The respiratory tract surface is covered by the ELF. In this example, inhaled ozone (O₃) first dissolves in the ELF aqueous phase, followed by facile reaction with antioxidants (e.g., reduced ascorbate, AH₂, and reduced glutathione, GSH), which can lead to secondary ROS production. Competing reactions between ROS and ELF unsaturated lipids (ULs) produce specific oxidized (ozonation) products. Influences of ELF protein reactions remain undefined. Due to its reactivity, it is unlikely that ozone directly contacts cellular membranes. ROS and lipid autoxidation initiated by decomposition of ozonation products lead to the generation nonspecific oxidized lipids. Secondary oxidants formed in the ELF may drive membrane unsaturated lipid oxidation, which likely contributes to the overall pool of nonspecific oxidation products. Both ROS and oxidized lipids can directly injure epithelial cells and/or initiate signaling cascades that drive PMN influx. Based on the current report from Dahl et al. (10), AM SRAs bind and internalize oxidized lipids, thereby reducing their effects on the lung epithelium. The net result limits the extent of bioactive lipid–induced inflammation. The specifics of scavenger receptor–oxidized lipid recognition and binding affinities, effects of scavenger receptor polymorphism, dispositions of internalized lipids, and composite mechanisms of how scavenger receptor–oxidized lipid binding influence PMN influx and related lung surface perturbations await further characterization.