Several plausible mechanisms have been proposed to explain the adverse health effects of particulate matter (PM) in polluted ambient air [1]. To date, experimental support has been provided for the role of local and systemic inflammation, cytokine and chemokine production, increased bone marrow production of myeloid lineage cells, free oxygen radical production in the chest, endotoxin-mediated cellular and tissue responses, stimulation of irritant receptors, and covalent modification of key cellular enzymes [1, 2]. Best characterized in humans are the effects of PM on airway inflammation [3]. Several human and animal studies have shown that inhalation of diesel exhaust particles (DEP), a model particulate pollutant, and concentrated ambient particles elicit proinflammatory effects, cytokine production, and enhancement of allergic responses in the upper and lower airways [2–4]. The mechanistic link between the PM exposure and inflammation depends