Two cheap ways to prevent the spread of covid: Masks and soap

The virus that causes COVID-19, SARS-CoV-2, is highly infectious, and can be spread by physical contact or by aerosols, sprays of tiny droplets we expel when we cough, sneeze, or even talk. We know now that surgical masks can block the transmission of the virus, but at the beginning of the pandemic, experts weren’t advising most people to wear them. The reasons for this were complicated, and included shortages that posed a danger to health care workers if there was a sudden run on the mask market. However, experts are now advising us to use masks. And hand washing is of course always a good idea.

The danger of spread by aerosol

Recently, a group of over 200 experts, including clinicians, infectious-disease physicians, epidemiologists, and engineers published a commentary that urges us to acknowledge the danger of airborne transmission of SARS-CoV-2.

This has brought the issue to the fore, and convinced even the World Health Organization that this is an important source of spread of COVID-19. Until recently, it was generally assumed that such respiratory diseases are spread by large droplets that, once expelled, soon fall to the ground, or land on a solid surface such as a doorknob (which is why hand washing is important).

But there is good evidence that transmission of both COVID-19, and the earlier SARS-1 disease, is often due to virus particles borne by very small droplets that are ejected when someone coughs, breaths, or even talks loudly in a bar (as can happen) (1). The virus in these smaller droplets stays around much longer than it does in the larger (>5 micron) particles.

Ordinary speech produces a lot of aerosol particles (2). Engineers estimate that when a person coughs or breaths, anywhere between 900 and 300,000 liquid particles shoot out of their mouth. A cough can send them out at speeds of up to 60 mph. Such aerosols are thought to be responsible for an outbreak of COVID-19 at a choir rehearsal near Seattle in March. Thirty-three people became infected and two died, even though there was no physical contact – no hugs or handshakes. In another case, a group of 10 diners at a restaurant in Guangzhou, China, was apparently infected by air currents from one air-conditioning unit. There are other examples of similar events.

Masks work

There is accumulating evidence, both from epidemiological studies and direct experiments, that surgical masks diminish the rate of coronavirus spread.

In a direct test of mask efficacy, respiratory droplets exhaled by people with several kinds of viral illness, including a seasonal coronavirus, were collected while they either did, or didn’t, wear surgical masks (3).

The effect of the masks on production of seasonal coronavirus was striking: for all sizes of droplets, there were no detectable coronavirus particles out of 22 patients wearing masks, whereas 7 out of 20 produced virus when not wearing a mask.

This underscores the important conclusion that masks prevent an individual, whether symptomatic or not, from spreading coronavirus to other people. It’s a little puzzling that consensus on whether masks protect the wearer has been slow to emerge, at least in public. Health care workers exposed to patients with COVID-19 were urged and even required to wear masks from the very beginning, so presumably there was an expectation that they were protective.

A consensus that masks, of various kinds, help protect the wearer is now growing. In April, the WHO urged: “health care facility workers and home-care caregivers should wear a medical mask when entering a room where patients suspected or confirmed of being infected with 2019-nCoV.” quoted in the Globe and Mail, on April 26. And in an interview with NPR on July 20, Dr. Monica Gandhi, UCSF professor of medicine and the director of the UCSF Center for AIDS Research said, “The more virus you get into your system, the more likely you are to get sick. And these masks protect you.” She described how an outbreak of COVID-19 in a chicken factory and a seafood factory in the United States was 95% asymptomatic, because, she felt, everyone was masking.

The ‘life’ and ‘death’ of virus

In general, viruses are not very stable out in the open. The SARS-CoV-2 virus particle is a large aggregation of complex molecules, including its RNA genome and numerous copies of essential proteins such as the ‘spike’ protein that allows it to bind to and infect cells. The outer coat of the virus contains phospholipid molecules arranged in a bilayer similar to that of human cell membranes. These phospholipids are in part hydrophobic (fat-loving, water-hating) and part hydrophilic (what the name suggests). The hydrophobic parts are buried within the membrane; the hydrophilic ‘heads’ face the outside world and the interior viral environment. Proteins like the ‘spike’ protein that allows the virus to attach to cells and infect them are on the outside, but they also have hydrophobic components that interact with the membrane phospholipids.

The complex viral structure is not held together by sturdy covalent bonds of the kind that connect the atoms of a glucose molecule. Instead, the large molecules are linked by their hydrophobic affinity for each other. It’s as if the virus is held together by little Velcro strips attached to the various protein and phospholipid molecules. A strong detergent (below) will dissolve these associations and destroy the virus.

Agents that destroy a virus like SARS-CoV-2 include chemicals in the air, sunlight, gamma rays from outer space, or even the vibrations of the atoms in its structural components. Particularly effective is the molecule abbreviated SLES, which stands for sodium laureth sulfate. It sounds exotic, but it isn’t (below). All of these inactivating events or agents act randomly in time.

Because of the random decay of viral activity, it is a “first order” process: the rate of viral loss is proportional to the amount that is still active. What this means in practical terms is that if half the virus activity is gone in 4 hours, constituting a four-hour half-life, another half of what remains will be gone by 8 hours, leaving 25% of the starting activity (graph below). It does not mean that all of the activity is gone in 8 hours.

Viral half-life depends on its environment.

