Nicotine and COVID-19: The Research

Table of Contents

1. Research at a Glance
2. The Papers
3. PubMed Topic Searches
4. More Nicotine Research
5. Connections
6. Featured Videos

Research at a Glance

What kind of study each paper on this page is, and when the papers were published. Hover over a bar for its count.

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The Papers (33)

Newest first. Study types on this page — Human trial: 1 · Human observational study: 4 · Meta-analysis: 1 · Review: 15 · Animal study: 1 · Cell study: 3 · Other: 8. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Evidence update on the respiratory health effects of vaping e-cigarettes: A systematic review and meta-analysis

Meta-analysis, 2025. This is a systematic review and meta-analysis combining 119 studies (5 in the statistical pooling) on people, animals and cells, looking at whether nicotine e-cigarette or vaping use affects breathing and lung health. People who vaped but had never smoked had a higher risk of respiratory symptoms than people who never used either product, and a higher but not statistically significant risk of COPD. Vapers who had never smoked had a lower risk of respiratory symptoms than smokers, but people who both vaped and smoked had a higher risk of symptoms and more COPD than people who used neither, similar to smokers alone. The authors rated most of this evidence as very low to low certainty, though some non-pooled studies showed moderate-certainty evidence of more respiratory symptoms, COPD, asthma, and lung inflammation and damage in vapers, with mixed findings on COVID-19 and other infections and no clear link to e-cigarette-associated lung injury.

Kundu A, Feore A, Abu-Zarour N et al. (2025). Evidence update on the respiratory health effects of vaping e-cigarettes: A systematic review and meta-analysis. Tob Induc Dis. — PubMed PMID: 41268099 · doi:10.18332/tid/209954

COVID-19 Disease and Chronic Health Outcomes Associated with Nicotine Use in a Great Plains Tribal Community: A Community-Based Study

Human observational study, 2025. Researchers surveyed 562 adults from 289 households on the Cheyenne River Sioux reservation and compared self-reported health among people who used only e-cigarettes, only cigarettes, both, or neither. Over half of the participants (53%) used nicotine, and the median number of puffs per day was 15 for e-cigarette users, 100 for cigarette smokers and 20 for people who used both. Compared with non-users, nicotine users had lower odds of reporting COVID-19, high blood pressure and high cholesterol, and lower odds of severe COVID-19 infection, but higher odds of a longer COVID-19 recovery time. All health outcomes were self-reported in a survey, and the study looked at associations at one point in time rather than testing nicotine directly.

Tillery A, O'Leary R, Aherrera A et al. (2025). COVID-19 Disease and Chronic Health Outcomes Associated with Nicotine Use in a Great Plains Tribal Community: A Community-Based Study. J Racial Ethn Health Disparities. — PubMed PMID: 39256325 · doi:10.1007/s40615-024-02145-3

Nicotine: From Discovery to Biological Effects

Review, 2023. This review covers the history of tobacco and summarizes research on the biological effects of nicotine in mammalian cells, including its actions through nicotinic receptors (nAChRs), particularly a specific receptor subtype (alpha7). It describes effects such as new blood vessel formation, cell division, and cell proliferation triggered by nicotine. The paper states nicotine is highly addictive and hazardous, and notes that a possible link between nicotine and COVID-19 severity needs further study.

Sansone L, Milani F, Fabrizi R et al. (2023). Nicotine: From Discovery to Biological Effects. Int J Mol Sci. — PubMed PMID: 37834017 · doi:10.3390/ijms241914570

Increased Nicotine Consumption in Australia During the First Months of the COVID-19 Pandemic

Human observational study, 2023. This study used Australian wastewater testing and nicotine replacement therapy sales data from 2017 to 2020 to estimate population-wide nicotine consumption as a proxy for smoking. Nicotine consumption fell from 2017 to 2019 but rose about 30% in the first half of 2020, the start of the COVID-19 pandemic, compared with the prior period. Sales of nicotine replacement products also rose gradually over the same years. The authors suggest the 2020 increase may relate to pandemic stress and more opportunities to smoke or vape while working from home during lockdowns.

