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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 OZONE BACKGROUND INFORMATION PHYSICAL AND CHEMICAL PROPERTIES Structural formula: O3 Molecular weight: 48.0 CAS number: 10028–15–6 Boiling point: −111.9°C Density as a gas: 2.144 g/L at 0°C Density as a liquid: 1.514 g/ml at −195. 4°C General characteristics: A polymeric, highly reactive form of oxygen. It is a bluish explosive gas or blue liquid. It is a powerful oxidizing agent with deodorant and antiseptic properties. It is a respiratory, ocular, and nasal irritant with a characteristic odor. Conversion factors: ppm=0.5 (mg/m3) mg/m3=2.0 (ppm) OCCURRENCE AND USE Ozone is used in organic synthesis and for bleaching waxes, textiles, and oils. It is produced by the action of ultraviolet radiation in sunlight on oxygen. It can be prepared in the laboratory by passing dry air between two plate electrodes connected to an alternating current of several thousand volts. Airplanes flying at high altitudes may contain ozone at up to 0.5 ppm in the cabin (ACGIH, 1979; Windholz et al., 1976). Ozone in submarine atmospheres is in the parts-per-billion range (NRC, 1974). Possible ozone contaminants include oxides of nitrogen, hydrogen peroxide, and free radicals (HO2, OH, HO3, O4) (Svirbely and Saltzman, 1957). SUMMARY OF TOXICITY INFORMATION EFFECTS ON HUMANS Healthy men have been exposed deliberately to ozone at up to 0.75 ppm for 2 h (Bates et al., 1972; Folinsbee et al., 1975; Hazucha, 1974; Hazucha et al., 1973). Light exercise was also taken at this concentration. A reduction in ventilatory capacity (25% reduction in forced expiratory volume) was reported. Chamber exposures have since shown that a critical ozone concentration for a ventilatory response is probably around 0.3–0.5 ppm (Kleinman et al., 1981). Exposure of male volunteers at 0.4 ppm for 4 h combined with exercise (700 kg-m per minute) caused significant changes in forced vital capacity (FVC), maximal midexpiratory flow (MMF), and airway resistance (Hackney et al., 1975a). Some subjects with hyperreactive airways have responded to ozone at concentrations as low as 0.37 ppm. Most studies have failed to show any effect at 0.25 ppm. There is also a suggestion in the literature that effects may be greater on the
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 second day of exposure (Hackney et al., 1975b). A group of young male volunteers were exposed at 0.5 ppm for 2 h. There were only minimal effects on the first day. However, when the exposure was repeated on the next day, 5 of 7 subjects showed significant effects. Twenty subjects were exposed to ozone at 0.5 ppm for 6 h (Kerr et al., 1975). Medium exercise on a bicycle ergometer (100 W at 60 rpm) was used. The subjects experienced dry cough and chest discomfort after exposure. Chest discomfort ranged from tightness on full inspiration to generalized chest pain that was accentuated by exercise, cough, and irritation of the nose and throat. Significant changes from control values were reported for several lung-function tests (specific airway conductance, pulmonary resistance, FVC, and forced expiratory volume in 3 s). There has been some suggestion that ozone at low concentrations may be carcinogenic or mutagenic in man. Chromosomal abnormalities have been produced in plants and animals, sometimes after low ozone exposures (0.2 ppm for 5 h) (Zelac et al., 1971). Minor chromosomal abnormalities have also been observed in the circulating lymphocytes of humans who have been exposed experimentally at 0.5 ppm for 6–10 h (Merz et al., 1975). So far, however, there is no convincing evidence that ozone at low concentrations causes cancer or congenital malformations in man. EFFECTS ON ANIMALS Mittler et al. (1956) reported LC50s for 3-h exposures to ozone as follows: Mice: 21 ppm Rats: 21.8 ppm Cats: 34.5 