Abstract
This skin damage that is a result of pollution is one of the most universal but least considered dermatological health in the contemporary times and the World Health Organization reports that nine in ten people breathe air with pollutant levels high. The presented extensive review follows the molecular continuum of early acneiform lesions to deep wrinkles development after exposure to cutaneous pollutants, and a single mechanistic pathway is formed, based on the aryl hydrocarbon receptor (AhR)-reactive oxygen species (ROS)-inflammation axis. Conserved signaling cascades, such as canonical (CYP1 induction) and non-canonical (c-Src/EGFR), converge upon oxidative stress, matrix metalloproteinase activation, and impaired extracellular matrix synthesis, depending on the airborne presence of particulate matter, polycyclic aromatic hydrocarbons and gaseous pollutants. Importantly, we find a critical lack of literature, namely the lack of a temporospatial model of the relationship between acute pollutant-induced comedogenesis and chronic extracellular matrix degradation. We solve this problem by suggesting the concept of oxinflammatory memory, which is based on temporary pollution exposures that cause irreversible cellular changes in terms of epigenetic changes, mitochondrial dysfunction, and cell senescence. The review concludes with a critical analysis of the clinically-validated interventions, such as the widely-researched CF Mix antioxidant preparation (15% vitamin C, 1% vitamin E, 0.5% ferulic acid) which has shown protection of pollutant-induced barrier disruption and collagen degradation in controlled human studies, and new AhR-modulating agents and laser combination approaches. The combination of the mechanistic knowledge and evidence-based therapeutic approach makes this review offer a roadmap to dermatologists and researchers concerning the prevention and reversal of the cutaneous pathology caused by pollution at the clinical spectrum.