Two metres or one: what is the evidence for physical distancing in covid-19?
BMJ 2020; 370 doi: https://doi.org/10.1136/bmj.m3223 (Published 25 August 2020) Cite this as: BMJ 2020;370:m3223Read our latest coverage of the coronavirus outbreak
Editorial
Airborne transmission of covid-19
All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Dear Editor
This is an interesting article , and probably useful in a general way for suggesting ways to mitigate risk, and promoting plenty of more detailed and quantitative research.
One point which I don't feel to be addressed is hidden in the statement :
'Small droplets (later called aerosols or airborne droplets), typically invisible to the naked eye, evaporate more quickly than they fall. Without airflow, they cannot move far, remaining in the exhaler’s vicinity.'
This seems to imply that the droplets stay near the exhaler and therefore that by keeping away from the exhalers vicinity one could avoid the aerosol.
In real life, people move around , leaving behind a cloud of exhaled aerosol.
Another person walking behind the exhaler , or walking into the space they have just vacated would inevitably be exposed to some of the cloud.
How long would it be before the space vacated by an exhaler no longer contains enough virus to infect someone breathing it in ?
I can give an example of clear opportunity for infection in apparently safe situations:
Today I was out in the woods with my dogs , met another dogwalker on the path , which was quite wide,
I kept about 3 m away from him while standing and speaking a few words and then carried on past the man on the path he had just been on.
I considered I had been a very safe distance apart in an open outdoor setting .
About 5-10 paces after passing him, I got a strong smell of cigarette smoke.
Clearly I had inhaled some of his exhaled breath even after 5-10 paces.
The man was not actually smoking when I talked to him so he had either just extinguished the cigarette or had a lingering cigarette smell in his breath.
Two thoughts - 1. could virus still be in the air at that distance /time after exhalation. and 2. If cigarette odour lingers longer in the air, could virus be attached to the particles from the smoke and remain longer in the air on a 'carrier'?
Regards
Ian Crutchley MA Cantab
Competing interests: No competing interests
Dear Editor
I do really appreciate this illuminating and very clearly written Editorial, which has the additional merit of providing a reliable basis for investigating the role of "airborne particulate" (pm 10 and pm 2.5 "dust particles") in the spread as well as in the pathogenesis of SARS-CoV-2 infection. Indeed, as we are well aware, a big discussion has been undertaken for several months by the Scientific Community regarding the role played by the aforementioned "dust particles" and, more in general, by "airborne pollution" in SARS-CoV-2 infection's ecology and epidemiology, based upon the positive correlations apparently existing between the "airborne particulate" levels, on one side, and the number of viral infection's cases in given Countries (or in certain areas of the same Countries), on the other, coupled with the number of CoViD-19-associated/related deaths in those Countries.
This is the case, for instance, in Countries like Belgium, or State Regions like Lombardia (Northern Italy), where high SARS-CoV-2 infection case/fatality rates have been observed. We don't know yet in a precise manner "if" and, especially, "how" airborne pollution may contribute to the increased case/fatality rates detected in SARS-CoV-2-infected patients from the aforementioned (as well as from other) Countries or geographical areas. Within such context, the differently sized (pm 10 vs pm 2.5) dust particles floating in the air could act as "particulate nuclei" around which SARS-CoV-2-carrying "droplets" and/or "aerosols", once shed by infected individuals into the surrounding environment, could place themselves, thereby taking advantage from the possibility of a transfer for longer, if not much longer, distances.
Another component or, better said, pathogenetic mechanism through which "airborne dusts" could influence this viral infection - as well as other viral and non-viral infections - refers to SARS-CoV-2-host interaction dynamics. In this respect, the chronic inflammatory stimulus brought to the airways by the airborne particulate as well as by the chemical substances bound to/vehicled by it, could result, in its turn, in increased expression levels of ACE-2 - the SARS-CoV-2 host cell receptor - given the well-documented anti-inflammatory role played by such molecules. By doing so, the viral chances to infect an individual and to successfully propagate throughout her/his body would be increased.
