus 169.6 degrees F (minus 111.9 degrees C) and minus 314 degrees F (minus 192.7 degrees C), ozone is a dark blue liquid. Below minus 314 degrees F (minus 192.7 degrees C), it exists as blue-black crystals (EPA, 1985).

SOURCES

NATURAL: Produced by ultraviolet light action on oxygen. Maximum concentration occurs in the atmosphere at around 75,000 feet. Natural electrical discharges (such as lightning) also produce ozone (Beard, 1982).
Ozone is also formed in photochemical reactions between nitrogen oxides and hydrocarbon emissions from cars and trucks (HSDB , 1996).
Ozone occurs primarily outdoors (Speizer, 1985).
The concentration of ozone in air may vary. It occurs at approximately 0.05 ppm at sea level (HSDB , 1996).

Concentrations in urban air are higher. Levels can reach 0.5 ppm in urban photochemical smog (WHO, 1979), higher than the ACGIH-TLV and OSHA PEL.
Seasonal fluctuations occur, with levels being highest in the summer and lowest in the winter (Bates, 1989; Lioy & Dyba, 1989).
Fluctuations also occur in urban areas during the day; highest concentrations occur near mid-day or early afternoon (Lioy & Dyba, 1989).
Motor vehicle exhaust is seen to exhibit the highest photochemical ozone creation potential (POCP) of all hydrocarbon emissions tested (Derwent et al, 1996).

These daily, seasonal, and geographic fluctuations of ozone concentration should be taken into account in designing an appropriate monitoring scheme and work shift for occupational exposures, especially for persons working outdoors.
Arc welding shielded by inert gases such as argon and helium room air ozonizers, office photocopying machines, fumigation chambers, high voltage electrical apparatus, UV quartz lamps, and ozonizers for treatment of sewage (Jaffe, 1967) 1968).
Ozone has been measured at concentrations as high as 0.56 ppm in laser printer exhaust (HSDB , 1996).
The most likely sources of exposures to ozone in industry are leakage from ozone-using processes and high voltage electrical equipment and from electric arc welding. (The latter is more potently a sources of nitrogen oxides.) Aircraft flying at altitudes greater than 33,000 ft may take significant quantities of atmospheric ozone into their cabin ventilation (Beard, 1982).
FOOD TREATMENT: A study was done to examine the solubility and stability of ozone in shrimp-meat extract (SME) and the bacteriocidal effect of ozone on shrimp-meat microorganisms. Ozone produced a decomposition rate of 2.7%/min in the SME from a saturated solution (1.4 mg O3/L) at 5 and 25 degrees C. Nine bacterial strains were tested and Salmonella typhimurium was found to be the most resistant to ozone. No mutagen was observed in shrimp meat when it was ozonated in saline (Chen et al, 1992).
DECOMPOSITION OF 2,4-D: A laboratory study was conducted to determine the rate constants for degradation of herbicides by ozone. The half-life for removal of 2,4-D at pH 7.5 and in the presence of bicarbonate ions was 39.5 minutes at a dissolved ozone concentration of 10 micromolar. The addition of a second herbicide did not affect the relative degradation rate (Xiong & Graham, 1992).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

Ozone is a skin, eye, upper respiratory tract, and mucous membrane irritant. The primary symptoms after acute exposure are irritation of the eyes, nose, throat, and chest, as well as fatigue. Exposure to less than 0.5 ppm may produce symptoms and alter pulmonary function tests, but does not significantly decrease exercise potential.

The primary site of acute injury is the lung; injury is characterized by pulmonary congestion, edema, and hemorrhage.

Human systemic effects by inhalation: visual field changes, lacrimation, headache, decreased pulse rate, decreased blood pressure, dermatitis, cough, dyspnea, respiratory stimulation, and other pulmonary changes.

Ozone increases bronchial allergen responses in subjects with allergic asthma or rhinitis.

The toxicity of ozone is increased by its interaction with other environmental oxidants.

OZONE THERAPY: Intraarticular ozone infiltrations in 2 patients resulted in cortical blindness and seizures.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

TOXIC; may be fatal if inhaled or absorbed through skin.
Vapors may be irritating.
Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite.
Fire will produce irritating, corrosive and/or toxic gases.
Runoff from fire control may cause pollution.

