4 ms·

Interesting, but I see two big issues that render the data nearly meaningless: 1) does CO2 correlate well to spit droplets? they mention this (alleging that p

Interesting, but I see two big issues that render the data nearly meaningless: 1) does CO2 correlate well to spit droplets? they mention this (alleging that places with more talking have more spit droplets than ones without) but present no data. Also, does CO2 on public transport involve any exhaust from the vehicle? Are people in gyms breathing a lot with their mouth closed, producing more CO2 but not talking (or otherwise producing spit droplets) nearly as much. Lots of ways this could be not very correlated. 2) does quantity of spit droplets really correlate to likelihood of getting infected? Viruses are replicators. It is not at all obvious to me that 1/2 the number of viruses means 1/2 the risk of getting infected. It might not even result in a significant drop at all. Theoretically one droplet containing the virus is enough to infect you, and if infected it replicates. The operative factor is how well your immune system recognizes the threat and produces antibodies, not how many virus copies were there originally. One drop was enough to infect just over half of a young, healthy experimental subject group: https://www.science.org/content/article/scientists-deliberately-infected-people-coronavirus-here-s-what-happened https://www.science.org/content/article/scientists-deliberat...

pessimizer 4y ago
> The operative factor is how well your immune system recognizes the threat and produces antibodies, not how many virus copies were there originally. These probably aren't independent, and are occurring at the same time. So while a very small amount of virus is replicating, the immune system is mounting a defense, slowing down that replication. The virus may never get to a significant amount (although the immune response might knock you on your ass.) On the other hand, if you start with a ton of virus already, you'll be dealing with the immune response and the direct effects of the virus at the same time, and the virus may overwhelm or even limit the immune response.
- rossdavidh 4y ago
  True, but even a large number of droplets will not result in "a ton" of virus, if by "a ton" we mean "similar to what will result if you get sick". A sick person breathes out a lungful with every breath, so obviously a sick person contains far, far more copies of the virus than that. Put it another way. If your immune system recognizes the virus already, it matters little whether you get one droplet or a thousand, it will beat it because it has a several-day head start in doing so. If, on the other hand, your immune system does not already recognize it, then it will not begin to see the problem, and thus will not begin to react, until it has replicated up to a large amount, where "large" is some amount greater than either one droplet or one thousand will give you. So, the consequences of getting exposed to 1/2 or 1/10 of the number of copies of the virus, is basically nil, because an exponential rise will be needed in either case to get up to the level where your immune system notices a problem. Either your immune system already recognizes the virus as a problem, or it doesn't. I neither case does the dose matter, so long as the dose is big enough to start the process. And that probably doesn't take much.
  - PuppyTailWags 4y ago
    This isn't true. Even a robust immune system cannot prevent disease at large enough doses of virus because the immune system takes time to execute at any level of robustness. Similarly, a small enough dose will not necessarily cause disease, because the immune system can recognize the virus and eliminate it before it can replicate significantly. This is actually a time-based race: the speed of which the immune system can react vs the speed in which the virus can replicate in the body.
dentemple 4y ago
The article is focusing on ventilation and air circulation. Poor ventilation results in increased CO2 levels, and it does so in a predicatable, measurable amount. We also know that poor ventilation increases the likelihood of catching covid from an infected individual. So measuring the level of a space's ventilation is not meaningless data, even if it doesn't translate 1-to-1 with transmission rates.
mannykannot 4y ago
There are two scenarios in which halving the number of droplets inhaled has little effect on the risk of being infected, and two where it is moot. The ones where it is moot is those where either you you are already infected or no-one is. Halving the number of droplets will have no effect if droplet inhalation is not causal in transmission. In this case, there is plenty of evidence that it is, in fact, the primary mode of transmission. It would also be the case when, even at the lower droplet count, one is likely to become infected. This is essentially the scenario in your second point. None of the above are the case in a typical bus ride today, and for such, it is reasonable to suppose, as a first approximation absent further evidence, that risk is correlated with the degree to which one is rebreathing other people's exhalations, even though one can postulate that it is also correlated with other factors. One can question the source of the CO2 on a bus, but the measured values reported here are significantly above those measured by busy urban roads, where 1000ppm is considered vary high. If the bus is leaking CO2 into the cabin to any significant degree, there are more immediate health concerns. Demanding near-perfect data before considering its implications can be a way to avoid issues.
groby_b 4y ago
1) Spit droplets is much less of a problem than aerosols. You can solve that problem well with keeping distance. Aerosols are a bigger problem - they travel further and linger. All the studies I've seen so far correlate CO2 with aerosol levels. If spit droplets are a concern, I have no idea. 2) Covid studies so far have shown that there's a minimum level of viral load required for an initial infection, and they have also shown that there's a correlation between initial dose and severity of infection. So, yes, how many virus copies were there originally matters very much. In general, this has been explored in a large number of studies. I'd suggest at least a cursory research before claiming issues that "render the data near meaningless".
whoomp12342 4y ago
it would be implied. in an indoor setting most of CO2 comes from human exhaust

