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The Relationship Between e-Cigarette Exposure, Sex Steroids, and COVID-19

Throughout the global COVID-19 pandemic, there has been a noticeably higher mortality rate in males compared to females. Though the mechanism that causes this remains unknown, Dr. Pawan Sharma and Dr. Amir Zeki hypothesize that sex steroids combined with the higher population of male e-cigarette smokers could be the link.

The renin-angiotensin system (RAS) may be an interesting link between the effects of smoking on the endocrine system. The RAS system has angiotensin-converting enzymes (ACE-1, ACE-2) axes related to cardiopulmonary pathophysiology, therefore playing a key role in respiratory infections and inflammation. ACE-2 is also the only confirmed receptor that binds to the spike protein on SARS-CoV-2, allowing for virus entry. In some individuals, including smokers and COPD patients, ACE-2 expression is higher in airway epithelium, type 2 pneumocytes, tissue macrophages, and ciliated airway epithelial cells.

Dr. Sharma and Dr. Zeki set out to determine if vaping would induce lung and airway ACE-2 expression and if it would vary based on intrinsic gender and nicotine exposure. The team exposed 7–8 week-old mice to e-cigarette vapor (with and without nicotine) for 30 minutes twice a day for 21 days to test their hypothesis. After the last exposure, the team analyzed the immune response and measured lung mechanics. Using the flexiVent, the team analyzed basal inspiratory capacity and airway hyperresponsiveness to increasing concentrations of methacholine.

In their study, Dr. Sharma and Dr. Zeki show that e-cigarette vapor exposure increases airway inflammation, upregulates ACE-2 expression in the lung and impairs lung function. They also demonstrated that this occurs in a sex-dependent manner, showing that ACE-2 expression is higher in male mice and was driven by nicotine exposure. The decline in flexiVent lung function was shown by an increased resistance following e-cigarette vapor exposure in both sexes. However, resistance increased in males in a nicotine-independent manner versus the female mice, where increased airway resistance was nicotine-dependent. Additionally, a reduction in basal inspiratory capacity was seen as well using the flexiVent following vapor exposure, which appeared to be independent of sex or nicotine concentration.

Overall, the study showed that e-cigarette vapor exposure induced ACE-2 expression in murine lungs, which were further exacerbated when combined with nicotine exposure. Though the exact cause of this remains unknown, Dr. Sharma et al. suggest it could result from the nicotinic acetylcholine receptors (nAChR).

Read the full publication here.


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