For example, the human exposure study revealed that diesel exhaust, a model of traffic-related air pollution (TRAP), significantly altered 342 plasma proteins—particularly fractalkine (CX3CL1), apolipoproteins (APOB, APOM), IL18R1, MIP-3 (CCL23), and MMP-12—implicating inflammatory pathways (IL-6/IL-18 signaling) and lipid metabolism (APOB-mediated atherosclerosis) in TRAP-induced cardiovascular disease [48]. This evidence concerns the gene CCL23 and atherosclerosis.