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

Abstract

The pulmonary epithelium, like most aerial biosurfaces, is naturally protected against atmospheric ozone (O3) by fluid films that contain ascorbic acid (AH2) and related scavengers. This mechanism of protection will fail, however, if specific copollutants redirect AH2 and O3(g) to produce species that can transduce oxidative damage to underlying tissues. Here, the possibility that the synergistic adverse health effects of atmospheric O3(g) and acidic particulate matter revealed by epidemiological studies could be mediated by hitherto unidentified species is investigated by electrospray mass spectrometry of aqueous AH2 droplets exposed to O3(g). The products of AH2 ozonolysis at the relevant air–water interface shift from the innocuous dehydroascorbic acid at biological pH to a C4-hydroxy acid plus a previously unreported ascorbate ozonide (m/z = 223) below pH {approx}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.