Good question, Francesca. I have been reading contradictory information related to this question. To me the most plausible correlation between air quality and virus spread, especially the SARS-CoV-2, could be due to the effects of air pollution having physiological effects on the respiratory tract. WHO insists that the virus is not airborne transmitted, and I haven't seen any evidence on the contrary. Some researchers suggest that PM could be a carrier of the virus, but again, no hard evidence has been shown. And for our sake, I hope the WHO is right!

I would not expect a associaton of pollution and virus spread (except that population density and pollution might be correlated). But I would expect the occurence of more severe symptoms of COVID-19 associated with exposure to pollution. Same as any precondition due to smoking.

I also would not expect a direct asosciation of pollution form particulate matter and spread of COVID-19 because other factors are more directly related such as age distribution, population density, social uses. Iy is possible that prolonged exposition to atmospheric pollution could increase vulnerablity to severe symptoms. There has been a long discussion whithin the Italian Aerosol Association and it has been written a note signed by more than 70 resrecahers (http://www.iasaerosol.it/attachments/article/96/Nota_Informativa_IAS.pdf) discussing what I summarised here. There is an English summary available here ( https://www.sif.it/static/SIF/resources/public/images/email/news/2020-03/Nota_Informativa_IAS_EN.pdf )

I totally agree with what the other people say. Pollution, including PM but also NOx, ozone, may decrease lung defences thus increasing the risk of infections. Exposure to immunotoxic compounds shift the risk curve of getting sick to the left, increasing the number of people affected if they come in contact with the virus. Contracting an infection is the combination of defense capacity and microbial load.

Very interesting question, Francesca. I think there are two ways how air pollution might affect the COVID-19 pandemic. (1) as mentioned by the other air pollution might have already affected the upper and lower respiratory tract and thus, the susceptibility might be higher (see comment about smoking). (2) the recent reports about the association of COVID-19 with olfactory loss might be related to the deposition of the virus or maybe virus-loaded UFP in the nasal cavity. Here, supporting cells in the respiratory epithelia seem to be a more likely target as olfactory receptor neurons did not express two key genes involved in CoV-

2 entry, ACE2 and TMPRSS2 (https://www.biorxiv.org/content/10.1101/2020.03.25.009084v2).

However, currently I don't see epidemiological data supporting this view as air pollution seem to be not a good predictor of COVID-19 hot spots. Here, other factors seem to be more important. Would be an interesting research question for the future. Stay safe!

First of all, it is necessary to determine the mass character of the virus. We need to know later whether the spread of this virus is suitable for a fully inversion atmosphere, a settling inversion atmosphere, a radiation inversion atmosphere, or a combined inversion atmosphere. In the light of this information, we can calculate the spread of the virus according to the x, y and z coordinates with the necessary mathematical equations. Since I am an Environmental Engineer, I do not have the right to comment because I do not know the weight of viruses, but the most important factors are mass. If it is determined what its mass is, calculations are made in line with the direction, intensity and concentration of the wind.

Thanks Francesca for opening this question. As you know a few weeks ago we launched this position paper (which is not a paper for the scientific community, but addressed to decision makers) with which we said to pay attention to the relationship between the strange curves of contagion in northern Italy and the number of pm10 exceedances in the previous days of virus incubation http://www.simaonlus.it/wpsima/wp-content/uploads/2020/03/COVID_19_position-paper_ENG.pdf .The position paper went around the world we had to translate it into 5 languages. It is based on evidence already present in the literature since the 1960s, that the virus is in the air. I'm sorry for some colleagues who replied in this discussion, but even if WHO is still a denier, the scientific community that works in this domain is convinced of this, in fact today two interesting articles on Nature and Science have come out .... https://www.nature.com/articles/d41586-020-00974-w, https://www.sciencemag.org/news/2020/04/you-may-be-able-spread-coronavirus-just-breathing-new-report-finds

What we have added is that if the virus is in the air, in those territories where pm10 is very high, characterized by intense atmospheric stability and humidity, interaction phenomena between the particles already present in the atmosphere and the virus in the form of an aerosol can facilitate the spread of the virus. I hope WHO changes its mind

On one hand, I am not surprised that the virus might be airborne by itself. On the other hand, it might be attached to micron aerosols and be transmitted over long distances. Either ways, inhaling the virus as being airborne by itself or carried on an another particle is not the only factor for infection. What matters here are (1) the health status and (2) the body response to react for such foreign body (i.e. immune system ability to fight back).

Therefore, I agree with my colleagues here that Air Pollution (which might reduce the efficiency of the respiratory and immune system) might increase the probability of the infection by COVID-19.

Very interesting question, Francesca. In the southern hemisphere we are entering to the autumn and winter with low temperatures and high relative humidity, as well as high levels of fine and ultrafine particles due to severe use of residential biomass combustion, especially in urban areas of the Central and South of Chile. In these urban areas, biomass has been used for heating and cooking food in the last 25 years, where people are chronically exposed to high levels of polycyclic aromatic hydrocarbons (PAHs) that weaken their immune systems and respiratory tract. It would be very interesting to create a group of international scientists to analyze the effect of air pollution in severe cases of COVID19, and if the particles can spread this coronavirus. We have some articles where we compare the mortality and morbidity health risks of acute exposure to fine particles in cities polluted with wood smoke and cities polluted by other types of sources. Here is one of them http://www.aaqr.org/article/detail/AAQR-13-10-OA-0316 and here is one of ultrafine particles and health Article Health risks caused by short term exposure to ultrafine part...

Hello Everyone,

Yes, Francesca brought up an interesting question and I enjoyed reading and learning from those of you who responded. My expertise is remote sensing and I have published some papers on the correction of satellite images for atmospheric effects. From an atmospheric science point of view, they are rather simple corrections aimed at removing scattering (additive) and absorption (multiplicity) effects. One of the effects of the ‘stay-at-home’ policies is that the air quality of major urban areas has improved dramatically. Satellite images showing the improvements during ‘stay-at-home’ time periods have been posted by NASA, ESA, NOAA, and others.

I wonder if the level of air pollution does have a direct link to the spread of COVID-19 with the improvement of air quality during this period does it mean that the spread of the virus was slowed. If so can this be detected? My guess (and only a guess) is that if air quality does play a direct role in the spread of the virus it is a minor variable compared to some of the other variables already mentioned (e.g., population density) and it would be difficult to extract the correlation of that particular variable.

I wonder if the satellite images collected during the improvement of air quality, along with ground based data for PM and the spread of the virus could be used to investigate this question. Also, as a side note: satellite images show some of the dramatic dust storms that come out of northern Africa and the Middle East and wonder if dust could also transport the virus long distance or does the virus die by the time dust settles?

Pat

Depending on the humidity and the temperature, the virus can survive from few hours up to 7 days, so the chance to get caught on the aerosols is considerable!

