The impact of air pollution on atherosclerotic cardiovascular disease development

Br J Cardiol 2024;31(2)doi:10.5837/bjc.2024.013 Leave a comment
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First published online 16th April 2024

Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death worldwide, causing around 17.9 million deaths annually, a third of whom are adults aged <70 years.1 In addition to genetic and behavioural risk factors (unhealthy diet, physical inactivity, and tobacco and alcohol abuse), inhaling airborne pollutants, such as fine particulate matter (<2.5 µm [PM2.5] and <10 µm [PM10]), ultrafine particles (UFPs; <100 nm), nitrogen dioxide (NO2), ozone (O3), and sulphur dioxide (SO2), are associated with ASCVD among adults.2

Air pollution has been referred to as “the single most important environmental factor presenting a risk to health and represents a greater disease burden than polluted water, soil contamination and occupational exposures combined”.3 Air pollution is a silent killer and was highlighted as a significant public health concern in the recently published European Society of Cardiology (ESC) guidelines.4

The impact of urbanisation on air pollution levels is a critical concern for countries like Malta, which have adopted a city model to bolster their economies. Despite efforts to stimulate economic growth, the rise in urbanisation can pose risks to air quality. In London, mean PM2.5 concentrations stood at approximately 12.7 µg/m³ in 2017, 12.0 µg/m³ in 2018, and 11.4 µg/m³ in 2019.5 Conversely, Valletta, Malta’s capital, recorded mean PM2.5 concentrations of about 14 µg/m³ in 2017, 14.4 µg/m³ in 2018, and 14 µg/m³ in 2019.6 While both have seen improvements in their aggregated annual mean PM2.5 concentrations compared with the concentration levels recorded in the past decade, they still exceed the World Health Organisation (WHO) annual air quality guideline value by approximately 1.14 to 1.4 times, highlighting the persistent challenge of air pollution in urban environments.

How much does air pollution contribute to ASCVD development?

A meta-analysis showed that a low and high air pollution concentration contributes to ASCVD among adults; however, the higher the concentration, the higher the risk of irreparable damage, which can exacerbate morbidity and mortality levels.7 This meta-analysis found that heart rate variability decreased for every 10 µg/m3 increase in PM2.5 within both short- and long-term exposure groups, whereas ASCVD risk increased.

In observational studies, which took place in China, Canada, US and South Korea, the hazard ratio (HR) increased significantly in the exposure to different pollutants (UFPs, NO2, PM2.5, PM2.5–10, O3, O3 + NO2 [Ox], and carbon monoxide [CO]), especially in urbanisation and industrialisation zones, meaning an increase in the exposure increases ASCVD risk.8‑11 Liang et al.9 found that for every 10 µg/m3 increase in annual mean PM2.5, the HR increased by 1.251 for ASCVD incidence (p=0.001). Bai et al.11 reported that congestive heart failure incidence increased rapidly per 10.7 parts per billion increase in NO2 exposure (HR=1.06). Furthermore, they found that participants’ exposure to high levels of PM2.5, O3, and Ox was associated with a 5% (p=0.03), 4% (p=0.001), and 3% (p=0.001) increase in acute myocardial infarction risk, respectively.

Another observational study in Australia by Huynh et al.12 recruited adults aged 40–70 years and determined their coronary calcium score (CCS) and the annual air pollutant concentrations at their geo-coded residential address. They found a significant correlation between participants’ CCS scores and exposure levels for PM2.5 (odds ratio [OR] 1.55, 95% confidence interval [CI] 1.05 to 2.29, p=0.01) and NO2 (OR 1.23, 95%CI 1.07 to 1.51, p=0.01) pollutants.

Inhaling these pollutants can lead to inflammation, oxidative stress, and blood vessel damage, all of which can contribute to ASCVD development. Huynh et al.12 found that exposure to a lower level of PM2.5 (4 µg/m3) could still induce oxidative stress and endothelial dysfunction, contributing to ASCVD development.

The importance of governmental policies and regulations to reduce air pollution

The COVID-19 pandemic-induced lockdown measures, imposed worldwide, created cleaner air,13-17 resulting in fewer premature deaths than the average number in previous pre-pandemic years. Governmental policies should focus mainly on regulations aimed at reducing air pollution. Education should focus on action to attenuate the increase in air pollution, such as using active or public transport, shifting to electric scooters and cars, and taking environmentally friendly measures to mitigate the adverse impact of ambient air pollution (AAP). The practical and judicious use of a wide range of media outlets can help health professionals launch a successful nationwide information and consultation campaign highlighting the risks AAP poses to health and life-expectancy, thus stressing the adverse consequences of ASCVD. The UK and the European Union have established action plans to reduce pollution below harmful levels by 2050.18,19 While we acknowledge that these targets will take decades to reach, we will continue to strive for better, cleaner air. In practical terms, reducing the PM2.5 concentration by 10 µg/m3 would prevent 1,557,000 avoidable cases of cardiovascular disease.9 In the European Union, at least 18% of all ASCVD-related deaths are estimated to be due to exposure to air pollution.20

The urgency of addressing air pollution

The steady increase in AAP has grown into a substantial public health issue, resulting in an increasing number of adverse health impacts and ASCVD cases. This editorial has indicated that an individual’s ASCVD risk increases with the air pollution levels to which they are exposed. Alarmingly, there is evidence that even minimal exposure can increase ASCVD risk. Therefore, governments should make concerted efforts to devise and implement more rigorously effective action policies to reduce ambient air pollution more steadily and rapidly, creating cleaner air and promoting future healthier populations.

Conflicts of interest

None declared.

Funding

None.

References

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