No, Vaping Doesn’t Make You More Susceptible To Coronavirus

No, Vaping Doesn’t Make You More Susceptible To Coronavirus

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If you saw the headline ‘Vaping Increases Susceptibility to Coronavirus in Mice’ then your first thought might well be: “Why would a mouse vape?”

But after you read the scientific study behind that press release, it turns out the new research is serious — and its results are pretty interesting.

The SARS-CoV-2 virus targets cells in human lungs, which is why Covid is mainly a respiratory disease.

So the idea that inhaling vapor from e-cigarettes increases your risk of developing the disease makes intuitive sense. Is there any evidence to support that theory?

In fact, the link between vaping and Covid is controversial: although research showing an association has received widespread media coverage, studies producing null results have been largely ignored, leading to outcome reporting bias.

One large study you probably haven’t heard of was recently led by the Mayo Clinic and published in the Journal of Primary Care & Community Health.

The study involved almost 70,000 patients who were over 12 years old and smoked cigarettes or vaped. The demographic was relatively diverse, with 86% white, a 62:38 ratio of female to male, and an average age of 52. Those factors were considered when calculating how smoking might affect the chance of being diagnosed with Covid. Only 5% tested positive for SARS-CoV-2.

According to the Mayo Clinic study, people who only used e-cigarettes weren’t more likely to catch Covid, whereas traditional smokers had a decreased risk of disease. Those results suggest the common ingredient in both types of cigarette — nicotine — isn’t responsible for any alleged benefits to susceptibility.

As the study’s title concludes: ‘Electronic cigarette use is not associated with COVID-19 diagnosis’.

But while a large-scale human study should be conclusive, controversy over how vaping might influence susceptibility to infection by Coronavirus could continue — and will be further complicated by the research in mice.

The new study was carried out by researchers at Thomas Jefferson University in Philadelphia and published in the Journal of Investigative Medicine.

In the study, mice were exposed to vapor from e-cigarettes — with or without nicotine — for 30 minutes, twice a day over three weeks. Compared to a control group breathing room air, lung tissue from vaping mice had more inflammation and worked less efficiently.

The damage was done even when the vapor didn’t contain nicotine, which reinforces the fact that the chemicals in e-cigarettes are toxic and still not safe, regardless of vaping being less harmful than real cigarettes.

One result from studying the lungs is especially relevant to humans: exposure to e-cigarette vapor increased levels of ACE2 (Angiotensin-Converting Enzyme 2), the receptor on the surface of cells that SARS-CoV-2 uses to invade.

So the study has revealed a means by which vaping might raise the risk of Covid, and that mechanism involves the ACE2 receptor, which is what spike proteins on a virus particle must recognize and bind to in order to break into a human cell.

In mammals, the function of ACE2 is to work as a vasodilator and help control blood flow. The receptor is found all around the body but particularly common on the surface of pneumocytes, cells lining the lung’s air sacs, which explains why viral infection can lead to respiratory symptoms like pneumonia.

According to the mouse study, the increase in ACE2 levels was larger when e-cigarette vapor contained nicotine.

The research also found a difference between sexes, mirroring two observations in humans: men vape more than women and have a higher Covid mortality rate. Reflecting those findings, the increase in ACE2 levels due to nicotine was even greater in male mice, which points to potential physiological reasons for why one sex seems more susceptible to Coronavirus.

Imagine that a SARS-CoV-2 coronavirus particle is a burglar, a human cell is a house and ACE2 receptors are the windows: if vaping and nicotine means more receptors, those extra points of entry might make it easier for the virus to gain access.

Or at least, that’s the idea.

While the mechanism revealed by the new study is plausible, it’s important to remember that its results may not apply to people. After all, the experiments were performed in mice.



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