I see that it is very likely for the virus to prolong its life span on the dark aerosols particles based on their radiative forcing and thus their positive feedback (+0.6 watts/sq. m), in addition to the other anthropogenic forcing, i.e. CO2, NOx, CH4 etc.

Source of the figure:

https://www.epa.gov/climate-indicators/climate-change-indicators-climate-forcing

Dear Francesca thank you for sparking this interesting question and conversation. I also enjoyed reading the different replies. I do agree with the concept that air pollution impairs lung immune defences (as you know I have worked on it) therefore increasing the susceptibility of part of the population to the SARS-CoV-2 and develop Covid-19. I find also interesting what Christoph van Thriel suggest i.e. that nasal epithelium and mouth mucosa may be the first sites of infection (for the reduction of olfactory and taste sense). The presence of SARS-CoV-2 in the atmosphere is more challenging: its presence in term of RNA sequence should not be considered as a clear signal of its viability, the interaction with airborne particles is all but easy to understand (I found this paper of great interest N. Groulx et al. / Science of the Total Environment 628–629 (2018) 1101–1107), if the virus is spread in liquid droplets from sneezing, coughing or just talking should we assume that the particles on which the virus is attached are those more hydrophilic so, roughly speaking, excluding engine emitted ones (this question is for you and those working on aerosol properties)? Finally, the frequency of person to person interaction (or as proxy population density) should be considered as additional variable in regression models and a big issue that is missing is the importance, for contagion, of indoor environments rather that outdoor ones.

Dear Francie, thanks for igniting a vivid discussion around this itchy and fascinating issue. Presence of pathogens adherent to waterborne particulate has been demonstrated by classic microscope observation long ago; therefore in line of principle the question whether, at much smaller size, a virus may find a convenient mode of transport in airborne particulate may make some sense.

Direct observation of viruses adherent to or encapsulated in

Hi everyone,

Congratulations Francesca for making this good discussion possible

Have you seen this study by a Harvard group (still in MedRxiv)?

" We found that an increase of only 1 μg/m3 in PM2.5 is associated with a 15% increase in the COVID-19 death rate, 95% confidence interval (CI) (5%, 25%) "

https://projects.iq.harvard.edu/covid-pm

https://projects.iq.harvard.edu/files/covid-pm/files/pm_and_covid_mortality.pdf

Dear all,

thanks a lot for contributing to this extremely important discussion. I think that (correct me, please, if wrong) it is an evidence that the topic is far from being understood. You mentioned so many different aspects, all deserving further investigation. And this is precisely the conclusion we've reached within the working groups of our institute: there are too many open questions to be addressed before reaching conclusions.

Among these, our focus is now on:

1 - What is the influence of the atmospheric aerosol, including bioaerosol (pollen/bacteria vs virus), and more in general air pollution, in eliciting indirect systemic effects (linked to pro-inflammation and oxidation mechanisms of the lungs, and immunology alteration processes) increasing the vulnerability of the population to COVID-19? What are the factors discriminating indoors from outdoors (e.g., UV solar radiation, humidity, viral load)?

http://www.isac.cnr.it/sites/default/files/curricula/Summary_WG1_v07042020.pdf

2 - Transmission of SARS-CoV-2 via aerosols: Is it a plausible mechanism? If so, what is the probability of occurrence, and what the driving processes/mechanisms/forces, sources and spatio-temporal scales relevant for the interactions between viruses and aerosol particles? What are the factors discriminating indoors from outdoors (e.g., solar radiation, viral load)?

http://www.isac.cnr.it/sites/default/files/curricula/Summary_WG2_4_v07042020.pdf

Also, meteo factors clearly matter

http://www.isac.cnr.it/sites/default/files/curricula/WG3%20covid19_Meteo_IT_EN.pdf

Our next steps shall, therefore, be devoted to design future experiments aimed at providing a better understanding. Again, your view here, as well as the establishment of collaborations, are highly appreciated.

Dear Francesca and all,

yes, the mechanisms underlying this observation from the Harvard group (see

https://www.medrxiv.org/content/10.1101/2020.04.05.20054502v1) and our discussion are far from being understood.

The impact of air pollution in the context of bioaerosols needs a deeper investigation beyond SARS-CoV-2. Here, the data quality is often not sufficient to draw conclusions. Your general ideas about research and experiments are exactly what would be needed to understand these "carrier" and other "additive" effects in more details.

Stay safe!

Christoph

Dear Francesca,

In a recent study I found a fundamental gap in knowledge connected with the influence of air pollution on human health, an issue that is highly relevant to age-related risks associated with COVID-19.

Сold, rainy, or wet weather could dramatically increase the health risks connected with air pollution. I found that all program codes, models and estimates of deposition of “air pollution” in the lungs used by WHO (the World Health Organization) and all national centers for health protection and disease control have a critical error in their calculations and estimations - the risk is underestimated dozens of times, for winter/cold and humid weather conditions.

For instance:

3% - THIS is the risk of deposition of smoke particles (300nm) in the airways - according to standard classical estimates//

90-96% - THIS is the risk, which can actually be if a person is in cold or wet environments.

%$ deposition rises for hygroscopic and HYDROPHOBIC aerosols too (it is absolutely new finding)

Thus, One of the most important findings is that the supersaturation effect can be clearly correlated with the timing of influenza in different climatic conditions. Perhaps, the Supersaturation is the only factor that can be used for analyzing the timing of influenza in mid-latitudes and tropics at the same time.

@Supersaturation/oversaturation definitely is unusual and generally neglected effect that can be induced in the airways by cold air inhalation (T70%; T

Moreover, recently I pointed out the problem of dry mucosa in the elderly in a short message on the link: https://www.researchgate.net/publication/340006233_Supersaturation_in_the_Airways_and_Covid-19_New_Way_to_Understand

One of the main points is that the supersaturation and enhanced condensation of water vapor (as well as enhanced deposition of inhaled pollutants due to supersaturation) is a strictly localized process in the nose and upper airways.

This process occurs due to the mixing of air and mass transfer with the wet walls of the respiratory tract. If the mucous membranes of the walls of upper airways are dry (as in the elderly), then due to a violation of mass transfer with the walls, the localization of “Supersaturation” will shift to the lower section of airways.

Accordingly, the enhanced deposition of inhaled pollutants and infectious aerosols, as well as the physicochemical impact of the effect of supersaturation (pH of formed droplets under supersaturated conditions are 4.5-6.5), will affect the trachea and bronchioles in the elderly.

I believe that this may be one of the important factors for explaining the increased mortality among the elderly in Wuhan and Italy, where extreme levels of air pollution PM2.5 were observed at the same time.

Kind regards,

Alex

Dear Francesca,

Thank you for this interesting question.

I have the following "picture" - not sure whether it makes sense:

In order to become infected a healthy person needs to inhale a certain dose. Probably one virus is not enough, right? The higher the dose, the higher the probability for an infection.

