Inhalation of ozone

Inhalation of ozone should be avoided. A threshold limit value of 0.1 p.p.m. of ozone in air has been adopted by the American Conference of Governmental Industrial Hygienists. This represents the concentration of ozone in air considered safe for an... 

Intermittent Exposures. In an effort to discover means of reducing the unfavorable responses to ozone, the effect of intermittent exposure to ozone was investigated. Adult male white mice were subjected to inhalation of ozone at 4 p.p.m. for 30 minutes, alternated with 20-minute exposures to air. The total time of exposure to ozone was 4 hours, an exposure capable of killing at least 50% of the animals if administered without interruption for 4 hours. The results of a representative experiment (Table V) show that interrupted exposure to ozone reduces the fatal effects of ozone in mice and indicate a means of reducing the effects of this hazardous substance. 

Pendino, K., Punjabi, C. and Lavnikova, N. (1992). Inhalation of ozone stimulates nitric acid production by pulmonary and interstitial macrophages. Am. Rev. Respir. Dis. 145, A650. 

Nettesheim P, Szakal AK. 1972. The response of the lower respiratory tract of mice and hamsters to chronic inhalation of ozonized gasoline fumes A light microscopic and electron microscopical study. Ann Occup Hyg 15 263-269. 

Osebold JW, Gershwin LJ, Zee YC Studies on the enhancement of allergic lung sensitization by inhalation of ozone and sulfuric acid aerosol. J Environ Pathol Toxicol 1980 3 221-234. (NC)... 

The disinfection of water by ozone requires careful control of this gas because of its toxicity. Inhalation of ozone can be fatal. Ozone is a deep lung irritant and causes pulmonary edema, the accumulation of fluid in the lungs. Ozone is strongly irritating to the eyes and upper respiratory... 

Ozone, O3, has several toxic effects. At 1 ppm by volume in air, ozone causes severe irritation and headache and irritates the eyes, upper respiratory system, and lungs. Inhalation of ozone can sometimes cause fatal pulmonary edema (abnormal accumulation of fluid in lung tissue). Ozone generates free radicals in tissue that can cause lipid peroxidation, oxidation of sulfhydryl (-SH) groups, and other destructive oxidation processes. 

Hatch, G.E., Slade, R, Crissman, K., Norwood, J. and Koren, H. (1989). Vitamin E concentrations in bronchoalveolat lavage fluid of humans, rats and guinea-pigs effect of ozone inhalation. Am. Rev. Resp. Dis. 140, A279. 

Matsumura, Y., et al., The effects of ozone, nitrogen dioxide, and sulfur dioxide on experimentally induced allergic respiratory disorder in guinea pigs. IV. Effects on respiratory sensitivity to inhaled acetylcholine, Am. Rev. Respir. Dis. 105, 2, 262, 1972. 

Schelegle, E.S., et al., Repeated episodes of ozone inhalation amplifies the effects of allergen sensitization and inhalation on airway immune and structural development in Rhesus monkeys, Toxicol. Appl. Pharmacol., 191, 74, 2003. 

Hatch, G.E., Slade, R., Stead, A.G., and Graham, J.A. 1986. Species comparison of acute inhalation toxicity of ozone and phosgene. J. Toxicol. Environmental Health 19 43—53. 

The use of ozonizers for deodorizing indoor air has been discussed and evaluated with respect to potential health hazards. In a normal 40-m room, an ozone concentration of 0.1 ppm is established after 3.5 h of operation of one of these devices. Evidence on health effects was cited to support the conclusion that inhalation of the quantities of ozone produced by these air conditioners should be avoided and that certainly no beneficial effects should be attributed to ozone inhalation. 

The sites of action and effects of ozone and other photochemical oxidants are described in Chapters 8 and 9. Recent work with primates has suggested that ozone is absorbed along the entire respiratory tract, penetrates more into the peripheral nonciliated airways, and causes more lesions in the respiratory bronchioles and alveolar ducts as the inhaled ozone concentration increases from 0.2 to 0.8 ppm. The most common and most severe tissue damage was observed in the respiratory bronchioles. The ciliated cells in the terminal bronchioles and the Type 1 cells in the epithelial layer of the proximal alveoli of rats were the... 

Frank in dogs. The most likely explanation is that the model does not account for chemical reactions of ozone in the mucus and epithelial tissue. Another problem is that the nose is believed to behave more like a scrubbing tower with fresh liquid at each level, inasmuch as the blood supply is not continuous for the entire length of the nose, as assumed in the model. Neglecting the surface area, volume, flow, and thickness of the mucus layer in the nose will probably also give erroneous results for soluble gases with a small diffusion coefficient in mucus and for singlebreath inhalations of a low concentration of any gas. 

Potentiation of the action of acetylcholine, another bronchoconstrictive agent implicated as a mediator in asthma, has also been reported in guinea pigs exposed to ozone at at least 2 ppm for 30 min before inhalation of acetylcholine the effect was observed intermittently for up to 23 h after ozone exposure. 

Further indirect evidence of a role of lipid peroxidation in ozone toxicity has been obtained in studies in which animals deficient in vitamin E were found to be more susceptible to lethal concentrations of ozone and sublethal concentrations led to a more rapid utilization of this antioxidant vitamin. Although vitamin E deficiency potentiates the effects of ozone, it is not completely clear whether supranormal concentrations of vitamin E protect against ozone toxicity. Mice given tocopherol supplements were not protected against lethal concentrations of ozone, and the specific activity of lung hydrolases was found to be unrelated to dietary vitamin E concentration. However, other investigators have reported that additional supplementation with vitamin E above usual dietary concentrations lessens the extent of toxicity in animals that inhale ozone. ... 

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