“…These multifactorial characteristics make difficult to underline the exact mechanism of PM-induced respiratory adverse effects. However, several in vitro studies have suggested different cell mechanisms associated to certain PM constituents such as: 1) bacterial ENX may be responsible for the inflammatory response due to the activation of Toll-like receptor-4 (TLR4) and transcription factors (e.g., NF-kB) and the release of pro-inflammatory cytokines (e.g., IL-6 and IL-8); 2) TMET [e.g., aluminum (Al), arsenic (As), iron (Fe), cadmium (Cd), copper (Cu), nickel (Ni), mercury (Hg), lead (Pb) and vanadium (V)] may cause cellular lipids, proteins and DNA damage, mutagenicity and carcinogenicity by generating reactive oxygen species (ROS); 3) PAH may cause oxidative stress, aberrant changes in cell cycling, gene expression and DNA functions by generating toxic metabolites due to the activation of aryl hydrocarbon (Ah) receptors and induction of Phase I and II metabolizing enzymes; and 4) air pollutants such as nitro-, sulfurand oxygen-elements (e.g., NO 2 , SO 2 , H 2 S, O 3 ) may cause lung epithelial cell damage, oxidative cellular stress and carcinogenicity [3, 25-26,29,34,37-47]. Based on these and other published studies (Aust et al, 2002; Wang et al, 2013), inflammatory injury and oxidative damage are considered as common mechanisms of PM-induced health adverse effects.…”