Exhaled aerosol increases with COVID-19 infection, age, and obesity
David A. Edwards, Dennis Ausiello, Jonathan Salzman, Tom Devlin, View ORCID ProfileRobert Langer, View ORCID ProfileBrandon J. Beddingfield, Alyssa C. Fears, Lara A. Doyle-Meyers, Rachel K. Redmann, Stephanie Z. Killeen, View ORCID ProfileNicholas J. Maness, and Chad J. Roy
Significance
Superspreading events have distinguished the COVID-19 pandemic from the early outbreak of the disease. Our studies of exhaled aerosol suggest that a critical factor in these and other transmission events is the propensity of certain individuals to exhale large numbers of small respiratory droplets. Our findings indicate that the capacity of airway lining mucus to resist breakup on breathing varies significantly between individuals, with a trend to increasing with the advance of COVID-19 infection and body mass index multiplied by age (i.e., BMI-years). Understanding the source and variance of respiratory droplet generation, and controlling it via the stabilization of airway lining mucus surfaces, may lead to effective approaches to reducing COVID-19 infection and transmission.
Particles are a function of Obesity X Weight
<10% of people are superspreaders
Abstract
COVID-19 transmits by droplets generated from surfaces of airway mucus during processes of respiration within hosts infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. We studied respiratory droplet generation and exhalation in human and nonhuman primate subjects with and without COVID-19 infection to explore whether SARS-CoV-2 infection, and other changes in physiological state, translate into observable evolution of numbers and sizes of exhaled respiratory droplets in healthy and diseased subjects. In our observational cohort study of the exhaled breath particles of 194 healthy human subjects, and in our experimental infection study of eight nonhuman primates infected, by aerosol, with SARS-CoV-2, we found that exhaled aerosol particles vary between subjects by three orders of magnitude, with exhaled respiratory droplet number increasing with degree of COVID-19 infection and elevated BMI-years. We observed that 18% of human subjects (35) accounted for 80% of the exhaled bioaerosol of the group (194), reflecting a superspreader distribution of bioaerosol analogous to a classical 20:80 superspreader of infection distribution. These 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
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