Skin Physiology and Textiles Consideration of Basic Interactions

U. Wollinaa, M.B. Abdel-Naserb, S. Vermac aDepartment of Dermatology, Hospital Dresden-Friedrichstadt, Academic Teaching Hospital of the Technical University of Dresden, Dresden, Germany; bDepartment of Dermatology, Ain Shams University Cairo, Cairo, Egypt; cPrivate Practice, Baroda, India


The skin exerts a number of essential protective functions ensuring homeostasis of the whole body. In the present review barrier function of the skin, thermoregulation, antimicrobial defence and the skin-associated immune system are discussed. Barrier function is provided by the dynamic stratum corneum structure composed of lipids and corneocytes. The stratum corneum is a conditio sine qua non for terrestrial life. Impairment of barrier function can be due to injury and inflammatory skin diseases. Textiles, in particular clothing, interact with skin functions in a dynamic pattern. Mechanical properties like roughness of fabric surface are responsible for non-specific skin reactions like wool intolerance or keratosis follicu-laris. Thermoregulation, which is mediated by local blood flow and evaporation of sweat, is an important subject for textile-skin interactions. There are age-, gender- and activity-related differences in thermoregulation of skin that should be considered for the development of specifically designed fabrics. The skin is an important immune organ with non-specific and specific activities. Antimicrobial textiles may interfere with non-specific defence mechanisms like antimicrobial peptides of skin or the resident microflora. The use of antibacterial compounds like silver, copper or triclosan is a matter of debate despite their use for a very long period. Macromolecules with antimicrobial activity like chitosan that can be incorporated into textiles or inert material like carbon fibres or activated charcoal seem to be promising agents. Interaction of textiles with the specific immune system of skin is a rare event but may lead to allergic contact dermatitis. Electronic textiles and other smart textiles offer new areas of usage in health care and risk management but bear their own risks for allergies.

Copyright © 2006 S. Karger AG, Basel

The skin is a communicative, sensitive and protective organ. The skin surface with the stratum corneum represents a critical structure in the interaction of the human body with the environment. Without the horny layer a terrestrial life would be impossible. On the other hand, the stratum corneum becomes impaired in any kind of superficial or deep injuries. To retain body homeostasis, recovery of the stratum corneum is necessary.

Other important protective functions of the skin are protection against infection and irradiation, in particular ultraviolet irradiation, thermoregulation and synthesis of hormones and other bioactive substances. The skin has a great importance in social life and is a basis of attractiveness as well. Many of these functions are also related to an intact barrier function.

The epidermis derives from the ectoderm. Initially the epidermis comes as a monolayer. In the first trimester the epidermis is covered by a single-layered periderm. Epidermal stratification starts after 8 weeks. During the second trimester cornification is realized. Then the periderm disappears and becomes a constituent of the vernix caseosa. The epidermal thickness in an immature newborn is about 29 |xm, in mature newborns and adults the thickness is about 50 |xm. The skin surface of the newborn is covered by the protective gelatinous vernix caseosa, whereas the skin surface of adults is rather dry [1].

If one considers clothing as a protective measure of skin in human life, the vernix caseosa may be seen as the first 'clothing' in an individual's life produced by the mother's body to protect the newborn especially during the very first period of adaptation to terrestrial life.

Stratum Corneum Barrier and Skin Surface

The stratum corneum is the essential structure of the skin barrier. The major constituents of the stratum corneum are lipids and proteins. In a typical case about 20 layers of nucleus-free corneocytes densely packed with keratin filaments are surrounded by a matrix. The matrix is composed of filaggrin and its derivates, and lipid-rich lamellar bodies. Lamellar bodies fuse end to end, thereby forming lipid double layers [2].

The lipid constitutes are cholesterol, ceramides and free fatty acids. Ceramides stand for about 50% of horny layer lipids and are essential for the lamellar structure of the epidermis. Cholesterol regulates the phase behaviour of the stratum corneum. The free fatty acids are mostly long-chained molecules with more than 20 C atoms. Lipids are responsible for the hydrophobicity of the horny layer [3]. The water exchange occurs via migrating pores, i.e. polar transport pathways within the lipid mosaic [4]. The matrix develops under the influence of pH gradients, sodium ions and enzymes (synthetases, reductases, hydrolases, lipases) [3]. In a simplistic way, the stratum corneum can be described by the bricks-in-mortar model [2]. More recent studies discovered subunits of octahedrons of corneocytes within the horny layer which may migrate [4].

The horny layer is covered on its surface by a thin amorphous film contributing to stratum corneum structure and function. In newborns there is an almost neutral skin surface with a pH of 6.6 that changes within days or weeks into an acidic pH of 5.9 (acid skin surface film). This leads to activation of pH-dependent hydrolytic enzymes like (3-glucocerebrosidase and stratum corneum secretory phospholipase A2 [5, 6]. Skin surface pH is modulated by microbial harvest, eccrine and sebaceous gland secretions, and endogenous catabolic pathways. The acidification of the horny layer is necessary for barrier function [7]. Exposure of the horny layer to neutral buffers (i.e. wet work conditions) or blocking of acidification increases the pH. Hereby, serine proteases become activated that digest desmoglein 1. Desmoglein 1 is a major constituent of cor-neosomes. Metabolization of desmoglein 1 decreases cohesivity of corneocytes and enforces horny layer permeability [8].

