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Editor’s note, September 10, 2020, 11:50 am: A number of readers and other experts responded to the following article with comments and expressions of concern. We sought clarification from the authors and have updated the article with their response attached at the end.
Several international health agencies, such as the WHO, recommend a distance of three to six feet between people to minimise the chances of aerosol-based transmission. Recent scientific reports suggest that SARS-CoV-2, the causative agent of COVID-19, can remain infectious for hours in aerosols. We also know that aerosol particles – whether or not they’re laden with viral particles – can travel more than four-times as far as is considered to be ‘safe’. The available scientific data, however, unequivocally rules out such possibilities.
Aerosols are tiny droplets, 10 micrometers wide, of fluids. In comparison, a single human hair is approximately 100 micrometers wide. During everyday activities like talking, breathing, and coughing, we release thousands of these aerosol particles without realising it. The size of these particles varies from one activity to the other. For instance, sneezing and coughing would release more particles than breathing.
These aerosols undergo two immediate changes in their configuration within milliseconds of leaving the mouth. Most of them instantly dry out and form dense aerosol nuclei that float in the air of confined spaces, such as a room. Simultaneously, the opposite also happens – the smaller droplets fuse and form larger droplets that then settle down on surfaces in the room. More than 99% of respiratory droplets drop to the ground within a minute or two. Aerosol particles released from an infected person sometimes may contain a germ, such as the new coronavirus. It, therefore, seems logical that aerosol particles can spread COVID-19. The bulk of scientific evidence, however, seems to suggest otherwise, for several technical reasons.
First, aerosols form a small fraction (1%) of all respiratory particles. The vast majority of respiratory particles are larger droplets that quickly settle down due to gravity and form the basis of contact (scientifically known as a fomite) transmission.
Second, the human oral and nasal cavities are home to an enormous number of non-pathogenic microorganisms – a large proportion of them are commensal (or friendly) bacteria. Modern scientific techniques like next-generation sequencing have identified more than 700 different types of bacteria in the mouth of healthy people. One estimate suggests that the total number of bacteria in the oral cavity is close to a billion cells per millilitre of saliva. This means the infectious viruses must compete for space with these other, much larger organisms in the tiny aerosol particles. As a result, most aerosol particles can’t harbour infectious viruses. In fact, many aerosol particles are empty, not containing any germs, good or bad.
Also read: New Virus Lasts Hours on Surfaces, in Air but Proximity to Patients Is Riskier
Third, one common problem with all scientific studies involving aerosol particles is that they are all performed in an indoor setting, such as a laboratory designed to mimic a classroom or a hospital corridor. While the findings of these studies are accurate under these conditions, the results can’t be extrapolated to outdoor settings, where the wind and other environmental factors play a crucial role in diluting and destroying aerosol particles. Additionally, there is the ‘the open-air factor‘ – a collection of various parameters such as humidity, temperature, UV rays from the Sun, etc. that are all responsible for rapidly inactivating viruses in aerosols outdoors.
Fourth, aerosols are primarily generated at the front end of the mouth (near the tip of the tongue), whereas the virus particles are mainly located deep in the lungs or the lining of the trachea. That means, except for a deep cough or sneeze, most aerosol particles generated by other normal activities can’t contain infectious viruses because these viruses are not located where the aerosols form.
Fifth, a single viral particle can’t establish a new infection – unlike some bacteria, such as the bacteria that cause tuberculosis. Many RNA viral genomes bear genetic defects and are non-infectious. Additionally, the lungs have a protective mucous layer that acts as a protective shield. So a few hundred to thousands of virus particles are necessary to start a new infection. Most aerosol particles can’t have more than a few viral particles.
Sixth, most enveloped viruses are unstable in aerosol particles, particularly at high temperature and humidity. Viruses don’t have a protective cell wall, unlike bacteria or yeast. So viruses are more prone to drying and inactivation.
