Reminder : European Scientist is not a peer-reviewed scientific journal. The opinion below is only up to its authors.
Great public organisations like the WHO tend to lack proper contact with actual facts and to suffer from difficulties to address the relevant issues. Many oversized national scientific committees and their staff, often more familiar with ministry corridors than with medical reality, suffer from a similar illness, resulting in poor communication and loss of confidence from the public. This paper is based on our experience with everyday reality in hospitals, in reanimation services, and with the number and history of patients.
The strange COVID 19 epidemic clusters observed in slaughterhouses all over the world encourage us to focus our research on two types of questions:
• what is the cause of the severity of the disease,
• what is the influence of the conditions of contamination on this severity?
The degree of severity of the disease is often attributed to age and overweight issues, making COVID a metabolic disease. We shall take a different point of view, and suggest it is more relevant of a meteorological disease, where meteorological conditions are playing a major role in its severity, through how they influence the load of the virus inoculum.
Starting from how the epidemic has hit slaughterhouses, we develop the hypothesis that the conditions of contamination in slaughterhouses involve the existence of an intramuros microclimate: the aerobiological conditions in these premises are stable according to the criteria of scientific literature, and the aerobiological conditions found in a slaughterhouse make it a realistic scale model of the meteorological conditions that lead to seasonal epidemics of respiratory viral infections.
The suspected contamination process in slaughterhouses [1, 8] presents a striking similarity with the bioclimatic conditions observed in Alsace (France) or the valley of Po (Italy). These regions are famous for their seasonal fogs.
Our hypothesis of a similar contamination process provides a possible explanation of both the severity of the condition and its temporality. This meteorological point of view makes it possible to anticipate the occurrence, not of a proper second wave but of a regional succession of epidemic episodes.
An intimate understanding of the phenomenon of seasonality makes it possible to take preventive measures and justifies the implementation of a certain number of protective and eviction measures in order to avoid a generalised lockdown, which might not necessarily be imposed by authorities but possibly induced by generalised panic.
The adhesion of individuals to this preventative policy can only be supported by the existence of a rational explanation.
Below, we propose a theory according to which it is the massive aerosol3 contamination that explains both the seasonality and the severity of the condition. This major risk should be assessed in the light of the so-called Spanish flu pandemic, which between 1918 and 1919 contaminated a third of humanity and killed between 20 and 100 million people.
For those of us who are everyday facing the consequences of deliberate risk-taking, we intend to alert the authorities about the unassessed risk of a delusive end to a benign summer epidemic, that could lead to a disaster in autumn.
2 The slaughterhouse mystery
Having taken part to systematic screening in slaughterhouses, we, like others, were able to observe massive contaminations that are difficult to explain. There is no equivalent of these outbreaks in other professions where there is some definite promiscuity. This is a worldwide observation. The same phenomenon has been observed in Germany, the USA, France etc… The existence of these epidemic outbreaks has even ruined a few American farmers who were unable to slaughter their animals. Their slaughterhouses had to close following the contamination of hundreds of employees. At the time of writing, a major outbreak of contamination has been announced in a Danish slaughterhouse and yet it is not questionable that in a slaughterhouse important precautions are taken to avoid contaminating the meat.
The animals did not contaminate the farmers, amd therefore are not directly responsible for these mass contaminations, as one might have imagined with a virus with a low species specificity. We therefore wondered what the regions from which the epidemic originated and these slaughterhouses had in common. A simple visit to these slaughterhouses immediately suggests an answer: it is both cold and damp [9, 12]. We still had to draw the consequences and come up with a hypothesis with a credible physical basis. As we cannot rely solely on intuition, we turned to physicists .
3 The “missing link” between slaughterhouses and mid-season: the stable aerosol
We found a bioclimatic similarity between these epidemic outbreaks and the seasonality of respiratory viral diseases: it became clear to us that the carrier of the contamination is most likely airborne, as for respiratory diseases in general; however it is mainly due not to the large Pfügge droplets which only contaminate within a small range, but to a stable aerosol [5, 6, 10, 11, 13]. We believe that in a slaughterhouse where the circulating air is cooled down, the supply of warm water vapour at animal temperature resulting from slaughter and quartering gives the perfect conditions for water vapour to condensate as an aerosol and the creation of a continuum of contamination, if by some misfortune it is fed by an employee carrying the virus, The aerosol would thus be the physical medium which, in the event of a patient in the slaughterhouse excreting SARS-CoV-2, enables a large number of employees to be contaminated, the phenomenon being linked to the double effect of persistence and convection movements linked to ventilation.
