Global Product Liability
Product Liability Alert

Vaping and COVID-19: Plausibility and causality

02 November 2020, by David Jaroslaw, Christopher Gismondi and Naira Gorovits

The first case of coronavirus disease 2019 (COVID-19) in the United States was reported in January 2020. As of this writing, of the US has the world’s highest number of COVID-19 cases, with nearly 7.5 million of the more than 35 million reported worldwide. Given that COVID-19 is primarily a respiratory disease, and that vaping involves drawing a heated vapor through the mouth and into the lungs, it was perhaps inevitable that some scientific researchers would ask whether vaping increases susceptibility to, or severity of, COVID-19. It was perhaps equally inevitable that even the possibility that such a relationship might exist would lead to liability claims against vape product manufacturers. However, the very newness of the disease, and our accordingly limited understanding of the mechanisms and epidemiology of the disease, raise a question as to whether plaintiffs bringing cases alleging a nexus between vaping and COVID-19 will be able to prove causality, as required under tort law principles, or if instead they will able to prove only what is, in essence, plausibility.

In fact, less than three months elapsed between the first reported COVID-19 case in the US and the first vaping-and-COVID-19 liability claim. In April 2020, an allegation that vaping put persons who contracted COVID-19 at greater risk of more serious complications was added to the claims asserted in the federal court multi-district litigation pending in the Northern District of California against JUUL Labs and other vape manufacturers and distributors (JUUL MDL).

In most exposure-related product liability litigation, there is a substantial body of epidemiological and biological literature regarding the relationship between the exposure and the disease at issue. Think of cigarette smoking and lung cancer, or asbestos and mesothelioma, or benzene and acute myeloid leukemia. While the parties to these disputes frequently disagree about whether the data support a causal relationship between the exposure and outcome at issue, and even more frequently dispute the claim that the exposure caused the outcome in any individual, but they still are working from a well-developed base of scientific and medical data. In the case of vaping and COVID-19, where knowledge of the disease is in its infancy, the science has not had time to catch up to the events.

The published epidemiological literature contains very little information regarding the correlation of vaping and the likelihood of developing COVID-19.  A single study, published in August 2020, reported that persons aged 13-24 who had ever used vape products were five times as likely to be diagnosed with COVID-19 than controls (similarly-aged persons who had never used vape or tobacco products).[1]However, the study also reported no statistically significant difference in COVID-19 incidence between persons who had vaped in the past 30 days compared to the control group, and that both ever-vapers and past-30-day vapers were more likely to get tested than controls. Finally, the study did not adjust for factors (other than vaping) that differ in prevalence between the "vaping" and "control" groups. If these factors are themselves related to the risk of developing COVID-19, they are referred to in the epidemiological literature as "confounders"; such confounders can account for some or all of the observed difference in risk between vapers and controls.  The only other epidemiological study we are aware of is a study (which has not yet been subject to peer review) comparing vaping rates in each US state with COVID-19 incidence and death rates in that state, and finding a positive correlation.[2] This type of study, which does not have data regarding the vaping status of any individual who contracted (or died of) COVID-19, is of limited value in examining causation.

There is considerably more data regarding cigarette smoking and COVID-19 than there is regarding vaping and the disease – there are far more cigarette smokers in the world than there are vapers, and patient data is far more likely to include information regarding smoking status than vaping status. Therefore, to date, most claims in the scientific and medical community that vaping increases the susceptibility to, or the severity of, COVID-19 are based on studies of nicotine and/or cigarette smoking, not studies of vaping itself. 

These studies have led some researchers to propose mechanisms by which vaping might contribute to progression of COVID-19. In particular, it has been asserted that nicotine increases the expression of an enzyme known as ACE-2, which is found on the surface membranes of cells in the lungs and other organs[3],[4], through its effect on a nicotinic receptor, known as nAChR-α7, found on certain bronchial cells.[5] ACE-2 is believed to be the site at which SARS-Cov-2, the virus that causes COVID-19, enters cells in the lung.  We are aware of only one study that has compared ACE-2 expression in persons who vape versus non-vaping controls, and that study (which has not yet been peer reviewed) reported that vapers did not have increased levels of ACE-2.[6] The remaining studies have not examined whether vaping itself causes the observed effects; rather, they assert, as one author put it, that, "[g]iven the role of the nicotine receptor, vaping may also lead to the upregulation of ACE2 [sic]." In effect, these studies assert that a causal relationship between vaping and ACE-2 expression, and possibly to COVID-19, is plausible, but do little to establish such a relationship.