Finally, the host immune system has many molecular sensors to detect, identify and destroy pathogens. Establishing an infection is not an easy task for a virus through the aerosol route. While it may seem possible, it is not probable.
These facts collectively suggest that much of the hype surrounding aerosols is mostly unwarranted.
Given these realities, prevention is better than cure, and there are multiple precautionary measures available to minimise the chances of contracting an infection of the new coronavirus. Aerosol particles may transmit viruses only in close proximity, especially in crowded rooms without ventilation. The use of a face mask in proximity is critical. Masks, however, offer only limited protection. So avoiding congested areas, including social events, parties, passenger cars, air-conditioned coaches, departmental stores, etc. is important.
One need not use a face-mask when working alone in the office or driving a car alone. If there are co-passengers in the vehicle, wear face masks and roll down the windows to promote ventilation that will remove aerosols. In public toilets, the process of flushing can generate a large volume of aerosol called toilet plume above the pot. Wearing a face mask in a public toilet is a must. In contrast, wearing a face mask is not necessary in open spaces, such as parks, gardens, well-ventilated corridors and large rooms.
Family members spend a lot of time together, so wearing a face-mask at home can’t help much. While exercising, don’t wear face masks; they will reduce oxygen uptake. Viruses can’t travel between buildings and infect people. Such fears are unreasonable. Newspapers dry aerosol particles at a faster rate because they are porous and absorbent, which is also true of building walls. It is practically not possible for viruses to infect people through newspapers or toilet papers. Additionally, cement and paint contain calcium-rich minerals. Viruses are readily inactivated on such surfaces, and disinfecting such surfaces is illogical.
Also read: India’s Epidemic: Why Do We Spray Bleach on the Road When It Won’t Help?
Adding a disinfectant, such as bleach, to clothes, while washing is not necessary. The concentration of detergent used for washing is so huge that the viruses and many bacteria are readily destroyed. Fruits and vegetables need not be disinfected using any special solutions. Washing them in water is all that is necessary.
The anxiety regarding the new coronavirus among non-experts is justified and understandable. The root cause of the concern lies more in the lack of scientific education and, importantly, the absence of a supportive administrative structure. Given the lack of necessary medical infrastructure, India is not in a position to face the challenges of the most severe medical calamity (thus far) of this century. The lack of an adequate healthcare support system is one of the primary reasons as to why every small risk associated with the SARS-CoV-2 virus appears to be magnified.
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Authors’ response to expressions of concern follows (published as received, with minor changes for style):
We are grateful for the opportunity to defend certain statements of our article. The conclusions drawn in our article have been substantiated by experimental data from the scientific literature. We understand and empathise with the confusion prevailing in the backdrop of the raging pandemic concerning facts on the mode of viral transmission.
In our article, we did not rule out the possibility of aerosol transmission of the new coronavirus; we only said that the probabilities are small. At present, scientific data have not yet emerged regarding this issue on the new coronavirus. However, based on the transmission properties of other enveloped viruses, especially those of the influenza virus and old coronaviruses, we have drawn several interpretations.
We are fully aware that several concepts in the field are less defined and controversial, especially the definition regarding aerosols versus droplet differences and the size of aerosols required for a lung infection. Several laboratories are currently working to address many of these concerns, and in the coming years, more clarity will be shed on these technical aspects.
Meanwhile, we have attempted to clarify the nature of aerosol transmission of the new coronavirus by extrapolating the available knowledge from other and similar viruses. Our conclusions are founded on comprehensive scientific data available from the areas of viral biology, molecular biology, epidemiology and the like. A balanced strategy is needed to ensure the unbiassed interpretation of the scientific data already available. Such analysis must be grounded in the broader experimental evidence available and not on any single discipline of science (from your email it appears that the objections are based on only epidemiological evidence).
The research articles and reviews we cite here have appeared in reputed and peer-reviewed, not spurious, journals. Although we mention only a few references under each clarification, there are very many additional reports available, if necessary. Events such as the Amoy Gardens Housing Estate in Hong Kong alert us that under specific circumstances, viruses can transmit through the drainage pipelines in buildings. However, the available data are only indirect evidence, and alternative proposals are available. Epidemiological events such as this should be interpreted with caution and must not be generalised.
