Urinary thromboxane, prostacyclin, cortisol, and 8-hydroxy-2 '-deoxyguanosine in nonsmokers exposed and not exposed to environmental tobacco smoke

This study tested the hypotheses that (1) increased platelet aggregation, a s measured by 2,3-dinor-thromboxane B-2 (Tx-M) and 2,3-dinor-6-keto-prostag landin F-1 alpha (PGI-M), and (2) increased oxidative stress, as measured b y 8-Hydroxy-2'-deoxyguanosine (8-OHdG), would occur in ETS-exposed nonsmoke rs as compared with non-ETS-exposed nonsmokers. The concentrations of the s table urinary metabolites of thromboxane (Tx-M) and prostacyclin (PGI-M), c ortisol and 8-OHdG were measured in a 24-h urine sample from 3 groups of su bjects: 21 nonsmokers with minimal (15 min or less per day) ETS exposure (t ermed non-ETS-exposed), 22 nonsmokers with at least 5 h per day of ETS expo sure (termed ETS-exposed), and 20 cigarette smokers who served as a positiv e control group. The self-reported levels of ETS exposure were verified by personal air monitors. As compared with either group of nonsmokers, cigaret te smokers excreted significantly more urinary Tx-M. Non-ETS-exposed nonsmo kers shelved a statistically significantly higher level of urinary Tx-M ove r that seen in nonsmokers with considerably more ETS exposure. Urinary conc entrations of PGI-M were marginally higher in the smokers and did not diffe r between the nonsmoker groups. Nonsmokers exposed to at least five h of ET S per day did not have significantly higher excretion of 8-OHdG than non-ET S-exposed nonsmokers. The results from this study suggest that platelet agg regation, as measured by the thromboxane metabolite Tx-M and prostacyclin m etabolite PGI-M, is not associated with ETS exposure. Therefore, platelet a ggregation is not a plausible or quantitatively consistent mechanism to exp lain the nonlinear dose-response hypothesis of cardiovascular disease and E TS exposure.