Viruses become airborne through droplets that are emitted by coughing, sneezing and talking. The longer the virus stays airborne and does not disappear by settling or diffusion the higher the probability of an infection. Depending on the droplet size distribution and the ambient conditions these droplets will evaporate more or less quickly. What remains will be agglomerates of viruses (and whatever is in the droplet that does not evaporate). In any case: The size distribution will be shifted significantly to smaller particles, resulting in a significant increase in diffusion coefficient. Which will result in a faster decrease of virus concentration as the virus cloud drifts apart.

If the particle concentration due to air pollution is high enough, airborne particles and virus(-agglomerates) will coagulate. As the resulting particle-virus -agglomerates are larger, their diffusion coefficient will decrease, which will reduce the decrease of local virus concentration.

The effect strongly will depend on the concentrations of both airborne viruses and particles. The level that is required to have an effect might be too high. And obviously whether the viruses stay viable.

Kind regards,

Thomas

thanks Thomas

we never met, but your 'picture' is the basis of our hypothesis...

There are some researches that are stating that.

Dear Thomas Krinke /

I allowed myself to describe the general mechanism for the spread of respiratory infections/

COUGHING and SNEEZING

Coughing and sneezing generate coarse bioaerosols (large-particles aerosols) containing droplets varying in size: geometric mean diameter below of 13.5 μm; for speaking it is 16 μm (Chao et al., 2009). It should be pointed that data on droplets size is various in the different studies (see review in (Chao et al., 2009)).

EVOPORATION

It is generally accepted that evaporation of exhaled droplets results in the formation of solid dry residue particles with concomitant particle shrinkage to about HALF the initial droplet size.

TIME

Laboratory experiments have shown that 90% of large size (Da > 50 mkm) water droplets rapidly settled at a distance of 1-2 m from the point of emission. Only about 4-10% of droplets remain suspended in room air (Da < 10 mkm), and the evaporation time of droplets 5-10 mkm was less than 0.1 s [37].

DEPOSITION IN THE AIRWAYS

Even after evoparation such droplets and dry particles may deposit in the upper airways (the probability to reach the lower airways is too small), but such droplets/partilces settle rapidly in the environmental air and are transmitted only over short time and distance( Hall, 2007).

TIDAL BREATHING AS GENERATION MECHANISM

Infected people generate infectious bioaerosols (size of the exhaled particles below 1μm) during tidal breathing (Milton et al., 2013; Cowling et al., 2013; Lindsley et al., 2016). Such bioaerosols practically do not settle in the environmental air and can be transmitted over long distance(Hall, 2007).

CONCENTRATION AND DOSE

The high concentration of exhaled infectious aerosols near an infected person (about 1 m).

“The size distribution will be shifted significantly to smaller particles, resulting in a significant increase in diffusion coefficient.” — I don't think so.

“If the particle concentration due to air pollution is high enough, airborne particles and virus(-agglomerates) will coagulate.” — I don't think so. Such a scenario is absolutely impossible. For coagulation processes, the concentration of particles should be very high and close to concentration of tobacco smoke when puffed.

“And obviously whether the viruses stay viable.”

I think that for the scenario of @inhaled dose near the infected person@ this question has no sense …. because every second new aerosol will be generated during breathing and talking.

Dear all,

we are pleased to share this paper just published:

"Does air pollution influence COVID19 outbreaks? "

https://www.researchgate.net/publication/340607324_Does_Air_Pollution_Influence_COVID-19_Outbreaks_httpswwwmdpicom2073-4433114377?isFromSharing=1

Thank you for this essential discussion.

UFP might be hold the covid virus in atmosphere and transport it. But I think in city where covid cases are higher than others, the population density, meteorology more associated to the virus spreading. Due to high air pollution in these area covid cases can be seen more.

Dear Francesca

I note with great regret that our position paper, which inspired, this discussion was not even quoted by your editorial, while the response of the ias to our paper is cited. Yet in this discussion there are colleagues who are confirming the plausibility of our hypothesis. This once again demonstrates the lack of ethics of science of a part of the Italian scientific community that prefers to devote itself to gang warfare rather than seeking the truth.

SARS-CoV-2 can be detected in the air up to 4 meters from COVID-19 patients

A recent study from Wuhan China indicates that SARS-CoV-2 virus is widely distributed on floors, computer mice, trash cans, and sickbed handrails and can be detected in air ≈4 meters from COVID-19 patients.

https://wwwnc.cdc.gov/eid/article/26/7/20-0885_article

https://www.medrxiv.org/content/10.1101/2020.04.15.20065995v1

I agree that air pollutants influence indirectly the pandemia as discussed by

Daniele and Francesca in their paper. But, I think there is also a synergy with weather factors.

It is hard to find such links in the literature but here I have found one.

This is from the book: A Change of Air: Climate and Health by Dr. William Thompson who said the following on Chapter on Chap. 14 (Climate and infection):

"...low temperature and humidity may affect the protecting cells lining the entrance of the lungs. Among these cells are the cilia cells, small lash-like processes which can maintain movement in the fluid moving over them in order to expel anything that may be damaging to the lungs, including microorganisms".

In the same Chapter, Dr. Thompson writes that

"1 deg. F (0.5C) fall in external temperature corresponds to 1% rise in the incidence of colds" (based on studies from Health Services at the time).

Of course COVID-19 is not the same virus as a cold but there are similar impact of weather and pollution, I would think: e.g. a negative correlation between the number of colds and outdoor temperature would also likely applies to COVID-19.

In Wuhan, during the epidemy there, mean daily temperatures are usually below 10C (according to climatological values for Dec-Feb). Now it is getting much above 10C, nowadays.

So there was a triple environmental stress at the start of the pandemia: 1) the virus, 2) air pollution (which was reduced later due to the confinement), 3) lowest temperatures and absolute humidity (during the winter months).

I am not saying air pllution and weather are dominant factors but they exacerbate things.

Air pollution causes inflammation and hyper-responsiveness of lungs and low temperatures makes the immune system weaker.

The seasonal variation of SARS (see picture) is quite close to that of COVID-19 so far.

Luis Alonso Diaz-Robles

Dear Luis,

thanks for the comment. I do support your suggestion "to create a group of international scientists to analyze the effect of air pollution in severe cases of COVID19, and if the particles can spread this coronavirus". Shall we start from people involved in this chat?

Allow me, please, to add a note regarding you comment "on health risks of acute exposure to fine particles in cities polluted with wood smoke and cities polluted by other types of sources". We have started working on the topic in 2017, and here is the last paper published (references to all previous papers therein):

https://www.mdpi.com/2073-4433/11/4/414

Ultrafine Particle Features Associated with Pro-Inflammatory and Oxidative Responses: Implications for Health Studies

Christoph van Thriel

Dear Christoph,

thanks for commenting. I've just read the very interesting paper you mentioned regarding possible associations between COVID-19, olfactory loss, and virus-loaded UFP in the nasal cavity. To my limited understanding, it could make sense, indeed, but still a lot of research is needed to obtain robust evidence on it. Am I wrong?