Thai PK, Tscharke BJ, O'Brien J et al. (2023). Increased Nicotine Consumption in Australia During the First Months of the COVID-19 Pandemic. Nicotine Tob Res. — PubMed PMID: 36889356 · doi:10.1093/ntr/ntac275

Is the post-COVID-19 syndrome a severe impairment of acetylcholine-orchestrated neuromodulation that responds to nicotine administration?

Human trial, 2023. Researchers proposed that the COVID-19 spike protein can attach to nicotinic acetylcholine receptors in the nervous system, which may disrupt normal nerve signaling and help explain the brain fog, muscle weakness, pain, breathlessness and mood changes seen in post-COVID-19 syndrome. Because nicotine binds these same receptors much more strongly than the body's natural acetylcholine, the authors suggested it might displace the virus from the receptor and restore normal signaling. In a small number of people with post-COVID-19 syndrome treated with a nicotine patch, the authors reported improvements ranging from rapid partial relief to complete resolution of symptoms within days.

Leitzke M (2023). Is the post-COVID-19 syndrome a severe impairment of acetylcholine-orchestrated neuromodulation that responds to nicotine administration?. Bioelectron Med. — PubMed PMID: 36650574 · doi:10.1186/s42234-023-00104-7

Nicotine in Combination with SARS-CoV-2 Affects Cells Viability, Inflammatory Response and Ultrastructural Integrity

Cell study, 2022. Researchers treated human lung cells grown in the lab with nicotine. They then exposed the cells to substances that mimic bacterial or viral infection, or infected them with SARS-CoV-2, the virus that causes COVID-19. With the infection-mimicking substances, nicotine lowered two inflammatory signals (IL6 and TNFα). With the real virus, nicotine made things worse: it increased the virus's damage to the cells, raised inflammatory signals, and caused severe cell injury that looked like two kinds of inflammatory cell death. These results come from cells only, but the authors concluded that nicotine has no protective role in COVID-19.

Sansone L, de Iure A, Cristina M et al. (2022). Nicotine in Combination with SARS-CoV-2 Affects Cells Viability, Inflammatory Response and Ultrastructural Integrity. Int J Mol Sci. — PubMed PMID: 36012747 · doi:10.3390/ijms23169488

Impact of vaping on respiratory health

Review, 2022. This is a review article discussing what is known about vaping and lung health, including the 2019 outbreak of vaping-associated lung injury (EVALI) and effects of long-term vaping on the respiratory system and COVID-19 outcomes. The authors conclude that vaping carries respiratory risks and that more research is needed to guide public policy, but they note the role of vaping in smoking cessation and harm reduction remains controversial.

Jonas A (2022). Impact of vaping on respiratory health. BMJ. — PubMed PMID: 35851281 · doi:10.1136/bmj-2021-065997

Cholinergic anti-inflammatory pathway and COVID-19

Review, 2022. This short commentary discusses a body signaling pathway called the cholinergic anti-inflammatory pathway, which some researchers have proposed as a way nicotine from tobacco might reduce the severity of COVID-19, even though smoking itself has generally been seen as making COVID-19 worse. The paper describes possible treatment approaches that work through this same pathway, such as stimulating the vagus nerve or using drugs that selectively activate a specific nicotine-receptor subtype, as potential COVID-19 therapies.

Mehranfard D, Speth RC (2022). Cholinergic anti-inflammatory pathway and COVID-19. Bioimpacts. — PubMed PMID: 35411295 · doi:10.34172/bi.2022.23980

Substance abuse and neurotransmission

Review, 2022. This book chapter reviews what is known about how drugs of abuse change brain signaling pathways, covering cocaine, amphetamines, opioids, alcohol, and nicotine together, plus how HIV-1 or COVID-19 infection interacts with substance abuse to affect the brain. It also discusses strategies for developing new drug-addiction treatments. Nicotine is covered as one of several substances of abuse rather than as the paper's sole focus.