Here, we provide many scientific citations to substantiate our statements. We are open to admitting the limitations of our assertions if anyone can offer empirical and comprehensive scientific evidence to counter our conclusions.
1. “Most enveloped viruses are unstable in aerosol particles, particularly at high temperature and humidity”
There have been multiple reports supporting the above statement, including a WHO commissioned report (see citation below). It is general knowledge that enveloped viruses lose infectivity at high humidity and high temperature.
i. Yang et. al, Applied & Environmental Microbiology, 2012 – page 6786
“Viruses that require acidification before fusion are less stable at 50 to 90% RH than at RHs outside this range. Such examples include IAV, SFV, Langat virus, Venezuelan equine encephalomyelitis virus, and SARS coronavirus.”
“However, it is worth noting that temperature is another factor that may influence the relationship beyond the direct effect of temperature on virus viability. RH is a function of temperature because ambient temperature determines the saturation vapour pressure of water.”
ii. Pan et. Al, Journal of Applied Microbiology, 2019 – page 1604
“In contrast, lipid-enveloped viruses such as vaccinia virus may have reduced stability in air if RH is above 70% (Cox 1987; Tellier 2006). These observations fit well with the general belief that phospholipid-protein complexes in enveloped viruses are usually more likely to denature in the air at medium to high RH, whereas the protein coats of non-enveloped viruses are more readily to denature at low RH” (Cox and Wathes 1995).
iii. Ramond Tellier, Emerging Infectious Diseases, 2006 – page 1658
“In experiments that used homogeneous aerosolised influenza virus suspensions (mean diameter 6 µm), virus infectivity (assessed by in vitro culture) at a fixed relative humidity undergoes an exponential decay; this decay is characterised by very low death rate constants, provided that the relative humidity was in the low range of 15%-40%.”
“Generally, viruses with higher lipid content tend to be more persistent at lower relative humidity, while viruses with lesser or no lipid content are more stable at higher relative humidities” (Coronaviruses are enveloped viruses, therefore are rich in lipid content.)
“Measles and influenza, both enveloped viruses, survive best in aerosols at low relative humidity (de Jong, 1964 #424; Hemmes, 1960 #423). Similarly, Japanese encephalitis virus has been demonstrated to be most stable in stabilised aerosols at low relative humidity, with half lives of 28, 38, and 62 minutes at 80, 55, and 30%, respectively (Larson, 1980 #281).”
“Generally virus survival varies inversely with temperature.”
We can provide more citations if you need to substantiate this statement further.
2. “While exercising, don’t wear face masks; they will reduce oxygen uptake.”
Masks trap exhaled air, which will be partly inhaled again, especially when the masks are wet after absorbing moisture from breath. While exercising, one needs more breathing activity and more oxygen. One can not breathe effectively wearing a mask. Therefore, it is common advice from medical experts not to wear a mask while exercising; we are surprised that objections are raised against such foregone conclusions.
i. Fikenzer et. al, Clinical Research in Cardiology, 2020 – page 7, Discussion
“This first randomised cross-over study assessing the effect of surgical masks and FFP2/N95 masks on cardiopulmoNary exercise capacity yields clear results. Both masks have a marked negative impact on exercise parameters such as maximum power output (Pmax) and the maximum oxygen uptake VO2max kg). FFP2/N95 masks show consistently more pronounced negative effects compared to surgical masks. Both masks significantly reduce pulmonary parameters at rest (FVC, FEV1, PEF) and at maximum load (VE,BF, TV). Furthermore, wearing the masks was perceived as very uncomfortable with a marked effect on subjective breathing resistance with the FFP2/N95 mask.”
ii. Johnson et.al, American Industrial Hygiene Association Journal – page 467
“Masks have been known to increase the oxygen cost of exercise, probably due to increased weight, constriction of normal breathing patterns, and the increased cost of respiratory work.”
iii. Chandrashekharan et. al, Medical hypothesis, 2020 – page 1
“Though WHO supports facemasks only for COVID-19 patients, healthy social exercisers” too exercise strenuously with customised facemasks or N95, which hypothesised to pose more significant health risks and tax various physiological systems especially pulmonary, circulatory, and immune systems. Exercising with facemasks may reduce available oxygen and increase air trapping preventing substantial carbon dioxide exchange.”
