Undoubtedly reduced transmission of COVID-19 followed the institution of social distancing. Besides reducing human to human viral transmission, physical distancing diminished levels of human and economic activity with consequential reduced pollution levels2. Coal consumption in China after lockdown decreased by approximately 50%, from 80 thousand tonnes daily to 40 thousand tonnes per day23 . In India, reductions of the order of 43% and 31% were noted for PM2.5 and PM10 respectively, during lockdown period compared to previous years. During the same period carbon monoxide decreased by 10% and nitrous oxide decreased by 18%. The air quality index (AQI) improved throughout India following lockdown24.
Before statutory lockdown, there may have been synergism between high PM2.5 levels and COVID-19 in infection transmission. This synergism may have also determined the severity of COVID-19 sequelae. Pathological synergism between PM2.5 and respiratory infection has been shown in animal studies. Preclinical studies, exposing mice to cigarette smoke demonstrated that following intratracheal injection of streptococcus pneumoniae, bacterial counts in murine lungs were higher than the control group25. Another study showed that air pollution could result in dysfunction of rat tracheal cilia, causing mucus stasis and resultant infection. Moreover a declined nonspecific immune defense, was noted making the rats more prone to secondary infection26. Viability and phagocytic activity of alveolar macrophages decreased significantly following the instillation of PM2.5 particles in Wistar rats27,28.
Similar deleterious effects of PM2.5 have been found in the respiratory system of humans. PM2.5 releases free radicals, metal and the organic components inducing free radical production leading to oxidation of lung tissue29. Through PM2.5’s propensity to produce free radicals, peroxidation of lipids on the cell membrane occurs, with consequent elevation of intracellular calcium. High levels of intracellular calcium increases inflammatory cytokine production (Kim et al 1997). PM2.5- induced inflammation led to an increase in the number of neutrophils, eosinophils, T cells and mastocytes30.31. All these cells can result in inflammatory cytokine production and resultant cytokine storm has been responsible for a significant number of COVID-19 related deaths32
Addressing this synergism may protect the populations from airborne infections such as the COVID-19 infection and simultaneously foster respiratory health. Prior to the outbreak of COVID-19 in Wuhan, Qom and Bergamo the Air Quality Index demonstrated strikingly elevated pollution levels of PM2.533. These elevated levels of PM2.5 occurred during the winter months possibly due to combustion of fuel for residential heating purposes.
Inferring from the fact that coastal cities have been in the main been spared from high COVID-19 infection, another environmental factor may come into play in the form of the level of atmospheric salt content. Chloride ion wet deposition, a variable reflecting the ambient salinity could be obtained from a colour-coded map of the distribution of the earth's salt content.13
Wuhan has been noted to be one of the cities in China with the least salt content in the air14. The cities hard hit by COVID-19 infection are distant from the sea and consequently have low salt content levels14-22. Rotterdam with an elevated salt content PM2.5 (0.4µg/m3) had lower rates of COVID-19 compared to Vredepeel in the inland Limburg region (0.2µg/m3). Beijing with a high salted PM2.5 (1.3µg/m3) had lower levels than Wuhan (0.3µg/m3). It is imperative that the impact of physical distancing due to enforced quarantine be factored in when considering infection rates. South West region of the U.K. with higher saline levels had lower COVID-19 infection rates compared to London which appears to have a lower chloride ion wet deposition. Similarly in Italy whereby the saline deficient Lombardy region was severely affected by COVID-19 infection, while the more saline rich south of Italy have very low infection rates.
Healthy levels of airway salt content protect the respiratory system disease. Hypertonic saline has been shown to have anti-infective properties34. Tracheo- bronchial ciliary action is accentuated when the saline content of the endobronchial tree is optimal. Optimal levels of tracheal sodium chloride are mucolytic making bronchial mucus is less viscous with. Patients with respiratory condition such as asthma and cystic fibrosis benefit from endo-bronchially nebulized saline35
A protein component of COVID-19 virus is hydrophobic10,11. Viral cell entry is mediated through extensive post-receptor-binding structural readjustments on the cell membrane. The hydrophobic peptides include the C-terminal of a fusion peptide11,12. Low concentrations of chlorinated solutions are lethal to the virus37. Atmospheric salt content may be another environmental factor that may have protected some populations preventing airborne infection from the COVID-19.
Variable amounts of sodium chloride are found on PM2.5 species9. The PM2.5 species vary from city to city, and there are also seasonal changes in the sea salt component of the PM2.5. As a corollary to the variable amount of PM2.5 sodium chloride component, there also a variable degree of hygroscopicity related to the sea salt-derived water content9. Besides the lethal effect of sodium chloride on the virus, there may be a connection with aerosol adhesion due to sodium chloride with the pollutant PM2.5. Recent evidence suggests that COVID-19 may adhere to PM2.5 particles to evade the bronchial tree defences and colonize the alveoli8. The presence of hygroscopic sodium chloride on PM2.5 may act as a deterrent against the adhesion of the hydrophobic proteins of COVID-19 to these particles, protecting populations living in regions with salt-rich PM2.5 prevalent high salt content regions.
CONCLUSION: The COVID-19 pandemic may have occurred due to the combination of a number of environmental factors besides the virulence of the virus. A decrease in airborne pollution in particular PM2.5 and possibly the sodium chloride rich species of PM2.5 may have protected some populations from the COVID-19 pandemic.