Toxicological Sciences 59, 316-323 (2001)
Copyright © 2001 by the Society of Toxicology
RESPIRATORY TOXICOLOGY |
Urinary Thromboxane, Prostacyclin, Cortisol, and 8-Hydroxy-2'-deoxyguanosine in Nonsmokers Exposed and Not Exposed to Environmental Tobacco Smoke
,1
* Research and Development, R. J. Reynolds Tobacco Company, Bowman Gray Technical Center, Winston-Salem, North Carolina 27102; and
Center for Thrombosis and Hemostasis, University of North Carolina, Chapel Hill, North Carolina
This study tested the hypotheses that (1) increased platelet aggregation, as measured by 2,3-dinor-thromboxane B2 (Tx-M) and 2,3-dinor-6-keto-prostaglandin F1
(PGI-M), and (2) increased oxidative stress, as measured by 8-Hydroxy-2'-deoxyguanosine (8-OHdG), would occur in ETS-exposed nonsmokers as compared with non-ETS-exposed nonsmokers. The concentrations of the stable urinary metabolites of thromboxane (Tx-M) and prostacyclin (PGI-M), cortisol and 8-OHdG were measured in a 24-h urine sample from 3 groups of subjects: 21 nonsmokers with minimal (15 min or less per day) ETS exposure (termed non-ETS-exposed), 22 nonsmokers with at least 5 h per day of ETS exposure (termed ETS-exposed), and 20 cigarette smokers who served as a positive control group. The self-reported levels of ETS exposure were verified by personal air monitors. As compared with either group of nonsmokers, cigarette smokers excreted significantly more urinary Tx-M. Non-ETS-exposed nonsmokers showed a statistically significantly higher level of urinary Tx-M over that seen in nonsmokers with considerably more ETS exposure. Urinary concentrations of PGI-M were marginally higher in the smokers and did not differ between the nonsmoker groups. Nonsmokers exposed to at least five h of ETS per day did not have significantly higher excretion of 8-OHdG than non-ETS-exposed nonsmokers. The results from this study suggest that platelet aggregation, as measured by the thromboxane metabolite Tx-M and prostacyclin metabolite PGI-M, is not associated with ETS exposure. Therefore, platelet aggregation is not a plausible or quantitatively consistent mechanism to explain the nonlinear dose-response hypothesis of cardiovascular disease and ETS exposure.
Key Words: environmental tobacco smoke; platelets; thromboxane; cardiovascular disease.
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