Acute and chronic exposure to air pollution in relation with incidence, prevalence, severity and mortality of COVID-19: a rapid systematic review

Abstract

Background: Air pollution is one of the world's leading mortality risk factors contributing to seven million deaths annually. COVID-19 pandemic has claimed about one million deaths in less than a year. However, it is unclear whether exposure to acute and chronic air pollution influences the COVID-19 epidemiologic curve.

Methods: We searched for relevant studies listed in six electronic databases between December 2019 and September 2020. We applied no language or publication status limits. Studies presented as original articles, studies that assessed risk, incidence, prevalence, or lethality of COVID-19 in relation with exposure to either short-term or long-term exposure to ambient air pollution were included. All patients regardless of age, sex and location diagnosed as having COVID-19 of any severity were taken into consideration. We synthesised results using harvest plots based on effect direction.

Results: Included studies were cross-sectional (n = 10), retrospective cohorts (n = 9), ecological (n = 6 of which two were time-series) and hypothesis (n = 1). Of these studies, 52 and 48% assessed the effect of short-term and long-term pollutant exposure, respectively and one evaluated both. Pollutants mostly studied were PM_2.5 (64%), NO₂ (50%), PM₁₀ (43%) and O₃ (29%) for acute effects and PM_2.5 (85%), NO₂ (39%) and O₃ (23%) then PM₁₀ (15%) for chronic effects. Most assessed COVID-19 outcomes were incidence and mortality rate. Acutely, pollutants independently associated with COVID-19 incidence and mortality were first PM_2.5 then PM₁₀, NO₂ and O₃ (only for incident cases). Chronically, similar relationships were found for PM_2.5 and NO₂. High overall risk of bias judgments (86 and 39% in short-term and long-term exposure studies, respectively) was predominantly due to a failure to adjust aggregated data for important confounders, and to a lesser extent because of a lack of comparative analysis.

Conclusion: The body of evidence indicates that both acute and chronic exposure to air pollution can affect COVID-19 epidemiology. The evidence is unclear for acute exposure due to a higher level of bias in existing studies as compared to moderate evidence with chronic exposure. Public health interventions that help minimize anthropogenic pollutant source and socio-economic injustice/disparities may reduce the planetary threat posed by both COVID-19 and air pollution pandemics.

Keywords: Burden; Lethality; Long-term air pollution; SARS-CoV-2; Short-term; Susceptibility.

Fig. 1

Interplay of Air pollution, Lockdown and SARS-CoV-2: An Epidemiological View. Model built following synthesis of current litterature [, , , –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; PM_2.5 (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

Fig. 2

PRISMA Flow Diagram. Note: One study has assessed both short-term and long-term air pollution

Fig. 3

Risk of bias. Summary of authors’ judgments on each domain for each included study (Panel a) and as percentages across included studies (Panel b). About one quarter of the studies had a low risk of bias

Fig. 4

Harvest plots displaying level of evidence between short-term exposure to air pollution and risk, severity, incidence, and lethality for COVID-19 Pandemic

Fig. 5

Harvest plots displaying level of evidence between long-term exposure to air pollution and risk, severity, incidence, and lethality for COVID-19 Pandemic