Mechanisms of anionic surfactant penetration into human skin: Investigating monomer, micelle, and submicellar aggregate penetration theories.

Objective Once penetrated into the stratum corneum, anionic surfactants bind to and denature stratum corneum proteins as well as intercalate into and extract intercellular lipids. With repeated exposures, this leads to skin dryness and irritation, compromising barrier function and skin health. The mechanisms of anionic surfactant penetration into the skin, however, are still widely debated. The objective of this study was to evaluate current theories of surfactant penetration into human skin. Methods A test set comprising 15 anionic surfactant systems and one non-ionic surfactant, all having either dodecyl or lauryl alkyl chains, was tested for surfactant penetration into split-thickness human cadaver skin in vitro using radiolabelled sodium dodecyl sulphate (C-14-SDS). Select physical properties of these formulations thought to be associated with skin penetration including critical micelle concentration, micelle diameter, filtrate concentration and zeta potential were also measured. Results C-14-SDS penetration into human cadaver skin from surfactant systems in vitro was found to correlate well with CMC (R-2 = 0.34, P < 0.05), filtrate concentration (R-2 = 0.36, P < 0.05) and zeta potential (R-2 = 0.76, P < 0.001), but poorly with micelle diameter (R-2 = 0.12). Furthermore, the latter measure correlated inversely with penetration compared to what would be expected based on the micelle penetration theory. Conclusion Neither monomer nor micelle penetration theories are sufficient to explain anionic surfactant penetration into human skin. Submicellar (or premicellar) aggregate penetration theory is difficult to defend at relevant surfactant concentrations. We propose a new hypothesis for this mechanism in which short-term penetration is based on monomer concentration and longer term penetration is based on surfactant-induced damage to the skin barrier.