Ryan Hisner Profile picture
Apr 22, 2021 17 tweets 7 min read Read on X
1/ The @nytimes has a good interactive story on the safety of flying during the pandemic, but they didn’t discuss boarding & deboarding. Judging by CO2 readings I saw on recent flights, this is the most dangerous part of flying. #covidco2 #COVIDisairborne
nytimes.com/interactive/20…
2/ By now there is overwhelming evidence #COVIDisAirborne. It’s transmitted mainly by shared air, i.e. inhaling the air others have exhaled, which contain aerosols—tiny, liquid particles that float suspended in air for seconds to hours, depending on size.
3/ There’s no easy way to measure virus levels in the air, but CO2 is a good proxy measure of risk. Outdoor CO2 levels are ~410 ppm, but since we exhale CO2, indoor concentrations are higher. The higher the CO2 level, the more air you’re sharing.
4/ I used an Aranet CO2 meter, which was tested & recommended by @jljcolorado, a top aerosol expert. I flew from Ft. Wayne, IN (FWA), to Rochester, MN (RST) with a layover at Chicago. FWA was not busy, & the CO2 ranged from 516 to 546 ppm.
5/ When we first sat down on the plane, the CO2 level was at 1424. Four minutes later, it was 1470. Over the course of the next 6 minutes, the CO2 concentration rose steadily.
6/ In the next four minutes, the CO2 level rose from 1654 ppm to 1899 to 2027 to 2255. Most IAQ experts, including @linseymarr, recommend keeping CO2 below 700 for a multitude of reasons.
7/ The next two pictures are quite blurry because the plane started to move, but you can tell the CO2 rose to 2343, then 2351 ppm.
8/ I think the ventilation system started bringing in outdoor air when the plane began taxiing but that it took a couple minutes for the CO2 to begin to decline. Two minutes after peaking at 2351 ppm, it had decreased to 2026, and two minutes after that it was 1738.
9/ By the time we took off the CO2 was around 1400 ppm, and it stayed right around that level for the entire flight.
10/ Chicago’s O’Hare Airport appeared to have quite good ventilation. The CO2 level stayed in the low-600 range where I was. I did not venture into the crowded cafeteria area nearby, where I imagine the levels were significantly higher.
11/ The next flight was to Rochester, MN, also on American Airlines. Immediately after boarding, the CO2 was already at 2096 ppm.
12/ Five minutes later, the CO2 concentration had risen to 2393 ppm, and in the next two minutes it rose further, to 2548 before peaking at 2650 ppm.
13/ At this point there was a revving noise, and CO2 levels started to decline, falling to 1820 ppm seven minutes later. 20 minutes after the peak 2650 reading, CO2 had declined to 1292 when we started taxiing.
14/ After taxiing for several minutes, we stopped. CO2 once again rose, but only to 1546, after which the plane started rolling again and levels declined.
15/ During this flight, which seemed equally crowded as the first flight and on a similarly small plane, CO2 concentrations were lower, ranging between 900-1030 ppm. Notably, relative humidity got as low as 12% later on in the flight.
16/ The Rochester Airport wasn’t very crowded, but with CO2 at 492 ppm, it still must have had good ventilation. Doors about 10 meters away likely helped.
17/ I’ll stop there for now. Later I’ll add info about the CO2 levels at Mayo Clinic and our hotel. Our return flights, again with a layover at O’Hare, are later today, and it will be interesting to see how they compare.

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Ryan Hisner

Ryan Hisner Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @LongDesertTrain

Jan 2
Two quick notes on the state of chronic-infection SARS-CoV-2 seqs

#1) ~3 years after its peak, BA.1 is still showing up in nasal swab seqs—despite reduced surveillance—most recently a mid-late Dec BA.1 from Nebraska.

#2) Chronic JN.1 seqs now more common, w/1 peculiarity

1/12
While BA.1 still show up semi-regularly, pre-Omicron seqs are much rarer. Why? I think there are four major reasons, two obvious & two less obvious.

A) Time.
This one’s obvious: Over time, some chronic infections are cleared, while in other cases, the host dies.

