Short answer: A controlled laboratory study found that raising carbon dioxide (CO₂) from about 500 parts per million (ppm) to 800 ppm made SARS‑CoV‑2 remain infectious longer in suspended droplets. The effect appeared at 800 ppm, including a reported 36.8% increase in Delta infectivity after 120 seconds in the stated comparison. After 40 minutes, approximately an order of magnitude more infectious Delta virus remained under elevated CO₂ than under ambient conditions.
Those are measurements of levitated droplets, not infection rates in a room. The study used those measurements in a Wells–Riley model to estimate how conditions might alter transmission. Its modeled results should not be read as proof that a person in a room with a particular CO₂ reading faces a precisely calculated increase in risk.
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What the study actually tested
Haddrell and colleagues published “Ambient carbon dioxide concentration correlates with SARS-CoV-2 aerostability and infection risk” in Nature Communications on April 25, 2024 (volume 15, article 3487; DOI 10.1038/s41467-024-47777-5). The experiment used CELEBS, short for Controlled Electrodynamic Levitation and Extraction of Bioaerosol onto a Substrate. This apparatus holds individual aerosol droplets in the air while investigators control gas composition, relative humidity and other conditions, then measures how much infectious virus remains.
The team examined the Delta and Omicron BA.2 variants. Some comparisons also included Beta. Delta supplied the higher viral titres needed for much of the broad-condition and long-duration work, so not every result has identical variant coverage.
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The central comparison changed ambient CO₂ while other experimental variables were controlled. The authors report that increasing CO₂ from approximately 500 ppm to 800 ppm significantly increased Delta aerostability after two minutes. In that particular comparison, they found no significant difference between 800 ppm and 6,500 ppm. That result applies to the stated time point, droplets and test conditions; it does not establish that all concentrations behave the same way in every room, aerosol size or variant.
The headline numbers, with their qualifications
| Finding | What was measured | How to interpret it |
|---|---|---|
| 800 ppm | Delta aerostability was significantly higher than at approximately 500 ppm after two minutes in the CELEBS setup. | This is a controlled droplet result, not a room-safety threshold. |
| 36.8% | Reported increase in Delta infectivity at 120 seconds under elevated CO₂ in the paper’s comparison. | A relative infectivity measurement, not a 36.8% increase in human infections. |
| 23.4% | Reported increase for Beta at 120 seconds. | Applies to the stated comparison and experimental conditions. |
| 11.7% | Reported increase for Omicron BA.2 at 120 seconds. | Variant-specific laboratory measurement. |
| Approximately one order of magnitude after 40 minutes | More infectious Delta virus remained in aerosol at elevated CO₂ than under ambient conditions in the longer-duration comparison. | “About ten times” describes infectious particles recovered from the experiment, not tenfold personal infection risk. |
The percentages compare infectious virus remaining after 120 seconds, rather than counting people who became infected. Infectivity can change as droplets dry and their chemistry shifts, so a larger fraction of virus surviving in a sample is not equivalent to a fixed increase in the probability that any individual will become ill.
Why CO₂ could change viral survival
Respiratory fluid contains bicarbonate and other components that determine a droplet’s acidity. Once a person exhales, carbon dioxide can leave the droplet. That loss changes the bicarbonate equilibrium and can drive the pH upward. The paper describes higher pH as a major driver of viral inactivation. Surrounding the droplet with more CO₂ can alter that gas exchange and slow the chemical shift that otherwise damages infectivity.
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Allen Haddrell, the University of Bristol aerosol scientist identified as lead author by Chemistry World, explained the mechanism this way: “To understand viral decay in respiratory aerosol, one needs to understand the complex pH dynamics occurring in the respiratory droplet.” He also said: “There is a significant amount of bicarbonate in respiratory fluid. When the bicarbonate leaves the aerosol in the form of CO2, it takes with it a large amount of acid. This results in a dramatic shift in pH of the droplet from neutral to more than 10.”
This is a physicochemical explanation for the laboratory observation, not evidence that CO₂ is the only—or necessarily the dominant—factor controlling transmission in occupied buildings. Humidity, temperature, droplet composition, particle size, ventilation, exposure time and the amount of virus emitted all matter as well.
Does higher indoor CO₂ make COVID transmission more likely?
The paper supports a qualified “possibly,” not a universal risk multiplier. People are the source of exhaled CO₂ and respiratory aerosol, so poor ventilation can raise both at the same time. If elevated CO₂ also helps preserve infectivity through droplet chemistry, it could add an effect beyond its usual role as a ventilation indicator. The experiment measured that added effect under controlled conditions; it did not follow people through naturally occupied rooms.
To connect decay measurements with transmission, the authors used the Wells–Riley framework. That model estimates infection probability from factors such as infectious aerosol concentration, breathing and exposure time, removal by ventilation, and viral decay. The paper assumes a uniformly mixed room. Real rooms have gradients, short-circuiting airflow, local exhaust, doors opening, and people at different distances from an emitter, so the model is an approximation rather than a direct observation.
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Chemistry World reported the authors’ estimate that exposure in a poorly ventilated classroom could produce a fourfold greater likelihood of infection after ten minutes than exposure in a well-ventilated classroom. That is a model-based estimate derived from the laboratory observations, not a measured classroom outcome or a guarantee that every poorly ventilated room carries exactly four times the risk.