Some of the aerosol containing virus particles, such as is expelled when we sneeze, may fall to the floor and start to lose activity quickly. But small-particle aerosols (5 micron diameters and less) do not, and are an important mechanism of virus spread. And if a virus-containing aerosol lands on a solid surface, it may survive for a much longer time (in other words, it has a longer half-life). A recent, peer-reviewed, publication in the New England Journal of Medicine (4) showed what happens to the SARS-CoV-2 virus in various circumstances.

Figure 1. Decay of SARS-CoV-2 viral activity in aerosol, or on various surfaces. The ordinate refers to the number of virus particles, as reflected by ability to infect cells in culture. Because decay is a first-order process it is not linear with time.

Virus particles in aerosols, small droplets such as are released when people cough, or even speak loudly in a bar, as they often do, have a half-life of about 1 hour. An hour is of course plenty of time for the virus to find a new victim. Virus particles deposited on solids such as cardboard, plastic, or steel have longer half-lives, up to 7 hours on plastic. A route of infection might be aerosol to metal doorknob to hand to face.

How many virus particles constitute an “infectious dose”? For some viruses, even a tiny dose is enough to cause an infection. For example, for half of infected people, it takes just 18 particles of norovirus to cause “stomach flu” and produce the symptoms of vomiting and nausea. (“Stomach flu” is unrelated to influenza.) The minimum infectious dose of SARS-CoV-2 is still unknown, but researchers suspect it is a low number. “The virus is spread through very, very casual interpersonal contact”, according to W. David Hardy, a professor of infectious disease at Johns Hopkins University School of Medicine. Researchers predict that aerosolized bits of saliva would easily infect other people if this happened in public indoor spaces like a bank, restaurant or pharmacy.

For the coronavirus that causes SARS-1, the estimated infective dose is just a few hundred particles. For MERS (Middle East Respiratory Syndrome), the infective dose is much higher, on the order of thousands of particles. But the SARS-CoV-2 virus is more similar to the SARS-1 – causing virus than MERS, and therefore, the infectious dose may be just hundreds of particles, according to the Columbia University virologist Dr. Angela Rasmussen.

Is the initial dose of SARS-CoV-2 related to subsequent Covid-19 severity? We don’t know for sure. The only way to answer this question definitively would be by “experimental challenge studies”, intentionally infecting healthy volunteers. Such studies are ethically forbidden because of the potential severity of the disease, and the lack of a therapy. But from the experience of Dr. Monica Ghandi of UCSF quoted earlier, more virus leads to worse health outcome.

Good old soap and water

It can take a long time for virus on a doorknob to decay; waiting for enough half-lives may simply take too long. So wiping surfaces that may have become contaminated with soap (or disinfectant) is important. The experts tell us that it’s relatively easy to inactivate the virus with ordinary hand soap (anti-bacterial agents found in some soaps is irrelevant; so is all of the other stuff that manufacturers put into hand soap to get you to buy it). The key ingredient is sodium laureth sulfate (SLES), already mentioned, which is a component of almost all hand soaps.


Figure 2. SLES. This common component of soaps and shampoos has a highly hydrophobic (fat-loving) part (crimson), made up of CH2 (hydrocarbon) groups, and a charged, polar, hydrophilic part (green), made up of ether-linked CH2-CH2 groups plus a polar and charged sulfate group at the end. As such, SLES binds to other hydrophobic groups such as the phospholipid envelope of the SARS-CoV-2 virus and dissolves them in water.

SLES, like the phospholipid and protein components of the coronavirus outer shell, has both a hydrophobic and a hydrophilic (water-loving) component. As such, it snuggles up to the viral components, and breaks the bonds, the Velcro strips, that hold the virus together. The result is destruction of the virus. There’s a good, readable description in The Guardian newspaper, written by an Australian chemist, Pall Thordarson (5), whose Twitter description of it went viral.

Political science

Politics is currently suppressing good science in the USA. On September 22, the New York Times carried an article saying that the Centers for Disease Control and Prevention had withdrawn, after just 3 days, a post on its web site that said that the SARS-CoV-2 virus is spread through aerosols. Studies such as those cited above show that aerosols do spread virus, particularly in high-density social situations. Warnings about aerosol spread should be prominent. But there was pressure, and the warning was removed. Sic transit veritas.

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Work cited

  1. Morawska, L., and J. Cao. 2020. Airborne transmission of SARS-CoV-2: The world should face the reality. Environ Int 139:105730-105730.
  2. Stadnytskyi, V., C. E. Bax, A. Bax, and P. Anfinrud. 2020. The airborne lifetime of small speech droplets and their potential importance in SARS-CoV-2 transmission. Proc Natl Acad Sci U S A 117:11875-11877.
  3. Leung, N. H. L., D. K. W. Chu, E. Y. C. Shiu, K. H. Chan, J. J. McDevitt, B. J. P. Hau, H. L. Yen, et al. 2020. Respiratory virus shedding in exhaled breath and efficacy of face masks. Nat Med 26:676-680.
  4. van Doremalen, N., T. Bushmaker, D. H. Morris, M. G. Holbrook, A. Gamble, B. N. Williamson, A. Tamin, et al. 2020. Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1. medRxiv : the preprint server for health sciences.
  5. Thordarson, P. 2020. The science of soap – here’s how it kills the coronavirus. The Guardian March 12, 2020.