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Ozone versus human health – a review

Umapati Sahay*
Former Head, Dept. of Zoology, Ranchi University, Ranchi, Jharkhand
& Dean, Faculty of Science, R.U., Ranchi
Received , 10th December, 2014; Revised: 24th January, 2015

Abstract : Ozone is a triatomic form of Oxygen. Its molecular formula is O3 and is found in stratosphere. It extends from about 6 Km at poles, 17 Km at equator & 50 Km above the earth’s surface. In normal condition, it is present in the atmosphere at about 0.5 ppm at sea level, though variations from an average of 0.02 ppm in winter to about 0.07 ppm in summer have been noted. When ultra violet light strikes an oxygen molecule, the photon splits the oxygen molecule into highly reactive oxygen atoms, these readily combine with an oxygen molecule & forms Ozone.
UV light
O2—————>20 + 2H

O + O2——–. O3

Ozone on the one hand protects the lives on earth surface from the lethal and harmful effects of UV-β radiations emerging from Sun’s rays by providing a giant umbrella which filters out radiations below 3000 A0 and controls the thermal budget yet acts as an ubiquitous urban pollutant causing damage to alveolar epithelium. Inhalation of ozone to a tune of 0.1 to 0.2 ppm is sufficient to cause toxicity leading to edema, hyperresponsiveness, impaired host defensive mechanism, psoriasis, skin cancers, increase in the level of malondialdehyde (MDA) in the skin etc. Exposure to ozone results into the release of archidonic acid eicosanoids (Prostaglandins and their related compounds prostacyclin PGI, thermoboxanes TXA, leukotriens LT & lipoxins are collectively called eicosanoids.) and platelet activating factors from a variety of pulmonary cell types reports Samet et al (1992) and Mekinnon et al (1995). Acute inhalation of Ozone is associated with an inflammatory response showing accumulation of macrophages at the injury site. The macrophages and alveolar epithelial cells get activated & release cytotoxic and pro-inflammatory mediators. In this review the author has compiled informations from the works of Laskin et al (1998) and Cross et al (1998) and few other workers and explained how pro-inflammatory cytokines like TNF-α (tumor necrosis factor), interleukin (IL-Iβ) and bacterially derived LPS (Lipopolysaccharide) singly or jointly modulate the cellular function by shifting the oxidation reduction equilibrium or modulate the regulatory protein which initiate gene transcription. The author has also dealt with how NF-β transcription factor binding to: NOS gene is the root cause of production responsible for pulmonary toxicity leading to inflammation (via JAk-STAT pathway).

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