Further, reliance on studies of cigarette smoking to examine vaping and COVID-19 is questionable, not only because vaping differs from smoking, but also because the data from studies investigating whether cigarette smoking increases susceptibility to, or severity of, COVID-19 might best be described as equivocal.  Some studies report a positive correlation between cigarette smoking and the likelihood that COVID-19 infection will progress to severe disease[7],[8],[9],[10], others report no statistical association between the two[11],[12], and still others report that cigarette smokers have a reduced likelihood of disease progression.[13],[14],[15]  It is, therefore, not surprising that the scientific literature already contains a substantial body of criticism of the methodologies and conclusions of these various studies.[16],[17]

So how is a court to evaluate a claim like the one in the JUUL MDL?  The specific allegation in the master complaint is that "JUUL users are… at greater risk of suffering more serious complications if they contract the coronavirus."[18]The master complaint does not refer to any scientific studies purporting to describe a causal relationship between vaping and the severity of COVID-19.  Rather, the complaint points to (i) a statement by Michael Felberbaum, a Food and Drug Administration spokesman, who commented in March 2020 that "[e]-cigarettes can damage lung cells," and expose people who "smoke and/or vape tobacco or nicotine-containing products" to more "serious complications from COVID-19" (though it should be noted that the FDA subsequently modified this position, stating that it was unknown "whether [vape product] exposure[] increase[s] the risk of COVID-19"[19], and (ii) a statement from the National Institute on Drug Abuse that COVID-19 posed an "especially serious threat" to persons who vape "[b]ecause [COVID-19] attacks the lungs."[20]

In a courtroom, these assertions must be analyzed not in the context of public health, but of tort law. To establish general causation, a plaintiff must prove that it is more probable than not that an exposure is capable of causing or contributing to the disease in question; a mere showing that the relationship is plausible is legally insufficient.[21] Further, "[t]o prove general causation, scientists frequently rely on epidemiological data to first establish an association between a chemical and a disease or set of symptoms which they then probe to determine if the association warrants being described as cause-effect relationship."[22]

By this standard, assertions like those in the JUUL MDL appear to be insufficient to support a viable claim. There is no epidemiological or toxicological data that might help assess the question of whether it is "more likely than not" that vaping causes, or increases the severity of, COVID-19. Standing alone, the assertions do not meet the tort law requirement of an in-depth assessment of causality. The assertions are classic statements of plausibility, not of causation. However, while cases always unfold in real time, in this case, the science is doing so as well. Whether courts will allow cases to proceed, on the theory that as the cases progress the science will as well, remains to be seen.

Learn more about this issue by contacting any of the authors.

An earlier version of this article appeared on Law360 on October 22, 2020.