ppm Rabbits: 36 ppm Guinea pigs: 51.7 ppm Svirbely and Saltzman (1957) reported LC50s for 4-h exposures as follows: Mice: 2.1–9.9 ppm Rats: 7.2–12.3 ppm Hamsters: 15.8 ppm Diggle and Gage (1955) investigated toxicity in rats and mice after 4-h exposures to ozone and concluded that the LC50 was around 10–12 ppm. Generally, lethal exposures to ozone are accompanied by dyspnea and lethargy, and autopsy reveals lung edema. Eye effects of ozone exposure were studied in rabbits by Mettier et al. (1960) and Hine et al. (1960). Exposure of rabbits for 1.9–2.8 ppm for 4 h produced no ocular effects, and exposure at 2 ppm 4 h/d was also without eye effects. Morphologic changes have been reported in the respiratory tracts of animals as a result of exposure to ozone at 0.2–0.25 ppm. Cats were exposed at 0.25, 0.5, and 1.0 ppm for 4.7–6.6 h (Boatman et al., 1974). At all three concentrations, there was considerable
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 desquamation of the ciliated airway lining cells, the degree of damage being roughly proportional to the ozone concentration. Cytoplasmic vacuolization of ciliated cells and condensation of mitochondria were the most consistent morphologic changes. The mitrochondrial alterations were seen after exposure at all concentrations and were most frequent in the medium-sized airways, 0.8–1.7 mm in diameter. In rats exposed at 0.2 ppm for 3 h (Stephens et al., 1974), degenerative changes were observed in Type I cells, which were replaced by Type II cells. Morphologic changes have also been reported by Mellick et al. (1977) in rhesus monkeys after exposure at 0.5 ppm for 8 h; similar but milder changes were observed in Bonnet monkeys after exposure at 0.2 ppm. Enzyme alterations have been reported in the respiratory tracts of various animals at about these concentrations. Increased activity of lung glutathione peroxidase and glutathione reductase and increased succinate-dependent lung mitochondrial oxygen consumption have been reported in rats exposed continuously for a week at 0.2 (Chow et al., 1974; Mustafa et al., 1975). Decreases in lysozyme, acid phosphatase, and ß-glucuronidase activity in alveolar macrophages (which appear to be related to dose up to 1 ppm) have been observed in rabbits exposed at 0.25–0.5 ppm ozone for 3 h (Hurst et al., 1970). Decreased red cell acetylcholinesterase and increased osmotic fragility have also been reported in man after exposure at 0.37–0.5 ppm for 2 h (Hackney et al., 1975b) Whether the increased fragility is due to the enzyme alterations or to the spherocytosis that may also occur at this concentration seems debatable. An increased susceptibility to pulmonary streptococcal infection has been shown to result from exposure to ozone at as low as 0.08 ppm for 3 h (Coffin and Blommer, 1970). This could be due in part to impairment of the bactericidal capabilities of the macrophage, which appears to occur as a result of exposures at about 0.3 ppm. EPIDEMIOLOGIC STUDIES Attempts have been made to relate mortality (California Dept. of Public Health, 1955, 1956, 1957) and morbidity (Brant and Hill, 1964; Wayne and Wehrle, 1969) to daily concentrations of oxidant in California. Mortality was at first thought to be related to oxidant concentration; but more refined analyses have shown that the increased temperatures with which the oxidant is positively correlated probably accounts for any association. Morbidity, as indicated by hospital admissions, has not been convincingly shown to be correlated with oxidant concentration. Attempts to correlate oxidant exposure with influenza or other respiratory infections have not been successful. There is some evidence that some asthmatics may have attacks when peak concentrations of oxidant reach 0.25 ppm (Renzetti, 1955), with maximal hourly concentrations of 0.05 or 0.06 ppm. A study that carried considerable weight in reaching the initial ozone ambient air quality standard of 0.08 ppm was based on the performance of cross-country runners in California (Wayne et al., 1967). A significant relationship was observed between the oxidant concentrations during and 1–3 h before the race and the percentage of runners whose performance decreased compared with that in the previous
