Exhaled respiratory droplets increase with the onset of COVID-19 infection and with aging and obesity

Superspreading events have distinguished the COVID-19 pandemic from the early outbreak of the disease. Now, research from Harvard University, Tulane University, MIT and Massachusetts General Hospital finds that a critical factor in these and other transmission events is the propensity of certain individuals to exhale large numbers of small respiratory droplets. The researchers found that age, obesity and COVID-19 infection all correlate with a propensity to breathe out more respiratory droplets.

Understanding the source and variance of respiratory droplet generation may lead to effective approaches to reducing COVID-19 infection and transmission.

The study was published yesterday in the Proceedings of the National Academy of Sciences.

“Respiratory droplet generation in the airways varies between people depending on their phenotype,” said David Edwards, Associate in Bioengineering at the Harvard John A. Paulson School of Engineering and Applied Sciences and co-author of the study.  “While our results show that the young and healthy tend to generate far fewer droplets than the older and less healthy, they also show, in combination with the results from nonhuman primates, that any of us, when infected by COVID-19, may be at risk of producing a large number of respiratory droplets. This is an important finding in that the majority of these droplets are smaller than a single micron, meaning they can carry infection deep into our lungs and propagate infection very far in poorly circulated indoor settings.”

Using data from an observational study of 194 healthy people, ages 19 to 66, and an experimental study of nonhuman primates with COVID-19, researchers found that exhaled aerosol particles vary greatly between subjects. Those who were older with higher body mass indexes (BMI) and increasing degree of COVID-19 infection had three times the number of exhaled respiratory droplets as others in the study group.

The researchers found that 18 percent of human subjects accounted for 80 percent of the exhaled particles of the group, reflecting a distribution of exhaled aerosol particles analogous to a classical 20:80 “super-spreader” distribution of airborne infection.  The findings suggest that quantitative assessment and control of exhaled aerosol may be critical to slowing the airborne spread of COVID-19 in the absence of an effective and widely disseminated vaccine. 

“Our nonhuman primate studies suggest that within a few days of infection by SARS-CoV-2 aerosol, exhaled aerosol increases with the rise of viral replication in the airways, reaching a peak within about a week from first infection — and then diminishing in magnitude as the infection is cleared to return to baseline within two weeks post infection,” said co-author Chad Roy, Professor of Microbiology and Immunology at Tulane School of Medicine and a core scientist at the Tulane National Primate Research Center at Tulane University.  “We observed these same phenomena with TB-infected nonhuman primates.  It seems likely that viral and bacterial infection of the airway weaken airway mucus in similar ways and promote airborne movement of infection — with risks to ourselves and those around us.” 

The authors argue that management of COVID-19 through the restoration of airway lining mucus barrier function, and, monitoring of exhaled aerosol numbers might be important strategies in the control of transmission and infection of COVID-19, and other respiratory infectious diseases, including TB and influenza.

The research was co-authored by Dennis Ausiello, of Massachusetts General Hospital and Harvard Medical School; Jonathan Salzman and Tom Devlin, of Sensory Cloud; Robert Langer, of the Massachusetts Institute of Technology; and Brandon J. Beddingfield, Alyssa C. Fears, Lara A. Doyle-Meyers, Rachel K. Redmann, Stephanie Z. Killeen and Nicholas J. Maness, of Tulane National Primate Research Center .

It was supported in part by National Institute of Allergy and Infectious Disease (Grant # HHSN272201700033I), the National Institutes of Health (Grant # OD01110) and the Bill & Melinda Gates Foundation