Review Article
Biochemical basis of ozone toxicity

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Abstract

Ozone (O3) is the major oxidant of photochemical smog. Its biological effect is attributed to its stability to cause oxidation or peroxidation of biomolecules directly and/or via free radical reactions. A sequence of events may included lipid peroxidation and loss of functional groups of enzymes, alteration of membrane permeability, and cell injury or death. An acute exposure to O3 causes lung injury involving the ciliated cell in the airways and the type 1 epithelial cells in the alveolar region. The effects are particularly localized at the junction of terminal bronchioles and alveolar ducts, as evident from a loss of cells and accumulation of inflammatory cells. In a typical short-term exposure the lung tissue response is biphasic: an initial injury-phase characterized by cell damage and loss of enzyme activities, followed by a repair-phase associated with increased metabolic activities, which coincide with a proliferation of metabolically active cells, for example, the alveolar type 2 cells and the bronchiolar Clara cells. A chronic exposure to O3 can cause or exacerbate lung diseases, including perhaps an increased lung tumor incidence in susceptible animal models. Ozone exposure also causes extrapulmonary effect involving the blood, spleen, central nervous system, and other organs. A combination of O3 and NO2, both of which occur in photochemical smog, can produce effects which may be additive or synergistic. A synergistic lung injury occurs possibly due to a formation of more powerful radicals and chemical intermediates. Dietary antioxidants, for example, vitamin E, vitamin C, and selenium, can offer a protection against O3 effects.

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      Air pollution on the near earth's surface is a major concern due to the hazardous toxic air pollutants [1]. Ozone (O3), a colorless harmful gas for living life which generally forms in association with other oxidant components such as hydrogen peroxide, nitrogen dioxide (NO2), formaldehyde and formic acid, nitrous and nitric acids, peroxyacyl nitrates (PAN), so on [2]. It has a strong oxidizing ability which is detrimental to human health, plants, and animals [3].

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    Mohammad G. Mustafa (b. 1940, Bangladesh; Ph.D., 1969 in Biochemistry), is Professor of Environmental Health Sciences, University of California, Los Angeles (UCLA). He worked with the Pulmonary (Air Pollution) Research Group at the U.C. Davis until his move to UCLA in 1975. His current researches focus on pulmonary effects of oxidant air pollutants (ozone, NO2) and other areas of inhalation toxicology.

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