ACUTE CLINICAL EFFECTS

Decreased blood pressure and pulse may occur in humans during ozone inhalation (Sax & Lewis, 1992). Ozone is a powerful oxidizer which may cause ocular irritation. Ozone produced eye irritation in the rabbit in the Standard Draize Test (RTECS, 1996). Dryness of the eyes and mucous membranes of the nose and throat has been reported (Griswald et al, 1957; ACGIH, 1991).

Reported cardiovascular effects have been secondary to respiratory changes (Menzel, 1984). Humans have developed ozone-related increases in pulmonary resistance following administration of histamine, methacholine, or acetylcholine (Holtzman et al, 1979; Menzel, 1984).

Both humans and experimental animals have increased respiratory rates and shallow breathing, which decreases 30 minutes after ozone exposure. The maximum effect is at 12 to 24 hours postexposure (Menzel, 1984; HSDB , 1996).

Pulmonary symptoms include bronchopneumonia, exertional dyspnea, substernal chest pain or soreness on deep inspiration, chest tightness (Kleinfield, 1975; (Clayton & Clayton, 1994) RTECS, 1996), bronchitis, bronchiolitis (Jaffe, 1967) 1968), and pulmonary edema and hemorrhage (Scheel et al, 1959; Hathaway et al, 1991; Clayton & Clayton, 1994; HSDB , 1996).

Nose versus mouth breathing made no difference on pulmonary functions in a study of 17 healthy nonsmoking volunteers exposed to 0.4 ppm of ozone for 30 minutes while exercising (Hynes et al, 1988).

Airway hyperresponsiveness from acute exposure may persist for some time. Reductions in FVC, FEV(1.0), and FEV(3.0) were greater after a second exposure to 0.45 ppm of ozone than from an initial exposure 2 days earlier, suggesting that the acute respiratory effects of ozone may persist for at least 48 hours (Bedi et al, 1985).

Airway hyperresponsiveness was apparent within 12 hours after an initial exposure to 0.25 ppm of ozone, but had disappeared by 72 hours (Folinsbee & Horvath, 1986). Individuals with allergic rhinitis have been no more sensitive to ozone than normal subjects when exposed to 0.18 ppm (McDonnell et al, 1987).

Healthy persons engaged in light exercise are likely to experience chest discomfort and cough and to have measurable impairment of expiratory pulmonary functions when exposed for 2 hours or less to ozone concentrations of less than 0.37 ppm. Some healthy persons have significant responses to 1 hour ozone exposures at 0.15 ppm or less during light exercise. More strenuous exercise increases the responses substantially (Beard, 1982).

Respiratory tract necrosis is a commonly reported finding in experimental animal studies. Inflammation is seen in all species, but the degree varies considerably. At airborne concentrations less than 1 ppm, damage is primarily to the junction of the alveoli and connecting air passages (Menzel, 1984).

Type 1 pneumocytes are killed at concentrations of 0.8 ppm for 12 hours (Castleman et al, 1980). Proliferation of Type 2 pneumocytes is a classic sign of ozone toxicity, regardless of species (Menzel, 1984).

Rapid, shallow breathing occurs in both humans and experimental animals after exposure to as little as 0.26 ppm for 2 hours (Amdur et al, 1978). Maximum effects are often delayed until 1 day after exposure (Menzel, 1984).

Ozone is associated with increased susceptibility to infection in experimental animals (Gardner, 1982). Increased human susceptibility to infection due to ambient air ozone concentrations has not been demonstrated (Menzel, 1984).

Very short, high-level exposures (0.5 ppm for 5 minutes) were sufficient to produce increases in pulmonary resistance in baboons. Cromolyn sodium significantly prevented these increases, but did not affect respiratory mechanics during control periods, suggesting that ozone affects the surface epithelial cells (Fouke et al, 1988).

Pulmonary lesions were more abundant and more severe in rats exposed to ozone during exercise than in those exposed during rest. The increased effect was greater than predicted from the estimated effective dose (Mautz et al, 1985).

