title: The Cellular Toxicity of PM2.5 Emitted from Coal Combustion in Human Umbilical Vein Endothelial Cells.
abstract: OBJECTIVE
  To explore the relationship between different components of fine particulate matter (PM2.5) emitted from coal combustion and their cytotoxic effect in the vascular endothelial cells.
  
  
  METHODS
  Coal-fired PM(2.5) was 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 PM(2.5) suspension was extracted using an ultrasonic water-bath method and then human umbilical vein endothelial cells (EA.hy926) were treated with various concentrations of the PM(2.5) suspension. Cell proliferation, oxidative DNA damage, and global DNA methylation levels were used to measure the cellular toxicity of PM(2.5) emitted from coal combustion.
  
  
  RESULTS
  Compared to other types of coal-fired PM(2.5) preparations, the PM2.5 suspension from Yinchuan coal had the highest cytotoxicity. PM(2.5) suspension from Datong coal had the highest toxic effect while that from Yinchuan coal had the lowest. Exposure to coal-fired PM(2.5) from Jingxi coal resulted in lower 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. At the same dose, PM(2.5) emitted from coal combustion could produce more severe DNA impairment compared to that produced by carbon black. Cell survival rate was negatively correlated with chloride and potassium ions content. The 5-methylcytosine (5-mC) level was positively correlated with Mn and negatively correlated with Zn levels. The 8 OHdG% level was positively correlated with both Mn and Fe.
  
  
  CONCLUSIONS
  PM(2.5) emitted from coal combustion can decrease cell viability, increase global DNA methylation, and cause oxidative DNA damage in EA.hy926 cells. Metal components may be important factors that influence cellular toxicity.
authors.affiliation: Department of Toxicology, School of Public Health, Peking University, Beijing 100191, China; State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China.
authors.forename: Fei Fei
authors.initials: FF
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China.
authors.forename: Chun Mei
authors.initials: CM
authors.lastname: Geng
authors.affiliation: Department of Toxicology, School of Public Health, Peking University, Beijing 100191, China.
authors.forename: Wei Dong
authors.initials: WD
authors.lastname: Hao
authors.affiliation: State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China; Department of Toxicology, Baotou Medical College of Public Health, Baotou 014040, Inner Mongolia, China.
authors.forename: Yong Dong
authors.initials: YD
authors.lastname: Zhao
authors.affiliation: State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Li
authors.affiliation: State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China.
authors.forename: Hong Mei
authors.initials: HM
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Qian
mesh_terms: D049109:Cell Proliferation; D060729:Coal Ash / Q000633:toxicity*; D004249:DNA Damage; D019175:DNA Methylation; D061307:Human Umbilical Vein Endothelial Cells; D018675:Toxicity Tests
chemical_list: D060729:Coal Ash
keywords: Coal combustion; Cytotoxicity; DNA methylation; PM2.5; Vascular endothelial cell