As noted earlier, the hydrolipid film on the surface of the skin is important for maintaining skin health. Epidermal lipids, which serve as the “mortar” between the corneocyte “bricks” in the stratum corneum, are also important to maintaining skin health and stratum corneum barrier function (53-55). Patient populations that exhibit heightened sensitivity to personal cleansing products, such as individuals with atopic dermatitis, often exhibit aberrant epidermal lipid composition or structure (56,57), and di Nardo et al. found an inverse relationship between susceptibility to irritation from SLS and levels of certain stratum corneum ceramides in normals (58). Visscher et al. reported an increase in transepidermal water loss rate, consistent with stratum corneum barrier compromise, following acetone/ether extraction of lipid from the skin surface and upper stratum corneum (59). Findings such as these, coupled with surfactants’ natural ability to emulsify oils and lipids, suggest that surfactants’ negative impact on skin could result from delipidization or selective removal of lipid components from the stratum corneum.
Kirk examined the amount of casual lipid, i. e., lipid on the skin surface, removed by one minute of controlled hand washing (60). Results from washing with water and with several bar cleansers are summarized in Figure 6. As expected, water is relatively inefficient at removing skin surface lipid. The surfactant bars are more efficient but still do not completely strip the skin surface of lipid. However, even partial removal of the hydrolipid film may effect changes in skin condition. Morganti reported that washing the skin with water decreases surface lipids by about 24%, while washing with soap reduces surface lipids by about 36% (61). Surprisingly, using a syndet bar to wash the skin reduced surface lipids by about 50%. Removal of skin surface lipids was hypothesized to decrease the skin’s ability to retain natural moisturizing factors (NMF), ultimately leading to dry skin. Sauermann et al. also reported removal of NMF by exposure to water and to soap or syndet solutions, but these authors did not measure lipid removal (13).
|
|
|
|
|
|
|
|
|
Bechor et al. reported > 70% relative change in casual sebum levels after washing the cheek for 30 seconds with water or various personal cleansing products (62). Sebum removal was not linked with clinical symptoms in this study, and sebum levels returned to baseline values in about one to two hours. Gfatter et al. examined the effect of washing on skin surface lipid content in a group of infants aged two weeks to 16 months (mean age 3.2 months) (63). Treatment consisted of a one-minute wash performed on each child’s chest and buttock with tap water (control), a synthetic detergent liquid, a synthetic detergent bar, or a soap bar. Skin surface lipid content and several other parameters were measured 10 minutes after washing. All of the washes removed a significant amount of skin surface lipid. Not unexpectedly the least removal was observed for the control group ( — 0.93 mg/cm2), the greatest removal for the soap bar group ( — 4.81 mg/cm2). The authors conclude that removal of surface lipid might reduce stratum corneum hydration and lead to dryness and scaling.
Personal cleansers can also induce changes in epidermal lipids, which are responsible for maintaining the skin’s barrier function. Imokawa et al. reported that the stratum corneum lipid lamellar structure of forearm skin was disrupted following a 30-minute exposure to 5% aqueous sodium dodecyl sulfate (64). Post-exposure analysis showed a selective loss of various lipid components including cholesterol, cholesterol ester, free fatty acids, and sphingolipid. The authors noted that surfactant exposure produced an enduring chapped, scaly appearance and reduced hydration. Recovery studies conducted by applying isolated lipid fractions to surfactant-treated skin suggested a role for sphingolipids in helping to restore the skin’s ability to retain water. Rawlings et al. examined lipid structure and composition in the normal skin of adult females and in xerotic skin induced by soap washing (65). Xerotic skin samples were obtained by tape stripping the backs of subjects’ hands following one week of three-times-daily washing with soap; normal skin samples were obtained from a control group of subjects. The authors noted an apparent perturbation of desmosomal degradation, with intact desmosomes persisting to higher levels in the stratum corneum in soap-treated skin. The lipid bilayer structure in the outer stratum corneum was degraded in both skin types, but the normal and soap-treated structures had a different appearance. The authors found a decreased stratum corneum
ceramide content in soap-treated skin, with a progressive, deeper loss accompanying more severe dry skin grades. However, the relative levels of the various ceramide species were not different in the two skin types. The authors concluded that alterations in stratum corneum lipid composition and organization, along with reduced desmosomal degradation, are responsible for the scaling that accompanies soap washing.
Fulmer and Kramer compared lipid content in normal and surfactant-induced dry skin in a paired, dry leg study (66). Subjects washed one randomly assigned leg three times daily with 4% sodium dodecyl sulfate solution for a period of two weeks; the other leg remained untreated as a control. At the end of treatment shave biopsies were taken for lipid analysis. In contrast to the results reported by some other groups, no alteration in the total amount of lipid per gram of stratum corneum protein resulted from the surfactant washing. In particular, the total ceramide level was not changed. However, ceramide, cholesterol, and free fatty acid profiles were altered in the surfactant-treated skin compared to control. The authors concluded that surfactant washing affects the quality, but not the quantity, of stratum corneum lipids, suggesting that surfactants’ role in the dry skin process is related to perturbation of the stratum corneum formation process, not lipid extraction.
Other studies also call the hypothesized relationship between lipid extraction and surfactant-induced skin damage into question. Scheuplein and Ross examined the effect of three classes of compounds on human epidermal membrane permeability to tritiated water: lipid solvents (e. g., chloroform:methanol), hydrogen-bonded solvents (e. g., water, DMSO), and surfactants (sodium laurate, SLS) (67). Lipid extraction decreased the dry weight of the stratum corneum by up to 20% even though its gross appearance remained unchanged. Solvent extraction of epidermal lipids resulted in a large increase in membrane permeability; this effect was irreversible. Hydrogen-bonded solvents also increased permeability, which was attributed to resolvation and membrane expansion. Unlike solvent extraction, the increase in permeability from hydrogen-bonded solvents was largely reversible. Exposure to surfactant caused visible expansion in the plane of the tissue, suggesting that the anionic surfactants initiate uncoiling of alpha-keratin molecules to form beta-keratin. The effect was reversible for mild surfactant exposures but irreversible for more severe exposures. Follow-up work by Dugard and Scheuplein again showed reversible changes in human epidermal membrane permeability following exposure to surfactants belonging to three n-alkyl homologous series (48). They concluded that extraction of lipids or other epidermal components was not the primary mechanism responsible for the increased membrane permeability, and instead suggested that surfactants act on membrane proteins. Rhein et al. reported that the swelling response of stratum corneum exposed to surfactant solutions was reversible, again suggesting a limited role for lipid extraction in surfactant interactions with skin (23). Froebe et al. examined in vitro stratum corneum lipid removal by SLS and linear alkyl benzene sulfonate (68). Both materials removed detectable levels of lipid only above their CMC, demonstrating that lipid removal is a micellar phenomenon. The primary lipid species involved were cholesterol and free fatty acids; little or no ceramide was extracted. Even at the highest surfactant concentration used (2%), the amount of lipid material removed from the skin represented less than 7% of the total stratum corneum lipid, indicating that delipidization, or at least the removal of sizable amounts of stratum corneum lipid, is not a primary mechanism for surfactant-induced irritation.