Air
pollution exposure is a risk factor for arrhythmia. The atrioventricular
(AV) conduction axis is key for the passage of electrical signals
to ventricles. We investigated whether environmental nanoparticles
(NPs) reach the AV axis and whether they are associated with ultrastructural
cell damage. Here, we demonstrate the detection of the shape, size,
and composition of NPs by transmission electron microscopy (TEM) and
energy-dispersive X-ray spectrometry (EDX) in 10 subjects from Metropolitan
Mexico City (MMC) with a mean age of 25.3 ± 5.9 and a 71-year-old
subject without cardiac pathology. We found that in every case, Fe,
Ti, Al, Hg, Cu, Bi, and/or Si spherical or acicular NPs with a mean
size of 36 ± 17 nm were present in the AV axis in situ, freely
and as conglomerates, within the mitochondria, sarcomeres, lysosomes,
lipofuscin, and/or intercalated disks and gap junctions of Purkinje
and transitional cells, telocytes, macrophages, endothelium, and adjacent
atrial and ventricular fibers. Erythrocytes were found to transfer
NPs to the endothelium. Purkinje fibers with increased lysosomal activity
and totally disordered myofilaments and fragmented Z-disks exhibited
NP conglomerates in association with gap junctions and intercalated
disks. AV conduction axis pathology caused by environmental NPs is
a plausible and modifiable risk factor for understanding common arrhythmias
and reentrant tachycardia. Anthropogenic, industrial, e-waste, and
indoor NPs reach pacemaker regions, thereby increasing potential mechanisms
that disrupt the electrical impulse pathways of the heart. The cardiotoxic,
oxidative, and abnormal electric performance effects of NPs in pacemaker
locations warrant extensive research. Cardiac arrhythmias associated
with nanoparticle effects could be preventable.