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 home meet. Deterioration began at concentrations around 0.03 ppm—appreciably lower than the national standard. A threshold concentration of 0.012 ppm was later suggested. This study is very hard to interpret. The validity of the suggested threshold is highly questionable, and the conclusion that the deterioration in performance was due to the oxidant concentrations is debatable. All in all, the study seems most unsuitable for standard-setting. INHALATION EXPOSURE LIMITS According to ACGIH (1979), the TLV-TWA for ozone is 0.1 ppm and the TLV-STEL is 0.3 ppm. The TLV-TWA for ozone was revised downward from an original recommendation of 1 ppm. ACGIH stated that a TLV-TWA of 0.1 ppm “represents a limit which, although it results in no ostensible injury, may result in premature aging in a manner similar to that from continued exposure to ionizing radiation, if exposure is sufficiently prolonged.” OSHA (1982) has established the Federal Standard for ozone in the work environment at 0.1 ppm. On the basis of a review of air quality criteria for photochemical oxidants, (U.S. Dept. of HEW, 1970) a 1-h National Primary Ambient Air Quality Standard for ozone was set at 0.08 ppm in 1971. This was revised in 1979 to 0.12 ppm (EPA, 1979). A panel of the NRC Committee on Medical and Biologic Effects of Environmental Pollutants revised the 0.08-ppm standard for the U.S. Senate Committee on Public Works (NRC, 1977). The panel summarized its assessment of the health risk from 0.08 ppm as follows: (1) There are risks that may not be negligible, and (2) they are not dangerously high. COMMITTEE RECOMMENDATIONS EXPOSURE LIMITS The ACGIH TLV-TWA differs from the EELs and CEL for ozone previously suggested by the Committee in 1966, which were 1.0 ppm for 1 h, 0.1 ppm for 24 h, and 0.02 ppm for 90 d. Specifically, 1.0 ppm for 1 h is much less restrictive than the ACGIH TLV-STEL of 0.1 ppm for 15 min. However, 0.1 ppm for 24 h is more stringent than the ACGIH TLV-TWA of 0.1 ppm for a 40-h workweek, except that the working shifts are interspersed with periods of lower (i.e., nonworking background) exposure. It seems unlikely that rare exposure at the present EEL of 1.0 ppm for 1 h will result in serious effects. This is not much higher than the 0.75 ppm at which human volunteers have been exposed in a number of chamber experiments. As far as the Committee has been able to learn, no one has been deliberately exposed to ozone at 0.1 ppm for 24 h. The nearest approach was a study in which two groups of 6 males were exposed at 0.2 and 0.5 ppm 3 h/d, 6 d/wk, for 12 wk (Bennett, 1962). No change in vital capacity or forced expiratory volume and no increase in upper respiratory infections per person, compared with controls, were
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 observed at 0.2 ppm. At 0.5 ppm, there were reversible signs of irritation of terminal bronchi and bronchioles (Bennett, 1962). Comparison of Seventh Day Adventists living in San Diego (daily maximal hourly average oxidant concentration, 0.07 ppm) with those living in the San Gabriel Valley (comparable concentration, 0.14 ppm) showed no differences in the prevalence of respiratory disease symptoms and chronic bronchitis or in lung function. These data suggest that the current 24-h EEL of 0.1 ppm is adequate. The 90-d CEL for ozone of 0.02 ppm does not appear to pose a hazard. Airborne concentrations in a number of cities are above this, and the