During the recent past, the risk of passive smoking has been widely recognized. Passive smoking has been demonstrated //to exert a variety of deleterious effects, associated with an increased risk of coronary heart disease eventually resulting in vascular damage.

Isoprostanes, a reliable marker of in vivo oxidation injury, have been shown to increase in active cigarette smoking. However, the data for passive smoking are lacking.

Recently, researchers from Austria and Greeec examined the isoprostane 8-epi-PGF2a in 12 smokers and non-smokers exposed daily to passive cigarette smoke for 12 days. Plasma samples stored at liquid nitrogen from people having been examined earlier were used.

Prevalues of 8-epi-PGF2a were found to be higher in cigarette smokers. Exposure to passive smoking caused a significant increase in 8-epi-PGF2a in non-smokers, while in smokers there was only a trendwise increase. After repeated passive smoke exposure, 8-epi-PGF2a in non-smokers approached the respective values of smokers.

There was a significant correlation of 8-epi-PGF2a to the thromboxane (plasma, serum, conversion from exogenous precursor, 11-dehydro-TXB2) parameters (MDA, HHT- conversion) examined in these patients before.

The findings, to be published in the journal Life Sciences (available online 13 September 2005) document a significant temporary increase in in vivo oxidation injury due to passive smoke favouring development and/or progression of vascular disease.

Apparently, repeated but not single exposure to passive smoking introduces a significantly large number of radicals into the human body. After rapid consumption of antioxidants lipid peroxidation products including isoprostanes are accumulated in blood and finally in vascular tissue exerting deleterious effects.

The authors conclude that besides activation of platelet function and the thromboxane synthesis, in vivo oxidation injury may be an i
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