Davis S, Zhu J (2022). Substance abuse and neurotransmission. Adv Pharmacol. — PubMed PMID: 35341573 · doi:10.1016/bs.apha.2021.10.007

Mitochondrial nicotinic acetylcholine receptors: Mechanisms of functioning and biological significance

Review, 2022. This review discusses nicotinic acetylcholine receptors that are found not just on cell surfaces but inside mitochondria, where they help control the release of substances linked to cell death, such as cytochrome c and reactive oxygen species. It summarizes laboratory research from the past five years on how these mitochondrial receptors signal using kinases, including studies with mice lacking certain receptor subunits, and discusses their role in several diseases including neuroinflammation, liver damage, and SARS-CoV-2 infection.

Skok M (2022). Mitochondrial nicotinic acetylcholine receptors: Mechanisms of functioning and biological significance. Int J Biochem Cell Biol. — PubMed PMID: 34929396 · doi:10.1016/j.biocel.2021.106138

Electronic Cigarette Use Is Not Associated with COVID-19 Diagnosis

Human observational study, 2021. Researchers looked at health records of 69,264 patients age 12+ who smoked cigarettes or vaped and sought care at a medical center between September 2019 and November 2020. People who used only e-cigarettes were no more or less likely to be diagnosed with COVID-19 than others, while people who only smoked cigarettes actually had a lower chance of a COVID-19 diagnosis, and people who did both fell in between. The authors noted that because nicotine is in both cigarettes and e-cigarettes but only cigarette smoking showed a lower risk, any protective effect of cigarette smoking against infection is probably not caused by nicotine itself.

Jose T, Croghan IT, Hays JT et al. (2021). Electronic Cigarette Use Is Not Associated with COVID-19 Diagnosis. J Prim Care Community Health. — PubMed PMID: 34109870 · doi:10.1177/21501327211024391

Regulation of the acetylcholine/α7nAChR anti-inflammatory pathway in COVID-19 patients

Human observational study, 2021. Researchers studied blood samples from 37 people hospitalized with COVID-19 (10 moderate, 11 severe, 16 critical) and 14 healthy people of similar age, measuring genes related to the body's nicotinic/acetylcholine anti-inflammatory system. A specific gene variant called CHRFAM7A, which is linked to the alpha-7 nicotinic receptor that nicotine acts on, was expressed significantly less often in the critically ill patients than in healthy controls. Patients who did not express this gene had higher inflammation markers (CRP), more lung damage, lower lymphocyte counts, and higher activity of an inflammation-promoting pathway (TNF). The authors concluded that this reduced expression should be taken into account before considering nicotine as a way to target this pathway in COVID-19.

Courties A, Boussier J, Hadjadj J et al. (2021). Regulation of the acetylcholine/α7nAChR anti-inflammatory pathway in COVID-19 patients. Sci Rep. — PubMed PMID: 34088975 · doi:10.1038/s41598-021-91417-7

An updated overview of e-cigarette impact on human health

Review, 2021. This review looks at research on how e-cigarettes affect human health, including adjustable nicotine content as one of their features. It reports that lab studies in cells and animals suggest e-cigarettes may be safer than conventional cigarettes, but that short-term use has been shown to cause harmful effects, and long-term effects have barely been studied. The heating process itself can also create new chemical byproducts of uncertain toxicity.

Marques P, Piqueras L, Sanz MJ (2021). An updated overview of e-cigarette impact on human health. Respir Res. — PubMed PMID: 34006276 · doi:10.1186/s12931-021-01737-5

E-cigarette vape and lung ACE2 expression: Implications for coronavirus vulnerability

Animal study, 2021. Mice were exposed to inhaled nicotine vapor from e-cigarettes to see how it affects a lung protein called ACE2, which the coronavirus uses to enter cells. In male mice, nicotine vapor increased ACE2 in the lungs, but this was not seen in female mice. Both nicotine and the vapor base lowered one type of nicotinic receptor (alpha5) in both sexes, with no change in another type (alpha7). Blood levels of ACE2 did not change, suggesting a blood test would not reflect what was happening in the lungs.