Maurizio Gualtieri

Dear Maurizio,

thanks for the relevant comment.

I do agree on what you wrote about Christoph van Thriel 's suggestion.

Also, I found very interesting the comment on the importance to consider particle properties. This is key to me, as you well know. In this regard, please, have a look to this paper (Fig.3 is amazing):

Akhrymuk et al., 2020. Magnetic nanotrap particles preserve the stability of venezuelan equine encephalitis virus in blood for laboratory detection. Doi 10.3389/fvets.2019.0050

Findings, indeed, suggest binds to proteins through hydrophobic and electrostatic interactions.

Thomas Krinke

Dear Thomas,

thanks for the comment. I think Daniele Contini and I addressed some of your points in the article Article Does Air Pollution Influence COVID-19 Outbreaks? (https://ww...

Allow me to add a note about coagulation (you mentioned it in your comment). I found it very interesting. Based on my limited understanding, there might be a certain plausibility; however, there are more questions than answers here. In particular, if coagulation is involved, what are the forces driving the process ? Electrical forces? Chemical affinity? Concentration gradients? Turbulence????? Aqueous-phase chemistry (droplet mode)?

This would be strictly linked to aerosol particles physicochemical properties, as wrote to Maurizio Gualtieri.

What do you think?

Dear Francesca,

The Coagulation function: K(r1,r2) = 4π·(r1+r2) ·(D1+D2)

r: Radius of the Particle

D: Diffusion Coefficent of the Particle

describes the probability that particles of (dis)similar size coagulate. At a given size distributions particles of similar size have a much lower probability to find each other than particles with a large difference in size.

( http://cost733class.geo.uni-augsburg.de/moin/iguawiki/data/pages/KursmaterialWS1213_HsKlivar/attachments/Roedel_Die_Atmosphaere.pdf )

The driver for coagulation is the Brownian motion of the particles. Van der Waals forces are responsible for the particles sticking to each other once they met.

The charge level of an aged atmospheric aerosol is usually close to Boltzmann equilibrium. For this reason I would assume that Coulomb or Dipol forces can be neglected.

From my perspective it is crucial to understand what happens to an infectious droplet once it is released to the atmosphere. The liquid containing the viruses is not pure water, so does it really evaporate? What is the size distribution after evaporation of the volatile compounds?

Just for completeness: What is the charge level of droplets that are emitted during speaking, laughing, sneezing, coughing,....? We know that during dispersion of polar liquids (like water) in aerosol generators highly charged droplets are generated. If the unipolar charge level is high enough, during evaporation repulsive Coulomb forces in the droplets will increase and might cause so-called Coulomb explosions. The result is a decrease in droplet size and an increase in number concentration.

Dear Thomas and dear Francesca, thank you for this discussion. However, I am wondering about one apsect. Small droplets are released during respiration and speechs and these could evaporate (partly or totally leaving more or less dried residue) and they are sifficiently small to be suspended in atmosphere and transported/dispersed like the other particle. So the question is why they should be "carried" by oher partcles in air? They will also be transported by themselves like any other particle.

https://www.mdpi.com/1660-4601/17/8/2932

Dear Thomas,

thanks for the explanation. In my previous comment, I meant to ask about a (" plausible") force, which can possibly drive coagulation processes between airborne viable virus-laden accumulation mode particles and "non-virus-laden" aerosol particles in the air.

In my limited understanding, I believe that, if any, several factors may play a role, including (but not limited to) physicochemical aerosol properties.

Importantly, would this coagulation mechanism modify some factors relevant for COVID19, including viral load, minimum dose, transmission route, entering path and impact in the human body? This is important to me to understand if there may be a direct effect (other than linked to inflammation, immunotoxicity,etc) in COVID19 related to non-virus-laden aerosol particles.

It would be good to have the opinion of virologists, toxicologists, biologists here.

Indeed, it seems to me that this is a point that goes beyond aerosol science, isn't it?

Thanks Gianluigi for sharing your paper with us.

By the way, it seems to me that we are still far from a complete understanding.

About Thomas Krinke topic

from Atmospheric Chemistry and Physics: From Air Pollution to Climate Change,

John H. Seinfeld, Spyros N. Pandis

MH in Po Valley

Dear Francesca Costabile and Readers,

The list of links between air quality and the spread of SARS-COV-2 includes many factors, both direct and indirect. Previous exposure to pollutants is certainly relevant, as noted in the articles mentioned during the discussion in this thread.

There are, however, some other factors such as atmospheric stability which are not often mentioned explicitly. Based on my observations of the movement of contaminants in street canyons and some numerical estimates, I am convinced that the risk of transmission of SARS-COV-2 is maximized under certain atmospheric stability regimes. This “control of the spread” is due to the direct effects of turbulent mixing as well as modulation of the terms in the stochastic coagulation equation.

The second factor affecting infection rates is the UV flux at the ground. Based on extensive studies of different viruses we can speculate that the Coronaviridae family is susceptible to the damage caused by UV radiation. It is well known that the tropospheric ozone is one of the factors that reduce the UV flux and increase the asthmatic reactions of the most vulnerable part of the population. In my opinion the tropospheric ozone factor is absolutely crucial.

In summary, it is useful to acquire data on low and high level cloudiness, the concentration of ozone in the planetary boundary layer and the atmospheric stability class information to supplement the standard data used in articles published in recent weeks.

According to the models used for the simulation of epidemic diseases with environmental factors, we can hope that the approaching summer can lead to the isolation of the current pandemics in several hotspots and to a possible elimination of the virus.

The main concern I have right now is that we are currently in the solar minimum phase. Some researchers speculate that the viral mutation may be correlated with the 11-year cycle of solar activity. The most interesting observation is described in the attached document stating that the pandemic warning was given last year.

Even if this claim is not yet substantiated, it shows that virus epidemics are caused by imbalances created in the complex earth system including chemical pollution and changing the habitats of some species.

https://www.mdpi.com/1660-4601/17/9/2986

Dear all,

a paper just published by Nature Research about SARS-CoV-2 airborne transmission indoors:

https://www.nature.com/articles/s41586-020-2271-3

Note the aerodynamic size range (0.25-0.5 micrometer) with the highest concentration. Also, note that the virus infectivity was not established.

Your view?

Hi Francesca. Interesting report, but it is impossible to have any strong conclusion out of it. For what is presented, it is quite evident that the authors only measured the presence of the RNA of the virus, and therefore it is not possible to evaluate infectivity. Based on what is presented, I would hypothesize that the outdoor situation would be even weaker. I am still convinced that the main role of air pollution on the SARS-CoV-2 situation is mainly related to the adverse effects of the pollution on the airways and lungs, giving the virus a better chance to infect and leading to more severe cases.

