Exposure to DEPs is an environmental and occupational health concern, and epidemiological, clinical and toxicological data indicate that exposure to DEPs induces both hypersensitive disease and cancer. Considering the fact that hypersensitive disease and cancer involve different immune responses, we investigated the relationship between the physicochemical properties of DEPs and the biological responses induced by DEP exposure. DEPs are composed of a carbonaceous core with adsorbed organic compounds, sulfates, and trace elements. Soluble organic compounds, including PAHs, can represent up to 60% of the mass of the particle. The main targets of DEPs introduced into the body via the bronchial tubes are immune cells in the BAL fluid and airway epithelial cells. The human epithelium contains several types of polarized cells with specific functions. The permeability of a molecule depends mainly on its electric charge of the molecule and to a lesser extent on its molar mass. Therefore, neutrally charged, small particles may pass the cell membrane more easily than charged, large ones. The total cells in BAL fluid increased at all times tested, indicating that DEPs did not induce apoptosis or necrosis. The rapid increase in the burden of hypersensitive disease has undeniably occurred in parallel with rapid industrialization and urbanization in many parts of the world. Several studies have shown that DEPs act as adjuvants to CYT387 allergens and hence increase the sensitization response. Furthermore, Ma and Ma reported that the organic component of DEPs may skew the immunity toward a Th2 response, whereas the particulate component of DEPs may stimulate both the Th1 and Th2 responses. In this study, DEP exposure was found to cause an obvious increase in the TNF-a levels in the BAL fluid to 4.1-fold that in the control, with a marked increase in CD8+ T-cell distribution on day 1 after treatment, but induced B-cell dominance with rapid recovery of the ratio of CD4+/CD8+ T cells on day 7. In addition, on day 7, the concentrations of IL-1, IL-6, and IL-5 in the blood were 4.1-, 12.8-, and 5.2-fold that in the control, respectively, whereas the IL-12 concentration in the BAL fluid increased to 10.4-fold that in the control. Considering the fact that the cellular response in the blood stream was caused by exposure to DEPs engulfed by immune cells, we suggest that the changes observed from day 1, i.e., Th1-type inflammatory response and CD8+ T-cell dominance, may have been effected by the surface charge and surface chemicals, and those from day 7, i.e., Th2-type inflammatory response, may be attributed to the release of the soluble chemical components of DEPs engulfed into immune cells. Our suggestions are supported by the rapid decrease in the levels of IL-12 and the rapid increase in the levels of IL-10 and IL-17 in the BAL fluid after complete phagocytosis of DEPs by immune cells in the BAL fluid on day 28. However, there is a possibility that other cells in the lung including epithelial cells will also release some cytokines and measurement in BAL fluid cannot differentiate them from immune cells.