Is COVID-19 "airborne"?
finding nuance amongst the scaremongering
You may have heard speculation that SARS-CoV-2, the virus causing the COVID-19 pandemic, is “airborne”. Sounds scary! You may have also heard public health officials reassure you that it’s not. But the “airborne” question bedevils scientists trying to communicate with the public. It combines a locus of substantial public fear with a question of true scientific nuance—a recipe for a misinformation mess. In brief: it’s probably not as easily trasmitted as something like measles, but people should absolutely maintain distance, wear masks to protect others, and try to stay in well-ventilated places, and doctors absolutely need appropriate protective equipment.
Many viruses—from measles to flu, and including SARS-CoV-2—are “airborne” in the sense that one way of getting sick is is to inhale virus particles (“virions”) sneezed or coughed into the air within respiratory secretions. Some secretions are on the bigger end, and we tend to call those “droplets”. Others are smaller, and we tend to call them “aerosols”. Of course, secretion size is in fact a continuous spectrum.
The tricky crux of the matter is that when people say “airborne”, what they often mean is “you’re at risk from virus particles hanging in the air—or being kicked back up into the air after falling to the ground—long, long after an infectious person sneezed them out”. That’s much more of a risk for smaller, “aerosol”-end-of-the-spectrum secretions. And it turns out that it’s more of a risk for some viruses than for others. Big, big risk for measles (which is part of why it is so transmissible). Less of a risk for flu (though probably not zero), even though both measles and flu can in principle be found both in aerosol-like and in droplet-like secretions. So far, scientists mainly think COVID looks more like flu.
But there’s still nuance. The WHO has strongly emphasized the role of droplet-sized particles in everyday SARS-CoV-2 transmission. Other experts are not sure we can be quite so confident just yet. See comments from Prof. Linsey Marr, an expert on these matters, in this NY Times article.
If my explanations don’t satisfy you, she is a great person to look up. She’s a true expert on this problem; I’m not. What’s more, she explains these things very clearly (see her twitter for many such good explanations)
Where nobody disagrees is that there are frighteningly plausible aerosol transmission risks in hospital settings, since medical procedures performed to treat severe COVID can produce aerosols. This is a major reason why hospitals are in such critical need of appropriate protective equipment for frontline healthcare workers (e.g. N95 masks).
This article is fairly long and in depth, but gives a good and relatively accessible overview, and it’s endorsed by Prof. Marr.
One final note of crucial nuance, and one where my own expertise is more relevant. Much reporting on our study of the aerosol and surface stability of SARS-CoV-2 has emphasized absolute times up until which we could detect viable virus. But that’s not really the appropriate number for assessing human infection risk, for two major reasons:
- We don’t know what concentration of infectious virus needs to be present to pose a risk of human infection.
- As you might expect, a larger initial deposited quantity of virus will result in a longer time until no viable virus is left.
This is why we calculated half lives rather than just reporting raw times to decay. The absolute time until viable virus is undetectable unsurprisingly depends upon how much viable virus you initially put there. The value of knowing decay rates (or, equivalently, half lives) is that you can estimate how long an arbitrary initial quantity will stick around, rather than being wedded to guesses about the particular quantity with which you were able to experiment. So if you look at our numbers, look at the half-lives.
A journalist I spoke with at the Philly Inquirer did a very nice job of summarizing these last few points.