The coronavirus disease 2019 (COVID-19) pandemic has caused untold disruption throughout the world. Understanding the mechanisms for transmission of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is key to preventing further spread, but there is confusion over the meaning of ‘airborne’ whenever transmission is discussed. Scientific ambivalence originates from evidence published many years ago which has generated mythological beliefs that obscure current thinking. This article collates and explores some of the most commonly held dogmas on airborne transmission in order to stimulate revision of the science in the light of current evidence. Six ‘myths’ are presented, explained and ultimately refuted on the basis of recently published papers and expert opinion from previous work related to similar viruses. There is little doubt that SARS-CoV-2 is transmitted via a range of airborne particle sizes subject to all the usual ventilation parameters and human behaviour. Experts from specialties encompassing aerosol studies, ventilation, engineering, physics, virology and clinical medicine have joined together to produce this review to consolidate the evidence for airborne transmission mechanisms, and offer justification for modern strategies for prevention and control of COVID-19 in health care and the community.

During the 2020 COVID-19 pandemic, an outbreak occurred following attendance of a symptomatic index case at a weekly rehearsal on 10 March of the Skagit Valley Chorale (SVC). After that rehearsal, 53 members of the SVC among 61 in attendance were confirmed or strongly suspected to have contracted COVID-19 and two died. Transmission by the aerosol route is likely; it appears unlikely that either fomite or ballistic droplet transmission could explain a substantial fraction of the cases. It is vital to identify features of cases such as this to better understand the factors that promote superspreading events. Based on a conditional assumption that transmission during this outbreak was dominated by inhalation of respiratory aerosol generated by one index case, we use the available evidence to infer the emission rate of aerosol infectious quanta. We explore how the risk of infection would vary with several influential factors: ventilation rate, duration of event, and deposition onto surfaces. The results indicate a best-estimate emission rate of 970 ± 390 quanta/h. Infection risk would be reduced by a factor of two by increasing the aerosol loss rate to 5 h⁻¹ and shortening the event duration from 2.5 to 1 h.