150 JOURNAL OF COSMETIC SCIENCE Barrier protection and barrier recovery Commonly used barrier creams, which are either W/O emulsions or emollients with lipophilic character, are claimed to protect against hydrophilic irritants. On the other hand, barrier creams that are O/W emulsion systems, or that act like hydrophilic systems, are thought to protect against lipophilic irritants. Pre-exposure skin care includes the use of O/W- and W/O-emulsions, tannery substances, zinc oxide, talcum, perfluorpolyethers, chelating agents, and UV-protectors. However, cleansing products and post-exposure skin care are two other important components of skin protection. The post-exposure skin care is based on emollients, moisturizers, humectants and lipid-rich formulations. Cumulative stress tests with repetitive application of irritants appear to be the best conditions for approximating work conditions [12-14]. Emollients or vehicle alone often shows a significant improvement of the clinical skin conditions as well as the S.C. hydration [15]. These authors proposed that a strict distinction between skin care and skin protection products should not be maintained [15]. A recent study discussed whether claims could be made with respect to protective and preventive properties of topically applied body lotions and barrier creams [16]. Moisturizer-containing emollients prevent irritant skin reactions induced by detergents, and may also accelerate regeneration of barrier function in irritated skin [5, 17]. Emollients with moisturizing properties, usually contain either singly or in combination(s) humectants, such as urocanic acid, ammonia, lactic acid, pyrrolidone carboxylic acid, urea, citrate, glycerol, sorbitol and hydroxy acids. These agents belong to a group considered "natural moisturizing factors" (NMF), and/or moisturizers. Their properties include the increase of hydration and the enhancement of water binding capacity in the upper S.C., while reduced NMF can diminish water absorption capacity and may result in perturbation of comeodesmolysis leading to hyperkeratosis. Emollients in atopic dermatitis The utility of emollients in the treatment of atopic dermatitis is well recognized. In atopic dermatitis S.C. hydration and water binding capacity are reduced [18-19], and impaired barrier function is readily observed in both involved and uninvolved skin [18]. These patients also are more prone to develop an irritant contact dermatitis [20]. In atopic dermatitis S.C. the content of barrier lipids is reduced, most prominently that of ceramide I and ceramide 3 [21-22]. This reduction of ceramide levels may result from the over- action of the epidermis-unique enzyme, sphingomyelin deacylase [23-24]. Sebaceous gland activity also is reduced in these patients [25]. Moreover, in atopic dermatitis S.C., the lamellar bodies are incompletely extruded and organized. This, along with the altered S.C. lipid content, may explain the impaired barrier function in these patients. Thus, emollients for patients with atopic dermatitis should improve barrier function and hydration, should have protective properties and contain an antibacterial compound (e.g. triclosan) [26]. These demands are met by emollients showing W/O emulsions properties with a high water content, containing a moisturizer (e.g. glycerol) [5], and/or those based upon physiological lipid mixture, which are ceramide-dominant [10-11,27]. References 1. CW Blichmann, J Serup, A Winther. Acta Derm Venereo169:327-330, 1989. 2. M Loden. Acta Derm Venereo172:327-330, 1992. 3. JWFluhr, GVrzak, MGloor. ZHautkr73:210-214, 1997. 4. L Lehmann, M Gloor, S Schlierbach, W Gehring. Z Hautkr 73:585-590, 1997. 5. JW Fluhr, M Gloor, L Lehmann, S Lazzerini, F Distante, E Berardesca. Acta Derm Venereo179:418-421, 1999. 6. PM Elias, KR Feingold. Semin Dermatol 11:176-182, 1992. 7. M Mao-Qiang, PM Elias, KR Feingold. J Clin b•vest 92:791-798, 1993. 8. WM Holieran, MQ Man, WN Gao, GK Menon, PM Elias, KR Feingold. J Clin Invest 88:1338-1345, 1991. 9. KR Feingold, MQMan, GKMenon, SSCho, BEBrown, PMElias. JClinb•vest86:1738-1745, 1990 10. M Mao-Qiang, BE Brown, S Wu-Pong, KR Feingold, PM Elias. Arch Dermatol 131:809-816, 1995. 11. MM Man, KR Feingold, CR Thomfeldt, PM Elias. J Im,est Dermatol 106:1096-1101, 1996 12. AM Grunewald, M Gloor, W Gehring, P Kleesz. Co•tact Dermatitis 32:225-232, 1995. 13. W Wigger-Alberti, A Rougier, A Richard, P Elsner. Acta Derm Venereo178:270-273, 1998. 14. PJ Frosch, A Kurte, B Pilz. Contact Dermatitis 29:113-118, 1993. 15. U Bemdt, W Wigger-Alberti, B Gabard, P Elsnet. Contact Dermatitis 42:77-80, 2000. 16. K de Paepe, MP Derde, D Roseeuw, V Rogiers. Contact Dermatitis 42:227-234, 2000. 17. DW Ramsing, T Agner. Acta Derm Venereo177:335-337, 1997. 18. M Loden, H Olsson, T Axell, YW Linde. BrJDermatol 126:137-141, 1992. 19. E Berardesca, D Fideli, G Borroni, G Rabbiosi, H Maibach. Acta Derm Venereo170:400-404, 1990. 20. W Gehring, M Gloor, P Kleesz. Contact Dermatitis 39:8-13, 1998. 21. A Di Nardo, P Wertz, A Giannetti, S Seidenari. Acta Derm Venereo178:27-30, 1998. 22. G Imokawa, A Abe, K Jin, Y Higaki, M Kawashima, A Hidano. Jlnvest Dermato196:523-526, 1991. 23 J Hara, K Higuchi, R Okamoto, M Kawashima, G Imokawa. J Invest Dermatol 115:406-413, 2000. 24. K Higuchi, J Hara, R Okamoto, M Kawashima, G Imokawa. Biochem J 350:747-756, 2000. 25. H Wirth, M Gloor, D Stoika. Arch Dermatol Res 270:167-169, 1981. 26. W Gehring, T Forssman, G Jost, M Gloor. Akt Dermato122:28-31, 1996. 27. Chamlin SL, Frieden IJ, Fowler A, Williams M, Kao J, Sheu M, Elias PM. Arch Dermatol 137:1110-1112, 2001