The impact of troposphere ozone (O(3)), the major oxidant in photochemical smog, on the overall wellbeing of skin is of considerable interest. To date, limited information is available on the impact of O(3) on human skin. Using a specially designed O(3) exposure chamber, we provide the first evidence that exposure of human skin to O(3) (0.8 ppm, 2-h time-weighted average) significantly reduced vitamin E by 70% and concomitantly increased lipid hydroperoxides by 2.3 fold in the superficial stratum corneum (SC). Although the dose of O(3) used here reduced the resident microflora population by 50% and created a state of oxidative stress within the SC, it did not affect several key enzymes involved in SC homeostasis including the redox-sensitive transglutaminase and the SC tryptic (KLK5) and chymotryptic (KLK7) proteases. Importantly, no signs of skin dryness or erythema were observed. We hypothesize that the limited effects of low doses of O(3) on SC function is attributable to several factors including: (i) protection provided by the anti-oxidant defence system; (ii) inability of O(3) to penetrate the SC; and (iii) limited water available to catalyse the Criegee reaction. Although chronic exposure to O(3) may produce a different outcome than that reported here, our data suggest that exposure to environmentally relevant doses of O(3), at best, induces a moderate state of oxidative stress, without producing a visible clinical response. In our opinion, exposure of skin to UV radiation is a much more significant threat than exposure to ground-level O(3).
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