Effects of Smoking Cessation on Eight Urinary Tobacco Carcinogen and Toxicant Biomarkers

Abstract

We determined the persistence at various times (3,7,14,21,28,42 and 56 days) of eight tobacco smoke carcinogen and toxicant biomarkers in the urine of 17 smokers who stopped smoking. The biomarkers were 1-hydroxy-2-(N-acetylcysteinyl)-3-butene (1) and 1-(N-acetylcysteinyl)-2-hydroxy-3-butene (2) [collectively called MHBMA for monohydroxybutyl mercapturic acid] and 1,2-dihydroxy-4-(N-acetylcysteinyl)butane (3) [DHBMA for dihydroxybutyl mercapturic acid], metabolites of 1,3-butadiene; 1-(N-acetylcysteinyl)-propan-3-ol (4, HPMA for 3-hydroxypropyl mercapturic acid), a metabolite of acrolein; 2-(N-acetylcysteinyl)butan-4-ol (5, HBMA for 4-hydroxybut-2-yl mercapturic acid), a metabolite of crotonaldehyde; (N-acetylcysteinyl)benzene (6, SPMA for S-phenyl mercapturic acid), a metabolite of benzene; (N-acetylcysteinyl)ethanol (7, HEMA for 2-hydroxyethyl mercapturic acid), a metabolite of ethylene oxide; 1-hydroxypyrene (8) and its glucuronides (1-HOP), metabolites of pyrene; and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (9) and its glucuronides (total NNAL), a biomarker of exposure to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). These biomarkers represent some of the major carcinogens and toxicants in cigarette smoke: 1,3-butadiene, acrolein, crotonaldehyde, benzene, ethylene oxide, polycyclic aromatic hydrocarbons (PAH), and NNK. With the exception of DHBMA, levels of which did not change after cessation of smoking, all other biomarkers decreased significantly after 3 days of cessation (P<0.001). The decreases in MHBMA, HPMA, HBMA, SPMA, and HEMA were rapid, nearly reaching their ultimate levels (81 -91% reduction) after 3 days. The decrease in total NNAL was gradual, reaching 92% after 42 days, while reduction in 1-HOP was variable among subjects to about 50% of baseline. Since DHBMA did not change upon smoking cessation, there appear to be sources of this metabolite other than 1,3-butadiene. The results of this study demonstrate that the tobacco smoke carcinogen/toxicant biomarkers MHBMA, HPMA, HBMA, SPMA, HEMA, 1-HOP, and NNAL are related to smoking and are good indicators of the impact of smoking on human exposure to 1,3-butadiene, acrolein, crotonaldehyde, benzene, ethylene oxide, PAH and NNK.

Exposure to Nicotine and Selected Toxicants in Cigarette Smokers Who Switched to Electronic Cigarettes: A Longitudinal Within-Subjects Observational Study

“…Moreover, the observed decline in various urine toxicant biomarker levels in our study was similar to decline among smokers who have quit smoking completely and did not substitute with any other product. 41 This observation suggests that e-cigarettes are not a significant source of exposure to those toxicants. Further evaluation should be undertaken on the impact of e-cigarettes on longer-term behaviors and effects of e-cigarettes that may contain low levels of toxicants.…”

Benzene Uptake in Hookah Smokers and Non-smokers Attending Hookah Social Events: Regulatory Implications

“…Urine samples were aliquoted and stored in a freezer (À20 C), then sent frozen in dry ice to two laboratories. The Masonic Cancer Center, University of Minnesota laboratory conducted urinary analyses for SPMA by LC-APCI-MS/MS-SRM with a limit of detection (LOD) of 0.03 pmol/mL as previously described (56). San Diego State University Laboratory conducted urinary analyses for creatinine by LC-MS/MS that was linear from 0.3 to 1,000 mg/dl (see supplementary Data for details on creatinine analyses).…”

Nicotine Reduction: Strategic Research Plan

“…These following biomarkers are suggested based on prior studies showing sensitivity to change in smoking status, differences across tobacco products and/or predictive validity (Carmella et al, 2009;Hatsukami, Benowitz, Rennard, Oncken, & Hecht, 2006;Hecht, Yuan, & Hatsukami, 2010;Yuan et al, 2011Yuan et al, , 2012, and targeting different pathophysiological mechanisms associated with disease (Hatsukami et al, 2006) …”