Drowsiness, dizziness, fatigue, loss of coordination, headache, malaise, and difficulty in articulating have been reported in ozone-exposed humans (Finkel, 1983; Anon, 1975; Hathaway et al, 1991; Clayton & Clayton, 1994). Substantiating evidence for extensive central nervous system depression has not been shown experimentally (Beard, 1982). Headache has been reported in persons with industrial exposure (Kleinfield et al, 1975).

Anorexia, nausea, and vomiting have been reported (Anon, 1975). Compounds generated by ozone (not ozone itself) have been implicated in causing hepatic damage in experimental animals. This has not been reported in humans (Menzel, 1984).

Decreases in RBC GSH content (Menzel, 1975) have been seen in humans exposed to 0.2 ppm for 30 to 60 minutes. RBC acetylcholinesterase decreases were seen in humans (Buckley et al, 1975) after exposure to 0.5 to 0.75 ppm for 2 to 5 hours.

In vivo exposure of RBCs to ozone changes their shape from disc-like to spherical. They may be hemolyzed more easily. Oxygen carrying capacity appears unchanged (Beard, 1982). Inhibition of oxygen dissociation from oxyhemoglobin may occur at the tissue level (ACGIH, 1986).

Frostbite injury can occur from direct contact with the cryogenic liquid or escaping gas (ILO, 1983; HSDB , 1996).

Sulfhydryl-containing enzymes are inhibited by exposure to 1 to 4 ppm for longer than 1 hour (De Lusia et al, 1972). Some enzymes, especially the glutathione peroxidase system of G-6-PD, glutathione reductase, and glutathione peroxidase systems are actually increased in the lungs of ozone-exposed experimental animals (Chow & Tappel, 1972).

CHRONIC CLINICAL EFFECTS

Repeated inhalation exposure under controlled conditions has produced a diminished response to ozone, called adaptation, by the fourth day of exposure (Folinsbee et al, 1983).

Whether or not an individual responds to ozone is consistent during different seasons of the year, when ambient ozone concentrations vary. "Responders" had lost much of their response by fall, toward the end of the period of high ambient ozone levels, but regained responsiveness by the following spring (Linn et al, 1988).

Amino acids in various proteins are oxidized by ozone. This is especially true of cysteine, methionine, and tryptophan (Menzel, 1984). Human alpha-1-proteinase inhibitor is ozonolysed in vitro, presumably by action on the amino acid. Johnson (1980) has proposed oxidation of alpha-1-proteinase as a factor in development of emphysema with long-term ozone exposure.

Immunosuppression has been reported in guinea pigs and mice with chronic low-level ozone exposure (Menzel, 1984). This effect has not been noted in humans.

There is some evidence that humans may develop a tolerance to the effects of low concentrations (Beard, 1982). The effects of ozone combined with other common air pollutants have been contradictory. When combined with nitrogen dioxide and sulfur dioxide, ozone did not increase airway resistance more than nitrogen dioxide alone in human volunteers (Von Nieding, 1979). In adolescent asthmatics, 0.12 ppm ozone or 0.3 ppm nitrogen dioxide alone decreased FVC, but combined exposure did not (Koenig et al, 1988).

Prior exposure to 0.12 ppm of ozone increased airway reactivity to 0.1 ppm of sulfur dioxide in adolescent asthmatics (Koenig JQ, 1988). Chronic exposure has caused bronchiolitis and bronchitis in experimental animals (ACGIH, 1991).

Chronic exposure in experimental animals has also caused bronchiolar fibrosis, pneumonitis, occasional lesions in the trachea and major bronchi, abnormal lung growth, changes in the nasal secretory product, and development of nodules in the lung (Clayton & Clayton, 1994).

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with liquefied gas, thaw frosted parts with lukewarm water.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
Keep victim warm and quiet.
Keep victim under observation.
Effects of contact or inhalation may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID

Most exposures to ozone gas result in only mild fatigue, headache, and minor respiratory difficulties. Severe exposures may require hospitalization and observation for severe pulmonary complications.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

CONCENTRATION LEVEL

The lowest published lethal concentration via inhalation in humans is 50 ppm for 30 minutes (RTECS, 1996).
Damage has occurred at concentrations as low as 0.5 ppm for 2 hours of exposure (Stephens et al, 1974).
Type 1 pneumocytes may be killed at 0.8 ppm for 12 hours of exposure.
Clara cell damage occurs at 0.5 to 0.8 ppm for 90 to 180 days of 8 hours per day exposure (Boorman et al, 1980).
Patchy damage of the ciliated cells of the upper airway may be seen after exposures to 0.2 to 0.5 ppm for 7 days, 8 to 24 hours per day, in various experimental animal species (Menzel, 1984).

