Exhaled aerosol increases with COVID-19 infection, risk factors of disease symptom severity

David A Edwards, Dennis Ausiello, Robert Langer, Jonathan Salzman, Tom Devlin, Brandon J. Beddingfield, Alyssa C. Fears, Lara A. Doyle-Meyers, Rachel K. Redmann, Stephanie Z. Killeen, NIcholas J. Maness, View ORCID ProfileCHAD J ROY

doi: https://doi.org/10.1101/2020.09.30.20199828

This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.

PDF: https://www.medrxiv.org/content/10.1101/2020.09.30.20199828v1.full.pdf

Abstract

Coronavirus disease-19 (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, translates 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 74 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 increase one to three orders of magnitude with aging, high BMI, and COVID-19 infection. These variances appear to be related to changes in airway mucus surface composition and the propensity for mucus surfaces to breakup into small droplets during acts of breathing. We also observed that 20% of those participating in our human study accounted for 80% of the overall exhaled bioaerosol, reflecting a bioaerosol distribution analogous to a classical 20:80 super spreader distribution.

Competing Interest Statement

The authors have declared no competing interest.

Funding Statement

Funding. The work at the Tulane National Primate Research Center was supported in part by the National Institute of Allergy and Infectious Disease (NIAID) Contract No. HHSN272201700033I (CJR) and also supported in part by grant OD011104 from the Office of Research Infrastructure Programs (ORIP), Office of the Director, NIH.

https://www.medrxiv.org/content/10.1101/2020.09.30.20199828v1