396 JOURNAL OF COSMETIC SCIENCE Permeation of tobacco-smoke pollutants was monitored by control experiment using Franz cells and Strat-M® membranes, being nicotine the major pollutant present in both, Strat-M® membrane and receptor solution, with concentrations of 2.5 µg cm−2 and 11.6 µg L−1 after a 30-min exposition, respectively. In the case of infinite exposi- tion, nicotine concentration significantly increased to 50 µg cm−2 in Strat-M® mem- branes and 1,500 µg L−1 in the receptor solution, after 8 h exposure. The effect of three antipollution cosmetics was demonstrated using the developed conditions, decreasing the permeation of BTEX, styrene, p-Cymene, limonene, and nicotine for exposures of 1 and 2 h. In the case of longer exposure (till 8 h), antipollution effects of the evaluated cosmetics were insignificant, due to a saturation of cosmetic layer over the skin simu- lant. Thus, antipollution cosmetics should be re-applied from time to time to provide a lasting effect. ACKNOWLEDGMENTS We acknowledge the financial support obtained from RNB for the project ­ “Desarrollo de nuevos cosméticos antipolución, urbancream “under the Centro para el Desarrollo Tecno­ lógico Industrial (CDTI) funding project program (CPI-19-027) and that obtained from the Ministerio de Ciencia, Innovación y ­ Universidades, Spain (PID2019-110788GB-I00). CONFLICT OF INTEREST The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. REFERENCES (1) International Agency for Research on Cancer, World Health Organization, United Nations, Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans: Tobacco smoke and ­ involuntary smoking, International Agency for Research on Cancer, Lyon (2004). ISBN 92 832 1283 5. (2) S. K. Das, Harmful health effects of cigarette smoking, Mol. Cell. Biochem., 253, 159–165 (2003). (3) E. Randerath, D. Mittal, and K. Randerath, Tissue distribution of covalent DNA damage in mice treated dermally with cigarette “tar”: Preference for lung and heart DNA, Carcinogenesis, 9, 75–80 (1988). (4) W. A. Pryor, M. Tamura, and D. F. Church, ESR spin trapping study of the radicals produced in NOx/ olefin reactions: A mechanism for the production of the apparently long-lived radicals in AS phase cig- arette smoke, J. Am. Chem. Soc., 106, 5073–5079 (1984). (5) D. Bernhard, C. Moser, A. Backovic, and G. Wick, Cigarette smoke- an aging accelerator?, Exp. Geron- tol., 42(3), 160–165 (2007). (6) D. P. Kadunce, R. Gress, R. Kanner, J. L. Lyone, and J. Zone, Cigarette smoking: risk factor for prema- ture facial wrinkling, Ann. Intern. Med., 114(10), 840–844 (1991). (7) R. A. Norman and M. Rappaport, Smoking, Obesity/Nutrition, Sun, and the Skin. in Preventive Derma- tology, R. A. Norman. Ed. (Springer, London), pp. 17–20(2010). DOI: 10.1007/978-1-84996-021-2_2 (8) D. N. Doshi, K. K. Hanneman, and K. D. Cooper, Smoking and skin aging in identical twins, Arch. Dermatol., 143(12), 1543–1546 (2007). (9) J. S. Koh, H. Kang, S. W. Choi, and H. O. Kim, Cigarette smoking associated with premature facial wrinkling: image analysis of facial skin replicas, Int. J. Dermatol., 41(1), 21–27 (2002).

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