Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2023 Jun 29;11(7):564.
doi: 10.3390/toxics11070564.

Changes in Biomarkers of Exposure and Potential Harm in Smokers Switched to Vuse Vibe or Vuse Ciro Electronic Nicotine Delivery Systems

Milly N Kanobe  1 , Paul R Nelson  2 , Buddy G Brown  3 , Peter Chen  1 , Patrudu Makena  1 , John W Caraway  1 , Gaddamanugu L Prasad  4   5 , Elaine K Round  6
Affiliations

Changes in Biomarkers of Exposure and Potential Harm in Smokers Switched to Vuse Vibe or Vuse Ciro Electronic Nicotine Delivery Systems

Milly N Kanobe et al. Toxics. .

Abstract

Electronic nicotine delivery systems (ENDS) have the potential to provide nicotine to tobacco consumers while reducing exposure to combustion-related toxicants. Here, we report changes in biomarkers of exposure (BoE) and biomarkers of potential harm (BoPH) in smokers who completely switched to Vuse Vibe and Vuse Ciro ENDS products, or to smoking abstinence in a randomized, controlled clinical study. Thirteen BoE (12 urinary and one blood) that indicate exposure to harmful and potentially harmful toxicants (HPHCs) were evaluated at baseline on day 5. Urinary BoPH linked to oxidative stress, platelet activation, and inflammation were also assessed at baseline, and on day 5 and day 7. Nicotine exposure was lower in Vuse Vibe and Vuse Ciro groups compared to baseline values. Urinary non-nicotine BoE decreased significantly (52.3-96.7%) in the Vuse ENDS groups, and the reductions were similar in magnitude to those observed in the abstinence group. Blood carboxyhemoglobin decreased 52.8-55.0% in all study groups. Decreases (10-50%) in BoPH were observed in all study groups. Thus, smokers who switch exclusively to Vuse Vibe or Vuse Ciro products or completely abstain from smoking are exposed to substantially lower levels of HPHCs, and experience improvements in BoPH of oxidative stress and inflammation pathways.

Keywords: BoE; BoPH; ENDS; abstinence; cigarette smokers; switching study.

PubMed Disclaimer

Conflict of interest statement

M.N.K., P.M., P.C. and J.W.C. are full-time employees of RAI Services Company, E.K.R. is a full-time employee of BAT (Investments) Limited, and B.G.B., G.L.P. and P.R.N. are former full-time employees of RAI Services Company. G.L.P. works as an independent scientific consultant. RAI Services Company is a wholly owned subsidiary of Reynolds American Inc., which is an indirect, wholly owned subsidiary of British American Tobacco plc.

Figures

Figure 1
Figure 1
Key events and timeline of the Vuse ENDS clinical study: Following randomization, enrolled subjects were assigned to using Vuse Vibe, Vuse Ciro, or smoking abstinence. Blood and urine samples were collected for biomarker analyses at baseline and Day 5 (BoE) and BoPH (Days 5 and 7).
Figure 2
Figure 2
Mean percent change in BoE in smokers switched to Vuse Vibe or Vuse Ciro products: Biomarkers of Exposure decline in smokers who switched to Vuse Vibe, Vuse Ciro or Abstinence for 5 days. Carboxyhemoglobin is a blood biomarker. Exposure to nicotine was determined by quantifying nicotine and its 5 metabolites, and reported as Total Nicotine Equivalents (NicEq-T). The BoE are indicated in the parentheses for the HPHCs evaluated, along with their acronyms: 1-AN (1-aminonaphthaline); 2-AN (2-aminonaphthalene); 4-ABP (4-aminobiphenyl); Acrylonitrile (2-cyanoethyl mercapturic acid [CEMA]); Crotonaldehyde (3-hydroxy-1-methylpropylmercapturic acid [HMPMA]; ); Acrolein (3-hydroxypropyl mercapturic acid [HPMA]); 1,3-Butadiene (Monohydroxybutenyl mercapturic acid [MHBMA]); Benzene (S-phenyl mercapturic acid [SPMA]); 3-OH-B[a]P (3-hydroxy-benzo[a]pyrene); NNK: (Nicotine-derived nitrosamine ketone; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol + glucuronides [Total NNAL]); NNN (N-nitrosonornicotine; N′-nitrosonornicotine + glucuronides [Total NNN]); COHb: carboxyhemoglobin. * Excluding participants with extreme data (data that were beyond the arithmetic mean ± 6 multiplied by standard deviation for each study endpoint).
See this image and copyright information in PMC

References

    1. Centers for Diseases Control and Prevention . How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Centers for Disease Control and Prevention; Atlanta, GA, USA: 2010. - PubMed
    1. Food and Drug Administration . US Department of Health and Human Services; Washington, DC, USA: 2012. [(accessed on 8 September 2022)]. Established List. Available online: https://www.govinfo.gov/content/pkg/FR-2012-04-03/pdf/2012-7727.pdf.
    1. United States Public Health Service Office of the Surgeon, General, Prevention National Center for Chronic Disease, Smoking Health Promotion Office On, and Health . Smoking Cessation: A Report of the Surgeon General. US Department of Health and Human Services; Washington, DC, USA: 2020. Publications and Reports of the Surgeon General.
    1. Institute of Medicine . Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction. The National Academies Press; Washington, DC, USA: 2001. - PubMed
    1. Zeller M., Hatsukami D. The Strategic Dialogue on Tobacco Harm Reduction Group. The Strategic Dialogue on Tobacco Harm Reduction: A vision and blueprint for action in the US. Tob. Control. 2009;18:324–332. doi: 10.1136/tc.2008.027318. - DOI - PMC - PubMed

LinkOut - more resources