background concentration of ozone in surface air at sea level is reported to be about 0.01–0.03 ppm (NRC, 1977). Given the fact that the CEL for ozone is in the range of ambient background concentrations, there was consideration to raising the 90-d exposure limit. However, because of the limited data on continuous exposure to ozone, the Committee believes that it would not now be prudent to suggest changes. When additional data on the effects of long-term continuous exposure to ozone at low airborne concentrations become available, the CEL should again be reviewed. In summary, the Committee does not recommend a change in the previously established EELs and CEL for ozone: 1-h EEL: 1 ppm 24-h EEL: 0.1 ppm 90-d CEL: 0.02 ppm
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 REFERENCES American Conference of Governmental Industrial Hygienists. 1979. Threshold Limit Values for Chemical Substances and Physical Agents in the Workroom Environment with Intended Changes for 1979. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. [94 p.] Bates, D.V., Bell, G.M., Burnham, C.D., Hazucha, M., Mantha, J., Pengelly, L.D., and Silverman, F. 1972. Short-term effects of ozone on the lung. J. Appl. Physiol. 32:176–181. Bennett, G. 1962. Ozone contamination of high altitute aircraft cabins. Aerosp. Med. 33:969–973. Boatman, E.S., Sato, S., and Frank, R. 1974. Acute effects of ozone on cat lungs. II. Structural. Am. Rev. Respir. Dis. 110:157–169. Brant, J.W.A., and Hill, S.R.G. 1964. Human respiratory diseases and atmospheric air pollution in Los Angeles, California. Int. J. Air Water Pollut. 8:259–277. California Department of Public Health. 1955. Clean Air for California. Initial Report of the Air Pollution Study Project. San Francisco: California Department of Public Health. [60 p.] California Department of Public Health. 1956. Clean Air for California. Second Report of the California Department of Public Health. Berkeley: California Department of Public Health, March 1956. [23 p.] California Department of Public Health. 1957. Report III…A Progress Report of the California Department of Public Health. Berkeley: California Department of Public Health, Feb., 1957. [32 p.] Chow, C.K., Dillard, C.J., and Tappel, A.L. 1974. Glutathione peroxidase system and lysozyme in rats exposed to ozone or nitrogen dioxide. Environ. Res. 7:311–319. Coffin, D.L., and Blommer, E.J. 1970. Alteration of the pathogenic role of streptococci group C in mice conferred by previous exposure to ozone. In I.H.Silver, ed. Aerobiology: Proceedings of the Third International Symposium held at the University of Sussex, England, 1969. New York: Academic Press, p. 54–61. Diggle, W.M., and Gage, J.C. 1955. The toxicity of ozone in the presence of oxides of nitrogen. Br. J. Ind. Med. 12:60–64. Environmental Protection Agency. 1979. National Primary and Secondary Ambient Air Quality Standards. Fed. Regist. 44(28):8202–8237.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Folinsbee, L.J., Silverman, F., and Shephard, R.J. 1975. Exercise responses following ozone exposure. J. Appl. Physiol. 38:996–1001. Hackney, J.D., Linn, W.S., Buckley, R.D., Pedersen, E.E., Karuza, S.K., Law, D.C., and Fischer, A. 1975a. Experimental studies on human health effects of air pollutants. I. Design considerations. Arch. Environ. Health 30:373–378. Hackney, J.D., Linn, W.S., Law, D.C., Karuza, S.K., Greenberg, H., Buckley, R.D., and Pedersen, E.E. 1975b. Experimental studies on human health effects of air pollutants. III. Two-hour exposure to ozone alone and in combination with other pollutant gases. Arch. Environ. Health 30:385–390. Hazucha, M. 1974. Effects of Ozone and Sulfur Dioxide on Pulmonary Function in Man. Ph.D. Thesis. McGill University (Canada). [Diss. Abstr. Int. 35B:2979-B, 1974] Hazucha, M., Silverman, F., Parent, C., Field, S., and Bates, D.V. 1973. Pulmonary function in man after short-term exposure to ozone. Arch. Environ. Health 27:183–188. Hine, C.H., Hogan, M.J., McEwen, W.K., Meyers, F.H., Mettier, S.R., and Boyer, H.K. 1960. Eye irritation from air pollution. J. Air Pollut. Control Assoc. 