Summary
Introduction:
This text summarizes the findings of two studies on the impact of electronic cigarette (E-cig) aerosol exposure on endothelial dysfunction (ED), a key measure of cardiovascular disease (CVD) risk. The first study focuses on the acute effects of E-cig aerosol exposure in rats, while the second study examines the chronic effects of E-cig use in human users. The text highlights the novel insights gained from these studies regarding the mechanisms of ED induced by E-cig aerosol exposure.
Key Points:
* The first study found that acute exposure to E-cig aerosol, as well as individual components like acrolein and acetaldehyde, impairs flow-mediated dilation (FMD) in rats, similar to the effects of combustible cigarette smoke.
* The study also found that bilateral vagotomy, which interrupts the nervous system's role in mediating ED, confirms the necessary role of the nervous system in E-cig aerosol-induced ED.
* The second study found that chronic E-cig use impairs FMD in humans, and sera of chronic E-cig users contains factors that impair endothelial nitric oxide (eNOS-derived NO) production and enhance permeability.
* Specific factors in E-cig users' sera, S100a8 and hMGB1, impair endothelial cell (EC) function via the Receptor of aGE (RaGE).
* The presence of elevated levels of RaGE ligands in E-cig users' sera does not bode well for vascular health.
* Limitations of the studies include the inability to assess the contribution of individual processes (production, destruction, or responsiveness) to the sum total of impairment and the absence of a "VSMC control" to confirm that vascular smooth muscle cell sensitivity to NO is not impaired.
* a unique observation of the second study is the novel pathway in E-cig users, but absent in smokers, wherein elevated S100a8 and hMGB1 increase EC permeability via RaGE.
Main Message:
The text emphasizes the importance of taking seriously any determinant that induces ED, as CVD is the leading cause of morbidity and mortality worldwide. The novel insights gained from these studies regarding the mechanisms of ED induced by E-cig aerosol exposure have implications for tracking progression and mitigating deleterious vascular effects of E-cig exposures. These answers may apply to a wide variety of environmental irritant exposures. The findings underscore the need for further research to understand how best to mitigate the harmful effects of E-cig exposures on vascular health.
Citation
Conklin DJ. how Irritating! Electronic Cigarettes Not “95% Safer” Than Combustible Cigarettes: Recent Mechanistic Insights Into Endothelial Dysfunction. arteriosclerosis, thrombosis, and vascular biology. 2022;42(11):1351-1354. doi:10.1161/aTVBaha.122.318468