3. “… whereas the virus particles are mainly located deep in the lungs or the lining of the trachea”
The above statement does not claim that the SARS-CoV-2 is absent in the saliva; it says that the bulk of the virus is deeper into the lungs. The virus primarily infects the deep lung tissues, tracheal lining, and upper respiratory tract. Taken by itself, this statement could be considered incorrect. However, in context of the article it is not so. As we have already explained in our second reason, the saliva contains abundant amounts of commensal microorganisms which have to compete for space in aerosols. The viral load in the oral cavity is low, and the viruses would be outcompeted. However, deeper inside the trachea and the lungs, this is not the case.
Schaefer et. al, Modern Pathology, 2020 – The entire paper details the detection of SARS-CoV-2 in the lungs and airways of patients.
4. “… a single viral particle can’t establish a new infection … So a few hundred to thousands of virus particles are necessary to start a new infection.”
This is an established fact in the community, and we are surprised that there are concerns regarding this fact. Cell infection studies or animal challenge experiments use virus stocks expressed in terms of Tissue Culture Infectious Dose-50 (TCID-50) or infectious dose to determine the minimum number of viruses required to infect 50% of target cells or animals. This is a number that is experimentally determined to measure the infectivity of any virus. People typically use 1 to several hundreds of such units of the virus in their experiments. Importantly, each TCID50 unit may contain hundreds of individual viral particles (see references below). To determine the number of infectious viral particles present in a TCID50 unit is not possible because the stock is a mixture of viable and non-viable viruses.
i. Alford RH et. al, Proc Soc Exp Biol Med. 1966 – The authors used 1 -120 TCID50 doses to infect human volunteers with influenza virus.
ii. van Elden LJ et al, J Clin Microbiol. 2001 – This study demonstrates that one TCID50 Unit contains 350-600 viral RNA molecules. Note that the RNA molecule number cannot be equated to viable and infectious viruses. It is evident that scientists have to use large quantities of viruses out of necessity, and such data may be interpreted with caution.
iii. Ward CL et. al, Journal of Clinical Virology, 2004 – This study shows that one TCID50 unit is equivalent to 1,000 viral RNA molecules.
iv. Jayaweera M et al, Environmental Research, 2020 – This is a recent computer modelling of SARS-CoV-2 which concludes that the virus may be transmitted in a confined environment. Please note that the study results cannot be extrapolated to open spaces and the authors do not make an assertive statement. Assertive data on SARS-CoV-2 is yet to emerge.
5. Establishing an infection is not an easy task for a virus through the aerosol route.”
A voluminous literature is available on this theme concerning every single virus. Viruses are obligate parasites and are dependent on the host for proliferation. Cells have developed an array of molecular sensors to detect virus-associated molecular patters to restrict their expansion (indeed, viruses have countermeasures).
i. Lim XY et al, Human Coronaviruses: A Review of Virus-Host Interactions, Diseases, 2020 – This is a review of host factors supporting and antagonising the proliferation of coronaviruses. Specific data regarding SARS-CoV-2 yet to emerge.
ii. King CR and Mehle A, The later stages of viral infection: An undiscovered country of host dependency factors. PLoS Pathogen, 2020 – This review describes many emerging experimental strategies to identify host restriction factors modulating the viral life cycle.
Udaykumar Ranga is a professor and Arun Panchapakesan is a PhD student – both in the HIV-AIDS Laboratory, Molecular Biology & Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru.