Although the exact components of PM and the exact mechanism leading to cardiovascular disease and cardiopulmonary disease mortality from exposure to PM are still unknown, several studies have shown that systemic inflammation may be a key step in these pathological processes through inflammatory mediators (Salvi et al. 1999) such as cyclooxygenase-2 (COX-2), interleukin (IL)-1β, and tumor necrosis factor-α(TNFα), which are among the most important mediators of the inflammatory response (Ross 1999) in the development of atherosclerotic vascular disease (Libby 2002). This evidence concerns the gene PTGS2 and cor pulmonale.