This study tested the hypothesis that environmental tobacco smoke (ETS
) exposure increases platelet activation. The concentration of the sta
ble urinary metabolites of thromboxane (Tx-M) and prostacyclin (PGI-M)
was measured in 3 groups of subjects: 27 nonsmokers who did not live
with a smoker, 21 nonsmokers who lived with at least 1 smoker, and 10
cigarette smokers who served as a positive control group. Urinary conc
entrations of the stable metabolites Tx-M and PGI-M did not differ bet
ween the nonsmokers living with at least one smoker and the nonsmokers
not living with a smoker (p = .39 for Tx-M; p = .42 for PGI-M). There
was a statistically significant increase in the urinary concentration
of PGI-M in the cigarette smokers when compared with either the nonsm
okers living with at least one smoker (p < .05) or the nonsmokers not
living with a smoker (p < .05). There was no significant difference in
Tx-M excretion in the cigarette smokers relative to either nonsmokers
living with a smoker (p = .99) or to nonsmokers in nonsmoking househo
lds (p = .53). In the 21 nonsmokers living with smokers, ETS exposure
did not result in platelet activation as measured by either thromboxan
e or prostacyclin release.