MAXIMUM TOLERATED EXPOSURE

CONCENTRATION LEVEL

The actual concentration at which ozone exerts toxic effects in any individual depends on many factors, including morphology of the airway passage, age, sex, dietary and hormonal status, pre-existing disease states such as asthma, and capacity of cellular protective systems based on superoxide dismutase, glutathion peroxidase, and catalase (Mehlman & Borek, 1987; Clayton & Clayton, 1994).
The extent of lung damage is generally a function of concentration of ozone rather than duration of exposure (Stephens et al, 1974b).
Heavy exercise increases sensitivity to ozone for forced respiratory function (Goldstein et al, 1985).
In one study, repeated exposure to 0.2 ppm ozone did not produce cumulative effects on respiratory function, exposure to 0.35 ppm produced greater decrements in FEV on day 3, but not days 4 and 5 of exposure, and effects were greater with 0.5 ppm, but were not present by the fourth day of exposure. The authors concluded that the respiratory effects of short-term exposure to ozone are cumulative, but that a period of adaptation follows after a few days of exposure. The adaptation involves not only improvement in pulmonary function, but also fewer subjective complaints (Folinsbee et al, 1980).

Effects of Ozone in Humans - Occupational Exposures (Beard, 1982) -

lZONE CONCENTRATION (ppm)	SUBJECTIVE COMPLAINTS
0.25	None
0.3 to 0.8	Throat irritation
0.9 peak	Throat irritation Lassitude, headache
0.8 to 1.7	Dry mouth and throat Irritation of nose and eyes Chest tightness
0.47	Mucosal irritation
0.94	Severe mucosal irritation sleepiness
Greater than 0.94	Pulse increase, Sleepiness Headache
0.1 to 0.6	Substernal pain, Cough, Mucous membrane irritation

Carcinogenicity Ratings for CAS10028-15-6 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Ozone, heavy work

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Ozone, light work

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Ozone, heavy, moderate, or light workloads (2 hours or less)

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Ozone, moderate work

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

EPA (U.S. Environmental Protection Agency, 2011): Not Listed
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
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Ozone
MAK (DFG, 2002): Category 3B ; Listed as: Ozone

Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)

NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS10028-15-6 (U.S. Environmental Protection Agency, 2011):

Not Listed

TOXICITY VALUES

References: (RTECS, 1996; Sax & Lewis, 1992
- LC50- (INHALATION)CAT:
- LC50- (INHALATION)GUINEA_PIG:
- LC50- (INHALATION)HAMSTER:
- LC50- (INHALATION)MOUSE:
- LC50- (INHALATION)RABBIT:
- LC50- (INHALATION)RAT:
- LCLo- (INHALATION)HUMAN:
- TCLo- (INHALATION)HUMAN:
- TCLo- (INHALATION)MOUSE:
- TCLo- (INHALATION)RAT:
- TDLo- (INHALATION)HUMAN:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS10028-15-6 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

Ozone, heavy work

TLV:

TLV-TWA: 0.05 ppm
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: Not Listed
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

TLV Basis - Critical Effect(s): Pulm func
Molecular Weight: 48

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Ozone, light work

TLV:

TLV-TWA: 0.1 ppm
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: Not Listed
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

TLV Basis - Critical Effect(s): Pulm func
Molecular Weight: 48

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Ozone, heavy, moderate, or light workloads (2 hours or less)

TLV:

TLV-TWA: 0.2 ppm
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: Not Listed
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

TLV Basis - Critical Effect(s): Pulm func
Molecular Weight: 48

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Ozone, moderate work

TLV:

TLV-TWA: 0.08 ppm
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: Not Listed
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

