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Tobacco Smoke and Endothelial Dysfunction: Role of Aldehydes?

  • Mechanisms of Hypertension and Target-Organ Damage (JE Hall and ME Hall, Section Editors)
  • Published:
Current Hypertension Reports Aims and scope Submit manuscript

Abstract

Purpose of Review

Tobacco smoking is the most significant modifiable risk factor in the development of cardiovascular disease (CVD). Exposure to mainstream cigarette smoke (MCS) is associated with CVD through the development of endothelial dysfunction, a condition characterized by an imbalance of vasoactive factors in the vasculature. This dysfunction is thought to be induced in part by aldehydes generated at high levels in MCS.

Recent Findings

Electronic cigarettes (e-cigs) may also pose CVD risk. Although the health effects of e-cigs are still largely unknown, the presence of aldehydes in e-cig aerosol suggests that e-cigs may induce adverse cardiovascular outcomes similar to those seen with MCS exposure.

Summary

Herein, we review studies of traditional and emerging tobacco product use, shared harmful and potentially harmful constituents, and measures of biomarkers of harm (endothelial dysfunction) to examine a potential and distinct role of aldehydes in cardiovascular harm associated with cigarette and e-cig use.

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Abbreviations

CAC:

Circulating angiogenic cell

CRP:

C-reactive protein

CVD:

Cardiovascular disease

E-cig:

Electronic cigarette

ENDS:

Electronic nicotine delivery systems

FMD:

Flow-mediated dilation

GRAS:

Generally regarded as safe

HPHCs:

Harmful or potentially harmful constituents

MCS:

Mainstream cigarette smoke

NO:

Nitric oxide

OS:

Oxidative stress

PG:

Propylene glycol

PM:

Particulate matter

ROS:

Reactive oxygen species

SHS:

Secondhand smoke

sICAM-1:

Soluble intercellular adhesion molecule 1

sVCAM-1:

Soluble vascular adhesion molecule 1

US FDA:

US Food and Drug Administration

VG:

Vegetable glycerin

WBCs:

White blood cells

WHO:

World Health Organization

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Acknowledgments

The authors thank the University of Louisville Diabetes and Obesity Center for support.

Funding

This work was supported by the National Institutes of Health (ES019217, GM127607, HL122676, HL149351, U54HL120163, T32ES011564) and the University of Louisville School of Medicine Integrated Programs in Biomedical Sciences (IPIBS).

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Authors and Affiliations

  1. Christina Lee Brown Envirome Institute, University of Louisville, Louisville, KY, 40292, USA

    Jordan Lynch, Lexiao Jin, Andre Richardson & Daniel J Conklin

  2. Diabetes & Obesity Center, University of Louisville, Louisville, KY, 40292, USA

    Jordan Lynch, Lexiao Jin, Andre Richardson & Daniel J Conklin

  3. University of Louisville American Heart Association – Tobacco Regulation and Addiction Center, Louisville, KY, 40202, USA

    Jordan Lynch, Andre Richardson & Daniel J Conklin

  4. Superfund Research Center, University of Louisville, Louisville, KY, 40202, USA

    Daniel J Conklin

  5. Department of Anesthesiology, Critical Care and Pain Medicine, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China

    Lexiao Jin

  6. Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, 40292, USA

    Daniel J Conklin

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Lynch, J., Jin, L., Richardson, A. et al. Tobacco Smoke and Endothelial Dysfunction: Role of Aldehydes?. Curr Hypertens Rep 22, 73 (2020). https://doi.org/10.1007/s11906-020-01085-7

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