ABSTRACT
The major target of ambient particulate air pollution is the lung. The lung is the portal of entry for any particulate matter (PM). The relation between increased concentrations of particulate air pollution and adverse health effects in general, as well as in sensitized subjects such as children, the elderly, and diseased people in particular, is documented well and in great detail (Brunekreef and Holgate 2002; Gehr et al. 2009; Latzin et al. 2009; Pope et al. 2009; Perez et al. 2010). Many experimental studies have thus far been performed to investigate how PM can enter the body, organs, tissues, and cells, to determine what effect they may have (Gehr et al. 2009). It is not surprising that it is the lung as an organ, the lung tissue, and lung cells that have been studied with preference to nd out why particles can have adverse health effects. In contrast to ne (i.e., micron-sized) particles that are taken up by cells by phagocytosis, nanosized particles (NPs; i.e., particles ≤0.1 μm in diameter) enter cells through an active endocytotic pathway or through a passive mechanism called adhesive interaction (Rothen-Rutishauser et al. 2007b; Wang et al. 2012). Evidence is growing that it is the nanosized fraction of PM that might be considered a particular health risk, on the one hand because of its high content of organic compounds and its pro-oxidative potential due to the high surface-to-volume ratio of the particles as compared with its bulk material (Peters et al. 1997; Oberdörster et al. 2005) and, on the other hand, because NPs could penetrate through tissues and cells and translocate in the lung periphery into capillary blood (Gehr et al. 1990; Schürch et al. 1990; Rothen-Rutishauser et al. 2007b). NPs could then be transported to all organs (Kreyling et al. 2002; Semmler et al. 2004). Many reports have shown that the main cellular effect of exposure to combustion-derived NPs is the production of reactive oxygen species (ROS) causing oxidative stress, which is a major factor in cellular inammatory reaction and toxicity (Donaldson et al. 2001; Brook et al. 2003).