TLV Basis - Critical Effect(s): Pulm func
Molecular Weight: 48

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS10028-15-6 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS10028-15-6 (National Institute for Occupational Safety and Health, 2007):

Listed as: Ozone
REL:

TWA:
STEL:
Ceiling: 0.1 ppm (0.2 mg/m(3))
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: Not Listed
Note(s):

IDLH:

IDLH: 5 ppm
Note(s): Not Listed

OSHA PEL Values for CAS10028-15-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Ozone
Table Z-1 for Ozone:

8-hour TWA:

ppm: 0.1

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 0.2

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS10028-15-6 (U.S. Occupational Safety and Health Administration, 2010):

Threshold Quantity, in pounds:100

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS10028-15-6 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS10028-15-6 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS10028-15-6 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS10028-15-6 (U.S. Environmental Protection Agency, 2010):

Listed as: Ozone
Reportable Quantity, in pounds: 100

Only the statutory or final RQ is shown. For more information, see 40 CFR table 302.4.

Threshold Planning Quantity, in pounds:

100
Amount necessary to be covered by this standard. See 40 CFR 355.30.

Note(s): Not Listed

EPA SARA Title III, Community Right-to-Know for CAS10028-15-6 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Ozone
Effective Date for Reporting Under 40 CFR 372.30: 1/1/95
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS10028-15-6 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS10028-15-6 (EPA, 2005):

Listed as: Ozone

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS10028-15-6 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

STORAGE

CONTAINER

Cylinders of dissolved ozone should be stored in refrigerated areas (HSDB , 1996).

ROOM/CABINET RECOMMENDATIONS

Commercially, ozone is typically generated onsite from air or oxygen and used immediately. This avoids the storage and handling problems usually associated with conventional oxidants (Freeman, 1989).

INCOMPATIBILITIES

Store away from all reducing agents, flammable materials, and substances such as iron, copper or chromium that may catalyze decomposition (HSDB , 1996).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 10028-15-6.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)
- Some may burn, but none ignite readily.
- Vapors from liquefied gas are initially heavier than air and spread along ground.
- Cylinders exposed to fire may vent and release toxic and/or corrosive gas through pressure relief devices.
- Containers may explode when heated.
- Ruptured cylinders may rocket.

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS10028-15-6 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

Dry chemical or CO2.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

Water spray, fog or regular foam.
Do not get water inside containers.
Move containers from fire area if you can do it without risk.
Damaged cylinders should be handled only by specialists.

TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Cool containers with flooding quantities of water until well after fire is out.
Do not direct water at source of leak or safety devices; icing may occur.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.

NFPA Extinguishing Methods for CAS10028-15-6 (NFPA, 2002):

Not Listed

COMBUSTION TOXICITY

No information on the combustion toxicity of ozone was found in available references at the time of this review.

EXPLOSION HAZARD

Ozone is a severe explosion hazard in liquid form when shocked, exposed to heat or flame, or in concentrated form by chemical reaction with powerful reducing agents (Sax & Lewis, 1992).

Solutions containing ozone explode on warming (Budavari, 1989).

Evaporation of a solution of ozone in liquid oxygen causes ozone enrichment and ultimately explosion (Bretherick, 1990).

Ozone reacts with non-saturated organic compounds to produce ozonides, which are unstable and may decompose with explosive violence (HSDB , 1996).

See the Reactivity Hazard Section for more information.

REACTIVITY HAZARD

Ozone is HIGHLY REACTIVE. It is a strong oxidizer and can explode upon contact with organic substances, especially strong reducing agents (EPA, 1985; Lewis, 1992).

Ozone forms a dangerous chemical reaction, often an explosive reaction, with the following (Lewis, 1993; Bretherick, 1990):

