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Urban atmospheric air pollution is considered a significant challenge for environmental Health (Brunekreef & Holgate, 2002; World Health Organization [WHO], 2003). Growing epidemiological evidence has supported the association between air pollution and cardiovascular morbidity and mortality (Brook et al., 2010). The biological mechanisms underlying these associations remain obscure (Kaufman 2010). One possible explanation to this association is that air pollution has been shown to cause pulmonary inflammation which is further associated with the production of local inflammatory mediators (Nurkiewicz et al., 2008; Nurkiewicz et al., 2009; Kido et al., 2011). These mediators in turn enter the systemic circulation and could contribute to the acceleration of atherothrombotic disease (Seaton et al., 1999; Ghio et al., 2000; Peters et al., 2001b; van Eeden & Hogg, 2002; Pope et al., 2004). Animal models of accelerated atherosclerosis following exposure to air pollution, strongly support this potential mechanism (Sun et al., 2005; Niwa et al., 2008). Low grade systemic inflammation has repeatedly been shown to be a contributing factor in the etiopathogenesis of atherothrombotic disease (Libby 2002; Danesh et al., 2005; Libby, 2006). A hint to the link between air pollution and systemic inflammation arises from studies demonstrating some type of correlation between inflammatory biomarkers, and the amount of outdoor atmospheric particles and volatile gases (Schwartz, 2001; Ghio et al., 2003; Liao et al., 2005; Diez Roux et al., 2006; Steinvil et al., 2008). Exposure to combustion-derived air pollution is associated as well to an early (1-2 h) and sustained (24 h) rise in cardiovascular morbidity and mortality (Peters et al., 2001a; Peters et al., 2004). Toxicological diesel exposure studies have demonstrated a selective and persistent impairment of endothelium-dependent vasodilatation that occurs in the presence of mild systemic inflammation (Mills et al., 2007; Tornqvist et al., 2007), coronary vasoconstriction (Cherng et al., 2009), as well as an increase in ex-vivo thrombus formation and invivo platelet activation (Lucking et al., 2008). Less attention has however been given to measuring pollutants and exposures near heavily-trafficked highways. The most widely reported pollutants in vehicular exhaust include carbon monoxide, nitrogen and sulfur oxides, unburned hydrocarbons (from fuel and crankcase oil), particulate matter, polycyclic aromatic hydrocarbons, and other organic compounds that derive from combustion (Brugge

Effect of Short-Term Exposure to Near Highway Pollutants in Motor Vehicle Exhaust on Inflammation Sensitive Biomarkers