Key result
Air pollution exposure is linked to increased CV morbidity and mortality, driven by pro-inflammatory pathways.
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Air pollution contributes to cardiovascular morbidity and mortality via systemic inflammation, oxidative stress, and direct effects of translocated ultrafine particles on the heart and vasculature.
Recent epidemiologic studies show that increased levels of air pollutants are positively associated with cardiovascular morbidity and mortality. Inhalation of air pollutants affects heart rate, heart rate variability, blood pressure, vascular tone, blood coagulability, and the progression of atherosclerosis. Several categories within the general population (i.e., people with pre-existing cardiovascular disease and diabetic and elderly individuals) are considered to be more susceptible to air pollution-mediated cardiovascular effects. Major mechanisms of inhalation-mediated cardiovascular toxicity include activation of pro-inflammatory pathways and generation of reactive oxygen species. Although most studies focus on the influence of systemic effects, recent studies indicate that ultrafine particles may be translocated into the circulation and directly transported to the vasculature and heart where they can induce cardiac arrhythmias and decrease cardiac contractility and coronary flow.
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Simkhovich et al. (2008) conducted a review in Cardiovascular injury. Air pollution was evaluated. Air pollution exposure is positively associated with cardiovascular morbidity and mortality, driven by pro-inflammatory pathways, reactive oxygen species, and direct vascular translocation of particles.
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