In vitro and in vivo studies have shown that PM can induce pulmonary inflammation, destroy lung function, cause emphysematous changes in PM10, and induce the release of proinflammatory cytokines (e.g., TNF-α and IL-1) and reactive oxygen radicals by alveolar macrophages in patients with COPD [31]. This evidence concerns the gene TNF and chronic obstructive pulmonary disease.