Vaping makes airways susceptible to infection
Following the vape trail through the body, the next stop is the lungs, where there’s mounting evidence that the chemicals in vape smoke might make the cells lining our airways an easier target for infection, as Queen Mary University of London’s Jonathan Grigg explains to Chris Smith…
Jonathan - So, what we do is grow cells that line the airways - the lower airways, deep in the lungs - grow them in the laboratory and put e-cigarette vapour onto them. And what we see is that those cells become stickier for bacteria that can cause really quite serious respiratory lung illnesses. And one of the commonest is called the pneumococcus. It actually causes quite serious pneumonia, actually can get across into the bloodstream. And we see more bugs of these bacteria sticking to the cells when they've been exposed to e-cigarette vapour. And one reason for that is that the e-cigarette vapour causes something called oxidative stress. In other words, it stresses the cells and the cells respond by making themselves stickier for these bugs to infect them.
Chris - Do you know if that stickiness actually has consequences though, because being a bit stickier might not translate into a greater or lesser disease risk? I mean, does it?
Jonathan - Well that's of course the key question of whether this happens in real life. Certainly what we call the receptor that the bugs use to stick onto is really a very important in a range of animal models. If the animals have more of this receptor in their airways, then they get more severe infection. We did follow it up by asking vapers to do a vaping session. And we brush the cells from their nose - and we think that the responses in the nose are probably very similar to the lower airway - and we found that with a vaping session, yes, the particular receptor that the bugs use did get up regulated. There was more of it after a vaping session. So it certainly happens in real life. We're not absolutely sure whether that's going to be translated into more vulnerability to severe infection, but it's certainly worrying to us.
Chris - Do you know how the vape is doing this to the cells? Is it just that oxidative stress reaction or are there specific chemicals in the vape that might be causing this to happen more, which would argue, well, if we don't use those chemicals or don't use those vapes, then we could reduce the risk?
Jonathan - Human vapers use a range of vaping implements, first, second, third generation vaping, different flavours. And we, we saw the same sort of response. We did look at nicotine-containing a nicotine-free vape, the same carrier, and we see the same effects whether nicotine is present or not. So it's not the nicotine itself that's causing it. We're probably certain that it's a generalisable phenomenon
Chris - And just bacteria, or could the effect also extend to fungi and possibly viruses?
Jonathan - We haven't looked. One study, which looked at the effect on a receptor that the SARS-CoV-2 virus uses to enter cells - that's called the ACE II receptor - certainly has been an initial report shown to be up regulated by e-cigarette vapour as well as cigarette smoke of course.
Chris - Now, if this is translating into a shift in clinical risk, given the uptake of vaping among younger people who are never normally smokers, are we seeing a link epidemiologically between vaping and possible more invasive chest infections with things like pneumonia?
Jonathan - The answer is not yet, but of course pneumonia is fortunately pretty rare in healthy young adults. It's taken us a very long time to show that active smoking was associated with pneumonia, invasive disease many, many years after the initial description of cancer. And it's confounded by the fact that people using different types of vape flavours, et cetera. And so epidemiological studies really haven't been done and we'd have, we don't know if there's a signal or not. But I think we have to say that these data are certainly worrying; that there are effects in the lower airway, which will make individuals more vulnerable to bacterial and possibly viral infections. But we haven't seen that signal yet.