While much more research is undoubtedly needed on these extremely challenging and intriguing issues, I would like to bring to your kind attention another related topic of interest, which has not been the subject thus far, to the best of my knowledge, of any in-depth studies. More in detail, what is the role, if any, exerted by "chemical environmental contaminants", with special emphasis on the so-called "persistent environmental pollutants" (such as "heavy metals" like methyl-mercury, "organochlorines" like DDTs, PCBs and dioxins, or "flame retardants" like PBDEs, etc.), in the pathogenesis of SARS-CoV-2 infection? We know for sure that many of the aforementioned compounds (as well as many others) have profound effects on the health and conservation of aquatic and terrestrial (vertebrate and invertebrate) organisms, given the prominent neuro-immunotoxicity and, even more importantly, the strong "endocrine-dysrupting activity" commonly displayed by them. As far as the latter is specifically concerned, a number or pathogenic interactions between these chemical contaminants and host's sex hormones, androgen and oestrogen receptors and carrier proteins have been reported (1).
Noteworthy, the majority of CoViD-19 cases, including those characterized by the most aggressive and severe disease forms, have been reported in male patients. This is most likely due to the fact that the activity of "transmembrane serine protease 2" (TMPRSS2), a key enzyme involved in the crucial interaction between SARS-CoV-2 spike (S) protein's "polybasic cleavage site" and the ACE2 receptor molecule on host's cell membrane, is an androgen/testosterone-dependant activity (2).
As a consequence, having this in mind, a critical question would be that related to the influence/modulation, if any, exerted by "reproduction hormone-interacting/dysrupting chemical pollutants" - many of which are also known to heavily accumulate and persist within the subcutaneous adipose tissue - on the pathogenetic evolution of SARS-CoV-2 infection.
This is another highly challenging, relevant, intriguing, and largely neglected issue, for which an "ad hoc" research effort is urgently needed.
1) Marine Mammal Ecotoxicology (2018), 1rst Edition, Maria Cristina Fossi & Cristina Panti (Editors), Elsevier.
2) Albini A., et al. (2020) - Internal and Emergency Medicine 15:759-766.
Competing interests: No competing interests
Dear Editor,
Can you further define "a short time" and "a long time" and "Low Occupancy" and "High Occupancy?" For example, would "a short time" be under 15 minutes and would "low occupancy" be 10 people or less? This would be valuable to know for those of us making decisions about indoor and outdoor meetings.
Thanks so much,
Scott
Competing interests: No competing interests
Dear Editor
Jones et al are to be congratulated on their paper, for highlighting the role of aerosol transmission of SARS-CoV-2. For far too long the dogma of large droplet-only spread has prevailed. with physical distancing to prevent large droplet spread as the be all and end all of mitigating measures against Covid-19, (along with hygiene measures). Distancing works, and is important, because it mainly protects against aerosol spread at close quarters rather than large droplets. (1) Distancing will not be protective however in enclosed indoor spaces with poor ventilation, as airborne spread considerably further than 2 metres can and does occur. Guenther et al, for example showed that spread over a distance of more than 8 metres occurrred in the superspreading event in the Tönnies meat packing plant in June. (2)
Concerning comments by other rapid response contributors about Jones' interpretation of Hamner's paper on the Skagit choir super-spreader event, Hamner does talk about fomite and large droplet spread being involved, but also mentions the possibility of aerosols from singing being involved. The same event was studied in great detail by Miller et al, in a preprint (3), who found:
"Inhalation of respiratory aerosol most likely dominated infection transmission during this event, as other modes of transmission are unlikely to account for the high secondary attack rate. For example, it seems infeasible that all attendees touched the same surface(s) as the index case. Furthermore, rehearsal attendees expressed that they had taken great care to minimize contact transmission (personal communication). There is no evidence to suggest that more than one person was infected at the time of the rehearsal. The index case would have spent extended time within a few meters of only a small proportion of the rehearsal attendees. Other close contact events that extend to a high proportion of the attendees would have been brief and incidental. Consequently, we believe it likely that shared air in the Fellowship Hall, combined with high emissions of respiratory aerosol from singing, were important contributing factors."