2/12
B) Number of infections.

BA.1 infected more people, more quickly than any previous variant. More infections = more chances to establish long-term infection.
3/12 Image
Read 12 tweets
Dec 23, 2024
Fantastic review on chronic SARS-CoV-2 infections by virological superstars Richard Neher & Alex Sigal in Nature Microbiology. I’ll do a short overview, outline a couple minor quibbles, & defend the honor of ORF9b w/some stats & 3 striking sequences from the past week.
1/64 Image
First, let me say that this is well-written, extremely readable, and accessible to non-experts, so you should go read the full paper yourself, if you can find a way to access it. (Just realized it’s paywalled, ugh.) 2/64nature.com/articles/s4157…
Neher & Sigal focus on the 2 most important aspects of SARS-CoV-2 persistence: its relationship to Long Covid (including increased risk of adverse health events) & its vital importance to the evolution of SARS-CoV-2 variants. I’ll focus on the evolutionary aspects.
3/64 Image
Read 64 tweets
Dec 6, 2024
In SARS-2 evolution, amino acid (AA) mutations get the lion’s share of attention—& rightfully so, as noncoding & synonymous nucleotide muts—which cause no AA change‚ are mostly inconsequential. But there are many exceptions, including a possible new one I find intriguing. 1/30
I’ll discuss four categories of such “silent” mutations, two of which might be involved in the recent growth of one synonymous mutation.

#1. Kozak sequence changes
#2. Secondary RNA structure
#3. TRS destruction/improvement
#4. TRS creation 2/30
Maybe the single most remarkable example of convergent evolution in SARS-CoV-2 involves noncoding mutations: the multitude of muts in major variants that have pulverized the nucleocapsid (N) Kozak sequence.
I wrote about this below & a few other 🧵s 3/
Read 33 tweets
Nov 24, 2024
@SolidEvidence There was yet another paper this week describing someone chronically infected, with serious symptoms, but who repeatedly tested negative for everything with nasopharyngeal swabs. On bronchoalveolar lavage (BAL), they were Covid-positive. 1/ ijidonline.com/article/S1201-…Image
@SolidEvidence BAL is very rarely performed, yet there must be dozens of documented cases now where NP-swab PRC-negative patients who were very ill tested positive by BAL. This has to be way more common than we realize.

If we had a similar GI test, I imagine we'd find something similar. 2/
@SolidEvidence Importantly, the patient was treated and improved, likely clearing the virus for good. Many, maybe most, chronic infections could be treated and cleared. But they have to know they're infected for that to happen. 3/
Read 4 tweets
Nov 22, 2024
Superb thread here by @jbloom_lab that meshes well with what we've seen over the last few months in SARS-CoV-2 spike evolution: not much.

IMO, nothing significant has happened since the NTD-glycan-adding muts (T22N, ∆S31) & Q493E appeared. This 🧵 explains why. 1/6
Read full 🧵for explanation, but the short story is that the best apparent escape mutations all interact w/something else—like a nearby spike protomer or other important AA—making mutations there prohibitively costly.

In short, the virus has mutated itself into a corner. 2/6
It's very hard to effectively mutate out such a local fitness peak via stepwise mutation in circulation since multiple simultaneous muts might be required to reach a higher fitness peak. 3/6

Read 6 tweets
Nov 10, 2024
It's an interesting thought. I think the evidence is strong that all new, divergent variants have derived from chronic infections. The first wave of such variants—Alpha, Beta, Gamma—IMO involved chronic infections lasting probably ~5-7 months. It's controversial to say.... 1/15
…that Delta originated in a chronic infection, but I think the evidence that it did is strong. One characteristic of chronic-infection branches is a high rate of non-synonymous nucleotide (nuc) substitutions (subs)—i.e. ones that result in an amino acid (AA) change. 2/15 Image
For example, if 80% of nuc subs in coding regions cause an AA change, that’s a very high nonsynonymous rate. The branch leading to Delta has 17 AA changes—from just *15* nuc subs! That’s over 100%. How is this possible? 3/15
Read 15 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us!

:(