The parallelism with the regions where the pandemic started is striking. These regions, the Rhine valley and the valley of Po, are known to have stable and long-lasting fogs in autumn and spring, and it is precisely in these areas that the epidemic developed most heavily. On the other hand, last winter in the West of France we had, in 2020, little condensation and few non-imported contaminations and very limited outbreaks.
We came to the following conclusion: this parallelism between weather conditions and the seasonal nature of the aerosols we can describe as “viral fogs”, is directly responsible for the massive transmission of the virus to a very large number of individuals, rapidly and during often long-lasting episodes.
4 A quick review of the conditions maintaining the virulence of SARS-CoV-2
The conditions of virulence of viral particles emitted in aerosols are poorly documented. The measurement of a determined number of copies is generally carried out with quantitative RT-PCR, which does not presume virulence, as few studies have been carried out by determining the number of viral particles on cell cultures.
The enveloped virus is fragile but seems to retain all its virulence within an aerosol. In any case, this is what the epidemic has just demonstrated.
Another element supporting the predominance of the aerosol in the contaminations is the seriousness of the pathology with the caregivers.
It is highly significant that caregivers who are particularly competent in hospital hygiene have been killed by this virus, thus 50 French doctors have died, 200 Peruvian doctors, etc. This heavy toll suggests that the most serious form of the disease is not carried by hand contact. Professionals are well trained into this type of prevention. In our opinion, this contamination is the result of massive respiratory contamination  directly linked to the absence of surgical masks worn by patients. These doctors were likely contaminated by air because their patients were not wearing masks.
Week after week, we are seeing an inexorable increase in the baseline number of positive genomic diagnoses for SARS-CoV-2. It seems strange and yet it makes sense.
This virulent epidemic resurgence seems disconnected from the generally observed lighter symptomatology. The undocumented, reckless conclusion drawn from this, is that it is less dangerous, with the risk of a delusive end to the epidemic. It is wrong to underestimate this virus and to think that the nature of the disease has changed. For months now, we have been often hearing inconsistent, out of touch with reality and inconsistent statements from media, representatives of political power and even the scientific community. It is not the purpose of this paper to summarise them, but here again they are most probably wrong.
From this lack of serious cases, deceptive optimistic conclusions are drawn, exposing that the infected population is rather young and the disease is symptomatic. Contrary to what happened last March in Europe, we do not actually observe the dramatic symptomatology at the origin of the saturation of the intensive care units. This is partly due to better management of the inflammatory side of the disease, which conditions the severity of the second phase of the disease. This is also due to smaller exposure to the inoculum resulting from the use of masks. But we suggest that the actual central process is the aerosol.
It is the load of the inoculum and the modalities of contamination which favour the serious lung disease. This is directly related to the viral load of the stable aerosol.
We propose to study, in the case of COVID, as has been demonstrated in other respiratory viral diseases, the major role of the degree of inoculum. The hypothesis has been put forward of a decrease in virulence of genomic origin, resulting from mutations. We suggest that the preferred mode of contamination, in summer, is direct or semi-direct contact by soiled surface or projection of microdroplets in the immediate vicinity of the contaminating patient. This type of transmission is therefore typical of a modern life of young people multiplying contacts. People at risk tend to remain sheltered in their homes. This type of contamination is very sensitive to the distance separating the contaminator from the contaminated person, so people at risk are excluded from the contamination process.
There used to be no relevant explanation for the seasonality of serious respiratory infections, but we now believe that the responsible is the season.