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References and citations

[1]Gaiha, S. M., Cheng, J., & Halpern-Felsher, B. (2020). Association Between Youth Smoking, Electronic Cigarette Use, and COVID-19. J Adolesc Health, 67(4), 519-523. doi:10.1016/j.jadohealth.2020.07.00ha et al., 2020.
[2]Li, D., Croft, D. P., Ossip, D. J., & Xie, Z. (2020). Are Vapers More Susceptible to COVID-19 Infection? medRxiv, 2020.2005.2005.20092379. doi:10.1101/2020.05.05.20092379.
[3] Leung, J. M., Yang, C. X., & Sin, D. D. (2020). COVID-19 and nicotine as a mediator of ACE-2. Eur Respir J, 55(6). doi:10.1183/13993003.01261-2020
[4] McAlinden, K. D., Eapen, M. S., Lu, W., Chia, C., Haug, G., & Sohal, S. S. (2020). COVID-19 and vaping: risk for increased susceptibility to SARS-CoV-2 infection? European Respiratory Journal, 56(1), 2001645. doi:10.1183/13993003.01645-2020.
[5] Russo, P., Bonassi, S., Giacconi, R., Malavolta, M., Tomino, C., & Maggi, F. (2020). COVID-19 and smoking: is nicotine the hidden link? Eur Respir J, 55(6). doi:10.1183/13993003.01116-2020.
[6] Lee, A. C., Chakladar, J., Li, W. T., Chen, C., Chang, E. Y., Wang-Rodriguez, J., & Ongkeko, W. M. (2020). Tobacco, but not nicotine and flavor-less electronic cigarettes, induces ACE2 and immune dysregulation. bioRxiv, 2020.2007.2013.198630. doi:10.1101/2020.07.13.198630.
[7] Alqahtani, J. S., Oyelade, T., Aldhahir, A. M., Alghamdi, S. M., Almehmadi, M., Alqahtani, A. S., Quaderi, S., Mandal, S., & Hurst, J. R. (2020). Prevalence, Severity and Mortality associated with COPD and Smoking in patients with COVID-19: A Rapid Systematic Review and Meta-Analysis. PLoS One, 15(5), e0233147. doi:10.1371/journal.pone.0233147.
[8] Guo, F. R. (2020). Smoking links to the severity of Covid-19: An update of a meta-analysis. J Med Virol. doi:10.1002/jmv.25967.
[9] Patanavanich, R., & Glantz, S. A. (2020). Smoking Is Associated With COVID-19 Progression: A Meta-analysis. Nicotine & Tobacco Research, 22(9), 1653-1656. doi:10.1093/ntr/ntaa082.
[10] Zhao, Q., Meng, M., Kumar, R., Wu, Y., Huang, J., Lian, N., Deng, Y., & Lin, S. (2020). The impact of COPD and smoking history on the severity of COVID-19: A systemic review and meta-analysis. J Med Virol. doi:10.1002/jmv.25889.
[11] Lippi, G., & Henry, B. M. (2020). Active smoking is not associated with severity of coronavirus disease 2019 (COVID-19). Eur J Intern Med. doi:10.1016/j.ejim.2020.03.014.
[12] Zheng, Z., Peng, F., Xu, B., Zhao, J., Liu, H., Peng, J., Li, Q., Jiang, C., Zhou, Y., Liu, S., Ye, C., Zhang, P., Xing, Y., Guo, H., & Tang, W. (2020). Risk factors of critical & mortal COVID-19 cases: A systematic literature review and meta-analysis. J Infect. doi:10.1016/j.jinf.2020.04.021.
[13] Cen, Y., Chen, X., Shen, Y., Zhang, X. H., Lei, Y., Xu, C., Jiang, W. R., Xu, H. T., Chen, Y., Zhu, J., Zhang, L. L., & Liu, Y. H. (2020). Risk factors for disease progression in patients with mild to moderate coronavirus disease 2019-a multi-centre observational study. Clin Microbiol Infect. doi:10.1016/j.cmi.2020.05.041.
[14] Miyara, M., Tubach, F., POURCHER, V., Morelot-Panzini, C., Pernet, J., Haroche, J., Lebbah, S., Morawiec, E., Gorochov, G., Caumes, E., Hausfater, P., COMBES, A., Similowski, T., & Amoura, Z. (2020). Low incidence of daily active tobacco smoking in patients with symptomatic COVID-19. Qeios, preprint v3. Retrieved from
[15] Petrilli, C. M., Jones, S. A., Yang, J., Rajagopalan, H., O'Donnell, L., Chernyak, Y., Tobin, K. A., Cerfolio, R. J., Francois, F., & Horwitz, L. I. (2020). Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study. BMJ, 369, m1966. doi:10.1136/bmj.m1966.
[16] Polosa, R., & Caci, G. (2020). COVID-19: counter-intuitive data on smoking prevalence and therapeutic implications for nicotine. Intern Emerg Med. doi:10.1007/s11739-020-02361-9.
[17] WHO. (June 30, 2020). Smoking and COVID-19. Retrieved from
[18] In re JUUL Labs, Inc. Marketing, Sales Practices, and Products Liability Litigation, MDL 2913 (C.D. Cal.), Amended Complaint April 6, 2020, ¶ 725.
[19] Bloomberg. (2020). FDA Shifts Its Covid-19 Stance on Vaping, Smoking Impact. Retrieved from
[20] In re JUUL Labs, Inc., Amended Complaint April 6, 2020, ¶ 726.
[21]Allen v. Pennsylvania Engineering Corp.,102 F. 3d 194, 198 (5th Cir. 1996) (regulatory agencies tasked with making "prophylactic rules governing human exposure" adopt a "preventive perspective" where the "threshold of proof is reasonably lower than that appropriate in tort law, which "traditionally make[s] more particularized inquiries into cause and effect" and requires a plaintiff to prove "that it is more likely than not that another individual has caused him or her harm") (quoting Wright v. Willamette Industries, Inc., 91 F.3d 1105, 1107 (8th Cir.1996)).
[22] Beyer v. Anchor Insulation Co., 238 F. Supp. 3d 270, 280 (D. Conn. 2017) (citing Federal Judicial Center, Reference Manual on Scientific Evidence 374 (2d ed. 2000)).

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