pessimizer 4y ago

> The operative factor is how well your immune system recognizes the threat and produces antibodies, not how many virus copies were there originally. These probably aren't independent, and are occurring at the same time. So while a very small amount of virus is replicating, the immune system is mounting a defense, slowing down that replication. The virus may never get to a significant amount (although the immune response might knock you on your ass.) On the other hand, if you start with a ton of virus already, you'll be dealing with the immune response and the direct effects of the virus at the same time, and the virus may overwhelm or even limit the immune response.

rossdavidh 4y ago
True, but even a large number of droplets will not result in "a ton" of virus, if by "a ton" we mean "similar to what will result if you get sick". A sick person breathes out a lungful with every breath, so obviously a sick person contains far, far more copies of the virus than that. Put it another way. If your immune system recognizes the virus already, it matters little whether you get one droplet or a thousand, it will beat it because it has a several-day head start in doing so. If, on the other hand, your immune system does not already recognize it, then it will not begin to see the problem, and thus will not begin to react, until it has replicated up to a large amount, where "large" is some amount greater than either one droplet or one thousand will give you. So, the consequences of getting exposed to 1/2 or 1/10 of the number of copies of the virus, is basically nil, because an exponential rise will be needed in either case to get up to the level where your immune system notices a problem. Either your immune system already recognizes the virus as a problem, or it doesn't. I neither case does the dose matter, so long as the dose is big enough to start the process. And that probably doesn't take much.
- PuppyTailWags 4y ago
  This isn't true. Even a robust immune system cannot prevent disease at large enough doses of virus because the immune system takes time to execute at any level of robustness. Similarly, a small enough dose will not necessarily cause disease, because the immune system can recognize the virus and eliminate it before it can replicate significantly. This is actually a time-based race: the speed of which the immune system can react vs the speed in which the virus can replicate in the body.

dentemple 4y ago

The article is focusing on ventilation and air circulation. Poor ventilation results in increased CO2 levels, and it does so in a predicatable, measurable amount. We also know that poor ventilation increases the likelihood of catching covid from an infected individual. So measuring the level of a space's ventilation is not meaningless data, even if it doesn't translate 1-to-1 with transmission rates.

mannykannot 4y ago

There are two scenarios in which halving the number of droplets inhaled has little effect on the risk of being infected, and two where it is moot. The ones where it is moot is those where either you you are already infected or no-one is. Halving the number of droplets will have no effect if droplet inhalation is not causal in transmission. In this case, there is plenty of evidence that it is, in fact, the primary mode of transmission. It would also be the case when, even at the lower droplet count, one is likely to become infected. This is essentially the scenario in your second point. None of the above are the case in a typical bus ride today, and for such, it is reasonable to suppose, as a first approximation absent further evidence, that risk is correlated with the degree to which one is rebreathing other people's exhalations, even though one can postulate that it is also correlated with other factors. One can question the source of the CO2 on a bus, but the measured values reported here are significantly above those measured by busy urban roads, where 1000ppm is considered vary high. If the bus is leaking CO2 into the cabin to any significant degree, there are more immediate health concerns. Demanding near-perfect data before considering its implications can be a way to avoid issues.

groby_b 4y ago

1) Spit droplets is much less of a problem than aerosols. You can solve that problem well with keeping distance. Aerosols are a bigger problem - they travel further and linger. All the studies I've seen so far correlate CO2 with aerosol levels. If spit droplets are a concern, I have no idea. 2) Covid studies so far have shown that there's a minimum level of viral load required for an initial infection, and they have also shown that there's a correlation between initial dose and severity of infection. So, yes, how many virus copies were there originally matters very much. In general, this has been explored in a large number of studies. I'd suggest at least a cursory research before claiming issues that "render the data near meaningless".

whoomp12342 4y ago

it would be implied. in an indoor setting most of CO2 comes from human exhaust