Effects of cessation of cigarette smoking on eicosanoid biomarkers of inflammation and oxidative damage

Joseph P. McElroy, Dayanjan S. Wijesinghe, Steven G. Carmella, Alisa K. Heskin, Mei Kuen Tang, Sharon E. Murphy, Sarah A. Reisinger, Joni A. Jensen, Dorothy K. Hatsukami, Stephen S. Hecht, Peter G. Shields

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17 Scopus citations


The urinary metabolites “prostaglandin E2 metabolite” (PGE-M) and (Z)-7-[1R,2R,3R,5S)-3,5-dihydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]cyclopentyl]hept-5-enoic acid (8-iso-PGF) are biomarkers of inflammation and oxidative damage, respectively, and are elevated in cigarette smokers. Relatively little is known about the effects of smoking cessation on these biomarkers. To investigate this, current cigarette smokers interested in quitting were recruited and invited to participate in a smoking cessation study where varenicline (Chantix) and brief supportive behavioral counseling were offered at each visit after baseline. Subjects returned to the clinic during the 12 week treatment phase for 9 visits post cessation on days 3, 7, 14, 21, 28, 42, 56, 70 and 84. Urine samples were collected at each visit and analyzed by liquid chromatography-tandem mass spectrometry for PGE-M, 8-iso-PGF2α, and cotinine. Cotinine values demonstrated that 15 of 38 subjects quit smoking for the entire 84 day period. Significant decreases in mean levels of PGE-M and 8-iso-PGF per milligram creatinine were observed in these subjects, by 44% (p = 0.0014) and 27% (p<0.001), respectively. The results of this study demonstrate that cessation of smoking for 84 days results in modest but significant declines in urinary PGE-M and 8-iso-PGF indicating reductions in systemic inflammation and oxidative damage. Given that levels were only modestly decreased, these markers are not specific to tobacco-smoke exposure. The modest declines in these biomarkers should be considered when planning studies with ex-smokers. There is a “hangover” from smoking that lasts at least 3 months.

Original languageEnglish (US)
Article numbere0218386
Pages (from-to)e0218386
JournalPloS one
Issue number6
StatePublished - Jun 28 2019

Bibliographical note

Funding Information:
This work was supported by the National Cancer Institute through N01 PC-064402 (TobPRAC) (PGS and DKH) and by the National Cancer Institute and the FDA Center for Tobacco Products through R01 CA 203851 (SSH and DKH). Mass spectrometry was carried out in the Analytical Biochemistry Core Facility of the Masonic Cancer Center, supported in part by National Cancer Institute Cancer Center Support Grant (CA-077598). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the Food and Drug Administration. We thank the subjects for their participation in this study.

Publisher Copyright:
© 2019 McElroy et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Copyright 2020 Elsevier B.V., All rights reserved.

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