Maintained hyperexcretion of thromboxane A2 metabolite in healthy young cigarette smokers: results from a prospective study in randomly sampled males with stable smoking habits

Summary. Although several studies have identified cigarette smoking as a factor increasing platelet formation of thromboxane A₂ (TxA₂), no prospective data on this issue have been presented in a defined population with stable smoking habits. Therefore, we analysed the relation between smoking habits and urinary excretion of the 2, 3-dinor metabolites of thromboxane A₂ (Tx-M) and prostacyclin (PGI-M) in 87 males, randomly sampled from a population of 18–19-year-old men, at two different occasions separated by 31–49 months. The daily cigarette consumption among the smokers was unchanged between the study occasions (11 vs. 11 cigarettes day^-1), but 9 of 43 initial smokers had quit. None of the initial non-smokers had begun smoking. Tx-M was higher in the smokers than in the non-smokers and correlated with the daily cigarette consumption both at the initial (176 vs. 123 pg mg^-1 creatinine; P = 0.01) and the second (214 vs. 164 pg mg^-1; P = 0.002) study occasion. Those who had quit smoking since the initial study did not differ in Tx-M from the non-smokers at the second study occasion. Urinary PGI-M did not differ between cigarette smokers, non-smokers and quitters at either of the study occasions. We conclude that cigarette smoking elicits an increased formation of thromboxane A₂, indicating platelet activation, that is stable during an observation period of up to 4 years. The increased platelet activity is reversible upon quitting.