The Role of Metal Components in the Cardiovascular Effects of PM2.5

Exposure to ambient fine particulate matter (PM2.5) increases risks for cardiovascular disorders (CVD). However, themechanisms  and  components  responsible  for  the  effects  are  poorly  understood.  Based  on  our  previous  murineexposure studies, a translational pilot study was conducted in female residents of Jinchang and Zhangye, China, totest the hypothesis that specific chemical component of PM2.5 is responsible for PM2.5 associated CVD. Daily ambientand personal exposures to PM2.5 and 35 elements were measured in the two cities. A total of 60 healthy nonsmokingadult  women  residents  were  recruited  for  measurements  of  inflammation  biomarkers.  In  addition,  circulatingendothelial  progenitor  cells  (CEPCs)  were  also  measured  in  20  subjects.  The  ambient  levels  of  PM2.5  werecomparable  between  Jinchang  and  Zhangye  (47.4  and  54.5μg/m3,  respectively).  However,  the  levels  of  nickel,copper, arsenic, and selenium in Jinchang were 82, 26, 12, and 6 fold higher than Zhangye, respectively. The levelsof  C-reactive  protein  (3.44±3.46  vs.  1.55±1.13),  interleukin-6  (1.65±1.17  vs.  1.09±0.60),  and  vascular  endothelialgrowth  factor  (117.6±217.0  vs.  22.7±21.3)  were  significantly  higher  in  Jinchang.  Furthermore,  all  phenotypes  ofCEPCs were significantly lower in subjects recruited from Jinchang than those from Zhangye. These results suggestthat specific metals may be important components responsible for PM2.5-induced cardiovascular effects and that thereduced capacity of endothelial repair may play a critical role.