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, 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 no...

Full description

Saved in:
Bibliographic Details
Published in:Toxicological sciences 2001-02, Vol.59 (2), p.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: Article
Language:English
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
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1096-6080
1096-0929
1096-0929
DOI:10.1093/toxsci/59.2.316