In addition to inducing oxidative stress in human aortic endothelial cells3, UFP exposure reduces anti-oxidant capacity of plasma high-density lipoprotein (HDL) and increases oxidative lipid metabolism to accelerate atherosclerosis in low-density lipoprotein (LDL) receptor-knockout (Ldlr−/−) mice4, 5. This evidence concerns the gene LDLR and atherosclerosis.