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Jose-Luis Jimenez of the University of Colorado Boulder, also quoted by Chemistry World, said: “While the authors had previously shown that CO2 did have an impact on virus survival, the fact that levels as low as 800ppm make a big difference is very surprising.” His comment highlights why the 800-ppm result attracted attention: it is close to concentrations that can occur indoors, yet the study does not establish 800 ppm as a universal boundary between safe and unsafe air.
Why the tenfold result is easy to misread
After 40 minutes, the investigators recovered approximately an order of magnitude more infectious Delta virus from aerosol under elevated CO₂ than under ambient conditions. “Order of magnitude” means roughly tenfold in that comparison. It does not mean that a person’s chance of infection automatically increases tenfold, because infection requires an exposure dose, a susceptible host, a route of inhalation and many other conditions.
The result also describes what remained infectious in sampled aerosol. It does not say that ten times as many particles were emitted, that ten times as much virus entered someone’s lungs, or that ten times as many people in a building would test positive. Those questions require human exposure and epidemiological data that this experiment did not collect.
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Laboratory droplets are not a whole room
The study used cultured virus in lab-generated droplets and levitated those droplets under controlled gas conditions. It was not a clinical trial, an outbreak investigation or a test of an occupied building. A chamber can isolate one variable in a way that is impossible in a school, office or train carriage, but that isolation also limits how directly the result transfers to everyday exposure.
The measured droplets started larger than many fine aerosols
The methods describe initially generated droplets larger than 50 micrometres. Under the study conditions they shrank to final radii of approximately 5–10 micrometres. The direct decay measurements therefore began with larger oral-mode droplets, while the Wells–Riley calculations addressed the smaller aerosol fraction relevant to airborne transmission.
The authors explicitly note that pH change depends on droplet size and total acid content. Extending the result from the measured droplets to all fine particles is consequently an uncertainty, not a settled fact.
Air composition and particle-size concerns
A May 17, 2024 report by Chemistry World recorded concerns from other researchers that the experimental air composition was not standardized and that the droplets were larger than the very small particles reported in some respiratory-aerosol studies. These are methodological concerns raised about how broadly the findings should be generalized; they do not erase the paper’s measured CO₂-associated changes in its own setup.
Variant and time differences matter
The 36.8%, 23.4% and 11.7% figures refer to Delta, Beta and Omicron BA.2, respectively, after 120 seconds in the stated comparison. The long-duration, 40-minute result focused on Delta because it produced higher titres for that work. One variant’s decay curve cannot automatically stand in for every current or future variant, and a two-minute percentage cannot be extrapolated linearly to an hour.
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What an indoor CO₂ reading can—and cannot—tell you
CO₂ monitoring remains useful as an indicator of ventilation because occupants exhale CO₂. A rising reading generally signals that exhaled air is accumulating faster than the room removes it. In the context of this paper, a reading may also indicate conditions in which CO₂-related droplet chemistry could matter.
However, a CO₂ monitor does not detect SARS-CoV-2, count infectious particles, identify who is infected or certify that a room is safe. The study did not test consumer monitor models, sensor accuracy, displays, data logging or air-cleaning devices. It also did not establish a single CO₂ number that guarantees protection.
If you use a monitor, treat it as a trend tool rather than a pass/fail test:
- Record readings while a room is empty and again during normal occupancy so you can see how quickly CO₂ accumulates.
- Note what changes the reading, such as opening windows, operating mechanical ventilation or changing the number of occupants.
- Look for sustained increases and slow recovery, which indicate that removal is not keeping pace with occupancy.
- Use the information to discuss ventilation with the building operator; do not use one low reading as proof that no infectious aerosol is present.
Because the paper did not validate any monitor or ventilation product as an infection-prevention measure, buying a meter alone cannot substitute for ventilation design, filtration, staying home when ill or other public-health measures appropriate to the situation.
What the findings mean for ventilation decisions
The strongest practical implication is to take indoor-air management seriously. Ventilation lowers occupants’ exhaled CO₂ and removes respiratory aerosol at the same time. The study suggests that CO₂ may have a second, direct influence on how quickly virus loses infectivity, which strengthens the case for avoiding stagnant indoor air. It does not replace established ventilation engineering with a new universal threshold.
Decisions should therefore consider the complete exposure picture: how many people share the space, how long they stay, whether air is mixed or supplied locally, whether filtration removes particles, and whether someone is actively emitting virus. A CO₂ number can help reveal changing ventilation conditions, but it cannot answer those questions by itself.
Bottom line on elevated CO₂ and SARS‑CoV‑2
Haddrell and colleagues found that elevated CO₂ preserved SARS‑CoV‑2 infectivity longer in levitated droplets, with a significant Delta effect reported when the test condition rose from about 500 ppm to 800 ppm. They measured variant-specific increases after 120 seconds and roughly an order of magnitude more infectious Delta virus after 40 minutes under elevated CO₂. The striking room-level implications came from a Wells–Riley model that assumes a uniformly mixed room and bridges measurements from larger droplets to smaller aerosols. Treat CO₂ as a ventilation signal—not a virus detector or a safety guarantee—and interpret the study as evidence that indoor-air conditions can influence viral stability, not as a precise calculator of any individual’s infection risk.
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Sources and publication details
- Haddrell et al., “Ambient carbon dioxide concentration correlates with SARS-CoV-2 aerostability and infection risk,” Nature Communications 15, 3487, published April 25, 2024. DOI: 10.1038/s41467-024-47777-5.
- Maria Burke, “Elevated carbon dioxide lets Sars-CoV-2 live far longer in droplets,” Chemistry World, May 17, 2024.
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