Exposure to ambient airborne particulate matter (PM) with an aerodynamic diameter less than 10 μm (PM10 ) links with public health hazards and increases risk for lung cancer and other diseases. Recent studies have suggested that oxidative stress is a key mechanism underlying the toxic effects of exposure to PM10 . Several components of water-soluble fraction of PM10 (sPM10 ) have been known to be capable of inducing oxidative stress in in vitro studies. In this study, we investigated if water-insoluble fraction of PM10 (iPM10 ) could be also capable of inducing oxidative stress and oxidative damage. Human lung epithelial A549 cells were exposed to 10 μg/mL of sPM10 , iPM10 or total PM10 (tPM10 ) preparation for 24 h. Here, we observed that all three PM10 preparations reduced cell viability and induced apoptotic cell death in A549 cells. We further found that, similar to the exposure to sPM10 and tPM10 , the intracellular level of hydrogen peroxide (H2 O2 ) in the iPM10 -exposed cells was increased significantly; meanwhile the activity of catalase was decreased significantly as compared with the unexposed control cells, resulting in significant DNA damage. Our data obtained from inductively coupled plasma-mass spectrometry (ICP-MS) assays showed that iron is the most abundant metal in all three PM10 preparations. Thus, we have demonstrated that, similar to sPM10 , iPM10 is also capable of inducing oxidative stress by probably inducing generation of H2 O2 and impairing enzymatic antioxidant defense, resulting in oxidative DNA damage and even apoptotic cell death through the iron-catalyzed Fenton reaction.
Keywords: DNA damage; PM10; apoptosis; cytotoxicity; lung epithelial cells; oxidative stress.
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