Introduction: Constantly increasing air pollution (AP) poses a concern negatively affecting our health including the skin. A typical manifestation of the skin damage induced by AP is its premature aging, irritation, skin barrier impairment, pigmentation disorders and development or exacerbation of various skin diseases. For these reasons, it is crucial to protect the skin from the negative effects of AP. In this study we evaluated the ability of some compounds commonly used in dermatological or cosmetic preparations with various biological activities to reduce AP-induced skin damage. Methods: We established a new experimental model using porcine skin explants exposed to cigarette smoke (CS) where we determined the level of reactive oxygen species (ROS) in the stratum corneum, skin barrier lipids peroxidation and gene expression of the pro-inflammatory cytokine IL-6 in the epidermis. We then tested several polysaccharides and their derivatives such as sodium hyaluronate (SH) of different molecular weights (MW, 1,6 MDa, 300 kDa, 15 kDa, 5 kDa), yeast glucomannan, schizophyllan and carboxymethyl β-glucan, a vitamin C derivative sodium ascorbyl phosphate, niacinamide and D-panthenol for their ability to prevent CS-induced skin damage. For the evaluation and comparison of their mechanism of action, film-forming effect was determined by TEWL and gloss measurements and the antioxidant properties were assessed by DPPH assay. Results: In the skin samples exposed to CS we observed significant negative changes such as the presence of large amount of ROS in the stratum corneum, a high level of skin barrier lipids peroxidation and upregulated IL6 gene expression. Pretreatment of the skin samples with all the tested substances significantly prevented CS-induced skin damage. The most effective was high MW SH probably due to its best film-forming effect and sodium ascorbyl phosphate with the best antioxidant properties. Conclusion: AP leads to a significant skin damage which can be effectively prevented by using some conventional cosmetic and dermatological ingredients with various mechanisms of action.

The negative impact of cigarette smoking on the skin includes accelerated aging, pigmentation disorders, and impaired wound healing, but its effect on the skin barrier is not completely understood. Here, we studied the changes in selected epidermal proteins and lipids between smokers (45–66 years, smoking > 10 years, > 10 cigarettes per day) and non-smokers. Volar forearm epidermal and stratum corneum samples, obtained by suction blister and tape stripping, respectively, showed increased thickness in smokers. In the epidermis of smokers, we observed a significant upregulation of filaggrin, loricrin, and a trend of increased involucrin but no differences were found in the case of transglutaminase 1 and kallikrein-related peptidase 7, on the gene and protein levels. No significant changes were observed in the major skin barrier lipids, except for increased cholesterol sulfate in smokers. Liquid chromatography coupled with mass spectrometry revealed shorter acyl chains in ceramides, and an increased proportion of sphingosine and 6-hydroxysphingosine ceramides (with C4 trans-double bond) over dihydrosphingosine and phytosphingosine ceramides in smokers, suggesting altered desaturase 1 activity. Smokers had more ordered lipid chains found by infrared spectroscopy. In conclusion, cigarette smoking perturbs the homeostasis of the barrier proteins and lipids even at a site not directly exposed to smoke.

Four in vitro oxidative‐stress models were used to study the antioxidant/antipollution effects of all‐trans‐astaxanthin and crocin compared to synthetic antioxidants. DPPH‐scavenging activity of astaxanthin (5 μM) was 2.4, 1.3, 1.4, 1.1 and 0.9‐fold higher than that of alpha‐tocopherol (AT), butylhydroxytoluene, butylhydroxyanisole, gallic acid and Trolox, respectively. Crocin scavenged the same radicals amount as butylhydroxytoluene and butylhydroxyanisole. Both carotenoids were more effective at reducing ferric ions than synthetic antioxidants and had a protective effect on the viability of stressed epidermal cells. Reactive oxygen species induced by hydrogen peroxide or cigarette smoke on a skin were quenched with astaxanthin and crocin to approximately the same extent as with AT. ASX was 3.8, 2.3 and 14‐fold better singlet oxygen scavenger than Trolox, AT and gallic acid, respectively. The polyunsaturated fatty acids in the astaxanthin’ emulsion were 6.5 and 2.5‐fold more resistant to oxidation than in the control emulsion and the AT’ emulsion, respectively.