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.

Conflict of interest statement

Competing interests

The authors declare no competing interests.

Figures

Fig. 1 |. Composition of particulate matter.

Primary aerosols include metals and other elements, whereas secondary aerosols result from the chemical conversion of gases to aerosols. Emerging evidence suggests that these components of particulate matter might have varying health effects. VOC, volatile organic compound. Reprinted with permission from REF, Urban Emissions.

Fig. 2 |. Association between PM2.5 levels and ischaemic heart disease and stroke mortality.

The relationships between fine particulate matter (PM2.5) and death from ischaemic heart disease or stroke were determined using the Integrated Exposure-Response (IER) and the Global Exposure Mortality Model (GEMM) methods. Adapted with permission from authors REF, EHP, and REF, PNAS.

Fig. 3 |. Mechanisms of air pollution-related cardiovascular disease.

Numerous molecular and physiological mechanisms mediate the effects of air pollution on the cardiovascular system. These mechanisms result in various interlinked cardiovascular manifestations, including atherosclerosis, vascular dysfunction and endothelial damage. HPA, hypothalamic-pituitary-adrenal.

Fig. 4 |. Personalized measures to reduce exposure to air pollution.

Personal face masks and home air-filtration systems are effective in decreasing exposure to air pollution. Behavioural changes (such as avoidance of polluted environments and staying indoors) can be adopted particularly during times of acutely worsened air quality. Exercise and certain dietary supplements (such as fish oil) might counteract the effects of air pollution on the cardiovascular system.