Acetylene
Alkenes
Alkylmetals (eg, dimethylzinc, diethylzinc)
Antimony
Aromatic compounds (eg, benzene, aniline)
Benzene + oxygen + rubber
Bromine
Charcoal + potassium iodide
Citronellic acid
Combustible gases (eg, carbon monoxide, ethylene, nitrogen oxide, ammonia, phosphine)
Diallyl methyl carbinol + acetic acid
Trans-2,3-dichloro-2-butene
Dicyanogen
Dienes + oxygen
Diethyl ether
1,1-Difluoroethylene
Dinitrogen pentoxide
Ethylene
Ethylene + formyl fluoride
Fluoroethylene
Liquid hydrogen
Hydrogen + oxygen difluoride
Hydrogen bromide
Hydrogen iodide
4-Hydroxy-4-methyl-1,6-heptadiene
23-Hydroxy-2,2,4-trimethyl-3-pentenoic acid lactone
Isopropylidene compounds
Nitrogen
Nitrogen dioxide
Nitrogen oxide
Nitrogen trichloride
Nitrogen triiodide
Nitroglycerin
Organic liquids
Organic matter
Oxygen + rubber powder
Oxygen fluorides (eg, dioxygen difluoride, dioxygen trifluoride)
Silica gel
Stibine
Tetrafluorohydrazine
Tetramethylammonium hydroxide
Trifluoroethylene
Unsaturated acetals

Ozone is incompatible with rubber and dinitrogen tetraoxide (Lewis, 1992).

Also see Explosion Hazard Section.

EVACUATION PROCEDURES

SUMMARY

Initial Isolation and Protective Action Distances (ERG, 2004)

Data presented from the Emergency Response Guidebook Table of Initial Isolation and Protective Action Distances are for use when a spill has occurred and there is no fire. If there is a fire, or if a fire is involved, evacuation information presented under FIRE - PUBLIC SAFETY EVACUATION DISTANCES should be used.
Generally, a small spill is one that involves a single, small package such as a drum containing up to approximately 200 liters, a small cylinder, or a small leak from a large package. A large spill is one that involves a spill from a large package, or multiple spills from many small packages.
Suggested distances to protect from vapors of toxic-by-inhalation and/or water-reactive materials during the first 30 minutes following the spill.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 100 meters (330 feet) in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions.
Keep unauthorized personnel away.
Stay upwind.
Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks).
Keep out of low areas.
Ventilate closed spaces before entering.

AIHA ERPG Values for CAS10028-15-6 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS10028-15-6 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Ozone
TEEL-0 (units = ppm): 0.1
TEEL-1 (units = ppm): 0.15
TEEL-2 (units = ppm): 1
TEEL-3 (units = ppm): 5
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS10028-15-6 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS10028-15-6 (National Institute for Occupational Safety and Health, 2007):

IDLH: 5 ppm
Note(s): Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)
- Fully encapsulating, vapor protective clothing should be worn for spills and leaks with no fire.
- Do not touch or walk through spilled material.
- Stop leak if you can do it without risk.
- If possible, turn leaking containers so that gas escapes rather than liquid.
- Prevent entry into waterways, sewers, basements or confined areas.
- Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to conact spilled material.
- Do not direct water at spill or source of leak.
- Isolate area until gas has dispersed.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 123 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

WASTE TREATMENT OPTIONS

CHEMICAL TREATMENT

CATALYTIC DECOMPOSITION: The catalytic decomposition of ozone was studied over an alpha-Fe2O3 catalyst between 23 and 65 degrees C. IR-spectroscopy was used to show that water vapor had no effect on the catalytic process, while the nitrogen oxide formed in the ozone generator caused a significant deactivation of the catalyst (Mehandjiev & Naidenov, 1992).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Ozone is formed in urban air by photochemical reactions between hydrocarbons and nitrogen oxides. It is a major photochemical air pollutant formed from emissions from cars, trucks, and other mobile sources of fossil fuel use (HSDB , 1996).

In urban photochemical smog, levels can reach 0.5 ppm, which is higher than the ACGIH-TLV and OSHA PEL (WHO, 1979).

Increased ozone (greater than 120 ppb) was accompanied by moderately high SO2 and NOx concentrations (10 to 20 ppb) over Lake Michigan. Emissions from urban regions near the southern and southwestern shores of Lake Michigan contributed to the increased ozone concentrations (Luria et al, 1992).

Levels of ozone and carbon monoxide provide estimates of anthropogenic sources of ozone. Anthropogenically derived ozone was greater than ozone from natural sources for three surface sites on the Atlantic coast of Canada (Parrish et al, 1993).

