Acidity enhances the formation of a persistent ozonide at aqueous ascorbate/ozone gas interfaces

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Abstract
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 ≈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.