10:17–20. Hurst, D.J., Gardner, D.E., and Coffin, D.L. 1970. Effect of ozone on acid hydrolases of the pulmonary alveolar macrophage. J. Reticuloendo. Soc. 8:288–300. Kerr, H.D., Kulle, T.J., McIlhany, M.L., and Swidersky, P. 1975. Effects of ozone on pulmonary function in normal subjects. An environmental-chamber study. Am. Rev. Respir. Dis. 111:763–773. Kleinman, M.T., Bailey, R.M., Chang, Y.-TC., Clark, K.W., Jones, M.P., Linn, W.S., and Hackney, J.D. 1981. Exposures of human volunteers to a controlled atmospheric mixture of ozone, sulfur dioxide and sulfuric acid. Am. Indust. Hyg. Assoc. J. 42:61–69. Mellick, P.W., Dungworth, D.L., Schwartz, L.W., and Tyler, W.S. 1977. Short term morphologic effects of high ambient levels of ozone on lungs of Rhesus monkeys. Lab. Invest. 36:82–90. Merz, T., Bender, M.A., Kerr, H.D., and Kulle, T.J. 1975. Observations of aberrations in chromosomes of lymphocytes from human subjects exposed to ozone at a concentration of 0.5 ppm for 6 and 10 hours. Mutat. Res. 31:299–302. Mettier, S.R., Jr., Boyer, H.K., Hine, C.H., and McEwen, W.K. 1960. A study of the effects of air pollutants on the eye. AMA Arch. Ind. Health 21:1–6. Mittler, S., Hedrick, D., King, M., and Gaynor, A. 1956. Toxicity of ozone I. Acute toxicity. Ind. Med. Surg. 25:301–306.
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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants, Volume 1 Mustafa, M.G., Macres, S.M., Tarkington, B.K., Chow, C.K., and Hussain, M.Z. 1975. Lung superoxide dismutase (SOD): Stimulation by low-level ozone exposure. Clin. Res. 23:138A [abstract] National Research Council. A Report by the Coordinating Committee on Air Quality Studies. 1974. Air Quality and Automobile Emission Control. Vol. 2. Health Effects of Air Pollutants. Washington, D.C.: Government Printing Office. [511 p.] (U.S. Senate Committee Print Serial No. 93–24) National Research Council, Committee on Medical and Biologic Effects of Environmental Pollutants. 1977. Ozone and Other Photochemical Oxidants. Washington, D.C.: National Academy of Sciences, [719 p.] Occupational Safety and Health Administation. 1982. Toxic and Hazardous Substances. 29 CFR 1910.1000. Renzetti, N.A., ed. 1955. An Aerometric Survey of the Los Angeles Basin, August-November, 1954. Air Pollution Foundation Technical Report No. 9. San Marino, Calif.: Air Pollution Foundation. [334 p.] Stephens, R.J., Sloan, M.F., Evans, M.J., and Freeman, G. 1974. Alveolar type I cell response to exposure to 0.5 ppm O3 for short periods. Exp. Mol. Pathol. 20:11–23. Svirbely, J.L., and Saltzman, B.E. 1957. Ozone toxicity and substances associated with its production. AMA Arch. Ind. Health 15:111–118. U.S. Department of Health, Education, and Welfare. 1970. Air Quality Criteria for Photochemical Oxidants. Washington, D.C.: Public Health Service, National Air Pollution Control Administration. [200 p.] (National Air Pollution Control Administration Publication No. AP 63) Wayne, W.S., and Wehrle, P.F. 1969. Oxidant air pollution and school absenteeism. Arch. Environ. Health 19:315 322. Wayne, W.S., Wehrle, P.F., and Carroll, R.E. 1967. Oxidant air pollution and athletic performance. J. Am. Med. Assoc. 199:901–904. Windholz, M., Budavari, S., Stroumtsos, L.Y., and Fertig, M.N. 1976. The Merck Index: An Encyclopedia of Chemicals and Drugs. 9th ed. Rahway, NJ: Merck and Co. Inc. p. 17. Zelac, R.E., Cromroy, H.L., Bolch, W.E., Jr., Dunavant, B.G., and Bevis, H.A. 1971. Inhaled ozone as a mutagen. I. Chromosome aberrations induced in Chinese hamster lymphocytes. Environ. Res. 4:262–282.
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