E-Cigarettes and Cardiovascular Disease Risk: Evaluation of Evidence, Policy Implications, and Recommendations
- 885 Downloads
Cardiovascular disease is the major cause of death in smokers. Although new tobacco products such as e-cigarettes do not generate many of the harmful or potentially harmful constituents (HPHCs), present in combustible tobacco products the cardiovascular effects of these devices are unknown and their efficacy in promoting and sustaining cessation remains unclear. Currently, these devices are being marketed as cleaner and safer alternative to smoking that could help smokers quit smoking. Nevertheless, e-cigarette aerosols contain appreciable levels of carbonyls, which within the concentration range reported in e-cigarettes, exert significant cardiovascular toxicity. Moreover, even by itself, nicotine is a sympathomimetic drug that elicits hemodynamic and metabolic changes that could increase the risk of acute cardiovascular events such as arrhythmias or plaque rupture and chronically increase cardiovascular disease risk by inducing dyslipidemia. The dose-response relationship between smoking and cardiovascular mortality is non-linear, suggesting that reduction in HPHC concentrations in e-cigarette aerosols may not result in proportional harm reduction and decreased HPHC exposure may be offset by increased use by individuals who believe that e-cigarettes are safer than conventional cigarettes. Thus, taken together, current evidence does not entirely support the notion that e-cigarettes are reduced harm products or effective smoking cessation devices.
KeywordsSmoking Acrolein Particulate matter Formaldehyde Acetaldehyde Blood pressure Atherosclerosis
This work was supported in part by the NIH grant HL120163 to the American Heart Association; however, the view presented does not reflect the policy of the American Heart Association or the Food and Drug Administration.
Compliance with Ethical Standards
Conflict of Interest
Dr. Bhatnagar declares no conflict of interest
Human and Animal Rights and Informed Consent
This article does not contain any studies with human or animal subjects performed by the author.
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
- 5.Centers for Disease C and Prevention. Current cigarette smoking prevalence among working adults--United States, 2004-2010. MMWR Morb Mortal Wkly Rep. 2011;60:1305–9.Google Scholar
- 7.The health consequences of smoking: a report of the surgeon general, Atlanta; 2004.Google Scholar
- 9.Piano MR, Benowitz NL, Fitzgerald GA. Corbridge S, Heath J, Hahn E, Pechacek TF, Howard G and American Heart Association Council on Cardiovascular N. Impact of smokeless tobacco products on cardiovascular disease: implications for policy, prevention, and treatment: a policy statement from the American Heart Association. Circulation. 2010;122:1520–44.CrossRefPubMedGoogle Scholar
- 15.••Pope 3rd CA, Burnett RT, Krewski D, Jerrett M, Shi Y, Calle EE, et al. Cardiovascular mortality and exposure to airborne fine particulate matter and cigarette smoke: shape of the exposure-response relationship. Circulation. 2009;120:941–8. The study report a non-linear dose response relationship between smoking and cardiovacular mortality.CrossRefPubMedGoogle Scholar
- 63.DeJarnett N, Conklin DJ, Riggs DW, Myers JA, O’Toole TE, Hamzeh I, et al. Acrolein exposure is associated with increased cardiovascular disease risk. J Am Heart Assoc. 2014;3.Google Scholar
- 64.•Andre E, Campi B, Materazzi S, Trevisani M, Amadesi S, Massi D, et al. Cigarette smoke-induced neurogenic inflammation is mediated by alpha,beta-unsaturated aldehydes and the TRPA1 receptor in rodents. J Clin Invest. 2008;118:2574–82. This study reports that acrolein mediates the neurogenic effects of cigarette smoke by stimulating TRPA1 receptors.PubMedPubMedCentralGoogle Scholar
- 67.Borchers MT, Wesselkamper SC, Deshmukh H, Beckman E, Medvedovic M, Sartor M, Leikauf GD and Committee HEIHR. The role of T cells in the regulation of acrolein-induced pulmonary inflammation and epithelial-cell pathology. Res Rep Health Eff Inst. 2009:5–29.Google Scholar
- 75.••Brook RD, Rajagopalan S, Pope 3rd CA, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation. 2010;121:2331–78. The statement discusses current evidence linking exposure to particulate matter to cardiovascular disease.CrossRefPubMedGoogle Scholar
- 83.Tierney PA, Karpinski CD, Brown JE, Luo W, Pankow JF. Flavour chemicals in electronic cigarette fluids. Tob Control. 2015.Google Scholar
- 96.•Lau PP, Li L, Merched AJ, Zhang AL, Ko KW, Chan L. Nicotine induces proinflammatory responses in macrophages and the aorta leading to acceleration of atherosclerosis in low-density lipoprotein receptor(−/−) mice. Arterioscler Thromb Vasc Biol. 2006;26:143–9. This study shows that exposure to nicotine increase atherosclerotic lesion formation.CrossRefPubMedGoogle Scholar
- 99.Farsalinos KE, Tsiapras D, Kyrzopoulos S, Savvopoulou M, Voudris V. Acute effects of using an electronic nicotine-delivery device (electronic cigarette) on myocardial function: comparison with the effects of regular cigarettes. BMC Cardiovasc Disord. 2014;14:78.CrossRefPubMedPubMedCentralGoogle Scholar