A critical role of ROS in mediating the effects of PM2.5 is supported by our observations that CAP exposure increased the levels of antioxidant enzymes, such as ecSOD, in the lungs and that PM2.5-induced vascular insulin resistance was prevented by TEMPOL, which catalyzes the disproportionation of superoxide (Krishna et al. 1996). The gene discussed is SOD3; the disease is Insulin resistance.