Freshly laid carpets emit several volatile organic compounds (VOC). Ozone addition to the air reduced the amount of certain VOC (eg, 4-phenylcyclohexane, 4-vinylcyclohexane, and styrene). The concentration of other compounds were found to increase (eg, formaldehyde, acetaldehyde, and aldehydes with between 5 and 10 carbons. This result suggests a reaction between the ozone and the higher weight compounds in carpets (Weschler et al, 1992).

ENVIRONMENTAL FATE AND KINETICS

Ozone has a half-life in ambient atmosphere of approximately 12 hours (Freeman, 1989).

WATER

SURFACE WATER
- Ozone has a half-life of 20 to 30 minutes in distilled water at 20 degrees C (Freeman, 1989).

SOIL

TERRESTRIAL
- The upper canopy of a Canadian deciduous forest in an acid rain area had a much higher ozone deposition rate than the lower canopy zones. Substantial ozone deposition occurred while the forest canopy was wet. The deposition rate was measured during daytime and nighttime hours. This observation was contrary to the assumptions used in most current deposition models (Fuentes et al, 1992).

ABIOTIC DEGRADATION

Photochemical reactions of atmospheric pollutants produce ozone. Moisture influences ozone deposition. Ozone's half-life in the ambient atmosphere is approximately a half a day. It causes toxic effects on several species of grass and clover, as well as a variety of tree species (Fredericksen et al, 1996; Fuentes et al, 1992; HSDB , 1996; Mohren et al, 1992; Mortensen, 1992; Retzlaff et al, 1992; Vollenweider et al, 2003).

ENVIRONMENTAL TOXICITY

GRASS, CLOVER: Visible ozone damage was observed in several species of grass and clover exposed to ozone at 55 nmols per mole in greenhouse conditions for 5 weeks. No injury was observed below 25 nmols per mole (Mortensen, 1992).

TOBACCO PLANTS: beta-1,3-Glucanase and chitinase were induced in ozone sensitive and tolerant tobacco cultivars by a pulse of ozone (0.15 mcL/L, 5 hours). The results show that near-ambient ozone concentrations can induce pathogenesis-related proteins and alter the disposition of plants toward pathogen attack. (Schraudner et al, 1992).

DOUGLAS FIR: Ozone may have significant effects on photosynthesis and respiration in stands with a low leaf area index (Mohren et al, 1992).

PLUM TREES: Casselman plums were exposed to varying partial pressures of ozone under experimental conditions for two years (Retzlaff et al, 1992).

The net leaf CO2 assimilation rate, the trunk cross sectional area growth and the fruit count per tree decreased when the partial pressure increased (Retzlaff et al, 1992)
Decrease in leaf gas exchange and loss of leaf surface area also contributed to decreases in trunk cross sectional area growth (Retzlaff et al, 1992)

BLACK CHERRY TREES IN PENNSYLVANIA

Ozone concentrations and visible foliar injury were measured in a forest in north-central Pennsylvania to determine the relationship between ozone uptake and visible symptoms (Fredericksen et al, 1996).

Visible leaf area injury was greatest for seedlings (46%), followed by canopy trees (20%), and saplings (15%) (Fredericksen et al, 1996).
Seedlings were more sensitive to ozone uptake due to the increased rate of stomatal conductance (Fredericksen et al, 1996).

BLACK CHERRY TREES IN MASSACHUSETTS

Ozone toxicity is a probable factor in low growth rates of ozone symptomatic black cherry trees in Massachusetts (Vollenweider et al, 2003).
Differences in stem growth rates over a 30-year period between symptomatic and asymptomatic mature black cherries in natural ecosystems were significant. Additional independent testing found that the significant differences were between growth rates and crown stippling (Vollenweider et al, 2003).

Ozone levels were positively correlated with elevation. Black cherry plot level ozone injury and the likelihood of observing injury on a plot were also positively correlated with elevation (Vollenweider et al, 2003).
Black cherry stands on better growth areas had more ozone symptom expression. These areas were at higher elevation on finely textured soil with relatively high available water capacity (Vollenweider et al, 2003).
Site factors significantly changed ozone symptom expression. Symptoms were more common on moister, cooler, western and more elevated sites, which lend toward better growing black cherry stands. Moisture availability in the soil is a key factor in whether injury symptoms are displayed and the severity of the symptoms (Vollenweider et al, 2003).
Ozone exposure to natural tree stands could be an additional environmental restriction to growth, and affect tree stability over time. In combination with other stresses, physiological aging could accelerate (Vollenweider et al, 2003).

