Abstract
The popularity of electronic cigarettes (e-cigs) has grown at a startling rate since their introduction to the United States market in 2007, with sales expected to outpace tobacco products within a decade. Spurring this trend has been the notion that e-cigs are a safer alternative to tobacco-based cigarettes. However, the long-term health impacts of e-cigs are not yet known. Quantitative magnetic resonance imaging (MRI) approaches, developed in the authors’ laboratory, provide conclusive evidence of acute deleterious effects of e-cig aerosol inhalation in the absence of nicotine in tobacco-naïve subjects. Among the pathophysiologic effects observed are transient impairment of endothelial function, vascular reactivity, and oxygen metabolism. The culprits of this response are currently not fully understood but are likely due to an immune reaction caused by the aerosol containing thermal breakdown products of the e-liquid, including radicals and organic aldehydes, with particle concentrations similar to those emitted by conventional cigarettes. The acute effects observed following a single vaping episode persist for 1–3 h before subsiding to baseline and are paralleled by build-up of biological markers. Sparse data exist on long-term effects of vaping, and it is likely that repeated regular exposure to e-cig aerosol during vaping will lead to chronic conditions since there would be no return to baseline conditions as in the case of an isolated vaping episode. This brief review aims to highlight the potential of pairing MRI, with its extraordinary sensitivity to structure, physiology and metabolism at the holistic level, with biologic investigations targeting serum and cellular markers of inflammation and oxidative stress. Such a multi-modal framework should allow interpretation of the impact of e-cigarette vaping on vascular health at the organ level in the context of the underlying biological alterations. Applications of this approach to the study of other lifestyle-initiated pathologies including hypertension, hypercholesterolemia, and metabolic syndrome are indicated.
Highlights
The popularity of electronic cigarettes (e-cigs) has grown at a startling rate since their introduction to the United States market in 2007, with sales expected to outpace tobacco products within a decade
Besides nicotine, which has long been known to cause endothelial dysfunction (EDF) (Neunteufl et al, 2002), e-cig users are exposed to a host of toxic compounds generated by thermal degradation of solvents (Bekki et al, 2014; Jensen et al, 2017), and possibly flavorings (Omaiye et al, 2019), along with metal contaminants and ultrafine metal particles ejected by the heating element (Williams et al, 2013, 2017; Olmedo et al, 2018)
A decrease on the order of 20–30% in nitric oxide (NO) bioavailability was found in nonsmokers, whose brachial artery flow-mediated dilation (FMD) was reduced by almost 40% after exposure to nicotinized e-cigarette in two crossover studies comparing the effects of e-cig vaping to tobacco smoking (Carnevale et al, 2016; Biondi-Zoccai et al, 2019), where tobacco smoking was found to cause a larger decrement in both quantities)
Summary
The popularity of electronic cigarettes (e-cigs) has grown at a startling rate since their introduction to the United States market in 2007, with sales expected to outpace tobacco products within a decade. Recent findings from the authors’ laboratories indicate that a single vaping episode involving non-nicotinized e-liquid provoked an inflammatory immune response and oxidative stress along with reduced nitric oxide (NO) bioavailability (Chatterjee et al, 2019b) The latter manifested in impaired peripheral vascular reactivity and endothelial function as determined by a battery of quantitative magnetic resonance imaging (MRI) metrics (Caporale et al, 2019). Smokers had reduced endothelial function and vascular reactivity independent of subjects’ age In that work, both measures of post-occlusion hyperemia and femoral FMD were assessed with an upper leg cuff-occlusion protocol disrupting both arterial inflow and venous return, along with parameters describing the time-course of femoral vein oxygen saturation (SvO2). All data are highly significant and consistent with the notion that the aerosol (supplemented with tobacco flavor), or the breakdown products (Wang et al, 2017), possibly micro-particles emanating from the heating elements (Williams et al, 2013, 2017), cause an immune response [as shown by the authors’ data in Chatterjee et al (2019b)], leading to acute EDF
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