Respiratory aerosols from breathing and talking are an important transmission route for viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies have found that particles with diameters ranging from 10 nm to 145 μm are produced from different regions in the respiratory system and especially smaller particles can remain airborne for long periods while carrying viral RNA. We present the first study in which respiratory aerosols have been simultaneously measured with carbon dioxide (CO2) to establish the correlation between the two concentrations. CO2 concentrations are easily available through low-cost sensors and could be used to estimate viral exposure through this correlation, whereas source-specific aerosol measurements are complicated and not possible with low-cost sensors. The increase in both respiratory aerosols and CO2 was linear over ten minutes in a 2 m3 chamber for all participants, suggesting a strong correlation. On average, talking released more particles than breathing, with 14,600 ± 16,800 min−1 (one-σ standard deviation) and 6210 ± 5630 min−1 on average, respectively, while CO2 increased with 139 ± 33 ppm min−1 during talking and 143 ± 29 ppm min−1 during breathing. Assuming a typical viral load of 7×106 RNA copies per mL of oral fluid, ten minutes of talking and breathing are estimated to produce 1 and 16 suspended RNA copies, respectively, correlating to a CO2 concentration of around 1800 ppm in a 2 m3 chamber. However, viral loads can vary by several orders of magnitude depending on the stage of the disease and the individual. It was therefore concluded that, by measuring CO2 concentrations, only the number and volume concentrations of released particles can be estimated with reasonable certainty, while the number of suspended RNA copies cannot.
Respiratory Aerosols from breathing and talking have found wide acceptance as a transmission route for viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Previous studies have found particles with diameters ranging from 10 nm to 145 µm, exhibited from different regions in the respiratory system. We present the first chamber study, in which respiratory aerosols have been simultaneously measured with carbon dioxide (CO2) to establish the correlation between the two concentrations. CO2 concentrations are easily available through low-cost sensors and could be used to estimate viral exposure through this correlation, whereas source-specific aerosol measurements are complicated and not possible with low cost sensors. The increase in both PM10 and CO2 was linear over ten minutes in a 2 m3 chamber for all participants, suggesting a strong correlation. On average, talking released more particles than breathing, with 14,600 ± 16,800 min-1 (one-σ standard deviation) and 6,210 ± 5,630 min-1 on average, respectively, while CO2 increased with 139 ± 33 ppm min-1 during talking and 143 ± 29 ppm min-1 during breathing. Assuming a typical viral load of 7 × 106 RNA copies per ml of oral fluid, ten minutes of talking and breathing are estimated to produce 7 and 16 suspended RNA copies, respectively, correlating to a CO2 concentration of around 1.800 ppm in a 2 m3 chamber. This provides a strong argument for keeping indoor spaces well ventilated and shows how CO2 concentrations, measured with low-cost sensors, could be used as a proxy for viral exposure.
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