This paper was already available as a preprint and we discussed its implications in our Editorial on the Journal Atmosphere. I agree with the conclusion of Ernesto Alfaro-Moreno. Concentratons in air in outdoor are at the limit of detection, and only a little larger in specific indoor environments (hospitals) in which it could be present a little larger risk but information on infectivity and lifetime of virus in air are missing and they are important to actually evaluate probability of airborne transmission.

Daniele Contini it is very important what you are pointing, regarding that the measurements are within the limits of detection. I have read many posts on different places where some people are quite concerned with the implications of air pollution on the pandemics. As scientists and experts in air pollution and health effects, we must be very careful to keep our statements based on hard science and being very clear when putting across our hypothesis. We have a social responsibility not to create panic. It is already hard enough the situation as it is.

Ernesto Alfaro-Moreno I completely agree. Myself and several other colleagues in Italy are doing exactly that. Spreading a note of caution in easy interpretation of data that could lead to panic and wrong reactions before having solid scientific information.

the aerodynamic size range (0.25-0.5 micrometer) says us that generation of such aerosols occurs during normal and tidal breathing //

Alex N Ishmatov they could be from respiratory emissions but could also be the residue of larger droplets after evaporation.

Daniele Contini, I was always surprised by the lack of photo images of particles of the dry residue of evaporation of respiratory drops (in micron and submicron diapason) // Article Physico-chemical characteristics of evaporating respiratory ...

After evaporation, the size of residue particle is equal to 1/2 of the "mother-droplet".

In 2007-2013 I had extensive experience in pulsed and explosive spraying of various aqueous solutions - electron microscopy of residue particles even after explosive spraying - I hardly saw any signs of particle destruction // I think it is very important to study the processes of evaporation of respiratory droplets under various conditions - at one time I even made a plan for experiments but did not work out, because I had to give up a scientist’s career)

Dear Alex. Thank you for your answer and the article suggested. I believe that the aspect of evaporation could be an interesting reserach topic. However, it is not to be excluded that a droplet around 1 or 2 micron could evaporate partly or totally leaving sbu-micrometric aerosol.

Hi Dr. Commondo, I came across this interesting study and it seems like there is a good correlation between pollutants and Covid19.

https://projects.iq.harvard.edu/covid-pm

Hello Alberto,

thanks for joining the discussion.

In fact, there is a general agreement in the scientific community that associations between air pollution and COVID19 are plausible. The point , however, is finding scientific and robust evidences elucidating the underlying causes, mechanisms and processes (beyond correlations).

In my view, this is an imperative step to translate scientific findings into clear mitigation actions (for policy-makers and legislators) for the future.

Dear All, I’m afraid that I accidentally discovered a new way in understanding the role of air pollution in mortality from covid-19 .. moreover, it seems to me that this way may be related to understanding increased mortality in elderly.

Preprint Age- and gender-related changes in the upper airways correla...

This is the first draft of the manuscript. Text processing and proofreading are required. I will be glad to any discussion and help in improving the manuscript, as well as advice on publishing in a journal.

The role of Air pollution on mortality is very obvious, because long term exposure with high NOX, PM regions, infect human respiratory system. These regions are prone to larger mortality like Europe, USA, etc. Long term climatology of NO2 shows peak over these regions. Moreover, generally these kind of virus also shows seasonal behaviour. Till now, it is not confirm for COVID-19.

Dear Prashant Kumar , What do you think, is it possible in this case to somehow relate high pollution levels to relatively low mortality in India, as well as relatively low mortality in China, South Korea, Japan, and possibly in the African republics? Why is there a gender and racial stratification in mortality and how we can connect this with air pollution from the classical point of view? ... I thought about these issues for a long time and discovered that this is a significant knowledge gap.

Dear Alex, It is just one possibility. There may be many other reason for high mortality like implementation of lockdowns, lockdown strictness, average age of patients, connectivity with China and other prone areas, etc. are also possible points to think. But , one point that is very clear is that if someone lives in air polluted regions (majorly NO2,) for a longer duration, their respiratory system is infected. And, any virus transmission like COVID-19, influence that region badly.

Dears,

the fascinating " EXPOSOME " concept has been created to look at all these questions in a new way. Have you had a look at it?

We can expand the EXPOSOME concept and build an immune system for the planet. This is essential in order to avoid the situation experienced during the present pandemics. For further details please kindly consult the following site:

https://www.atlanticcouncil.org/blogs/geotech-cues/we-can-build-an-immune-system-for-the-planet/

There are different aspects to consider:

1. The effect of living in a pollutant area on the pre-existing condtion of the resiratory system (before coming in contact with COVID)

2. The effect of humidity and pollutants on the maximum distance that covid can travel ( is it more than the 2m interpersonal distance so far suggested?)

3- How deep PM bearing COVID can penetrate our lungs

After reading some literature on these topics, I write down some aspects which I found relevant and, may be, deserve some further thinking. They affect mainly point 2 and 3:

Humidity decreases the evaporation time of a droplet.

PM 2.5 can enhance the growth of mist droplets.

In carbon-water suspensions after a first vaporation stage, a solid crust is formed.

Soot particles in Padania are coated with organics, nitrates, ammonia, sulfate

Hydrofillicty/hydrophobicity can be affected.

In foggy environment the morphology of soot changes (becomes less irregular, more spheircal)

I woder : maybe the safety distances should not be taken as 2m for all situations.

It may change according to the region, the season and also the day time.

The factor, used in epidemiological models, to describe the transmission rate, could be correlated to the frequency of collisions of people within a radius R=the safety distance. Maybe this could explain the differnet violence of the epidemy among regions

Dears,

from our point of view, virus-laden aerosols are part of the complex cocktail forming the ambient aerosol. Indeed, ambient aerosol particles are not a homogeneous substance, but a mixture of very different aerosol populations/types, including the bioaerosol and including virus-laden aerosol particles.

The confusion, likely, arises from the metrics used for the ambient aerosol: the PM2.5 mass concentration (or PM1 or PM10). We believe that aerosols need more than one single metric - whereas only mass concentration can be likely enough for gas compounds.

Therefore, we have now the vision to include virus-laden particles in the ambient aerosol, and not to keep them separated.

The question now is how to measure separately and properly different ambient aerosol populations (e.g., soot, dust, virus-laden particles, combustion-related UFPs) with no artefacts...

Dear Francesca, very good question indeed. This is something for aerobiologists to take over. Great efforts have been done in the past to use molecular biology techniques to quantify the presence of different organisms in PM, such as bacteria and fungi. I guess that quantitative real-time PCR would give the answer to what are you suggesting, but I am not an aerobiologist.

Hello Everyone,

I made a comment early into this discussion about how examples of satellite images have documented the improvement of air quality at different urban areas around the world, including northern Italy. If the virus is spread by the level of air quality would this mean that because of the air quality improvement brought about by 'stay-at-home' policies the spread is slowed down? I suggested the use of satellite image data and ground based sensor data to investigate this possible affect (also stated that population density may over helm this signature).

