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

• Published in: Toxicological sciences Vol. 59; no. 2; pp. 316 - 323
• Main Authors: SMITH, Carr J, FISCHER, Thomas H, HEAVNER, David L, RUMPLE, Melissa A, BOWMAN, Denise L, BROWN, Buddy G, MORTON, Michael J, DOOLITTLE, David J
• Format: Journal Article
• Language: English
• Published: Cary, NC Oxford University Press 01-02-2001
• Subjects: 8-Hydroxy-2'-deoxyguanosine; Adult; Air Pollutants - analysis; Biological and medical sciences; Biomarkers - urine; cortisol; Creatinine - urine; Deoxyguanosine - analogs & derivatives; Deoxyguanosine - urine; Epoprostenol - urine; Female; Humans; Hydrocortisone - urine; Male; Medical sciences; Meta-Analysis as Topic; Middle Aged; Platelet Aggregation - physiology; prostacyclin; Smoking - blood; thromboxanes; Thromboxanes - urine; Tobacco Smoke Pollution - analysis; Tobacco, tobacco smoking; Toxicology; Human; Urine; Blood coagulation; Oxidative stress; Prostaglandin I2; Metabolite; Toxicity; Elimination; Sex; Biological marker; Cardiovascular disease; Hydrocortisone; Inhalation; Tobacco; Platelet; Passive smoking; Thromboxane; Fumes
• ISSN: 1096-6080; 1096-0929; 1096-0929
• DOI: 10.1093/toxsci/59.2.316

This study tested the hypotheses that (1) increased platelet aggregation, as measured by 2,3-dinor-thromboxane B(2) (Tx-M) and 2,3-dinor-6-keto-prostaglandin F(1alpha) (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.