Transepidermal water loss (TEWL) and damage to the skin barrier

July 21, 2020 0 Comments

Transepidermal water loss (TEWL) and damage to the skin barrier

Transepidermal water loss (TEWL) is the loss of water from the stratum corneum.  And it’s one of the major factors responsible for dry, scaly skin and irritant dermatitis.

The stratum corneum receives water from the dermis and some from the environment.

Numerous external factors can cause TEWL.

The water content of the stratum corneum fluctuates with environmental humidity levels. There is accentuation of dry skin with exposure to cold, wind and low humidity.

Other external factors damage the stratum corneum barrier by denaturing keratin protein, removing natural moisturizing factors and interrupting the lipid bilayers. These factors include solvents, detergents, excessive use of water and soap, and other irritating chemicals.

The severity of the damage is dependent on the type and intensity of exposure to these irritating factors.

When the skin is exposed to solvents such as toluene, n-hexane, or carbon tetrachloride, which remove barrier lipids, the TEWL is increased.

It may require repeated and prolonged exposure to an irritant to see the actual damage.

Cleansers are designed to remove unwanted materials from the skin such as dirt, oils, and sebum. However, the use of harsh surfactants damages the skin barrier; increases the skin’s susceptibility to environmental sources of irritation and sensitization; and reduces skin moisture and smoothness.

  • Charged surfactants, such as anionic and cationic, are the most aggressive. Sodium lauryl sulfate (SLS) is a harsh surfactant that, given its small hydrodynamic radius, is the only surfactant that can extract the intercellular lipids and disrupt the lipid bilayer. It, along with most of the charged surfactants, adsorb skin proteins, causing them to denature and swell. The extent of protein denaturation is dependent on the surfactant monomer concentration and exposure time. As surfactants denature skin proteins, enzymatic reactions that control desquamation, inflammation, and oxidation processes are negatively impacted. The resulting enhanced barrier permeability leads to skin dryness, roughness, cracking, and inflammation.  Surfactants also negatively impact the skin hydration properties by removing NMF. Research showed that when isolated human stratum corneum was exposed to 1% solutions of soap, alkyl sulfate or alkyl benzylsulfonate, all surfactants reduced the ability of the tissue to absorb water from the atmosphere, relative to water. This water-holding capacity is correlated with the loss of NMF. A similar correlation has been found between natural saponified soaps and mild synthetic surfactants using confocal Raman spectroscopy.

However, there are a number of surfactants used commercially that are mild to the skin. These include mostly nonionic and amphoteric variants and the anionic variants: highly ethoxylated (at least 5-EO) alkyl sulfates, sulfosuccinates, isethionates, sarcosinates, taurates, alkyl phosphates, and alkyl glutamates. The aggressiveness of charged surfactants can be minimized by reducing the concentration of the surfactant’s monomer species, reducing the charge by incorporating various counterions and/or cosurfactants to form mixed micelles, and introducing ethoxylation. The improved mildness reduces the incidence of barrier damage, which aids in the maintenance of hydrated skin (i.e., nondrying cleansers).

The temperature of the water can increase the irritant capacity of skin cleansers by causing increased absorption of the cleanser with warmer temperatures. There is greater removal of the protective lipids with hotter water.

  • There is evidence that prolonged contact with water can negatively affect SC barrier function, similar to surfactants. In addition to eliciting erythema, inflammation, and intense dermatitis, excess water exposure can increase SC swelling and suppleness, weaken SC corneocyte cohesion, and increase the permeability of all substances, especially water. Overexposure of skin to water causes a disruption of the SC intercellular lamellar bilayer ultrastructure in vitro as well as in vivo. Similar to surfactant exposure, the swelling response was time dependent, and wide intracellular clefts between corneocytes were observed. These studies as well as others show that prolonged hydration of the SC can directly disrupt the barrier lipids, leading to compromised skin.  Significant water exposure causes the loss of the soluble natural moisturizing factors and some of the protective lipids paradoxically resulting in TEWL. Persistent hydration of the skin from exposure to water results in: Penetration of foreign substances and contribute to allergic and irritant contact dermatitis and Changes in the normal ecological environment in/on the skin, which can support the overgrowth of pathological organisms on the skin.

The end result of prolonged use of water and cleansing agents is alteration of the water-holding capacity of the skin and an increased TEWL. Dry, scaly skin that is less pliable and damaged is the physical result.

There are also endogenous factors that make one more susceptible to damaged skin by external factors. These factors include having active skin disease such as psoriasis, eczema, inherited dry skin conditions (ichthyosis), a previous history of skin diseases (childhood eczema), sensitive skin and/or older age. These endogenous factors may exacerbate dryness of the skin and increase one’s susceptibility to dermatitis.

The exposure to irritants with the resulting transepidermal water loss compromises the barrier function of the stratum corneum and decreases its ability to protect the skin against environmental influences.  The harsher the cleansers or solvents, and/or prolonged exposure to irritants, the greater removal of protective lipids, proteins, natural moisturizing factors and water loss. With decreased water capacity, there is also loss of function of the normal enzymes to desquamate the corneocytes. If the water content of the skin is less than 10%, these interacting factors are disturbed and the result is dry, scaly, and less pliable skin.

  •  Moisturizing the stratum corneum using lotions and creams is typically the best way to hydrate the skin. This is typically accomplished by using emulsion formulas, which contain humectants, emollients, and/or occlusive agents. Humectants attract and hold on to water. Occlusive agents form a barrier across the skin, reducing the TEWL.
  • “Emollient” comes from a Latin derivation meaning a material designed to soften and soothe the skin.  Emollients can be occlusive or semiocclusive meaning they may not be very effective at preventing evaporative water loss, but are effective in smoothing skin. Glycerol and urea are well-known humectants. Glycerol also prevents the crystallization of stratum corneum lipids at low relative humidity, which leads to less TEWL and higher water content of the skin. Previous studies evaluated the influence of glycerol on the recovery of damaged stratum corneum induced by repeated washings with SLS. The authors found that glycerol created a stimulus for barrier repair and improved stratum corneum hydration.
  •  Petrolatum is a common occlusive agent. Application of hydrophobic materials such as petrolatum to prevent skin dryness may be as old as mankind itself. In recent times, however, manufacturers are incorporating lipids that can form lamellar bilayers in their formulations to enhance the barrier properties of the skin. They typically use ceramides or ceramidelike molecules to accomplish this goal and have found even greater benefit when they combine the lipid technology with glycerol. Niacinamide has also been shown to enhance lipid biosynthesis, which again improves barrier function. As in the above situation, the addition of glycerol further improves the clinical dry-skin condition.

*Source: Handbook of Cosmetic Science and Technology*

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