Why the study?
Does passive smoking increase platelet thromboxane production in smokers and nonsmokers?
Does passive smoking increase platelet thromboxane production in smokers and nonsmokers?
Passive smoking enhances thromboxane A2 release from platelets, potentially contributing to hemostatic imbalance and increased cardiovascular risk.
Passive smoking may heighten thrombotic risk via thromboxane; hypothesis-generating and requires outcome trials before practice change.
Although active smoking is known to enhance platelet thromboxane production, no data on passive smoking are available yet. In an 18 m3 room, the influence of single and repeated exposure to passive smoke for 60 minutes was assessed in nonsmokers and smokers. Smokers and nonsmokers were matched for sex and age. All the evaluated parameters (plasma TXB2, serum TXB2, malondialdehyde, 11-dehydro-TXB2, conversion of exogenous arachidonic acid to hydroxy-5,8,10-heptadecatrienoic acid, and TXB2) were higher in smokers than nonsmokers at baseline conditions, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of nonsmokers rendered their platelets more activated, so they became closer to the behavior of smokers. Contributing to the development of hemostatic imbalance, these results indicate that passive smoking may enhance thromboxane A2 release from the platelets.
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Kritz et al. (2005) studied this question.
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