Air pollution link to some COVID-19 deaths

About 15% of COVID-19 deaths globally could be attributed to long-term exposure to air pollution, a new study claims today.

Cardiovascular Research publishes the findings of the first research to estimate the proportion of deaths from the virus that could be attributed to air pollution for every country in the world.

The research team, which includes academics from Germany, USA, Italy and the UK, estimates that the average global proportion was 15%, but in East Asia it is about 27%, Europe 19% and in North America 17%.

They say these proportions are an estimate of “the fraction of COVID-19 deaths that could be avoided if the population were exposed to lower counterfactual air pollution levels without fossil fuel-related and other anthropogenic emissions.”

They also point out that the study does not imply a direct cause-effect relationship between air pollution and COVID-19 mortality, but refers to relationships between two, such as aggravating co-morbidities.

The study used epidemiological data from previous US and Chinese studies of air pollution and COVID-19 and from the 2003 SARS outbreak, and was supported by additional data from Italy.

The data were combined with satellite data that showed global exposure to PM2.5 particulate matter, information on atmospheric conditions and ground-based pollution monitoring networks, to create a model that could calculate the fraction of coronavirus deaths attributable to long-term exposure to PM2.5.

Professor Jos Lelieveld of the Max Planck Institute for Chemistry, Mainz, Germany, said: "Since the numbers of deaths from COVID-19 are increasing all the time, it’s not possible to give exact or final numbers of COVID-19 deaths per country that can be attributed to air pollution.

“However, as an example, in the UK there have been over 44,000 coronavirus deaths and we estimate that the fraction attributable to air pollution is 14%, meaning that more than 6,100 deaths could be attributed to air pollution."

Professor Thomas Münzel, from the University Medical Centre, of the Johannes Gutenberg University, Mainz, said: “PM2.5 particles migrate from the lungs to the blood and blood vessels, which cause inflammation and severe oxidative stress, leading to damage to the inner lining of arteries, the endothelium, as well as narrowing and stiffening of the arteries. The COVID-19 virus also enters the body via the lungs, causing similar damage to blood vessels, and is considered an endothelial disease.

"If both long-term exposure to air pollution and infection with the COVID-19 virus come together then we have an additive adverse effect on health, particularly with respect to the heart and blood vessels, which leads to greater vulnerability and less resilience to COVID-19,” he said.

“If you already have heart disease, then air pollution and coronavirus infection will cause trouble that can lead to heart attacks, heart failure and stroke.

“Particulate matter seems to increase the activity of a receptor on cell surfaces, called ACE-2, that is known to be involved in the way COVID-19 infects cells. So we have a ‘double hit’: air pollution damages the lungs and increases the activity of ACE-2, which in turn leads to enhanced uptake of the virus by the lungs and probably by the blood vessels and the heart.”

The authors acknowledge some limitations to the research: USA epidemiological data were collected at county level, and not from individuals, which means that it is more difficult to exclude confounding factors; data were collected in middle- to high-income countries; and the calculations were carried out for the whole world, meaning that the results for low-income countries may be less robust.

The results are based on epidemiological data collected up the third week in June 2020 and the researchers say a comprehensive evaluation will need to follow after the pandemic has subsided.

Pozzer A, Dominici F, Haines A et al. Regional and global contributions of air pollution to risk of death from COVID-19. Cardiovascular Research 27 October 2020; doi:10.1093/cvr/cvaa288

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