As for the statement by Axon that "Singing itself has now been shown to produce only a minimal increase in aerosol mass over speaking or breathing", this is a selective reading of Gregson et al's paper, which in fact says "Speaking and singing show steep increases in mass concentration with increase in volume (spanning a factor of 20-30 across the dynamic range measured, p<1×10-5). At the quietest volume (50 to 60 dB), neither singing (p=0.19) or speaking (p=0.20) were significantly different to breathing. At the loudest volume (90 to 100 dB), a statistically significant difference (p<1×10-5) is observed between singing and speaking, but with singing only generating a factor of between 1.5 and 3.4 more aerosol mass." While the difference between singing and speaking is not very large, greater volume and duration of vocalisation, whether singing or speaking, are clearly associated with much greater aerosol generation than quiet breathing.
I also do not share the concerns of other rapid response contributors about the risk chart in Jones' paper, showing risk according to distance, time, mask wearing, ventilation, number of people etc. It is not meant to be quantitative, but to show the major risk factors for spread and how these are additive. Perhaps there could be adjustments made to the colour scheme employed as suggested, but along with similar graphical displays of risk factors, these are warmly welcomed by the general public as an aid to understanding transmission risk.
The reason for public welcome is of course the dereliction of duty by the UK government and Public Health England, in failing to formally recognise aerosol transmission of SARS-CoV-2, explain it to the public and provide clear guidance on how to mitigate the risk. Evidence for airborne spread is now very convincing; the government's own expert advisory committees have been talking about it for several months. The Envrionmental Monitoring Group (which reports to SAGE) and SAGE itself have repeatedly warned of the risks of aerosol spread, yet there has been a deafening silence about this from the authorities. Schools have re-opened, people are being strongly encouraged to go back to work and universities are about to re-open; these are all enclosed indoor spaces posing risks for airborne spread, yet the advice they are given is all about social distancing and hygiene, and a passing, tokenistic mention to increase ventilation "where possible", with no explanation of why, or detail on how to assess ventilation requirement, and what measures should be taken.
Not surprisingly knowledge of indoor airborne spread is therefore limited, not only among the public, but also employers, regulatory authorities and indeed medical professionals, including public health officials. Factory outbreaks, of which there seems to be one or two new ones each week, are blamed on workers not observing distancing or hygiene measures, when no enquiry at all is made of the adequacy or otherwise of measures to mitigate airborne spread in the workplace, such as ventilation systems.
As Wilson et al said in their recent paper on airborne spread, (3) "guidelines and governments must acknowledge the evidence and take steps to protect the public". The transmission of Covid-19 is increasing, we are heading towards winter and will spend much more time indoors. We ignore indoor aerosol spread of Covid-19 at our peril.
(1) https://www.sciencedirect.com/science/article/abs/pii/S0360132320302183
(2) https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3654517
(3) https://www.medrxiv.org/content/10.1101/2020.06.15.20132027v2
(4) https://www.bmj.com/content/370/bmj.m3206
Competing interests: No competing interests
I read with interest as the authors detail how the two metres rule for physical distancing relies on an outdated and oversimplified understanding of droplet science. This lack of nuanced understanding results in policies which are supposed to be scientifically informed but wind up being nothing of the sort. Surprisingly, following this well-researched background, the authors proceed to propose a “More nuanced model” in which they commit the exact same mistakes that they are critical of.
Figure 3 claims to show graded levels of risk of SARS-CoV2 transmission. However, by failing to provide any objective criteria for the decision points (high versus low occupancy, prolonged versus short contact, well versus poorly ventilated), the figure is not only unscientific but functionally worthless. How can one use such a diagram to make a risk decision without understanding what the terms mean? Further baffling were the two situations deemed by the authors to represent a “borderline case that is highly dependent on quantitative definitions of distancing, number of individuals, and time of exposure.” Given the entirely subjective nature of the cut-offs and the many other potentially relevant variables detailed at length by the authors throughout the article (e.g., humidity, viral shedding, airflow patterns, etc…) it seems clear that EVERY SINGLE CASE detailed in the diagram falls into this borderline category. In other words, the diagram has nothing to add to scientific discussion on the topic. While I fully agree with the authors that “rules on distancing should reflect the multiple factors that affect risk” it’s hard to escape the conclusion that the authors avoided doing exactly this while crafting their graphic. Creating a scientifically validated risk model is a monumental challenge requiring the collaboration of numerous experts across many fields. Creating a made-up risk diagram based off the gut feelings of the authors is not only unhelpful but oversimplifies this scientific challenge to an astounding degree.
