Document rekXDx7N3j61yz8xYz6eZQgv

OZONE CAS: 10028-15-6 O, CEILING LIMIT, 0.1 ppm <= 0.2 mg/m3) Ozone is a liquid or gas, depending on temperature, each appear ing bluish in color. The gas possesses a characteristic odor in con centrations of less than 2 ppm."1 Physicochemical properties include: Molecular weight: 48.00 Density of gas: 1.6 (air - 1) Melting point -193C Boiling point: -111.9C Critical temperature: - 12.1 C Ozone is a powerful oxidizing agent. The liquid and concentrated solutions explode on warming. Ozone is used as a disinfectant for air and water, for bleaching textiles, oils and waxes, and in organic syntheses."1. It is also produced in welding arcs, corona discharges, and by ultraviolet radiation. Acutely, ozone is injurious or lethal at relatively low concentra tions and at short exposure periods (white rat, LD50 in 4 hrs - 4.8 ppm).,JI The primary site of acute injury is the lung, an injury characterized by pulmonary congestion, edema, and hemorrhage. There are indications in man that there are secondary sites of reac tion to ozone characterized by a defect in the dissociation of oxy gen from oxyhemoglobin.131 Chronic exposure to ozone has been reported to result in bronchiolitis and bronchitis in animals exposed daily for six hours over a period of one year, at concentrations slightly in excess of 1.0 ppm.141 )affe`!l, in a review paper, noted that ex posure at 0.1 and 0.2 ppm seven hours a day for three weeks result ed in increased neonatal mortality in mice. On the basis of a report of Griswold et a/,'" the susceptibility of man to ozone appears to be at least equal to that of the most sus ceptible animal species (mouse and rat). Human exposure for two hours at an average concentration of 1.5 ppm ozone resulted in a 20% reduction in timed vital capacity of the lung and other effects. Kleinfeld and Giel'71 reported pulmonary congestion in welders us ing the inert-gas shielded-arc process in which the ozone concen tration reached a maximum of 9 ppm. Challen and co-workers81 found similar effects in welders from exposure somewhat under 2 ppm, which disappeared when ozone levels were reduced to around 0.2 ppm. In addition to these serious effects of ozone, air concentrations of ozone in excess of a few tenths ppm cause occasional discomfort to exposed individuals in the form of headache, and dryness of throat and mucous membranes of the nose and eyes following exposures of short duration.1911" The important points to consider in the setting of a TLV for ex posure to ozone are: 1) whether pulmonary effects are a function of dose and whether exercise potentiates the effects of exposure, 2) whether effects of chronic exposure occur at concentrations below those causing acute effects, and 3) whether workers with chronic obstructive pulmonary disease are at greater risk than workers without pulmonary disease. Dose response characteristics of human exposure to ozone at steady state exercise levels are addressed by the work of McDonnell et a/.1"' Six groups of young men, ranging in number from 20 to 29, were exposed for 2.5 hours to one of six concentrations of ozone while undergoing intermittent exercise at a level that increased pul monary minute ventilation to approximately 35 Ipm/rrr of body sur face area. (This corresponds to a moderately heavy work load.) The six ozone concentrations were 0, 0.12, 0.18, 0.24, 0.30, and 0.40 ppm. Significant decreases in forced vital capacity (FVC) and forced expiratory volume in one second (FEV,) were seen at 0.12 ppm and were successively greater at the higher ozone concentrations. Cough ing was increased at 0.12 ppm as well as at the higher concentra tions. At ozone levels of 0.3 ppm, Adams et af'2' and Folinsbee et a/"31 demonstrated that concentration is more effective in reducing pulmonary function values than is increased minute ventilation or duration of exposure. The effect of exercise was demonstrated at ozone levels of 0.3 ppm in an animal model by Mautz et a/."41 Rats were exposed to 0.2 ppm under conditions of rest and treadmill exercise up to 30 Ipm at 20% grade. The abundance and severity of focal lung parenchymal lesions increased as exercise and duration of exposure were increased. At concentrations above 0.3 ppm, it was found that the concentra tion of ozone was the primary determinant of pulmonary effect, rather than the effective dose rate (estimated as concentration X minutevolume). At lower levels, the pulmonary effect was dependent