Summary Air pollution is composed of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide and ozone. PM is classified according to size into coarse particles (PM10), fine particles (PM2.5) and ultrafine particles. We aim to provide an original review of the scientific evidence from epidemiological and experimental studies examining the cardiovascular effects of outdoor air pollution. Pooled epidemiological studies reported that a 10 μg/m3 increase in long-term exposure to PM2.5 was associated with an 11% increase in cardiovascular mortality. Increased cardiovascular mortality was also related to long-term and short-term exposure to nitrogen dioxide. Exposure to air pollution and road traffic was associated with an increased risk of arteriosclerosis, as shown by premature aortic and coronary calcification. Short-term increases in air pollution were associated with an increased risk of myocardial infarction, stroke and acute heart failure. The risk was increased even when pollutant concentrations were below European standards. Reinforcing the evidence from epidemiological studies, numerous experimental studies demonstrated that air pollution promotes a systemic vascular oxidative stress reaction. Radical oxygen species induce endothelial dysfunction, monocyte activation and some proatherogenic changes in lipoproteins, which initiate plaque formation. Furthermore, air pollution favours thrombus formation, because of an increase in coagulation factors and platelet activation. Experimental studies also indicate that some pollutants have more harmful cardiovascular effects, such as combustion-derived PM2.5 and ultrafine particles. Air pollution is a major contributor to cardiovascular diseases. Promotion of safer air quality appears to be a new challenge in cardiovascular disease prevention.

Studies have pointed out that air pollution may be a contributing factor to the coronavirus disease 2019 (COVID-19) pandemic. However, the specific links between air pollution and severe acute respiratory syndrome-coronavirus-2 infection remain unclear. Here we provide evidence from in vitro, animal and human studies from the existing literature. Epidemiological investigations have related various air pollutants to COVID-19 morbidity and mortality at the population level, however, those studies suffer from several limitations. Air pollution may be linked to an increase in COVID-19 severity and lethality through its impact on chronic diseases, such as cardiopulmonary diseases and diabetes. Experimental studies have shown that exposure to air pollution leads to a decreased immune response, thus facilitating viral penetration and replication. Viruses may persist in air through complex interactions with particles and gases depending on: 1) chemical composition; 2) electric charges of particles; and 3) meteorological conditions such as relative humidity, ultraviolet (UV) radiation and temperature. In addition, by reducing UV radiation, air pollutants may promote viral persistence in air and reduce vitamin D synthesis. Further epidemiological studies are needed to better estimate the impact of air pollution on COVID-19. In vitro and in vivo studies are also strongly needed, in particular to more precisely explore the particle–virus interaction in air.

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An integrated exposomic view of the relation between environment and cardiovascular health should consider the effects of both air and non-air related environmental stressors. Cardiovascular impacts of ambient air temperature, indoor and outdoor air pollution were recently reviewed. We aim, in this second part, to address the cardiovascular effects of noise, food pollutants, radiation, and some other emerging environmental factors. Road traffic noise exposure is associated with increased risk of premature arteriosclerosis, coronary artery disease, and stroke. Numerous studies report an increased prevalence of hypertension in people exposed to noise, especially while sleeping. Sleep disturbances generated by nocturnal noise are followed by a neuroendocrine stress response. Some oxidative and inflammatory endothelial reactions are observed during experimental session of noise exposure. Moreover, throughout the alimentation, the cardiovascular system is exposed to persistent organic pollutants (POPs) as dioxins or pesticides, and plastic associated chemicals (PACs), such as bisphenol A. Epidemiological studies show positive associations of exposures to POPs and PACs with diabetes, arteriosclerosis and cardiovascular disease incidence. POPs and PACS share some abilities to interact with nuclear receptors activating different pathways leading to oxidative stress, insulin resistance and angiotensin potentiation. Regarding radiation, survivors of nuclear explosion have an excess risk of cardiovascular disease. Dose-effect relationships remain debated, but an increased cardiovascular risk at low dose of radiation exposure may be of concern. Some emerging environmental factors like electromagnetic fields, greenspace and light exposure may also require further attention. Non-air related environmental stressors also play an important role in the burden of cardiovascular disease. Specific methodologies should be developed to assess the interactions between air and non-air related pollutants.

The aim of this study, is to investigate the effects of a short-term exposure to air pollutants, as assessed by Nitrogen dioxide (NO2), Particulate Matter PM2,5 and PM10 concentrations, on coronary event onsets in Strasbourg, France. An observational, analytical, retrospective, epidemiological study was conducted in Strasbourg between 1 January 2012 and 31 December 2014. Higher daily coronary events rates were evidenced when NO2 concentrations were measured above 40 µg/m3 (1.258 (95% CI 1.142–1.374) vs. 1.110 (95% CI 1.033–1.186); p = 0.015). The NO2 concentration was higher than 30 µg/m3 for 677 days (61.8%). Higher daily coronary events rates were evidenced when NO2 concentrations were measured above 30 µg/m3 (1.208 (95% CI 1.128–1.289) vs. 1.067 (95% CI 0.961–1.172) p = 0.009). A marked seasonality of NO2, PM2.5, and PM10 concentrations characterized by an increase during winter and a decrease during the summer could be established. The seasonality of coronary events was evidenced simultaneously. After adjustments were made to account for the time and the month, no independent impact of NO2, PM2.5 or PM10 on daily coronary events could be demonstrated.