Competing interests: No competing interests
Dear Editor,
COVID-19 Is Transmitted Through Aerosols. We Have Enough Evidence, Now It Is Time to Act.
“…it seems clear that aerosols are more important when it comes to transmitting COVID-19 than we thought six months ago-and certainly more important than public health officials are currently making them out to be. The WHO and CDC, among others, must begin communicating the science suggesting aerosol spread of COVID-19-and the risk reduction strategies necessary as a result. If not, we hamper our ability to counter the growing health consequences and increasing death toll of COVID-19.”
COVID-19 is Transmitted Through Aerosols.We Have Enough Evidence, Now It Is Time to Act
A public health poster was part of a government campaign in New South Wales to limit the spread of the deadly Spanish flu pandemic of 1918-19, in which about 12,000 Australians died, 6300 of them in New South Wales. Soldiers returning from World War I and infected people were quarantined, wearing masks in public places was made compulsory, schools were closed, many public activities were banned or restricted and pharmacy prices were regulated.
https://www.naa.gov.au/learn/learning-resources/learning-resource-themes...
Competing interests: No competing interests
Dear Editor
A major problem in understanding the possible role of airborne transmission in the Covid-19 pandemic has been the need to combine research findings from the biomedical, physical and social sciences. Authors from each have tended to filter the others through their own understanding rather than establishing genuine interdisciplinary collaborations to integrate these different sources of expertise. In a brief response, it is not possible to detail all the flaws in Jones et al(1) and we have selected three for specific consideration.
The Images
The study of airborne transmission has been plagued by the widespread and uncritical reproduction of still and video images – and graphics from modelling – produced under a variety of conditions and with little recognition of their limitations. Many of these rest on the use of manikins to mimic human expiration under laboratory conditions that fail to reproduce real-world conditions. Such experiments are convenient to measure and photograph, but lack verisimilitude. The two images in this paper demonstrate some of these flaws.
Figure 1 does not have a scale bar to show the distance traveled by the cloud. However, this appears to be contained within the depth of the head i.e. 20-30 cm, commensurate with more recent work of Viola et al(2). The cloud is rising due to the buoyancy of the emitted droplets and the thermal plume created by human body warmth relative to environmental temperature. It might also be added that sneezing is not a recognized symptom of Covid-19(3). Figure 2 also purports to depict a sneeze, but there is no supporting detail of the original experiment. The cloud’s source is not shown and its density appears unrealistically high, although this could be due to the camera sensor’s saturation from a lengthy exposure or high ISO setting. The perspective is unexplained. The image is attributed to Bourouiba(4), but seems to be derived from Scharfman et al(5) (including Bourouiba). Although Scharfman et al gives details of an experimental set-up, this image does not appear in that paper. From Scharfman et al it is also possible that this image is associated with a third paper involving Bourouiba (though not Scharfman et al) (6), although again, the image in Fig. 2 does not appear. The similar experimental images in Bourouiba et al(6), and the corresponding modeling, show sneeze ejections traveling 70-80 cm, not 7-8 m. The shorter distance would be consistent with other recent work (2,7) and we wonder whether there has been a translation error with the units.