Lallai V, Manca L, Fowler CD (2021). E-cigarette vape and lung ACE2 expression: Implications for coronavirus vulnerability. Environ Toxicol Pharmacol. — PubMed PMID: 33838329 · doi:10.1016/j.etap.2021.103656

COVID-19 and Smoking: What Evidence Needs Our Attention?

Review, 2021. This is a review article discussing the relationship between smoking and COVID-19. It notes that nicotine increases the activity of the ACE2 receptor, which the virus uses to enter cells, potentially making smokers more susceptible to severe disease. The review also notes that while nicotine has some anti-inflammatory effects, no evidence supports using it to treat COVID-19, and smoking should not be seen as protective.

Xie J, Zhong R, Wang W et al. (2021). COVID-19 and Smoking: What Evidence Needs Our Attention?. Front Physiol. — PubMed PMID: 33815131 · doi:10.3389/fphys.2021.603850

Nicotinic cholinergic system and COVID-19: In silico identification of interactions between α7 nicotinic acetylcholine receptor and the cryptic epitopes of SARS-Co-V and SARS-CoV-2 Spike glycoproteins

Other, 2021. This was a computer modeling study only; no people, animals or cells were tested. The researchers used computer models to see how the spike proteins of SARS-CoV and SARS-CoV-2, the virus that causes COVID-19, might fit against the human α7 nicotinic acetylcholine receptor, a receptor that nicotine acts on. In every model, the contact area included a large part of the spike's 'toxin-like' section, which resembles part of a snake venom toxin, and the spot on the receptor where such toxins bind. The authors say this supports the idea that nicotine and similar substances that activate the same receptors might be protective, and that antibodies against this part of the spike protein should be studied further.

Lagoumintzis G, Chasapis CT, Alexandris N et al. (2021). Nicotinic cholinergic system and COVID-19: In silico identification of interactions between α7 nicotinic acetylcholine receptor and the cryptic epitopes of SARS-Co-V and SARS-CoV-2 Spike glycoproteins. Food Chem Toxicol. — PubMed PMID: 33503469 · doi:10.1016/j.fct.2021.112009

Is there a smoker's paradox in COVID-19?

Review, 2021. This review looked at earlier studies on whether smokers are underrepresented among COVID-19 patients, a pattern some called a 'smoker's paradox.' The authors found several biases and gaps in the existing data that could create a false impression that smoking protects against COVID-19, and concluded that the evidence for this protective effect is limited and questionable. They discuss possible biological mechanisms that have been proposed, including an anti-inflammatory effect of nicotine, a dampened immune response in smokers, and increased nitric oxide in the airways, but caution that smoking could just as easily worsen COVID-19 risk and outcomes, as it does with other respiratory infections.

Usman MS, Siddiqi TJ, Khan MS et al. (2021). Is there a smoker's paradox in COVID-19?. BMJ Evid Based Med. — PubMed PMID: 32788164 · doi:10.1136/bmjebm-2020-111492

Activation of the Cholinergic Anti-Inflammatory Pathway as a Novel Therapeutic Strategy for COVID-19

Review, 2020. This is a discussion paper proposing that activating a nerve-based anti-inflammatory pathway could help treat COVID-19. It states that nicotine, along with another compound called anisodamine and certain herbal medicines, has been shown in lab and animal studies to activate this pathway and reduce inflammation. The authors suggest this approach, including vagus nerve stimulation and acupuncture, is worth testing for safety and effectiveness in COVID-19 patients, but no actual patient trial is reported in this paper.

