PASSIVE SMOKING AND PLATELET THROMBOXANE

While active smoking is known to enhance platelet thromboxane producti on, no data on passive smoking is available yet. The influence of sing le and repeated exposure to passive smoke for 60 minutes in a 18 m(3) room was assessed in non-smokers as compared to sex and age matched sm okers. All the evaluated measures (malondialdehyde, plasma thromboxane B-2, 11-dehydro-thromboxane B-2, serum thromboxane B-2 conversion of exogenous arachidonic acid to thromboxane B-2 and to hydroxy-5, 8,10-h eptadecatrienoic acid) were higher in smokers than non-smokers at base line, immediately and 6 hours after passive exposure to cigarette smok e. Repeated exposure of non-smokers rendered their platelets more acti vated becoming close to the behaviour of smokers. These results indica te that passive smoking may activate thromboxane A(2) release from the platelets, contributing to the development of hemostatic imbalance.