Emission, Ventilation, Exposure
The section ‘Force of emission, ventilation, exposure time’ relies mainly on case studies. The previous section, discussing air sampling studies, cautions that these ‘were small, observational, and heterogeneous in terms of setting, participants, sample collection, and handling methods [and] prone to recall bias…’. The same restraint is not evident here, although the additional risks of confounding call for it. The Skagit County choir, for example, has been widely cited as evidence for airborne transmission.(8) The original authors, however, left open questions about the social interactions between choir members, and the sharing of plates of fruit and cookies, indicating the possibility of contact or fomite transmission. Singing itself has now been shown to produce only a minimal increase in aerosol mass over speaking or breathing.(9) The same is true for the various case studies of call centres and restaurants. While air flow patterns from air-conditioning or extraction systems (ventilation) may have had an effect, they are also confounded by a lack of knowledge relating to possible contact or fomite transmission. Localized air flow patterns may have an effect on the distribution of non-settling particles, but it appears as though the authors see ventilation as adding to the distribution of particles. The express purpose of ventilation is to extract non-settling particles altogether. If the flow rate is reasonable – a few times greater than the (per capita) volume humans breathe at – there is too little time to inhale infective particles before they are removed.
The Risk Assessment Chart
The main source for the assessment of distance and transmission risk appears to be Chu et al. (10) Although Jones et al acknowledge that this review has limitations, this glosses over the many severe, and likely fatal, flaws in the meta-analysis detailed by Heneghan and Jefferson(11): “As experienced reviewers, we looked at the evidence and could not replicate the distance estimates reported in the Lancet paper”. Moreover, Chu et al appear not to take account of the differing ventilation conditions of the sources for their meta-analysis – which is crucial for the compilation of Figure 3. While this purports to be a usable took for risk assessment, there is no evidence of engagement with the long-established risk analysis methods(12–14) used in various sectors (including health care). The authors admit that their assessment is qualitative, but the variables are either ill-defined or undefined e.g. low/high occupancy, good/poor ventilation, volume level of the activity, short/prolonged contact time, or most importantly low/medium/high risk of transmission. The judgements used to develop the traffic-light system are not supported by any analytic methodology nor any scientific literature, including that of the indoor air quality research community(15). The authors have ended-up creating what can be considered as a set of risk matrices, which have well-documented flaws but can be a useful tool if properly designed(16–19). The figure is solely the opinions of the authors, reflecting their pre-existing biases – advocacy-based evidence rather than evidence-based advocacy(20).
Conclusions
While Jones et al have sought to reconcile physical and biomedical approaches, the result goes mainly to show the limitations of one discipline’s superficial understanding of another and the need to embrace the knowledge of a third. Using an evocative image with no explanation is unacceptable in a scientific manuscript. Frankly, this adhoc approach to risk analysis is what gives qualitative methods a bad name. The risk assessment should be supported by literature, (preferably) quantitative analysis, and it must be within an accepted methodological framework for risk assessment.
References
1. Jones NR, Qureshi ZU, Temple RJ, Larwood JPJ, Greenhalgh T, Bourouiba L. Two metres or one: what is the evidence for physical distancing in covid-19? BMJ [Internet]. 2020 Aug 25 [cited 2020 Aug 27];370. Available from: https://www.bmj.com/content/370/bmj.m3223
2. Viola IM, Peterson B, Pisetta G, Pavar G, Akhtar H, Menoloascina F, et al. Face Coverings, Aerosol Dispersion and Mitigation of Virus Transmission Risk. arXiv:200510720. 2020;
3. Sudre CH, Lee K, Lochlainn MN, Varsavsky T, Murray B, Graham MS, et al. Symptom clusters in Covid19: A potential clinical prediction tool from the COVID Symptom study app. medRxiv. 2020 Jun 16;2020.06.12.20129056.
4. Bourouiba L. Turbulent Gas Clouds and Respiratory Pathogen Emissions: Potential Implications for Reducing Transmission of COVID-19. JAMA. 2020 May 12;323(18):1837–8.
5. Scharfman BE, Techet AH, Bush JWM, Bourouiba L. Visualization of sneeze ejecta: steps of fluid fragmentation leading to respiratory droplets. Exp Fluids. 2016 Feb;57(2):24.
6. Bourouiba L, Dehandschoewercker E, Bush JWM. Violent expiratory events: on coughing and sneezing. J Fluid Mech. 2014 Apr 25;745:537–63.