As I mentioned, my expertise is remote sensing and very different from the expertise of most of you. I am finding this discussion very interesting and I am learning a lot. A question I have is:

Since it appears that perhaps sun light (guessing the uv wavelengths) affects and kills the virus rather quickly (in tens of minutes?) will this limit the spread of the virus by bad air quality since the sun light will kill before it goes to far or will something like PM10 size particles protect the virus from the sun light?

Again, I am well outside my expertise and this might be a 'non-issue / question' for the discussion being carried out here.

Pat

Dear Pat. Your mention of the study of the relationships of better air quality due lockdown and the reduced spread of Covid19 is interesting but quite difficult to be demonstrated or at least not practical. The lockdown obviously slowed the spread because of the lower number of social contacts and it clearly also improved air quality. Therefore there is an obvious correlation between air quality and spread of covid19 that does not indicate cause-effect relationships because it is the lockdown that drives both time series.

It is true that the lockdown contributed both to the reduction of the primary infection rate and to the decrease of pollution through the massive voluntary emission cuts (this is probably the first known to me such a massive emission control experiment).

We should recognize, however, that the decrease of pollution levels leads to a drastic increase of the UV flux measured at the surface. Considering the fact that this radiation is the principal virucide for coronaviridae, there is definite correlation between the secondary transmission rates (from the contaminated surfaces) for this infection and reduction of pollution. This correlation is further compounded by the feedback loop between the aerosol concentration and the height of the Planetary Boundary Layer (PBL). Even a slight reduction of the concentration of aerosols increases the solar flux; this leads to a deeper PBL and further reduction of the pollution level and even higher sanitizing doses of UV.

In conclusion we should consider the feedback between UV, pollution and the secondary infection rates in the overall assessment of the infection dynamics.

Dear Pat, very interesting details.

Regarding your sun light points, as per available details,

The COVID-19 virus can be transmitted in ALL AREAS, including areas with hot and humid weather.

There is no evidence that sun light kills the new coronavirus. https://www.who.int/news-room/q-a-detail/q-a-coronaviruses

Dear Prashant Kumar

Please kindly consult the following site

https://sites.nationalacademies.org/BasedOnScience/covid-19-does-ultraviolet-light-kill-the-coronavirus/index.htm

Yes, but UV light is not safe

Dear Prashant Kumar

Yes, it is true. The medical use of UV in the historical context is discussed in the following article

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789813/

The medical uses of UV should not be confused with the UV radiation from the Sun acting as the natural cleansing agent. The environmental UV radiation regulated by pollution is one of the crucial factors controlling viruses deposited on all surfaces contributing to the secondary infections. There is a significant body of literature on this subjects.

The new generation of the numerical models simulating the spread of epidemic diseases should include the feedbacks mentioned in my comment.

Dear Francesca, this study might be interesting?

SARS-Cov-2 RNA Found on Particulate Matter of Bergamo in Northern Italy: First Preliminary Evidence. Not yet peer reviewed article, and there is still a lot to be cleared.

https://medrxiv.org/content/10.1101/2020.04.15.20065995v2

My understanding of UV destroying germs applies to UVC (the most powerful ones) or short-wave UV These do not reach the terrestrial surface because absorbed by the ozone layer completely in most cases. Pollution or no-pollution they never reach the earth's surface in most situations. UVC kills germs but you need a special apparatus to do that which performs germicidal irradiation.

https://en.wikipedia.org/wiki/Ultraviolet_germicidal_irradiation

I do not think we can count too much on the sun's UV. However, by evaporating the water (droplets containing the virus), the virus cannot live very long and probably die. So humidity in the air is very important here as well as the sun's rays to evaporate the water droplets surrounding the virus.

Best regards

Dear Alain Robichaud

UV radiation from the sun is the main cleansing agent in the environment. The review of reports on 254-nm UV inactivation of RNA-containing virus families shows that the radiation reaching the Earth's surface is very effective in decontamination of all types of surfaces.

I don't think there is any correlation between air quality and Covid 19 spread speed of at least until now

Marcel Severijnen : Thanks for sharing. I do believe that science is now ready to look at evidences for causations and mechanisms, rather than associations and correlations. That's challenging, indeed, but that's the only way to improve our understanding for the future.

Dear Janusz,

I agree with you that UVs in the range 200-280 nm kills germs, microbes, etc.

But this range belongs to UVC range. How much % reaches the surface of the Earth (because most is blocked by ozone layer). That is my point.

Regards

Dear Alain,

Please kindly consult the initial section in the following report

https://www.ncbi.nlm.nih.gov/books/NBK401588/pdf/Bookshelf_NBK401588.pdf

(Fig. 5 gives a direct answer)

In general the amount of UV radiation is not only sufficient to eliminate the coronaviridae on some surfaces at the ground, but can also damage unprotected skin during prolonged exposure.

Best regards.

Francesca Costabile and Readers,

The recent paper prepared by Sanchez-Lorenzo et al. (2020): “Anomalous atmospheric circulation favored the spread of COVID-19 in Europe” links the particular virulence of the epidemics in Italy and Spain to the persistent anticyclonic circulation over southwestern Europe during February 2020. Perhaps the stratification in the lower part of the Planetary Boundary Layer in the high pressure area promoted the "fumigation effects" during the transport of a virus in droplets and dry aggregates. If we accept this hypothesis, we can safely assume that high pollution levels were not directly responsible for the severity of the epidemic. This conjecture can be verified by calculations with the appropriate transport models on a very small scale.

I don't think there is any correlation between air quality and Covid 19 spread speed but I think there is a correlation between air quality/reduction in air pollution and COVID-19 lockdown. However, there are now emerging researches to sustantiate that.

Janusz Pudykiewicz

Thanks for sharing the e-print. The conclusions are about plausibility that " the strong atmospheric stability and associated dry conditions may have favored the virus’s propagation, by short-range droplet transmission as well as likely by long-range aerosol (airborne) transmission " .

As a scientist, I am open to every possible causation here, and indeed I guess that there is a complex mixture of factors to be explored, including this.

A quick note. To my limited understanding, beyond plausibility and associations, science has still provided no robust evidence for airborne transmission of an infectious/viable SARS-CoV-2 (i.e., having a viral load able to infect cells and hence impact on the COVID-19 spread within humans). I personally believe that this is going to take a long time, perhaps years.

An old, but still good letter to Nature on it:

https://www.seme.org/site/docs/covid-19/Lewis_090420_Coronav_airborne_No_experts_agree.pdf

Dear Francesca Costabile and Readers,

Thank you for your comments. The problem of airborne transmission of an infectious/viable SARS-CoV-2 is mainly a subject of numerous debates and this is not surprising considering the lack of data and limitations of our theoretical models. At this moment, we have to assemble a multi-scale analytical model (scale range: 100m - 1 cm) simulating transport of the pathogen from the infected person including the dynamics of the droplets, their drying and the creation of aggregates of viral particles with the different forms of organic matter. The model should also include the effects of stratification which have proven to be extremely important in the analysis of the epidemic in Europe, as indicated by the recent study mentioned in my post.

