The pulmonary epithelium, like most aerial biosurfaces, is naturally protected against atmospheric ozone (O(3)) by fluid films that contain ascorbic acid (AH(2)) and related scavengers. This mechanism of protection will fail, however, if specific copollutants redirect AH(2) and O(3)(g) to produce species that can transduce oxidative damage to underlying tissues. Here, the possibility that the synergistic adverse health effects of atmospheric O(3)(g) and acidic particulate matter revealed by epidemiological studies could be mediated by hitherto unidentified species is investigated by electrospray mass spectrometry of aqueous AH(2) droplets exposed to O(3)(g). The products of AH(2) ozonolysis at the relevant air-water interface shift from the innocuous dehydroascorbic acid at biological pH to a C(4)-hydroxy acid plus a previously unreported ascorbate ozonide (m/z = 223) below pH approximately 5. The structure of this ozonide is confirmed by tandem mass spectrometry and its mechanism of formation delineated by kinetic studies. Present results imply enhanced production of a persistent ozonide in airway-lining fluids acidified by preexisting pathologies or inhaled particulate matter. Ozonides are known to generate cytotoxic free radicals in vivo and can, therefore, transduce oxidative damage.