Just a while ago, the Italian Society of Environmental Medicine (SIMA) released a preprint version of its paper confirming the presence of coronavirus RNA in particle pollution samples collected in industrial areas of Northern Italy.
These preliminary results sparked a great debate… Not on the possible implications in case of their confirmation, but on how the press announced the results.
Following SIMA’s publication, many scientific journalists, bloggers, and professional debunkers raced to highlight the lack of scientific objectivity in defining “official” SIMA’s preliminary results.
The paper is indeed a preprint, meaning it has not yet completed the peer review process envisaged for publication in scientific journals. Furthermore, the presence of coronavirus RNA in particle pollution samples would say nothing about its actual contagiousness and therefore about its possible contribution to spreading coronavirus.
Hence the criticisms: nothing conclusive can be said to affirm the role of particulate matter as the carrier of the virus.
True. But is this the principal issue?
Recently, some scientific papers supported the thesis that air pollution could be a contributing factor to the high death rate of coronavirus.
Given the short time frame since the beginning of coronavirus emergency, most of them are either letters to the editor or brief reports aiming more at describing and discussing the scientific validity of a hypothesis that needs to be demonstrated with subsequent more detailed studies, or preprint versions of more extensive studies still undergoing peer review.
Then why are those made public earlier and widely spread by the media? We are in the midst of a global pandemic crisis and the effectiveness of measures taken to fight it depends on how well we interpret its causes and contributing factors.
SIMA’s study poses a crucial question: why 80% of the victims and 65% of ICU admissions are in the Po Valley?
After more than a month since the first SIMA position paper was released, nothing happened. Environmental factors are largely ignored by strategies to deal with the crisis as well as by mainstream media.
Still, Harvard’s preprint study claims that an increase in long-term exposure to fine particulate matter (PM2.5) leads to a significant increase in the mortality rate from coronavirus. An increase of only 1 µg / m3 in PM2.5 is associated with a 15% increase in COVID-19 mortality.
The paper (this time published) from the University of Århus argues that the high level of pollution in northern Italy should be considered an additional cofactor of the high level of mortality recorded in that area.
Lastly, the San Raffaele letter to the editor re-launched the hypothesis of particulate matter as a carrier, hoping for further studies and quoting the recent publication in The New England Journal of Medicine which testified the plausibility of the transmission of the virus via aerosol.
We also have the many data of scientific literature cited by the ARPA study which shows that particulate matters amplify the effects of infections (boosters), defining it as a possible cofactor in supporting the virus-induced inflammation process. Studies on the population highlight how particulate matter leads to systemic inflammation and how SARS-CoV-2 infection induces the recall of numerous molecules of the immune system contributing to the compromised inflammatory state of patients.
The same study, however, indicates the lack of scientific literature to support the hypothesis of particulate matter as a carrier (defined as “incomplete”) and of scientific works demonstrating the presence on samples of atmospheric particulate matter of SARS-CoV-2 or other types of coronavirus. A deficiency to which the SIMA study should respond, albeit partially and preliminarily. Nevertheless, several studies are cited that have found experimental findings or statistical associations between concentrations of environmental particulate matter and the spread of influenza viruses and the role of particulate matter in the transmission of viruses in animal flu epidemics.
In conclusion, the hypothesis that particulate matter acts as a carrier (carrier), as well as booster, certainly needs more insights. So far, this hypothesis has not been investigated enough and the SIMA study is a laudable also isolated, attempt to confirm (or exclude) the presence of the virus in the particulates and its role in the spread of the infection.
It should be remembered, however, that Italy holds the negative record in Europe for premature deaths from nitrogen dioxide and ozone and the second place for fine particulate matter (PM2.5) with 58600 premature deaths.
Whether the particulate matter is a carrier, a contributing factor in the inflammation process (booster), or both, an approach based on the precautionary principle would suggest taking environmental factors more seriously.
Keeping emissions of particulates and other kinds of pollution low to avoid the risk of paving the way for new peaks of coronavirus infection is a more than reasonable request.
Also because the great risk we are facing is that the management of the emergency and the post-COVID-19 economic crisis might end up putting aside the protection of the environment by sacrificing it on the altar of economic recovery. Just as it is happening in the United States and France.
In Italy there are already rumours from the Ministry of Transport thinking of cancelling the constraint provided for by the National Strategic Plan for Sustainable Mobility, leaving operators free to choose any motorization for bus fleets, even the most polluting ones. Given that a bus has an average life of 12 years, this would mean losing a good opportunity to help reduce polluting emissions.
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