Personal protective equipment and concerns over airborne transmission of COVID-19: a reply.

Thanks to Drs Brown and Pope [1] for their interest in my review [2]. The crux of their letter is the question of whether coughing and sneezing create a risk of infection from aerosols and how this compares with procedure‐related aerosol generation. This area is complex, difficult to study and, in many areas, lacking a strong evidence base. Recommendations based on the limited evidence are at times opaque, inconsistent and rapidly changing. Such a situation generates strong opinions and discussion without likelihood of resolution.

The issue of which procedures are ‘aerosol generating’ is frequently raised but I focus more on those which risk infection of healthcare workers; in this regard the evidence highlights tracheal intubation over all other procedures, with mask ventilation, tracheostomy and non‐invasive ventilation also of higher risk [3]. Risk with other procedures is open to interpretation and likely ranks lower in the hierarchy.

There is no doubt that coughing and sneezing create a respiratory aerosol [4], although the dichotomy into particles larger or smaller than 5 µm is likely to be too simplistic a concept. What is less clear is the extent of the aerosol, its content in terms of viable viral particles and whether the volume is sufficient to create a high risk of infection. Factors to consider include: the individual's response to the virus (i.e. the extent of viral shedding and coughing); the mucus content and type; the disease severity and stage; and the location within the respiratory tract from which the aerosol arises [5]. Furthermore, the composition, duration and impact of the aerosol depend on environmental factors: temperature; local and general humidity; and whether indoors or outdoors. Within hospital the rates of viral clearance are impacted by air exchange rates which vary considerably between locations. It is widely stated that each air exchange clears 63% of viral content, although finding supportive evidence is problematic, but in better ventilated areas (e.g. all operating theatre and most intensive care units) aerosols will be cleared rapidly. If the patient wears a mask this too will dramatically reduce infectious risk [6]. So, the fact an aerosol is generated is not sufficient to determine that it is an infective risk or that it contributes significantly to disease transmission.

Perhaps most importantly the mechanism of disease transmission remains, as judged by expert groups, to be predominantly via contact (fomite) and droplet infection with airborne infection judged only a minor contributor. Of note, UK guidance is not notably different from that of the World Health Organization, but is more location specific.

The debate over more widespread use of masks in the community and more widespread use of filtering face pieces in hospitals will continue. It is notoriously difficult to prove lack of risk, but whether the ‘precautionary principle’ is the right one to follow is not a simple decision. Recent reports suggest that those in high‐risk areas are disproportionately under‐represented in reports of fatalities from COVID‐19 but also that healthcare workers are not overall at disproportionate risk of fatality.

The discussion must not distract from ensuring healthcare workers rigorously practice standard infection control procedures and correct transmission‐based precautions to protect against known routes of transmission; droplet and contact. The decision on where best to deploy limited stocks of personal protective equipment (PPE) will remain complicated and it is certainly a valid question as to whether there should be wider use of airborne precautions on the wards and within social care facilities. It is likely that the PPE supply issue will be exacerbated by easing of lockdown and use of PPE in industry and the community, so any decision needs to be carefully considered and should not be to the detriment of those in demonstrably high‐risk areas.