The situation observed in Europe is in many ways similar to the evolution of events in China. After analyzing the mean sea level pressure patterns over Asia in the time preceding the outbreak in Wuhan, I realized that the epidemic was exacerbated by the abnormally high static stability. The analysis of this problem is quite important when comparing this outbreak to the similar events observed in the past.

The dynamics of the initial stages of pandemics is a nonlinear, intermittent process and when searching for the triggering mechanisms, we must take into account all factors such as the source/sources of the virus, the patterns of human interactions and the meteorological conditions.

as for the air transmission of any coronaviruses, this is absolutely beyond doubt

/// the main question in the contact transmission - and in my opinion, it is in this aspect that there are a lot of questions and there is no evidence base - it is possible that this method has almost no effect

// as for airborne transmission - the dose is important here

// accordingly, the largest dose near the source of infection - the farther the lower the dose

// decrease is inversely proportional to the square of the distance from the source. (dose - 1 / m2)

// if we take into account that breathing is a source of aerosol - it is not surprising that most of the recorded cases of infection occurred after close and prolonged contact (to be near the object)

I liked the article about the transmission of infection in a restaurant

https://www.medrxiv.org/content/10.1101/2020.04.16.20067728v1.full.pdf

Dear Janusz,

On the document you send, I look at Figure 5 but there is no evidence that UVC reaches the surface of the earth. Or maybe I am missing something.

On the other hand on Table 5, it is clear that UVC is filtered out from natural sunlight and only apparatus such as mercury arc sunlamp can produce UVC.

For the natural sunlight, Table 5 shows:

Radiation emission Contribution to tanning

UVA UVB UVC UVA UVB UVC

95% 5% 0% 20% 80% 0%

UVC is not present in natural sunlight (0%) and contributes to 0% of tanning.

My understanding is that coronavirus needs UVC to be destroyed and only special lamp can produce it.

Dear Alain,

According to Lytle and Sagripanti (2005) (JOURNAL OF VIROLOGY, Nov. 2005, p. 14244–14252 ) the UV radiation from the Sun at terrestrial surfaces is sufficient to deactivate many viruses including the coronaviridae. The abstract from this paper is included below:

“UV radiation from the sun is the primary germicide in the environment. The goal of this study was to estimate inactivation of viruses by solar exposure. We reviewed published reports on 254-nm UV inactivation and tabulated the sensitivities of a wide variety of viruses, including those with double-stranded DNA, single-stranded DNA, double-stranded RNA, or single-stranded RNA genomes. We calculated D37 values (fluence producing on average one lethal hit per virion and reducing viable virus to 37%) from all available data. We defined “size-normalized sensitivity” (SnS) by multiplying UV254 sensitivities (D37 values) by the genome size, and SnS values were relatively constant for viruses with similar genetic composition. In addition, SnS values were similar for complete virions and their defective particles, even when the corresponding D37 values were significantly different. We used SnS to estimate the UV254 sensitivities of viruses for which the genome composition and size were known but no UV inactivation data were available, including smallpox virus, Ebola, Marburg, Crimean-Congo, Junin, and other hemorrhagic viruses, and Venezuelan equine encephalitis and other encephalitis viruses. We compiled available data on virus inactivation as a function of wavelength and calculated a composite action spectrum that allowed extrapolation from the 254-nm data to solar UV. We combined our estimates of virus sensitivity with solar measurements at different geographical locations to predict virus inactivation. Our predictions agreed with the available experimental data. This work should be a useful step to understanding and eventually predicting the survival of viruses after their release in the environment”

Dear all,

according to the data presented in by O’Reilly et al in the Lancet Planetary Health- - see Figure in the supplementary material, ref below - it seems that seasonality cannot be considered a key modulating factor of SARS-CoV-2 transmissibility. Your view, please?

https://www.thelancet.com/cms/10.1016/S2542-5196(20)30106-6/attachment/0fbf4780-0843-45f4-a099-c8c49df2c694/mmc1.pdf

Dear Francesca Costabile ,

I am in the process of writing a letter in response to this study (see text below). I do not have much hope for publication, but I believe that this letter can clarify this issue. I will be happy for any advice or comments regarding the letter.

Alex

Letter/Correspondence in response to

O'Reilly, K. M., Auzenbergs, M., Jafari, Y., Liu, Y., Flasche, S., Lowe, R. (May 06, 2020). Effective transmission across the globe: the role of climate in COVID-19 mitigation strategies. The Lancet Planetary Health, Volume 4, Issue 5, e172. https://doi.org/10.1016/S2542-5196(20)30106-6.

The authors touched one of the most important epidemiological problems in their work. I believe that the new aspect below may improve our understanding of causations and mechanisms, rather than associations and correlations.

The effectiveness of COVID-19 transmission, as well as other respiratory viruses and pathogens, depends on the factors of population susceptibility. High susceptibility to the virus is due to several host factors (local immune response, mucociliary clearance, etc.). In turn, these host factors depend on some external conditions (cold air, air pollution, and etc.) (Moriyama et al., 2020).

There is a clear seasonality for the effects of cold in some regions, but cold cannot be connected with tropical countries at first glance. That is why often doubts about the COVID-19 seasonality which was reflected by the authors of (O'Reilly et al., 2020).

But, and this is important, in accordance with the recent research concept of “Supersaturation in the airways” (Ishmatov, 2020) there is a clear seasonality of the dramatic increase in the deposition of air pollutants especially in submicron and ultrafine size range, spanning all climatic zones, from cold and dry to hot and humid regions.

In particular, the total deposition of submicron and ultrafine particles in the human airways during inhalation may rise from ~3–20% up to ~90% due to the enhanced condensational growth under supersaturated conditions in the airways. It was found that such unusually high underestimation of deposition efficiency is typical for the most methods and approaches commonly used (Ishmatov, 2019; 2020).

The boundary environmental conditions for enhanced deposition of inhaled pollutants in the airways are air temperature of T

The observation that the virus is transmitted in areas with high air temperatures is not sufficient to support any speculation regarding the seasonality of SARS 2 coronavirus disease. The main reason is that we don't have a seasonality theory yet, even for relatively well known viruses.

In order to create a solid foundation for future projections, we should perform a study similar to that reported in Lancet but with some additional environmental parameters, including

Stratification of the PBL

Ventilation factor in the PBL

Solar radiation at the surface

Cloud cover

Convective mass fluxes

Earth magnetic field

The above selection represents the absolute minimum required.

We should look also at the transportation system from the point of view of graph theory and establish the intensity of virus mutation rates depending on the region.

