Pollution as an individual and collective cardiovascular risk factor

“One must be a sea, to receive a polluted stream without becoming impure” Friedrich Nietzsche

A key foundation of modern cardiovascular practice is the concept of cardiovascular risk factor, which can be operatively defined as a condition which increases the likelihood of subsequent cardiovascular disease, even if not always representing a disease by itself.(1) Indeed, while diabetes mellitus is both a disease and a cardiovascular risk factor, defining arterial hypertension might be more debatable. Of course, family history of premature atherothrombosis can only be considered a risk factor. Despite these premises, we still focus mainly on individual risk factors, which may have limited impact given their relative rarity.

Modern cardiovascular epidemiology sees risk factors in a continuum of individual and collective effects which may be irreversible or sanctionable, also at individual level, collective level, or both.(2) Climate and weather have long been shown to be important factors for adverse cardiovascular outcomes, including death, myocardial infarction, and stroke.(3-5) While the effects are typically relatively limited to short term, persisting untoward effects also apply. In particular, extreme heat, extreme cold, and sudden changes in temperature and humidity may all have adverse cardiovascular effects, and lead to fatal as well as non-fatal outcomes.(6)

Another important piece of the puzzle is pollution, which is indeed becoming a major global threat to health and prosperity.(2) Indeed, pollutants are evidently best viewed as collective risk factors, sanctionable at collective level first, but important also at the individual level. Indeed, individuals can support politicians and decision makers and foster greener development and economic models. Most importantly, we could factor changes in pollutants as determinants in individualised risk scores. Another simple way to tame cardiovascular effects of pollutants is to enforce traffic bans.(7)

In general terms, all pollutants may have detrimental effects.(1) However, some pollutants may have a more damaging impact, and some may exert mainly short-term effects. Particulate matter, and in particular particulate matter with a diameter equal or less than 2.5 µm (PM2.5), is a major pollutant, with short-term as well as long-term adverse effects.(8-9) Indeed, it may lead to increases in blood pressure and vasoconstriction, but also promote low-grade chronic inflammation as well as platelet reactivity. It is crucial indeed to recognise, as highlighted in the current issue of the European Journal of Preventive Cardiology by Ishii et al, that even a few days of exposure to increased levels of pollutants may lead to an excess of adverse cardiovascular events, such as myocardial infarction.(10) The work reported by the JROAD Investigators is particularly important as it shows that pollution increases the risk of atherosclerotic myocardial infarction, but also infarction associated with non-significant coronary artery disease. Furthermore, this Japanese epidemiologic study highlights the fact that the most appropriate lag to gauge the adverse effects of pollution for this event is between two and four days. Intriguingly, PM2.5 seems the most detrimental pollutant, even adjusting for individual and weather characteristics. Finally, dose-effect analysis suggests that myocardial infarction with non-obstructive coronary arteries (MINOCA) may be associated with pollutant levels at a lower dose that atherothrombotic myocardial infarction.

In conclusion, notwithstanding the limitations of epidemiologic research and the need for additional studies, we must bear in mind that pollution should be considered a major cardiovascular risk factor.