Subacute episodic exposure to environmental levels of atmospheric particulate matter provokes subcellular disequilibrium instead of histological vascular damage

Hazardous impacts of subacute exposure to atmospheric particulate matter (PM) on the vascular system are not fully understood. Much emphasis has been put on apparent pathological alterations previously, but early checkpoints were scarcely centralized in the course of cardiovascular disequilibria, such as the cellular or/and subcellular visions. In the current study, a tertiary assessment was implemented, including aortic tissues, vascular cells and subcellular equilibrium. As a result, subacute PM aspiration exerted negligible effects on lipids deposition of vascular walls. However, adverse effects were determined at the cellular and subcellular levels, such as endothelial monolayer disintegration and organelle dysfunction. Specifically, endoplasmic reticulum (ER) stress and mitochondrial malfunction were provoked by PM stimulus. Furthermore, correlation analysis suggested a strong association between aortic ox-inflammatory cascade and vascular subcellular disequilibrium. Altogether, subcellular, cellular and histological levels were assessed to gain a comprehensive understanding of vascular toxicity by realistic concentrations of PM, from which even in the absence of pathological changes, vascular endothelial cells and subcellular structures were predominantly damaged. In particulate toxicology, the necessity of early checkpoints needs to be further strengthened.