Particulate matter and cardiac arrhythmias: From clinical observation to mechanistic insights at cardiac ion channels

Airborne particulate matter (PM) pollution comprises various air-colloidal particles including gases, organic and inorganic particles. Over the past few years, a growing number of studies have shown that PM has a disastrous effect on the human cardiovascular system, particularly in relation to cardiac arrhythmias. However, the mechanisms underlying these observed effects have not yet been clearly defined. In this review, the electronic database PubMed was used as the source of selected peer-reviewed research articles published in English. Both pre-clinical studies and clinical trials were obtained using particulate matter, cardiac arrhythmias, ion channel and cardiomyocytes as keywords. We present evidence pertinent to the potential mechanisms underlying PM-induced cardiac arrhythmias, drawing from results spanning in vitro to clinical studies, with a particular focus on the profile of vulnerable cardiac ion channels. At a cellular level, PM has been shown to up-regulate the expression of myocardial Ca2+ ion channel proteins, increase Ca2+ release from ryanodine 2 (RyR2) and decrease sarcoplasmic reticulum (SR) re-uptake of Ca2+, leading to intracellular Ca2+ overload. Additionally, the disruption of myocardial Ca2+ homeostasis has been shown to aggravate the production of mitochondrial ROS, inflammatory cytokines, and apoptotic cascades, which may potentially contribute to arrhythmic substrates, especially in high-risk patients. The upregulation of genes encoding sodium (Na+) and potassium (K+) channels caused by PM has been implicated in the induction of QT prolongation and alterations in action potentials related to cardiac arrhythmias. Finally, we discuss potential interventions to mitigate PM-induced cardiac pathology and propose future directions for these therapeutic strategies. © 2025 Elsevier Ltd