Qin Z, Xiang K, Su DF et al. (2020). Activation of the Cholinergic Anti-Inflammatory Pathway as a Novel Therapeutic Strategy for COVID-19. Front Immunol. — PubMed PMID: 33633726 · doi:10.3389/fimmu.2020.595342

Nicotine e-vaping and cardiovascular consequences: a case series and literature review

Other, 2020. This paper reviews the medical literature and reports three patient cases of people with existing peripheral artery disease who switched from heavy cigarette smoking to high-intensity nicotine e-vaping. All three developed further arterial complications within 6 to 30 months of making the switch. The authors also discuss a possible link between nicotine e-vaping and COVID-19 risk, though no specific findings on that link are given in the abstract.

Jessri M, Sultan AS, Magdy E et al. (2020). Nicotine e-vaping and cardiovascular consequences: a case series and literature review. Eur Heart J Case Rep. — PubMed PMID: 33437920 · doi:10.1093/ehjcr/ytaa330

Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity

Cell study, 2020. Researchers exposed human airway lining cells grown in the lab to nicotine at a concentration meant to match what a person takes in from one cigarette, for 1 hour, 48 hours or continuously. Acting through a nicotinic receptor called alpha-7, nicotine made the cells survive and multiply more, delayed their normal aging, lowered the protective protein p53, raised growth signals such as VEGF and EGFR, cut the cells' energy (ATP) production, and made them move more and grow without anchoring, changes linked to a more tumor-like state. These results come only from lab-grown cells, and the experiments did not use the virus. The authors still concluded, from these findings and earlier evidence, that nicotine is likely involved in how severe SARS-CoV-2 infection becomes.

Lupacchini L, Maggi F, Tomino C et al. (2020). Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity. Molecules. — PubMed PMID: 33379366 · doi:10.3390/molecules26010101

Neuroinvasion and Viral Reservoir in COVID-19

Review, 2020. This review article discusses theories about how COVID-19 may affect the nervous system, including direct invasion of the brain and crossing of the blood-brain barrier. One of the three theories it discusses is a 'nicotinic hypothesis,' which proposes that the virus interacts with nicotinic acetylcholine receptors as part of how it affects the body and nervous system. The paper does not report new experimental data; it summarizes existing ideas about these mechanisms.

Altable Pérez M, De la Serna JM (2020). Neuroinvasion and Viral Reservoir in COVID-19. Cureus. — PubMed PMID: 33214943 · doi:10.7759/cureus.11014

Nicotine and the nicotinic cholinergic system in COVID-19

Review, 2020. This review looks at how nicotine and the body's nicotinic receptor system might affect COVID-19. The authors agree that smoking does harm and support quitting smoking to lower COVID-19 risk. They also argue that nicotine itself, or drugs that act on nicotinic receptors, could have a possible treatment role, because these may affect mood and inflammation and might interfere with how the virus enters or copies itself in cells. The authors present this as a possibility and a hypothesis. The paper reports no new experiments in people, animals or cells.

Tizabi Y, Getachew B, Copeland RL et al. (2020). Nicotine and the nicotinic cholinergic system in COVID-19. FEBS J. — PubMed PMID: 32790936 · doi:10.1111/febs.15521

The rise of electronic nicotine delivery systems and the emergence of electronic-cigarette-driven disease

Review, 2020. This review article discusses electronic cigarette use and the 2019 outbreak of vaping-associated lung injury in the United States, which affected over 2,000 patients and caused 68 deaths. It describes how e-cigarette vapor has been shown to affect cell metabolism and cause DNA damage, and links e-cigarette use to higher risk of chronic obstructive pulmonary disease, increased severity of lung infections, and increased pneumonia risk. The paper notes that whether vaping affects susceptibility to viruses, including coronavirus, is not yet determined, and states that e-cigarettes have not been shown to help people quit smoking.

