Fig. 1
Interplay of Air pollution, Lockdown and SARS-CoV-2: An Epidemiological View. Model built following synthesis of current litterature [3, 13, 15, 30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51] . The airborne nature of SARS-CoV-2 transmission might be facilitated by air pollutants. Indirectly pollutant can increase host susceptibility to SARS-CoV-2 by directly induce respiratory epithelium/ endothelium lesions. Further, pollutants trigger oxidative stress, increase ACE-Receptors, and are independently associated with the risk, severity, and mortality for cardiorespiratory and metabolic diseases (COPD, tuberculosis, ARI, HTP, high BMI, diabetes, etc.). Patently, SARS-CoV-2 manifestation is linked to cytokine storm liberation, it binds to ACE-2 Receptors to penetrate host cell membrane and is more severe among people with the above evoked cardiorespiratory and metabolic conditions. In addition, pollutant can sustain cytokine storm triggered by SARS-CoV-2. Consequently, exposure to high level of pollutants potentiates SARS-CoV-2 effect resulting in increased risk, incidence, severity, and lethality with uncertain level of evidence related multiorgan sequelae. On the other hand, COVID-19 pandemic has resulted into a lockdown which has clearly improved the level of anthropogenic pollutants. Not such benefice is expected for household burning solid biomass fuel for domestic energy or containing a smoker as strict lockdown has resulted on the increased exposure-time. Abbreviations: SARS-CoV-2: severe acute respiratory syndrome coronavirus; PM2.5 (or 10): particulate matter of less than 2.5 (or 10) micrometers in diameter, NO2: nitrogen dioxide; O3: ozone; SO2: sulfur dioxide; TRAP: traffic related air pollution; HAP: household air pollution; ACE-2: angiotensin-converting enzyme 2 ARI: acute respiratory infection; COPD: chronic obstructive pulmonary diseases; HPT: hypertension; BMI: body mass index; CFR: case fatality rate; MR: mortality rate