Janusz

Interesting paper but nothing says if corona virus could be killed just by exposure to natural sunlight. For example, N95 mask needs very special attention to desinfect.

UV light to desinfect is widely known but my question was what kind of virus could solar light could kill and in which condition.

Thanks for the paper anyways.

Regards

Alain,

Thank you for your comments. Perhaps the information in the note

“Inside the secret DHS lab testing how long coronavirus can survive on shopping carts and in sunlight” can clarify your doubts.

Please kindly consult the following link

https://www.nbcnews.com/news/us-news/inside-secret-dhs-lab-testing-how-long-coronavirus-can-survive-n1201386

Dear Janusz,

thanks for sharing the link.

Interesting comments about inactivation within minutes of virus on surfaces and in the air in direct sunlight, about high temperature and relative humidity relations and transmission indoors.

Looking forward to seeing the scientific articles - unfortunately, that's only a journalistic interpretation.

Dear Francesca,

Thank you for your comment. The statement:

“What we have found so far is that sunlight seems to be very detrimental to the virus,” Dabisch explained. “And so within minutes, the majority of the virus is inactivated on surfaces and in the air in direct sunlight” is the expression of the opinion of a leading researcher, we can accept this assertion as a very reasonable estimate.

It is likely that the study will be published in the literature accessible to a wide scientific community.

In the meantime, we can still attempt to perform some back of the envelope estimates, although they are not easy because the physics involved in such work is still not yet fully developed. Very often I think that the attempt to explain the behavior of viruses can even set the scene for the new revolution in physics.

The entire discussion of the role of sunlight in disinfection brings us back to the initial question of air pollution which is largely driven by photochemistry. It is even possible that in some situations with a high ozone concentration we will observe the emergence of another factor detrimental for the virus.

photochemistry // sunlight + chemical components (air pollutants) = ozone //

"Higher levels of ambient ozone are associated with reduced influenza transmissibility" - see in https://erj.ersjournals.com/content/51/5/1800369

My two cents in discussion.

Here's the paper (Published: 20 May 2020):

Ratnesar-Shumate et al. Simulated Sunlight Rapidly Inactivates SARS-CoV-2 on Surfaces. The Journal of Infectious Diseases, 2020, https://doi.org/10.1093/infdis/jiaa274

https://academic.oup.com/jid/advance-article/doi/10.1093/infdis/jiaa274/5841129

Conclusions: " The present study provides the first evidence that sunlight may rapidly inactivate SARS-CoV-2 on surfaces, suggesting that persistence, and subsequently exposure risk, may vary significantly between indoor and outdoor environments. Additionally, these data indicate that natural sunlight may be effective as a disinfectant for contaminated non-porous materials. "

It is encouraging to see the results indicating the role of solar radiation in the deactivation of viruses.

The sun is always a major factor to consider in our studies of pandemics because of a disinfecting role of radiation. At the same time, the weakening of the interplanetary magnetic field associated with the current solar minimum increases the flow of energetic particles from cosmic rays and therefore the frequency of mutations of viruses.

The current pandemics was anticipated by some authors on the basis of monitoring of the Solar cycle

https://www.longdom.org/open-access/sunspot-cycle-minima-and-pandemics-the-case-for-vigilance-2332-2519-1000159.pdf

We cannot also exclude the influx of biological matter from space because of the weakening of this field.

In the article linked above, we can read:

>>Beginning of the quote

“It is also of interest to note that the first descent of viral-sized particles deposited in the stratosphere will occur at places where the stratosphere is thinnest; and by this argument populated areas of China lying eastward of the Himalayan mountain range would present the best candidates”

COVID-19 exacerbation depends on many factors as enumerated above.

It should not be forgotten that temperature is also a basic one, if not the most important environmental factor. First, the immune system is stronger (weaker) with increasing (decreasing) temperatures. Look of what happens now (Peru, Columbia, Brazil, etc): as fall and cooler temperatures affect South America, the contagion and number of deaths are increasing although confinement there started at roughly the same time as North America. With winter coming up soon, things will degrade further.

Second, with higher (lower) temperatures, people tend to open(close) window meaning that the indoor air is less (more) contaminated. i.e. poor ventilation is related to outdoor temperatures.

Third, under low temperatures and condensing moisture, the virus survive longer. In hot and dry climate, the droplets coughed out by patients and containing the virus quickly dry and the virus is unable to survive.

It is well known that short spells of low temperature greatly raise the incidence of broncho-pneumonia (Dr. Thompson. A change of air. Charles Scribner's SONS, New-York, 1979. Chap. 14 Climate and infection). Moreover, for each 0.5 deg C fall in outdoor temperature, there is a 1 % rise of the incidence of colds (idem ref.).

In addition of UV having a lethal action 9as mentioned by Janusz) , there is also negative air ions. There is evidence that positive air ions may facilitate infection. The most dangerous positive ion levels occurs in polluted environment.

https://scialert.net/fulltext/amp.php?doi=tasr.2011.130.133

Moreover, countries which have hot and sunny climate (e.g. Africa) have limited damage due to COVID-19.

Hot and sunny weathre "increases metabolism and catabolism of vitamin A (retinoic acid) and its effect on the Renin–Angiotensin System, ACE2 receptor of covid -19 ,immune modulation and immune response and speed of antibody formation " according to the following discussion:

https://www.researchgate.net/post/Mystery_of_low_Covid-19_death_rates_in_Africa_compared_with_European_countries

Also, the sun favors vitamin-D which is strongly suspected to help resisting the COVID-19 virus

https://www.webmd.com/lung/news/20200518/more-vitamin-d-lower-risk-of-severe-covid-19.

We often forget the climate and weather in explaining infectious disease.

There is no surprise as Big Pharma are the one who control the medical message.

Buen día, los saludo desde Hermosillo, Sonora México, acá estamos en primavera, casi iniciamos el verano, las temperaturas ambientales fluctúan entre los 34 y 42 °C con baja humedad, disminución de corrientes de aire en chorro, sin posibilidad de lluvias..

A la pregunta: De la existencia de la relación entre la polución del aire y la relación de propagación del coronavirus con su enfermedad covid19 no se ha estudiado, si se ha relacionado el incremento de la enfermedad por el no aislamiento de la gente y no uso de cubrebocas.

Saludos Cordiales.

Copat, C.; Cristaldi, A.; Fiore, M.; Grasso, A.; Zuccarello, P.; Oliveri Conti, G.; Signorelli, S.S.; Ferrante, M. A First Review to Explore the Association of Air Pollution (PM and NO2) on Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2). Preprints 2020, 2020050299 (doi: 10.20944/preprints202005.0299.v1).

https://www.pnas.org/content/early/2020/06/10/2009637117

The Need for a Tighter Particulate-Matter Air-Quality Standard /// https://www.nejm.org/doi/full/10.1056/NEJMsb2011009?query=recirc_top_ribbon_article_21#article_references