Airborne PM2.5 and the Emergence of 10 SARS-CoV-2 Variants The Multifaceted Influence of an Airborne Pollutant on Viral Natural Selection determining SARS-CoV-2 Evolution - An Environmental Wake-up Call or an Ecological Fallacy?
Authors: Baron Yves Muscat 
Published: July 2021

Background

Airborne particulate matter has been suggested as a co-factor for SARS-CoV-2 infection. Besides the deleterious effect this pollutant has on pulmonary immunity and the propagation of respiratory ACE-2 receptors (angiotensin converting enzyme II), the SARS-CoV-2’s point of entry, particulate matter has also been proposed as a vector for this virus’ transmission. Particulate matter may also be a marker for anthropogenic activity acting as a surrogate for increased human to human contact, increasing both transmission and the mutagenic viral load. Genes coding for SARS-CoV-2 have been detected on airborne particulate matter and its proximity to the virus, may have caused this pollutant to act as a mutagen causing the inception of SARS-CoV-2’s variants and simultaneously being genotoxic to the progenitor viruses, differentially favouring variant emergence.

Since the initial phases of the pandemic, a multitude of SARS-CoV-2 variants have been detected, but the few that survive to promulgate human infection have increased transmissibility. It also appears that there is a limited set of persistent mutations SARS-CoV-2 can produce. This set of mutations has been found in widely disparate and distant regions. This may suggest that besides intra-host mutation in an inflammatory ambience, an ubiquitous factor such as an environmental mutagen, may have resulted in convergent evolution leading to the emergence of similar variants. This paper examines a possible association in a multi-modal manner between the airborne pollutant PM2.5 and the emergence of ten of the most clinically and epidemiologically relevant SARS-CoV-2 variants.

Methods

The daily average levels of PM2.5 of a number of cities, where variants were detected, were obtained from the World Air Quality Index (WAQI), a real-time assessment of atmospheric pollution. PM2.5 levels were correlated with SARS-CoV-2 variants including Variants of Concern (VOC) or Variants of Interest (VOI). These variants included the G614 variant in Beijing, the 20A.EU1 variant in Valencia, the B.1.351 variant in South Africa, the B.1.1.7 variant in the UK, the USA variants B.1.429 in Los Angeles, B.1.2 in Louisiana and New Mexico, the B.1.526 variant found in New York, the variant B.1.1.248 in Brazil. During mid-March 2021, the B.1.617 variant first detected in October 2020, surged in Nagpur, India and the R.1 variant was detected in Kentucky U.S.A. The average daily PM2.5 levels were assessed, the evaluation initiating just before the occurrence of the first spike/s in this pollutant’s atmospheric concentration, till after the emergence of the variants. Where available the daily number of new cases of COVID-19 diagnosed was matched to the PM2.5 levels.

Results

There appears a common pattern of PM2.5 in most of the regions prior and during the emergence of the SARS-CoV-2 variants. An initial spike/s of PM2.5 were noted on average 50 days prior to the emergence of the variants and another smaller spike/s in PM2.5 were noted just before or contemporaneous with the emergence of the variant. Prior to the emergence of to the G614 variant in Beijing, the average PM2.5 level during its peaks was 153.4µg/m3 (SD+/-63.9) to settle to a baseline of 94.4µg/m3 (SD+/-47.8)(p<0.001). Before the appearance of the 20A.EU1 variant in Valencia, the PM2.5 spikes averaged at 61.3µg/m3 (SD+/-21.8) to decrease to a mean of 41.2µg/m3 (SD+/-15.5) (p<0.04). In Kent, U.K. a solitary PM2.5 spike averaged 82µg/m3 (SD+/-29) before the detection of the B.1.1.7 and following the PM2.5 spike the baseline level of this pollutant was 27.8µg/m3 (SD+/-18.0) (p<0.03). In Nelson Mandela Bay South Africa, where B.1.351 was first detected, the PM2.5 mean baseline level was reported as 40.4µg/m3 (SD+/-14.0), while prior to this variant’s emergence, the PM2.5 spike averaged 85.1µg/m3 (SD +/-17.3)(p<0.0001). In Brazil the average PM2.5 during its spike was 107.4µg/m3 (SD+/-34.2) before B.1.1.248 variant emerged and after the spike the baseline PM2.5 was 48.3µg/m3 (SD+/-18) (p<0.0001). In the USA the average PM2.5 peak levels prior to the emergence of the SARS-CoV-2 variants were 118µg/m3 (SD+/-28.8) in Los Angeles (baseline 66.1µg/m3 (SD+/-25.1), 75+/-27.8µg/m3 (baseline 43.3(SD+/-14.4)µg/m3 in Louisiana, 71.4+/-11.3µg/m3 (baseline 43.6(SD+/-12.4)µg/m3 New Mexico, 54.3+/-13.8µg/m3 (baseline 34.4(SD+/-11.6)µg/m3 in New York and 37.7+/-7µg/m3 (baseline 28.5 SD+/-6.8)µg/m3µg/m3 in Eastern Kentucky. All the spike patterns of PM2.5 levels noted in the USA were significantly higher when compared to their respective baselines (p<0.0001). Prior to the surge of the variant in India, the PM2.5 spike in Nagpur averaged 166.8+/-10.8µg/m3 (baseline 123.2SD+/-16.9µg/m3) (p<0.0001). 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 in most of the regions reviewed.

Conclusion

There appears to be an association between the levels of atmospheric PM2.5 and the emergence of SARS-CoV-2 variants. In most regions two groups of spike/s of PM2.5 were noted prior to the emergence of these variants. The first PM2.5 spike/s approximately 50 days before the variant’s emergence may suggest that anthropogenic activity was increased possibly reflecting augmented human to human contact, consequently increasing the viral burden of the progenitor virus. The first PM2.5 spike may also have made populations more susceptible to SARS-CoV-2 through the propagation of the respiratory ACE receptor. There is the potential that coronavirus-laden, PM2.5 induced mutagenesis in the SARS-CoV-2 genome resulted in establishing persistent variants and contemporaneously was genotoxic to the progenitor virus, expediting the latter’s disappearance. PM2.5 may have further diminished the pulmonary immunity inviting further viral invasion. The second spike/s prior to the emergence of variants, may suggest another anthropogenic spike in human activity. With the second spike/s in PM2.5, this airborne pollutant may have acted as a viral vector encouraging variant emergence. This may have not only led to increasing viral transmission, catalysed by the preceding risk factors, but resulted in an overwhelming viral load, providing fertile ground for variant emergence. The above findings suggest that antecedent spikes in PM2.5 prior to variant emergence not only contributed to transmission, but also impacted the immediate viral environs which resulted in its natural selection, effecting SARS-CoV-2’s evolution.