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

48.00

DESCRIPTION/PHYSICAL STATE

Ozone is a bluish gas with a slightly pungent odor, which may be detected at the 0.05-0.3 ppm level (Beard, 1982).

bluish gas or blue liquid (Budavari, 1989)

colorless to bluish gas, dark blue liquid, or blue-black crystals (EPA, 1985)

between -111.9 degrees C (-169.6 degrees F) and -192.7 degrees C (-314 degrees F), ozone is a dark blue liquid (EPA, 1985)

below -192.7 degrees C (-314 degrees F), ozone exists as blue-black crystals (EPA, 1985)

pleasant, characteristic odor in concentrations of less than 2 ppm (Budavari, 1989)

Concentrations of 1 ppm produce a disagreeable sulfur-like odor (Lewis, 1992).

DENSITY

STANDARD TEMPERATURE AND PRESSURE

(0 degrees C; 32 degrees F and 760 mmHg)
GAS: 2.144 g/L (HSDB, 2005; Budavari, 1989)

OTHER TEMPERATURE AND/OR PRESSURE

LIQUID: 1.614 g/mL (at -195.4 degrees C) (HSDB, 2005; Budavari, 1989)

FREEZING/MELTING POINT

MELTING POINT

-192.7 degrees C +/- 2 degrees C (HSDB, 2005)
-193 degrees C (Budavari, 1989)

BOILING POINT

-111.9 degrees C (HSDB, 2005; Budavari, 1989)

SOLUBILITY

IN WATER

0.49 mL/100 mL (at 0 degrees C) (Beard, 1982)
Ozone is more soluble in water than oxygen (Lewis, 1993).

IN ORGANIC SOLVENTS

soluble in alkaline solvents (HSDB , 1996)
soluble in oils (HSDB , 1996)

HENRY'S CONSTANT

3.9x10(3) atm-m(3)/mol (at 20 degrees C) (Corbitt, 1990)

-REFERENCES

GENERAL BIBLIOGRAPHY

40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.

40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.

49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.

49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.

62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.

65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.

66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.

67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.

68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.

69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.

ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.

AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.

Amdur MO, Ugro V, & Underhill DW: Respiratory response of guinea pigs to ozone alone and with sulfur dioxide. Am Ind Hyg Assoc J 1978; 39:958-961.

American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.

Anon: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1975.

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Bates DV: Ozone -- myth and reality. Environ Res 1989; 50:230-237.

Beard RR: Ozone, O3, in: Clayton GD & Clayton FE (Eds), Patty's Industrial Hygiene and Toxicology, Vol 2C, Toxicology, 3rd ed, Wiley Interscience Publications, New York, NY, 1982.

Bedi JF, Drechsler-Parks DM, & Horvath SM: Duration of increased pulmonary function sensitivity to an initial ozone exposure. Am Ind Hyg Assoc J 1985; 46:731-734.

Beltran FJ, Encinar JM, & Garciaaraya JF: Kinetic study of the ozonation of some industrial wastewaters. Ozone - Sci Engineer 1992; 14:303-327.

Bignami G, Musi B, & Dell'Omo G: Limited effects of ozone exposure during pregnancy on physical and neurobehavioral development of CD-1 mice. Toxicol Appl Pharmacol 1994; 129:264-271.

Boorman GA, Sills RC, & Grumbein S: Long-term toxicity studies of ozone in F344/N rats and B6C3F1 mice. Toxicol Lett 1995; 82-83:301-306.

Borek C, Ong A, & Cleaver J: DNA damage from ozone and radiation in human epithelial cells. Toxicol Ind Health 1988; 4:547-553.

Bretherick L: Bretherick's Handbook of Reactive Chemical Hazards, 4th ed, Butterworths, London, England, 1990.

Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.

Buckley RD, Hackney JD, & Clark: Ozone and human blood. Arch Environ Health 1975; 30:40-43.

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Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents