Environmental Fe, Ti, Al, Cu, Hg, Bi, and Si Nanoparticles in the Atrioventricular Conduction Axis and the Associated Ultrastructural Damage in Young Urbanites: Cardiac Arrhythmias Caused by Anthropogenic, Industrial, E-Waste, and Indoor Nanoparticles.
Lilian Calderón-GarcidueñasAngélica González-MacielRafael Reynoso-RoblesJosé Luis Rodríguez-LópezHector G Silva-PereyraGladis J Labrada-DelgadoBeatriz Pérez-GuilléRosa Eugenia Soriano-RosalesMiguel Angel Jiménez-Bravo LunaRafael Brito-AguilarPartha S MukherjeeCarlos Gayosso-ChávezRicardo Delgado-ChávezPublished in: Environmental science & technology (2021)
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.
Keyphrases
- air pollution
- electron microscopy
- catheter ablation
- oxide nanoparticles
- heavy metals
- left ventricular
- aqueous solution
- atrial fibrillation
- life cycle
- heart failure
- human health
- particulate matter
- congenital heart disease
- wastewater treatment
- metal organic framework
- oxidative stress
- single molecule
- cell death
- emergency department
- high resolution
- cell cycle arrest
- induced apoptosis
- single cell
- lung function
- cell proliferation
- magnetic resonance imaging
- left atrial
- ionic liquid
- room temperature
- risk assessment
- walled carbon nanotubes
- stem cells
- solid phase extraction
- mesenchymal stem cells
- quantum dots
- simultaneous determination
- pi k akt
- dual energy
- label free
- adverse drug
- mitral valve
- loop mediated isothermal amplification