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Environmental determinants of cardiovascular disease: lessons learned from air pollution

Abstract

Air pollution is well recognized as a major risk factor for chronic non-communicable diseases and has been estimated to contribute more to global morbidity and mortality than all other known environmental risk factors combined. Although air pollution contains a heterogeneous mixture of gases, the most robust evidence for detrimental effects on health is for fine particulate matter (particles ≤2.5 µm in diameter (PM2.5)) and ozone gas and, therefore, these species have been the main focus of environmental health research and regulatory standards. The evidence to date supports a strong link between the risk of cardiovascular events and all-cause mortality with PM2.5 across a range of exposure levels, including to levels below current regulatory standards, with no ‘safe’ lower exposure levels at the population level. In this comprehensive Review, the empirical evidence supporting the effects of air pollution on cardiovascular health are examined, potential mechanisms that lead to increased cardiovascular risk are described, and measures to reduce this risk and identify key gaps in our knowledge that could help address the increasing cardiovascular morbidity and mortality associated with air pollution are discussed.

Key points

  • Air pollution is the most important environmental cardiovascular risk factor, with fine particulate matter (PM2.5) and ozone gas being the most-studied air pollutants.

  • The health effects of air pollution might depend on chronic exposure, pre-existing medical conditions and sources or composition of the pollutants.

  • Multiple primary initiating and secondary effector mechanisms are responsible for the cardiovascular effects of air pollution.

  • Numerous animal and human studies have shown that inhalation of PM2.5 pollution can contribute to cardiovascular disease and mortality.

  • The most widely studied personalized approaches to reducing the cardiovascular risk of air pollution include the use of face masks and in-home air purifiers.

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Fig. 1: Composition of particulate matter.
Fig. 2: Association between PM2.5 levels and ischaemic heart disease and stroke mortality.
Fig. 3: Mechanisms of air pollution-related cardiovascular disease.
Fig. 4: Personalized measures to reduce exposure to air pollution.

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Acknowledgements

The authors were funded by the NIH grants 5R01ES019616 (S.R. and R.D.B.), 1R01ES026291 (S.R.) and U01ES026721 (S.B. and S.R.).

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Glossary

Ozone gas

An inorganic molecule composed of three atoms of oxygen, which mainly exists in the Earth’s stratosphere (ozone layer) and troposphere (low-level ozone).

Primary particulates

Particulates that are directly released into the atmosphere by the source (such as combustion).

Secondary particulates

Particulates that form in the atmosphere from primary gases (such as oxidation of nitrogen into nitric acid).

Primary combustion

The release of unburned combustible gases from wood burning with heat, as opposed to secondary combustion, which involves gases that react secondarily (oxidize) to form other pollutants.

Atmospheric stability

The measure of atmospheric resistance to vertical motion, which determines the movement of air and storm formation.

Integrated Exposure–Response

(IER). A meta-analytical approach integrating data from studies of ambient air pollution, second-hand smoking, household pollution and active smoking to estimate the shape of the association between air pollution and mortality.

Disability-adjusted life years

(DALYs). Number of years alive, adjusted for disability, which estimates the burden of life years lost to the disease.

Anthropogenic emissions

Emissions originating from human activity, such as burning of fossil fuels for cooking, mining and manufacturing.

Global Exposure Mortality Model

(GEMM). An integrated approach including only ambient air pollution studies to define the shape of the association between air pollution and mortality.

Harvesting effect

(Also known as mortality displacement). The hypothesis that excess deaths that occur after an environmental trigger (such as air pollution) would have occurred in the short term, regardless of the presence of the trigger.

Frustrated phagocytosis

Occurs when phagocytic cells do not internalize the target, resulting in its release into the environment.

Intratracheal instillation

Direct inoculation of a substance into the trachea.

Ankle–brachial index

A non-invasive marker of the presence of peripheral arterial disease, estimated using the ratio of lower-extremity to upper-extremity blood pressure.

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Al-Kindi, S.G., Brook, R.D., Biswal, S. et al. Environmental determinants of cardiovascular disease: lessons learned from air pollution. Nat Rev Cardiol 17, 656–672 (2020). https://doi.org/10.1038/s41569-020-0371-2

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