7. Bandiera L, Pavar G, Pisetta G, Otomo S, Mangano E, Seckl JR, et al. Face Coverings and Respiratory Tract Droplet Dispersion. medRxiv.
8. Hamner L, Dubbel P, Capron I, Ross A, Jordan A, Lee J, et al. High SARS-CoV-2 Attack Rate Following Exposure at a Choir Practice - Skagit County, Washington, March 2020. MMWR Morb Mortal Wkly Rep. 2020 May 15;69(19):606–10.
9. Gregson, Watson, Orton, Haddrell, McCarthy, Finnie, et al. Comparing the Respirable Aerosol Concentrations and Particle Size Distributions Generated by Singing, Speaking and Breathing. 2020 Aug 20 [cited 2020 Aug 30]; Available from: https://chemrxiv.org/articles/preprint/Comparing_the_Respirable_Aerosol_...
10. Chu DK, Akl EA, Duda S, Solo K, Yaacoub S, Schünemann HJ, et al. Physical distancing, face masks, and eye protection to prevent person-to-person transmission of SARS-CoV-2 and COVID-19: a systematic review and meta-analysis. The Lancet. 2020 Jun 27;395(10242):1973–87.
11. Heneghan C, Jefferson T. COVID-19 Evidence is lacking for 2 meter distancing [Internet]. Oxford, UK: The Centre for Evidence-Based Medicine, University of Oxford; 2020 Jun [cited 2020 Aug 28]. Available from: https://www.cebm.net/covid-19/covid-19-evidence-is-lacking-for-2-meter-d...
12. MacKenzie CA. Summarizing Risk Using Risk Measures and Risk Indices. Risk Anal. 2014 Dec 1;34(12):2143–62.
13. Aven T. Risk assessment and risk management: Review of recent advances on their foundation. Eur J Oper Res. 2016 Aug 16;253(1):1–13.
14. ISO. IEC 31010 Risk management -- Risk assessment techniques [Internet]. Geneva, Switzerland: International Standardization Organization; 2019 p. 164. 2nd Edition. Available from: https://www.iso.org/standard/72140.html
15. Ai ZT, Melikov AK. Airborne spread of expiratory droplet nuclei between the occupants of indoor environments: A review. Indoor Air. 2018 Jul;28(4):500–24.
16. Cox LA. What’s Wrong with Risk Matrices? Risk Anal. 2008 Apr 1;28(2):497–512.
17. Duijm NJ. Recommendations on the use and design of risk matrices. Saf Sci. 2015 Jul 1;76:21–31.
18. Peace C. The risk matrix: uncertain results? Policy Pract Health Saf. 2017 Jul 3;15(2):131–44.
19. Bao C, Li J, Wu D. A fuzzy mapping framework for risk aggregation based on risk matrices. J Risk Res. 2018 May 4;21(5):539–61.
20. Martin GP, Hanna E, McCartney M, Dingwall R. Science, society, and policy in the face of uncertainty: reflections on the debate around face coverings for the public during COVID-19. Crit Public Health. 2020 Aug 10;0(0):1–8.
Competing interests: No competing interests
Dear Editor
this paper appears to misrepresent an important reference on "27 Hamner L, Dubbel P, Capron I, etal. High SARS-CoV-2 attack rate following exposure at a choirpractice"
It is stated that: "findings from fluid dynamic studies help explain why at one choir practice in the US, a symptomatic person infected at least 32 other singers, with 20 further probable cases, despite physical distancing."
The actual words in the Hamner et al paper referred to are:
"Transmission was likely facilitated by close proximity (within 6 feet) during practice and augmented by the act of singing"
and
"The 2.5-hour singing practice provided several opportunities for droplet and fomite transmission, including members sitting close to one another, sharing snacks, and stacking chairs at the end of the practice. The act of singing, itself, might have contributed to transmission through emission of aerosols, which is affected by loudness of vocalization"
Flawed references will taint the public health message for genuine evidence-based measures.