Only a few days ago, Professor Didier Raoult stated, in accordance with a quasi-omnipresent consensus, that the reasons why epidemics due to respiratory viruses are generally seasonal remain unknown. We believe that it is not virology that will provide the answer but meteorology. A large number of communications currently attribute the number and severity of contaminations to the existence of an aerosol vector of small particles smaller than 5 micrometres [3,7]. We believe that it is precisely the persistence of this aerosol that significantly lengthens and intensifies the risk of transmission, contamination being all the more probable following a longer contact and a larger inoculum. This is referred to as the rate of contamination. The publications that report the infectivity of aerosols reaching the alveoli (particularly in influenza) suggest a maximum risk for small sized particles of the order of one micrometre. These particles must therefore stay in suspension for a sufficient time to remain contaminating, which requires favourable aerobiological conditions (temperature, humidity, barometric pressure).
We propose a theory of the route of contamination and the importance of the inoculum. This contamination is closely associated with the existence of a permanent aerosol.
Research focused on the analysis of the influence of seasonality should be encouraged. It appears to be the origin of both contagion and disease severity. This analysis, if confirmed, would make it possible to anticipate the evolution of an epidemic of respiratory viruses that appears to be necessarily seasonal and the foreseeable consequences, including geographical, on the Coronavirus pandemic. For example, it might make it possible to forecast epidemics during the monsoon season…
5 Consequences for the prevention of individual transmission
A certain number of so-called “barrier” measures such as the wearing of masks, eviction and basic hygiene rules should make it possible to avoid a disaster not triggered by an authoritative lockdown but by a de facto lockdown, caused by the fear of contamination and its adverse consequences on economy –and health. Wearing a surgical mask is fundamental [4, 14] because the aerosolised particles carrying the virus are often electrostatically charged [16, 18] and thus adsorbed independently of their size on the mask’s polymer fibres. This phenomenon is added to the passive filtering effect of the screen and even replaces it for particles of the order of one micrometre or less in size than the screen of the surgical mask. This has consequences on the prevention of epidemic outbreaks in confined spaces but also in health establishments.
A few months ago I intervened to warn about the risk linked to massive respiratory contamination by aerosols, in the sampling rooms of laboratories or in healthcare establishments. As a result, we refuse to take nasopharyngeal samples elsewhere than in the open air whenever possible. It seems risky to organise sampling by exposing successive patients in a confined space. During nasopharyngeal sampling, for example, the patient may likely sneeze and produce a very large aerosol, while it is not materially possible to completely clean these rooms during serial sampling.
It is therefore necessary to ventilate the premises extensively and avoid confined spaces such as lifts and toilets. In toilets, the vortex of evacuation is a generator of droplets and aerosols fed by the high viral load of the faecal matter.
Some people have questioned the possibility for an aerosol to remain in suspension long enough to contaminate large numbers of individuals. Among my activities, I have been involved in consulting missions in the nuclear sector where the question of maintaining radionuclides in suspension after nuclear incidents has been raised. Pierre Roupsard’s Ph.D. thesis  gives a bright demonstration of the influence of meteorological conditions on the stability of aerosols in urban environments.
The proposed mechanism implies short-term epidemiological consequences.
We can therefore legitimately fear, not a second wave, but an explosion of contamination when the meteorology allows it. What has been observed, despite the population transfers facilitated by modern means of transport, is that the massive infection is not mainly due to population movements but to meteorology, as it appears that the contamination in the two hemispheres is not synchronous.
The severity of the disease is a consequence of the aerosol nature of the inoculum.
The mutations of the virus observed are not very important and have no proven impact on its virulence. We have strong arguments for citing the aerosol as the seasonal origin of the contagion. We shall see that seasonality is very likely also the cause of the severe forms of the disease. Consequently the hypothesis of a benign evolution is an opinion which alas might well be contradicted as early as next fall.
Seasonality is the basis for the seriousness of the disease and there is no evidence that the virus would have evolved, even if it cannot be excluded.
Two things should be remembered. The virus in suspension is kept in a state of virulence in aerosol droplets. The virus is sensitive to desiccation and only this transport in droplets allows the integrity of its fragile envelope to be maintained, a condition of its virulence since it supports the S protein (Spike) which allows viral particles to enter the target cells carrying the membrane receptor ACE2. These receptors are present in many cells: nerve cells, digestive cells, the nasal mucosa, the throat, the vascular endothelium and especially the endothelium of the pulmonary alveoli.
