| Particulate matter (PM) | Cardiac inflammatory mediators | Effect | Reference |
| PM2.5 | IL-1β, IL-8, IL-12, TNF-α, CRP, COX | Decrease cell viability and increase inflammatory mediators | [79] | | TNF-α | Increase inflammation and blood coagulation markers | [80] | | CD4+, CD8+, CD14+ and CD16+, IL-6, IL-1β, MCP-1, MIP-1α/β, TNF-α | Increased endothelial cell apoptosis, proinflammatory cytokines, and antiangiogenic activity contribute to pathogenic atherogenesis and acute coronary events | [82] | | TRAF6, NF-κB | Increased reactive oxygen species (ROS), increased cardiomyocyte apoptosis, stimulated inflammatory cell infiltration, and enhanced inflammatory factors in AC16 cells and heart tissue | [55] | | EDN1, F3, IL-1, IL-6, TNF, TLR2 | Involved in systemic inflammation, coagulation, and vasoconstriction | [7] | Smaller PM size | IL-1β, IL-6, TNF-α | Increase inflammation marker | [81] | PM10 | CD14 and TLR4 | Inverse association of DNA methylation of inflammatory genes in overweight and obese patients | [78] | | TNF-α | Increase inflammation and blood coagulation markers | [80] | Ultrafine particle | 3-NT, CCXL2, EPGN, EREG, FOSL1, GREM1, HES1, IL-1α, IL-1β, IL-6, IL-24, NFE2L2, MAFF, MCP-1, p47phox, TGIF1, VEGF | Biological dysregulation in atherosclerosis, increase inflammation | [19]; [63]) | Black carbon (BC) | F3, ICAM-1 | Inflammation and thrombosis | [76] | Polycyclic aromatic hydrocarbons (PAHs) | IL-1β, IL-6, IL-10, TNF-α, IFN-γ, and hs-CRP | Inflammation and atherogenesis | [77] |
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