Yves Muscat Baron1* and Liberato Camilleri2
Background: The atmospheric pollutant PM2.5 has been implicated in the pathogenesis of COVID-19. Some of the variants of SARS-CoV-2 possess the attributes of increased transmissibility and immune escape and appear to have been naturally selected to promulgate the pandemic. Variants of SARS-CoV-2 resulted due to a number of persistent SARS-CoV-2 mutations found in widely disparate and distant regions. This paper examines a possible association between airborne pollutant PM2.5 and the emergence of ten SARS-CoV-2 variants.
Methods: The daily mean levels of PM2.5 of a number of cities, where SARS-CoV-2 variants were detected, were obtained from the World Air Quality Index (WAQI). The mean daily PM2.5 levels were evaluated just before the occurrence of the first cluster of PM2.5 peaks’ atmospheric concentration, till after the emergence of the SARS- CoV-2 variants. Where available the daily number of new cases of COVID-19 diagnosed was matched to the PM2.5 levels.
Results: There appears to be a common pattern of PM2.5 in most of the regions prior to the emergence of the SARS-CoV-2 variants. An initial cluster of PM2.5 peaks was noted on average 50 days prior to the emergence of the variants and another group of smaller peaks in PM2.5 were noted just before or contemporaneous with the emergence of the SARS-CoV-2 variants. In the regions where the quantity of daily new cases was available, a number of significant correlations were obtained between PM2.5 levels and the number of new cases of SARS-CoV-2 variants.
Conclusion: In most regions two clusters of PM2.5 peaks were noted prior to the emergence of SARS-CoV-2 variants. The first cluster of PM2.5 peaks may suggest that anthropogenic activity was increased possibly reflecting augmented human to human contact. Due to elevated levels of PM2.5, a consequent propagation of the respiratory ACE-2 receptor (port of viral entry into the cell) ensued. Coronavirus- laden PM2.5 may have induced intra-host mutagenesis in the SARS-CoV-2 genome, contemporaneously diminishing pulmonary immunity. With the second cluster of PM2.5 peaks, this airborne pollutant may have also acted as a viral vector. The above findings suggest that antecedent peaks in PM2.5 prior to SARS-CoV-2 variants’ emergence not only contributed to transmission, but also impacted the immediate viral environs which may have led to SARS-CoV-2’s natural selection.
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