Full Title: Cutaneous Responses to Tropospheric Ozone Exposure
Journal: Textbook of Aging Skin
Year of Publication: 2017
Publication Author(s): Giuseppe Valacchi
Living organisms are continuously exposed to environmental pollutants. Depending on their state, pollutants can be taken up by ingestion, inhalation, or contact with the skin. Because the skin is an interface between the body and the environment, it is chronically exposed to several forms of stress such as ultraviolet (UV) radiation and other environmental oxidants such as cigarette smoke and ozone (O3). UVB and, to a lesser degree, UVA induce various skin pathological conditions, including erythema, edema, hyperplasia, “sunburn cell” formation, photoaging, and photocarcinogenesis. There is abundant information that reactive oxygen species (ROS) such as hydroxyl radicals are involved in UV-induced skin damage, both by direct effects of UV and by subsequent phagocyte infiltration and activation. Oxidative environmental pollutants, such as cigarette smoke, O3, and oxides of nitrogen that have been studied in the respiratory tract (Kelly et al. Eur Respir J Suppl 40:70s–5, 2003), also represent a potential oxidant stress to the skin. In order of importance, the skin is the second most frequent route by which chemicals can enter into the body. The skin is the major target of liquid and gaseous pollutants, and the pollutant that reacts most specifically with the cutaneous tissues, besides UV radiation, hydrocarbon, and organic compounds, is O3. Ozone represents one of the major oxidants in photochemical smog, levels being highest in heavily polluted areas where exposure to UV is also high. In the last decade, many studies have shown the toxic effect of O3 on the skin (Valacchi et al. Biochem Biophys Res Commun 305:741–6, 2003; Valacchi et al. Br J Dermatol 153:1096–100, 2005), and more recently a clear correlation between O3 exposure and the development of skin pathologies has been demonstrated (Xu et al. Br J Dermatol 165:224–5, 2011).