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Vaping EVALI and COVID-19 link

COVID-19, Vaping & EVALI

COVID-19 has rapidly spread throughout the world and was declared a pandemic in March of 2020. Studies have identified certain demographics are more at risk for developing severe COVID-19. These demographic groups include the elderly, those with pre-existing health conditions, and those that smoke1 . Furthermore, there has been much speculation about the link between vaping, e-cigarette or vaping product use-associated lung injury (EVALI) and COVID-19 severity since the pandemic started.

Smoking negatively impacts the immune system and its responsiveness to viral and bacterial pathogens, making the smoker more susceptible to disease. Analysis of severe COVID-19 patients shows 3.4% were current smokers, and 6.9% were former smokers. None of the non-severe patients were current smokers, and 3.7% were former smokers2.

Our current understanding of COVID-19 is that SARS-CoV-2 enters cells by binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor, dysregulating the Renin-Angiotensin System (RAS). Normally, ACE2 would cleave the vasoconstrictive hormone (angiotensin-II) into vasodilator (angiotensin 1-7) in the RAS pathway1. Recent studies suggest that the levels of ACE2 influence disease progression and that smokers lungs express approximately 40-50% more ACE2 compared to non-smokers3. This increase may lead to a greater susceptibility of developing severe symptoms or hospitalization.

When considering, Electronic Nicotine Delivery (ENDS) may contain products like vitamin-E acetate, natural oils, and terpene, which have been identified in EVALI patients’ Broncho-Alveolar Lavage Fluid (BALF) samples. Chronic exposure to irritants like nicotine and vitamin-E acetate by ENDS is also known to disrupt the RAS pathway, suggesting a higher risk COVID-193.

More preclinical research regarding the associations between COVID-19 and smoking or vaping is needed. Noninvasive techniques, including the use of a Whole Body Plethysmograph (WBP), may be used to longitudinally quantify lung impairment in rodents after virus infection.

Additionally, invasive lung function outcomes offered by the flexiVent can offer detailed insight into the disease progression and pathophysical changes  caused by the virus.


  1. Smith, J. C., Sausville, E. L., Girish, V., Yuan, M. L., Vasudevan, A., John, K. M., & Sheltzer, J. M. (2020). Cigarette smoke exposure and inflammatory signaling increase the expression of the SARS-CoV-2 receptor ACE2 in the respiratory tractDevelopmental Cell.
  2. Zhang, J. J., Dong, X., Cao, Y. Y., Yuan, Y. D., Yang, Y. B., Yan, Y. Q., … & Gao, Y. D. (2020). Clinical characteristics of 140 patients infected with SARS‐CoV‐2 in Wuhan, ChinaAllergy.
  3. Pino, L. E., Triana, I., Pérez, C., Piotrostanalzki, A., Ruiz-Patiño, A., Lopes, G., & Cardona, A. F. (2020). Electronic nicotine delivery systems (ECs) and COVID-19: the perfect storm for young consumers. Clinical & Translational Oncology, 1.
  4. Kaur, G., Lungarella, G., & Rahman, I. (2020). SARS-CoV-2 COVID-19 susceptibility and lung inflammatory storm by smoking and vapingJournal of Inflammation17(1), 1-8.

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