McAlinden KD, Eapen MS, Lu W et al. (2020). The rise of electronic nicotine delivery systems and the emergence of electronic-cigarette-driven disease. Am J Physiol Lung Cell Mol Physiol. — PubMed PMID: 32726146 · doi:10.1152/ajplung.00160.2020

A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications

Other, 2020. This short article puts forward an idea, a hypothesis, about Covid-19 and does not report a new experiment. The authors cite early population data suggesting that people who currently smoked appeared less likely to be infected by the virus that causes Covid-19. From this they propose that the nicotinic acetylcholine receptor, the receptor that nicotine acts on, plays a key role in how the infection develops. They suggest the receptor could be a target for preventing and controlling Covid-19, but the article did not test this in people, animals or cells.

Changeux JP, Amoura Z, Rey FA et al. (2020). A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications. C R Biol. — PubMed PMID: 32720486 · doi:10.5802/crbiol.8

Nicotine and smoking in the COVID-19 era

Other, 2020. This brief report compared smoking rates reported in 12 published studies of COVID-19 patients against expected smoking rates in the general population of the same regions. The analysis found a lower proportion of COVID-19 patients with a smoking history than the regional population average would predict. The authors caution that the finding has important limitations and should be seen only as a preliminary observation to prompt further research, not a conclusion.

Tajlil A, Ghaffari S, Pourafkari L et al. (2020). Nicotine and smoking in the COVID-19 era. J Cardiovasc Thorac Res. — PubMed PMID: 32626554 · doi:10.34172/jcvtr.2020.22

The cholinergic anti-inflammatory pathway alleviates acute lung injury

Review, 2020. This is a commentary discussing how a protein called HMGB1, released by dying or stressed cells, drives lung inflammation. It describes a pathway in which the body's own nerve signaling (the cholinergic system) can reduce this inflammation, and highlights an earlier study in which a drug that activates the alpha7 nicotinic acetylcholine receptor reduced lung injury and HMGB1 buildup in an oxygen-induced lung injury model. The commentary suggests activating this same pathway might help with severe COVID-19 lung injury, but this is a proposed idea, not a result from new experiments in this paper.

Andersson U (2020). The cholinergic anti-inflammatory pathway alleviates acute lung injury. Mol Med. — PubMed PMID: 32600316 · doi:10.1186/s10020-020-00184-0

Cytokine Release Syndrome (CRS) and Nicotine in COVID-19 Patients: Trying to Calm the Storm

Other, 2020. This paper puts forward a hypothesis; it is not a study. Severe COVID-19 can set off a 'cytokine storm', in which the immune system releases too many inflammatory signals. The authors suggest nicotine might calm that storm, because it switches on a type of nicotinic receptor (α7) that is part of the body's own anti-inflammation pathway, and they note nicotine is already used in ulcerative colitis to reduce inflammation. They point to early clinical reports from China suggesting smokers were statistically less likely to be hospitalized, and they propose nicotine as a possible treatment for severely ill patients, but they did not test it in patients, animals or cells.

Gonzalez-Rubio J, Navarro-Lopez C, Lopez-Najera E et al. (2020). Cytokine Release Syndrome (CRS) and Nicotine in COVID-19 Patients: Trying to Calm the Storm. Front Immunol. — PubMed PMID: 32595653 · doi:10.3389/fimmu.2020.01359

How nicotine can inhibit cytokine storm in the lungs and prevent or lessen the severity of COVID-19 infection?

Other, 2020. This is a short letter that puts forward an idea; it is not a new experiment. It starts from survey reports suggesting that people who smoke were less likely to catch COVID-19, or had milder breathing symptoms, than non-smokers. The authors suggest nicotine may calm the inflammatory response in the lungs. Because immune cells in the lungs called macrophages largely shape how the body responds to and clears the virus, the letter reviews recent findings that could explain how nicotine might change the way these cells respond during COVID-19.

Kloc M, Ghobrial RM, Kubiak JZ (2020). How nicotine can inhibit cytokine storm in the lungs and prevent or lessen the severity of COVID-19 infection?. Immunol Lett. — PubMed PMID: 32522666 · doi:10.1016/j.imlet.2020.06.002

COVID-19 breakthroughs: separating fact from fiction

Review, 2020. This review article discusses several COVID-19-related claims and controversies, including the scientific evidence on whether nicotine affects how severe COVID-19 disease becomes, alongside separate topics like ibuprofen use, surface contamination, disparities in impact on minority groups, vitamin D, and differences in disease severity in children versus adults across countries.

Dhillon P, Breuer M, Hirst N (2020). COVID-19 breakthroughs: separating fact from fiction. FEBS J. — PubMed PMID: 32500928 · doi:10.1111/febs.15442

COVID-19 and the nicotinic cholinergic system

Other, 2020. This short letter discusses COVID-19 and the body's nicotinic cholinergic system, the network of receptors that nicotine acts on. The authors note that smoking appears to be uncommon among people hospitalised with COVID-19. They propose that some COVID-19 symptoms could be linked to a breakdown of the cholinergic anti-inflammatory pathway, a nerve-based system that helps calm inflammation. They suggest that substances that activate nicotinic receptors should be studied as possible treatments; the letter reports no new experiments or patient data.

Farsalinos K, Angelopoulou A, Alexandris N et al. (2020). COVID-19 and the nicotinic cholinergic system. Eur Respir J. — PubMed PMID: 32444400 · doi:10.1183/13993003.01589-2020

COVID-19 and nicotine as a mediator of ACE-2

Other, 2020. This is a short letter to a lung medicine journal, written early in the COVID-19 pandemic, about how nicotine might be connected to ACE-2. ACE-2 is the protein on the surface of cells that the COVID-19 virus uses to get in. The letter suggests that the alpha-7 nicotinic receptor, which nicotine acts on, may increase the amount of ACE-2 on cells. This is an idea put forward for discussion. The abstract reports no experiment, no participants and no measured results.

Leung JM, Yang CX, Sin DD (2020). COVID-19 and nicotine as a mediator of ACE-2. Eur Respir J. — PubMed PMID: 32350104 · doi:10.1183/13993003.01261-2020

COVID-19 and smoking: is nicotine the hidden link?

Cell study, 2020. This short letter asks whether nicotine itself could help explain a possible link between smoking and COVID-19. The authors report that, in human airway lining cells grown in the laboratory, nicotine acting through one type of nicotinic receptor (the alpha7 receptor) increased the amount of ACE-2, the protein the COVID-19 virus uses to enter cells. This result comes only from cells in a dish and was not tested in people.

Russo P, Bonassi S, Giacconi R et al. (2020). COVID-19 and smoking: is nicotine the hidden link?. Eur Respir J. — PubMed PMID: 32341101 · doi:10.1183/13993003.01116-2020

Is nicotine exposure linked to cardiopulmonary vulnerability to COVID-19 in the general population?

Review, 2020. This review, written early in the COVID-19 pandemic, looks at people who were exposed to nicotine before they caught the virus. The authors propose that these people may be 'primed' for a higher risk of serious illness, because nicotine can act directly on ACE2, the likely entry point the virus uses to get into cells, and can trigger harmful signalling in the cells that line the lungs. This is a prediction based on known biology. The review reports no new study in people that tests it.

Olds JL, Kabbani N (2020). Is nicotine exposure linked to cardiopulmonary vulnerability to COVID-19 in the general population?. FEBS J. — PubMed PMID: 32189428 · doi:10.1111/febs.15303

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PubMed Topic Searches

1. PubMed: COVID-19 and nicotine (the search this page is built from)

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Connections

• Immune Response — interactive animation
• Nicotine: The Research
• Dr. Bryan Ardis on this subject — his claims, presented on their own pages and kept separate from this research collection
• The Nicotine Patch, animated
• Nicotinic Acetylcholine Receptors
• Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
• Brain and Memory
• Mood and Mental Health
• Inflammation and Immunity
• Cancer Research
• Heart and Blood Vessels
• Metabolism and Weight
• Addiction and Withdrawal
• Patches, Gum and Delivery

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