Ozone toxicity

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 

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Mustafa, M.G. (1990). Biochemical basis of ozone toxicity. Free Radic. Biol. Med. 9, 245-265. 

This chapter first reviews and discusses selected research on local dose aspects of ozone toxicity, the morphology of the respiratoty tract and mucus layer, air and mucus flow, and the gas, liquid, and tissue components of mathematical models. Next, it discusses the approaches and results of the few models that exist. A similar review was recently done to defme an analytic framework for collating experiments on the effects of sulfur oxides on the lung. Pollutant gas concentrations are generally stated in parts per million in this chapter, because experimental uptake studies are generally quoted only to illustrate behavior predicted by theoretical models. Chapter 5 contains a detailed discussion of the conversion from one set of units to another. 

In a study of the mechanism whereby BordeteUa pertussis vaccine increased acute ozone toxicity in rats, Thompson ascribed the effects to /3-adrenergic blockade, and not to an immune-mediated response. It was further noted that both atropine and reserpine reduced mortality, whidi suggested that the acute lethal effects of ozone were due to shock and circulatory collapse, rather than pulmonary edema. 

The idea that Ozone toxicity is expressed through the formation of reactive free-radical intermediates was originally derived from studies that noted the similarity of the effects of ozone to those of radiation. Earlier studies... 

All these rapidly reacting intermediates are potentially harmful to the cell and might play a role in ozone toxicity. Furthermore, the potential for ozone-induced free-radical chain reactions exists. It appears likely that more than one radical is formed, either directly from ozone or as a result of the interaction of ozone with normal cellular constituents. 

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. ... 

The possibility that pulmonary membranes are a primary site of ozone toxicity is suggested by a number of lines of evidence, most of which are indirect. These include observations that the membrane is the major site of ozone toxicity in plants and bacteria morphologic evidence of pulmonary membrane damage after ozone exposure in a number of studies and in vitro experiments with human red cells and artificial lipid membranes. 

The supposition that ozone is mutagenic or carcinogenic in man is based primarily on information on the biochemical mechanism of ozone toxicity and to a lesser extent on in vitro and animal studies. The biochemical evidence is for the most part indirect and depends on an analogy between the free-radical nature of ozone toxicity and of radiation and other carcinogenic agents. 

The biochemical mechanism of ozone toxicity appears to have many similarities with those of other agents, particularly ionizing radiation, that ate known human carcinogens. 

Alpert, S. M., and T. R. Lewis. Unilateral pulmonary function study of ozone toxicity in rabbits. Arch. Environ. Health 23 451-458, 1971. 

Goldstein, B. D., M. R. Levine, R. Cuzzi-Spada, R. Cardenas, R. D. Buckley, and O. J. Balchum. p-Aminobenzok acid as a protective agent in ozone toxicity. Arch. Environ. Health 24 243-247, 1972. 

Pagnotto, L. D., and S. S. Epstein. Protection by antioxidants against ozone toxicity in mice. Experientia 25 703, 1%9. 

Stokinger, H. E., and L. D. Scheel. Ozone toxicity. Immunochemical and tder-ance-producing aspects. Arch. Environ. Health 4 327-334, 1962. 

Although it is widely believed that the effects of ozone on cell permeability are the basis of ozone toxicity,the chemical basis of the effects on membranes is still arguable. It is still not clear whether the first effect of ozone is on the protein or lipid components of the cell. 

Brerman, E., and I. A. Leone. Suppression of ozone toxicity symptoms in virus-infected tobacco. Phytopathology 59 263-264, 1%9. 

Hibben, C. R. Ozone toxicity to sugar maple. Phytopathology 59 1423-1428, 1%9. 

Leone, I. A., and E. Brennan. Ozone toxicity in tomato as modified by phosphorus nutrition. Phytopathology 60 1521-1524, 1970. 

When the fleck is examined closely, the lesion can be associated with contiguous stomata in the upper surface. Often, the first visible symptom of ozone toxicity is the death of the palisade parenchyma cells that line the cavities directly beneath the upper stomata. In the case of beans (Phaseolus vulgaris L.) or tobacco (Nicotiana tabacum L.) and perhaps other plants, the upper stomata lie in patterns of arcs or circles, while the lower stomata are scattered randomly and regularly across the epidermis. 

Negative Role of Nitrogen Oxides in Ozone Toxicity. There is an erroneous impression, unfortunately widespread, gained from the misinterpretation of certain studies 16, 17) that the contamination of ozone with oxides of nitrogen has been partly responsible for the observed toxicity and that ozone is not nearly so toxic as it has been thought to be ). There are at least two reasons for this misimpression. 

Interesting as the foregoing findings are, they scarcely compare in significance with the following two aspects of ozone toxicity effects of physical stress, and the marked tolerance acquired in animals following shortly after brief exposures to noninjurious levels of ozone. 

Table VII. Increase of Ozone Toxicity from Superimposed Exercise...

Perhaps the most striking and unusual feature of ozone toxicity is the marked tolerance to multilethal doses of ozone that develops in rodents after brief exposures to ozone. Increased tolerance to ozone was first observed in rats that had been previously exposed for many days to 1 p.p.m. of ozone and then challenged in the rotating... 

A physical burden during the exposure increases remarkably the sensitivity to ozone. Considerable tolerance may be developed. Nitrogen oxides do not affect the ozone toxicity. 

Ozone is known to reduce plant yield and its toxicity is largely due to its oxidising potential. Upon dissolving in water, activated oxygen species such as hydrogen peroxide and the superoxide and hydroxyl radicals are formed (3). It is predominantly through these reactive intermediates that ozone toxicity is thought to be expressed. 

Recovery after severe acute ozone toxicity is slow. Up to 10 tol4 days of hospitalization may be required. Minimal residual symptoms may be present for up to 9 months, but the victim should completely recover. 

Besides the skin, gut, and BBB, there are other coculture models exhibiting crosstalk between the cocultured cell types that were developed for measuring toxicity. For example, an epitheHal/fibroblast [Lang et al., 1998] coculture model of the bronchial epithelial was used to examine ozone toxicity. Bone resorption caused by PasteureUa multocida toxin was studied in an osteoclast/osteoblast direct contact coculture model [MuUan and Lax, 1998]. Brana et al. [1999] cultured 400-/um thick rat brain (hippocampal) slices on a membrane insert and cultured the murine macrophage cell line (RAW 264.7) underneath. When challenged with the HIV-1 derived Tat protein, neuronal cell death in the brain slice occurred only when cocultured with the macrophage cell line. This model could be used to identify neurotoxic soluble molecules released by macrophages. 

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