We believe that only a large inoculum of aerosolised particles reaching the alveoli simultaneously will be able to cause a major pathology of the entry portal, which requires the existence of an aerosol consisting of micro-droplets with a size of around one micrometre and reaching the alveola .
It is a constant fact that in this type of disease there is a first local barrier which can limit the physiopathological impact of an infestation through various mechanisms. The first one is mechanical, the particles with a large diameter, greater than 5 micrometres, are generally blocked before reaching the pulmonary alveoli, whose vascular microenvironment is the bed of the severity of the disease.
There is no doubt that, as has been demonstrated for other viruses, in the case of a low level of contamination, the organism is given time to organise a specific cellular and humoral immune defence which opposes, on the one hand, the dissemination of the virus throughout the organism and, on the other hand, the importance of this viral multiplication in situ.
Thus we think that the summer contagion route favours all cellular targets, except the pulmonary target which is not easily accessible. On the other hand, this target appears to be particularly exposed in the event of massive contamination by an aerosol which will be all the more dangerous as it will carry a high viral load. This supports the significant increase in both the number of contaminations and their severity in mass contaminations in dense housing.
Understanding the aerosol-based virus spreading mechanism is fundamental, as beyond the SARS-CoV-2 pandemic, it offers a coherent and cross-cutting explanation for the seasonality of all respiratory viral diseases. The oldest studies have been carried out on the transmission of tuberculosis. They were also carried out for influenza.
All the mechanisms leading to the production of aerosols must be understood in order to assess and minimise behavioural risks, some of which are unavoidable, such as the mechanics of bronchioles. Sneezing and coughing must be minimised and produced separately from the community. Speaking is an important source of aerosol production, and loud voice, shouting and singing do significantly increase this production.
The respect of barrier measures and in particular the generalisation of the use of masks are the most appropriate response to limit the gravity and number of contaminations. The general public will only be able to fully adhere if they understand why the surgeon wears a surgical mask: not to massively contaminate his patient by aerosols.
We believe that communication purporting to assert without evidence that people who are screened only carry debris nuclear material or non-infectious virions, presents a major public health danger by causing the general public to counteract common sense decisions, presented as political or conspiracy aberrations.
We are not optimistic: the observation of the summertime existence in France of a baseline involving a very large number of daily contaminations currently estimated at more than 9,000 cases. This implies the existence of a permanent contaminant potential that we can estimate at least at 90000 patients (3 days before the symptoms and 7 days after). This figure is underestimated by 30% since we have at least 30% false negatives in RT-PCR. We will therefore face the autumn not with patient zero but with almost 120,000 patients… this disease has already affected millions of people, resulting in the death of hundreds of thousands of patients, and a second season of the disease might well be much more serious than the first4. This is what happened in 1918. The so-called ‘Spanish flu’, which was probably linked to an H1N1 virus, killed many more people after August 1918, while the disease had appeared in France during spring 1917. The ‘Spanish flu’ killed more people than the First World War. The process was repeated in 1919.
It is therefore time to be vigilant and to implement preventive measures aimed at limiting the spread of the virus. The only relevant indicator remains the number of patients carrying the genomic markers of the virus.
Beyond this looming second season of the SARS-CoV-2 virus, we will have to be very vigilant and give ourselves the means to be. Collaboration between healthcare teams and laboratories will be essential. In the longer term, we will undoubtedly have to envisage syndromic vigilance using multiplex PCR in order to simultaneously identify the different viruses responsible for an epidemic, using what is known as the syndromic approach. This approach makes it possible to simultaneously identify a large number of respiratory pathogens. For the next season, there will be the SARS-CoV-2 virus, but also the slightly forgotten influenza, which was the virus that rightly frightened us and still deserves our vigilance, among others. We must learn the lessons from our inability to quickly adapt our laboratories to a major public health threat. It is fundamental to maintain the capacity of local laboratories to determine the nature of the viruses in circulation. This is the price of limiting the human and economic consequences of a new pandemic.
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