Respiratory exposure to PM, including DEP, causes airway epithelial cell damage according to deposits on bronchial epithelium and induces toxicity effects on airways and lung disease through releasing various cytokines including IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-6, IL-11, TNF-α, regulated on activated, normal T cell expressed and secreted (RANTES), intercellular cell adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin [40,41]. The gene discussed is IL1B; the disease is lung disorder.