Pulmonary generation of inflammatory stimuli that affect the systemic vasculature. Ozone exposure causes airway epithelial injury, induces oxidation reactions in airway lining fluid, and causes alveolar macrophage activation. Components of this inflammatory milieu gain access to the arterial circulation and can potentially consume low-molecular-weight antioxidants, induce low-density lipoprotein oxidation and modification following reaction with aldehydic products of lipid oxidation, and, finally, monocyte and neutrophil activation. This cascade of pulmonary-initiated systemic vascular events can lead to atherosclerotic plaque formation.

Photochemically induced ground level ozone generation. UV radiation from the sun induces homolytic cleavage of the primary pollutant nitrogen dioxide (·NO₂), forming nitric oxide (·NO) and atomic oxygen (O·) that undergoes reaction with molecular oxygen (O₂) to produce ozone (O₃).