In a recent study being reviewed in the journal Scientific Reports and published on the Research Square* preprint server, researchers assessed the risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection for indoor scenarios.
Study: Transmissibility of coronavirus and its variants from infected subjects in indoor environments. Image Credit: Elizaveta Galitckaia/Shutterstock
Besides super spread events, low and medium risk events also contribute to an increased risk of SARS-CoV-2 infection in the indoor environment. This is most likely because the aerosol pathway, including droplets and their residues, is the main transmission route for coronavirus disease 2019 (COVID-19).
Several models have quantified the risk posed by SARS-CoV-2 in indoor environments. However, previous single-shot models did not treat droplet inhalation as a discrete process, leading to difficulties in linking viral load in infected individuals to the likelihood of lung deposition in the susceptible individual. A dual Poisson model estimates the probability that an individual must inhale at least one droplet for a virion to deposit in the lungs and establish SARS-CoV-2 infection.
Additionally, previous hazard models assumed a constant final droplet diameter because accurately assessing the evaporation of droplets containing non-volatile salts is a complex process. However, the current study model dealt with the dispersion mechanism by the ventilation-dependent turbulent diffusion process.
In other words, the present study addresses the missing link between how increased viral load increases aerosol transmissibility of disease following a viral load-mechanical coupling of aerosols.
About the study
In the present study, researchers used a standard inhalation infection risk problem to demonstrate the applicability of the droplet evaporation-settling-dispersion model.
They used a 50 m3 chamber with an air exchange rate (AER) of 0.5 h -1 and released 1200, 100, 6.2, and 1.7 droplets of 4.2 µm, 9 µm, 14.6 µm, and 18.8 µm, respectively, during a coughing episode. They assumed a SARS-CoV-2 load of 5 x 10 6 at 5×10 ten RNA copies/mL with 0.1 h -1 inactivation rate.
Droplet lifetime in a typical indoor environment
Researchers linked viral load to the degree of SARS-CoV-2 dissemination by calculating the exposure time needed to reach the single risk for a given expiratory event, including breathing, speaking, coughing and sneezing. They incorporated several factors that may influence viral spread rates, such as the use of masks, the effect of ambient temperature, relative humidity (RH), and indoor air quality. In addition, they took into account the expiratory emission characteristics, such as droplet size distribution, emission frequency, and virion concentration in the emitted droplets.
The solids content of the saliva/droplet, outside of ambient conditions, affects the equilibrium droplet size. Thus, the researchers assumed a solids content of 8 g/L and precisely modeled the evaporation of the droplets coupled with the other processes. Importantly, they did not believe that droplets were instantly mixed into the room environment and accounted for the effect of ventilation-induced turbulence to simulate droplet dynamics in the room.
Different variants of SARS-CoV-2 infect different parts of the respiratory system, for example, Omicron infects and multiplies faster in the bronchi than the Delta variant. Therefore, the researchers considered both bronchial and pulmonary deposition events.
They compared the risk predictions of the current study model with those of Nicas et al. It should be noted that Nicas et al. proposed the first comprehensive model to study the aerosol infection pathway in 2005.
For 10 minutes in an indoor environment, when the viral load has gone from 2×10 8 RNA copies/mL at 2×10 ten RNA copies/mL, the risk of SARS-CoV-2 infection increased rapidly by 1-50%. The risk of infection remains below 1% for viral loads below 10 8 RNA copies/mL for one hour indoors.
As the viral load exceeded 10 ten RNA copies/mL, the model predicted a smooth transition at risk of approaching a higher value and reaching saturation. As SARS-CoV-2 Delta and Omicron variants produce a higher viral load than older wild-type SARS-CoV-2 variants, the study design rationalized the observed greater transmissibility of these variants. Since true disease severity is associated with variant infectivity, the present study demonstrated that the risk of infection was dependent on viral load, independent of variants.
The model also explored the effect of ventilation rate on indoor infection risks. When the AER was increased by 0.5 h -1 at 10 o ‘clock -1 for an exposure time of 10 minutes, the risk of a single hit decreased by about an order of one. A reasonable explanation is that ventilation removes airborne viruses from the indoor environment; however, as viral load increases, the effect of enhanced ventilation decreases because smaller particles also contribute to risk.
Ambient relative humidity had a negligible impact on the risk of SARS-CoV-2 infection. Therefore, higher RH led to larger droplet sizes with reduced lifetime, hence lower risk of infection. The observed variation in droplet lifetime with relative humidity was only significant for particles between 20 and 80 µm. Due to evaporation and gravity, the large particles have shrunk to about 1/5 of their original size.
The study remarkably highlighted the importance of the deployment of masks, air purifiers and external ventilation and their role in mitigating the risk of SARS-CoV-2 infection. The study model also looks attractive for assessing the cost-effectiveness of deploying the technology. Of all the parameters examined, viral load seemed to have the most dominant effect, and it was correlated with the type of variant. The analysis revealed that viral load and principles of aerosol physics governed viral deposition in the lungs.
Overall, the study made a valuable contribution to the topic of airborne disease risk assessment.
Research Square publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be considered conclusive, guide clinical practice/health-related behaviors, or treated as established information.
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