We have just had a study published in Clinical Infectious Diseases exploring the extent and magnitude of hospital surface and air contamination with SARS-CoV-2 during the (first!) peak of COVID-19 in London. The bottom line is that we identified pretty extensive surface and air contamination with SARS-CoV-2 RNA but did not culture viable virus. We concluded that this highlights the potential role of contaminated surfaces and air in the spread of SARS-CoV-2.
The transmission of SARS-CoV-2 is thought to occur mainly through infected droplets that generally travel a fairly short distance from infected individuals (hence the 2m (oh wait is that >1m?) physical distancing approach). In addition, there is a strong theoretical argument that contaminated surfaces play a role in indirect contact transmission of SARS-CoV-2. However, there isn’t a lot of information available on the extent to which surfaces and air in hospitals become contaminated with SARS-CoV-2. At the time that the work was undertaken, there were a few studies that had performed fairly limited sampling of surfaces and air in healthcare settings. Most had focussed on COVID-19 isolation rooms and cohort wards, and had used only PCR to identify SARS-CoV-2 in surface and air samples (rather than trying to culture viable virus). Therefore, we set out to sample surfaces and air in a broad range of clinical and non-clinical areas using both PCR and culture in parallel.
We chose a total of eight areas to sample: the adult emergency department, an acute admissions ward, two COVID-19 cohort wards, three theatres during tracheostomy procedures, an intensive care unit, a ward with a 6-bedded bay converted into a negative pressure area for management of continuous positive airway pressure (CPAP) on patients with COVID-19, and the entrance and public area of a main hospital building. All of the inpatient clinical areas were fully occupied with adult patients with confirmed or suspected COVID-19 at the time of the study (whilst we didn’t plan this – because nobody knew exactly when the peak would be – we happened to perform the sampling at the peak of the pandemic).
The sampling strategy was to take about four air samples in different places in each area sampled trying to reflect a range of perceived contamination risk. For example, in the emergency department, we took an air sample in the “green” part (for patients without suspected COVID-19), and the other samples in various sections of the “red” part (for patients with suspected COVID-19). We then took surface samples, focussing on high-touch surfaces, in the immediate vicinity of each air sample.
Overall, SARS-CoV-2 RNA was detected on 114/218 (52.3%) of surfaces and 14/31 (45.2%) air samples but no viable virus was cultured. The proportion of surface samples contaminated with viral RNA varied by item sampled (see Figure 1) and by clinical area. We found that keyboards were frequently contaminated. Most of the keyboards sampled were in shared staff workspaces, so highlight the need to have a disinfection strategy for keyboards (and not only to prevent the spread of COVID-19!).
SARS-CoV-2 RNA was detected on surfaces and in air in public areas of the hospital but was more likely to be found in areas immediately occupied by COVID-19 patients than in other areas (64% vs. 45%, p=0.025, Chi squared test). We did a laboratory evaluation in order to understand the “limit of detection” of SARS-CoV-2 dried onto surfaces, suggesting that Ct values of >30 (corresponding to an E gene copy number of <105 per mL) are unlikely to be culturable. This parallels studies of viral infectivity from clinical specimens. The high PCR Ct value for all air and surface samples (>30) indicated that the virus would not be culturable. Future studies might consider a first line RT-PCR on all environmental samples, and only attempt culture on those with a lower CT value.
Figure 1: Proportion of environmental samples suspected or positive by item sampled, with the number on the x axis representing the number of each item sampled. (Duplicate PCRs were run from each air or surface sample for the purposes of quantitation; if both were positive, the sample was designated ‘positive’, if one was positive and one was negative, the sample was designated ‘suspect’.)
We found SARS-CoV-2 air contamination in the parts of the hospital that were dedicated to aerosol generating procedures, but there was no difference in viral load compared with other parts of the hospital. There’s much current debate about particle size and transmission risk of SARS-CoV-2, fueled by this opinion piece also in CID (see the excellent Controversies blog in response here). However, important to recognize that the air sampling method that we used did not differentiate particle size, so we can’t comment and compare the extent of aerosol (i.e. particles < 5 µM) produced.
This is really only the start to answering some of the key questions that arise when discussing the potential role of surface and air contamination in the spread of SARS-CoV-2. Our findings only provide a “snapshot” of contamination on one particular day. The next set of studies should include longitudinal sampling to understand how the viral load on surfaces and in air changes over time – and ideally, how this corresponds with the risk of acquisition in patients and staff.
This was my first use of a pre-print server in the publication process (I know I know, I’m very behind the times). My experience was good. Pre-print publication was pretty straightforward, allowed the rapid dissemination of findings to colleagues, and did not prevent publication in a very decent journal.
We had lengthy discussions interpreting what our findings mean for applied infection prevention and control. On the one hand, the finding of SARS-CoV-2 on surfaces and in air is a concern and suggests that more interventions (e.g. more cleaning/disinfection, enhanced air handling, increased physical distancing, masks etc) are required. But on the other hand, no viable virus was cultured, suggesting that the risk of transmission from the detection of viral RNA detection is minimal. I’m pleased that we had the viral culture data, and the laboratory evaluation of the “limit of detection” of viability on surfaces to help us interpret our findings. On balance, we concluded that our findings highlight the potential risk from contaminated surface and air, but don’t demand an immediate change in prevention practices.