Competing interests: No competing interests
Dear Editor
Although the article “Two metres or one: what is the evidence for physical distancing in covid-19?” by Jones NR et al.,1 published in BMJ 2020;370:m3223 on 25 August 2020, reports sound and practical information on protecting people from SARS-CoV-2 infection, information on “occupancy or crowding level” and definitions of low and high occupancies are not provided. The Oxford Dictionary of English defines crowd as “a large number of people gathered together in a disorganized and unruly way”.2 This definition is insufficient for scientific studies, and specific measurements defining crowding are necessary.
The World Health Organization states that crowding in housing relates to the conditions of the dwelling and the space it offers, in addition to the number of people sharing the dwelling.3 This definition allows for relative comparisons. For example, which scenario is more crowded: three persons in a lift of 1 m2, 50 people in a 200 m2 supermarket or six healthcare workers doing ward rounds in 4 m2 patient rooms? Although there is no universally accepted measure for overcrowding, the U.S. Department of Housing and Urban Development Office of Policy Development and Research has reported on the benefits of several methods of measuring overcrowding, such as persons-per-room (PPR) and unit square footage-per-person (USFPP).4 Typically, the number of standing passengers per square meter is an objective standard measure for crowding used by many public transport services around the world.5 Presently, in public areas, such as public transport vehicles, bars and restaurants, and even in hospital wards, intensive care units, training meeting halls and operating theatres, there is ambiguity in the appropriate methods of protection against COVID-19 infection.6 The study conducted by Jones NR et al.1 provides useful information on protecting people from COVID-19 but, in order to best interpret the results of such a study involving crowd parameters, it is necessary to apply one of the crowd measurement methods reported in the literature.
References
1. Jones N, Qureshi Z, Temple R, et al. Two metres or one: what is the evidence for physical distancing in covid-19?. . BMJ 2020;370:m3223
2. Stevenson A. Oxford Dictionary of English. Third edition ed. Oxford: Oxford University Press 2010.
3. World Health Organization, editor. WHO Housing and health guidelines. Geneva: Licence: CC BY-NC-SA 3.0 IGO., 2018.
4. U.S. Department of Housing and Urban Development Office of Policy Development and Research. Measuring Overcrowding in Housing. Bethesda: Econometrica, Inc. 2007.
5. Zheng L, Hensher D. Crowding in Public Transport: A Review of Objective and Subjective Measures. Journal of Public Transportation 2013;16(2):107-34.
6. Ganau M, Netuka D, Broekman M, et al. Neurosurgeons and the fight with COVID-19: a position statement from the EANS Individual Membership Committee. Acta Neurochir (2020). https://doi.org/10.1007/s00701-020-04360-3. 2020
Yours sincerely,
Assoc. Prof. Naci Balak, MD, IFAANS
Department of Neurosurgery, Istanbul Medeniyet University, Göztepe Education and Research Hospital,
Kadiköy, Istanbul, Turkey
Competing interests: No competing interests
Re: Two metres or one: what is the evidence for physical distancing in covid-19?
Dear Editor
SARS-CoV-2 is transmitted mainly through short- and long-range airborne transmission.[1 2] Omicron, now dominant in many countries, shows faster transmission and greater vaccine escape than previous variants.[3] Further measures are needed to contain transmission.
In August 2020, we argued that “Rigid safe distancing rules are an oversimplification based on outdated science”.[4] We produced risk charts for SARS-CoV-2 transmission incorporating multiple variables: indoors versus outdoors (and, for the former, level of ventilation), room occupancy (low or high), time spent together (short or long), vocalisation (silent, speaking, shouting or singing), and masking (yes or no).
While these Covid risk charts have been translated into over 30 languages,[5] rapid responses to the article criticised the authors for providing relative, rather than absolute, estimates of risk levels. We knew, for example, that speaking and singing would transmit more airborne particles than remaining silent – but how much more, and over what length of time?
We have now developed a mathematical model to quantify further these relative risks with updated data.[6] Our model, which assumes a single enclosed space in which viral-containing aerosols exhaled by a single infected human become rapidly mixed, is based on models developed for infectious disease spread through the air (e.g. measles[7]). It takes account of the disease-specific emission rate of viral-carrying particles (quanta), the increase in emission of viral particles with vocalization and exercise, room volume, room occupancy (assumed to be stable and continuous), rate of particle removal either naturally (e.g. opening windows) or mechanically (e.g. replacement with outdoor air, filtration), and the efficiency with which virus-carrying particles penetrate masks.
