The Cellular Toxicity of PM2.5 Emitted from Coal Combustion in Human Umbilical Vein Endothelial Cells

Key words: 
• PM2.5 /
• Coal combustion /
• Vascular endothelial cell /
• Cytotoxicity /
• DNA methylation

Abstract: ObjectiveTo explore the relationship between different components offineparticulate matter (PM2.5) emitted from coal combustion and their cytotoxic effect in the vascular endothelial cells. MethodsCoal-fired PM2.5was sampled using a fixed-source dilution channel and flow sampler. The sample components were analyzed by ion chromatography and inductively coupled plasma atomic emission spectroscopy(ICP-AES). The PM2.5suspension was extracted using an ultrasonic water-bath method and thenhuman umbilical vein endothelial cells (EA.hy926) were treated withvarious concentrations of the PM2.5 suspension. Cell proliferation,oxidativeDNA damage, and global DNA methylation levelswere used to measurethe cellulartoxicity of PM2.5emitted fromcoalcombustion. ResultsComparedtoothertypesof coal-fired PM2.5preparations,thePM2.5 suspension from Yinchuan coal had the highest cytotoxicity.PM2.5 suspension from Datong coal hadthe highest toxic effectwhile that fromYinchuan coal had the lowest.Exposure to coal-fired PM2.5 from Jingxi coalresulted inlower 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. At the same dose, PM2.5 emitted from coal combustion could produce more severeDNAimpairmentcompared to that produced by carbon black.Cell survival rate was negatively correlated with chloride and potassiumionscontent.The5-methylcytosine(5-mC) level waspositively correlated withMnandnegatively correlated withZn levels.The 8-OHdG% level was positively correlated withboth MnandFe. ConclusionPM2.5 emitted from coal combustion can decrease cell viability, increase global DNA methylation, and causeoxidativeDNA damage inEA.hy926 cells. Metalcomponentsmay be important factors that influence cellular toxicity.