on both exercise rate and concentration. The question of whether effects from chronic exposure occur at concentrations of ozone below the threshold for acute effects prob ably cannot be answered directly, but is closely related to the issue of whether a TWA exposure is applicable to ozone. Since chronic effects from exposure to ozone at levels below 1.0 ppm have not been reported, inferences from animal studies and human short-term exposure studies may be useful. Freeman et aF151 showed that dogs exposed to 1.0 ppm ozone for 16 hours had less than half as much macrophage response in their airways as dogs exposed for only 8 hours to 2 ppm, even though the time-weighted average exposure was the same in both experiments. Similarly, dogs exposed to 1.0 ppm for 24 hours had about half of the response of dogs exposed for 8 hours to 3 ppm. Dungworth et a/1161 studied effects of ozone concentrations ranging from 0.2 to 0.8 ppm on rhesus and bonnet monkeys exposed 8 hours per day for 7 days. Histological examina tion of conducting airways of the bonnet monkeys revealed the lu minal surfaces coated with numerous macrophages, other cellular elements, and small quantities of debris. There were both hyperpla sia and hypertrophy of bronchiolar epithelium which resulted in replacement of the usual nonciliated cuboidal and squamous cells by low columnar cells rich in organelles. The authors state that the threshold for detectable morphological effect in bonnet monkeys is below 0.2 ppm and may be close to 0.1 ppm. However, changes evoked during the first three to four days bring about a state of adap tation whereby continued exposure results in little or no additional damage. With regard to populations with obstructive pulmonary disease, Linn et at"7' measured pulmonary function and biochemical parameters in 22 asthmatic volunteers exposed for two hours to ozone concentration approximating 0.2 ppm under conditions of heat stress and intermittant exercise. There were no significant changes in FEV,, FVC, lung volume, or single breath N2 indices. Statistically significant, but very small changes in a number of biochemical meas ures, such as glucose-6-phosphate dehydrogenase and acetyl cholinesterase, were reported. Based upon the information from man and animals, it appears that exposures to ozone in the order of 0.2 ppm produce mild acute, but not cumulative effects. Thus, control of exposure should not be DO 074777 CONFTDFNTTAl 453(87) based on the concept of cumulative dose as measured by the eighthour TWA. It also appears that exposures in the order of 0.1 ppm will be well tolerated by most workers including asthmatics. Based on all of the above information, a ceiling limit of 0.1 ppm is recommended. The intent of the Committee being that this ceil ing value has the effect of establishing a 15-minute time-weighted average of 0.1 ppm. References 1. The Merck Index, 10th ed., p. 1002, Merck & Co., Inc., Rahway, New Jersey (1983). 2. Stokinger, H.E.: Arch. Ind. Health 15:181 (1957). 3. Brinkman, R. and H.B. Lamberts; Nature 181:1202 (1958). 4. Stokinger, H.E., W.D. Wagner and O.J. Dobrogorski: Arch. Ind. Health 16:514 (1957). 5. Jaffe, L.S.: Am. Ind. Hyg. Assoc. I, 28:267 (1967). 6. Griswold, S., LA. Chambers and H.L Motley. Arch. Ind. Health 15:108 (1957). 7. Kleinfeld, M. and C.P. GW: Am. I. Med. So. 231:638 (1956). 8. Chailen, P.J.R., D.E. Hickish and |. Bedford: Br. I. Ind. Med. 15:276 (1958). 9. Wilska, S.: Acta. Chem. Scand. 5:359 (1951). 10. Troche, M.R.: Arch. Mai. Profess. 12:55 (1951). 11. McDonnell, W.F., D.H. Horstman, M.J. Hazucha et al: /. Appl. Phys iol. 54:1345 0983). 12. Adams, W.C., W.M. Savin and A.E. Christo: I. Appl. Physiol. Respirat Environ. Exercise Physiol. 51:415 (1981). 13. Folinsbee, L|., B.L Drinkwater, J.F. Bedi and S.M. Horvach: Environ mental Stress: Individual Human Adaptations, pp. 111-124. Academ ic, New York (1978). 14. Mautz, W.J., T.R. McClure, P. Reischl, R.F. Phalen and T.T. Crocker: A Toxicol. Environ. Health 16:841-854 (1985). 15. Freeman, G., R.J. Stephens, D.L Coffin and J. Stara: Arch. Environ Health 26:209 (1973). 16. Dungworth, D.L, W.L Castleman, C.K. Chow et al: Fed. Proc. 34 1670 (1975). 17. Linn, W.S., R.D. Buckley, C.E, Spier et al: Am. Rev. Respir. Disease (17.835 (1978). MAC, 1 ppm, 1946-1947 TLV-TWA, 1 ppm, 1948-1953 TLV-TWA, O.t ppm, 1954-1986 TLV-STEL, 0.3 ppm, 1976-1986 TLV-CEILING, 0.1 ppm, proposed 1987 Documentation reviewed/revised, 1987 454(87) DO 07477R CONFTDFNTTAL