Details of these calculations, which are consistent with the observed variation in attack rates across twelve widely-studied super-spreader events for Covid-19, and were also applied to other outbreaks of tuberculosis, influenza and measles, are published in the technical paper.6 One of the attack rate charts from the resultant model is reproduced in a linked table (https://docs.google.com/document/d/1BWWCpUWiPIlntWRFfPwqBSa1Z777KFIl/edit), with an interactive risk calculator made available online (http://tinyurl.com/COVID-Tables).[8]
The quantitative findings from the modelling study strongly affirm the validity of the low-, medium- and high-risk social situations set out in the original BMJ paper from August 2020.[4] We have added quantitative risks of transmission to all the original scenarios, including additional data on the risks of exercise whereby heavy breathing greatly increases viral emission from infected individuals. The model, however, does not account for all variables, notably overlapping breathing zones between individuals and known airflow heterogeneity indoors (see technical paper for details[6]).
As transmission escalates despite vaccination, fuelled by shedding from asymptomatic carriers,[9] we should note the perils of mixing unmasked in crowded and under-ventilated indoor spaces, especially when singing or exercising. When prevalence decreases after the current wave, more activities become low risk.
T. Greenhalgh [1], Zhe Peng [2], Jose L. Jimenez [2], W Bahnfleth [3], S Dancer [4,5], L. Bourouiba [6] (on behalf of 22 authors of the original paper)
1. Nuffield Department of Primary Care Health Sciences, University of Oxford, Oxford OX2 6GG, UK.
2. Dept. of Chemistry and Cooperative Institute for Research in Environmental Sciences; University of Colorado; Boulder, CO 80309, USA
3. Dept. of Architectural Engineering, The Pennsylvania State University, University Park, Pennsylvania 16802, United States
4. Dept. of Microbiology, NHS Lanarkshire, Glasgow, Scotland G75 8RG, U.K.
5. School of Applied Sciences, Edinburgh Napier University, Scotland EH11 4BN, U.K.
6. The Fluid Dynamics of Disease Transmission Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
References
1. Greenhalgh T, Jimenez JL, Prather KA, et al. Ten scientific reasons in support of airborne transmission of SARS-CoV-2. The Lancet 2021;397(10285):1603-05.
2. World Health Organisation. Coronavirus disease (COVID-19): How is it transmitted? (Updated 21st December 2021). Geneva: WHO. Accessed 27th December 2021 at https://www.who.int/news-room/questions-and-answers/item/coronavirus-dis... 2021.
3. Chen J, Wang R, Gilby NB, et al. Omicron (B. 1.1. 529): Infectivity, vaccine breakthrough, and antibody resistance. ArXiv 2021
4. Jones NR, Qureshi ZU, Temple RJ, et al. Two metres or one: what is the evidence for physical distancing in covid-19? bmj 2020;370
5. CovidStraightTalk. The #COVIDRISKCHART in 34 languages: CovidStraightTalk.org 2020.
6. Peng Z, Rojas ALP, Kropff E, et al. Practical Indicators for Risk of Airborne Transmission in Shared Indoor Environments and Their Application to COVID-19 Outbreaks. Environmental Science & Technology 2022;e-pub ahead of print doi: 10.1021/acs.est.1c06531
7. Riley E, Murphy G, Riley R. Airborne spread of measles in a suburban elementary school. American journal of epidemiology 1978;107(5):421-32.
8. Jimenez JL, Peng Z. COVID-19 aerosol transmission estimator. Colorado: University of Colorado. Accessed 27th December 2021 at https://tinyurl.com/covid-estimator 2021.
9. Johansson MA, Quandelacy TM, Kada S, et al. SARS-CoV-2 Transmission From People Without COVID-19 Symptoms. JAMA network open 2021;4(1):e2035057-e57.
Competing interests: No competing interests