Title:Air Pollution Exposure and Blood Pressure: An Updated Review of the Literature
Volume: 22
Issue: 1
Author(s): Paolo Giorgini, Paolo Di Giosia, Davide Grassi, Melvyn Rubenfire, Robert D. Brook and Claudio Ferri
Affiliation:
Keywords:
Air pollution, particulate matter, blood pressure, hypertension, cardiovascular risk, public health, epidemiology, endothelial
dysfunction.
Abstract: Both high arterial blood pressure (BP) and elevated levels of fine particulate matter (PM2.5) air pollution
have been associated with an increased risk for several cardiovascular (CV) diseases, including stroke, heart failure,
and myocardial infarction. Given that PM2.5 and high BP are each independently leading risk factors for premature
mortality worldwide, a potential relationship between these factors would have tremendous public health repercussions.
Therefore, the aim of this review is to summarize recent evidence linking air pollution and BP. Epidemiological
findings demonstrate that particulate pollutants cause significant increases in BP parameters in relation to
both short and long-term exposures, with robust evidence for exposures to PM2.5. Moreover, recent epidemiological
studies suggest a positive association between residence within regions with higher levels of ambient PM and an
increased incidence and prevalence of overt hypertension. Studies provide consistent results that elevated concentrations of pollutants increase
hospital admissions and/or emergency visits for hypertensive disorders and also support that PM levels increases BP in vulnerable
subsets of individuals (pregnant women, high CV risk individuals). In this context, PM-mediated BP elevations may be an important
pathway which acts as a potential triggering factor for acute CV events. Mechanistic evidence illustrates plausible pathways by which
acute and chronic exposures to air pollutants might disrupt hemodynamic balance favoring vasoconstriction, including autonomic imbalance
and augmented release of various pro-oxidative, inflammatory and/or hemodynamically-active mediators. Together these responses
may underlie PM-induced BP elevations; however, full details regarding the responsible mechanisms require further studies. As a consequence
of the ubiquity of air pollution, even a small effect on raising BP and/or the prevalence of hypertension, i.e. the major risk factor
for mortality and morbidity worldwide, would have enormous global public health implications.