The horny layer impairment as subclinical dryness of skin is quite common. It may have substantial impact on the whole body. Itching sensations are a common symptom [9]. Prolonged exposure of human skin to wetness (water) and/or occlusion leads to measurable disturbances of barrier function. The transepidermal water loss increases in relation to duration of exposure and temperature [10, 11].

Interaction of clothing with the skin surface is first a mechanical one with the skin surface structure. Friction and pressure are the major forces. Surface quality of textiles may directly interfere with skin integrity. This is of particular importance for socks. The plantar skin is not only the thickest of the whole human body with a well-developed multilayered stratum corneum, it has to stand repeated pressure and friction during the whole human life. Even the smallest peaks of pressure when occurring frequently enough - as caused by a seam for instance - may cause skin lesions in patients with impaired skin resistance (e.g. bullous disease or diabetes) [12]. Friction is also a major cause of the induction of keratosis follicularis on the thighs and the outer upper arms [13].

Xerosis cutis is a consequence of the reduction of epidermal water content (<10% of stratum corneum). An increased transepidermal water loss leads to itching, scaling, roughness and fissuring [14]. Xerosis might be a symptom of irritant contact dermatitis, atopic dermatitis or ichthyosis. In case of so-called sensitive skin which is often a dry skin as well, e.g. in atopic dermatitis, the tactile threshold is lowered. Rough textile surfaces, such as wool, can induce irresistible prickling and itching known as 'wool intolerance' [13, 15]. Smooth textile surfaces are often more comfortable irrespective of the fibres included. These qualities are of particular relevance in direct skin-textile interaction like in underwear. The perceived importance of fabrics and sweat as triggering exacerbating factors in atopic dermatitis is high. About 40% of 12- to 14-year-old schoolchildren believe that wool fabrics and sweating during exercise are worsening their skin condition [16].

Fig. 1. Mechanical irritation. a Mechanical irritation by clothing of the polyamide type; cotton was well tolerated. The lichenoid lesions healed only by changing the clothing. b Hair loss induced by tight polyester jeans. cThe traditional sari friction dermatosis causes hyperpigmentation and lichenoid papules in the hip region.

Fig. 1. Mechanical irritation. a Mechanical irritation by clothing of the polyamide type; cotton was well tolerated. The lichenoid lesions healed only by changing the clothing. b Hair loss induced by tight polyester jeans. cThe traditional sari friction dermatosis causes hyperpigmentation and lichenoid papules in the hip region.

Atopic dermatitis and dry skin often flare up during wintertime, but the mechanisms of winter deterioration of dry and atopic skin are not fully understood. Dryness of textile-protected skin in particular is prominent around the shoulders (fig. 1). Change of washing clothing with anionic, additive-enriched detergents to a non-ionic, additive-reduced detergent for a period of 2 weeks improved skin conditions in Japanese patients who had worn cotton underwear and used to wash it with cold tap water. Under these conditions residues of common washing detergents/surfactants in cotton underclothes may contribute to winter worsening of dry or atopic skin [17]. In an experimental study on professional laundry, a broad variety of surfactant residues according to the type and amount could be identified on cotton-based textiles. The skin reaction during patch testing in healthy and skin-sensitive adults was not strictly correlated with a threshold limit or the concentration of surfactants. Non-ionic surfactants were better tolerated than anionic ones [18].

Clothing and Thermoregulation

In neonates body temperature rapidly drops soon after birth. In order to survive, neonates must accelerate heat production by lipolysis in brown adipose tissue, i.e. non-shivering thermogenesis. This process is oxygen dependent [19]. Clothing has to function as insulation and therefore supports thermoregulation. Heat loss prevention is a major task in the delivery room and thereafter, which is of particular relevance in preterm neonates.

The cutaneous thermosensitivity is not evenly distributed over the body. Local thermosensitivity can be calculated from changes in sweat rates and thermal discomfort. The highest cold sensitivity is found on facial skin, 2-5 times higher than in any other part of the body. Facial skin has also the highest warm sensitivity. In contrast, the limb extremities are the least thermosensitive segment for warming and cooling [20].

A key function of clothing is insulation. Thickness of the material and therefore the volume of air enclosed in the fabric appears to be the major determinant. Dry heat transfer through fabrics consists mainly of conduction and radiation. During exercise or in extremes of environment (cold and heat), the interaction of body thermoregulation with clothing gains even greater importance. Recent developments with phase-changing materials open the opportunity for buffering heat [21].

The total body as well as per body surface sweating rate increases after puberty. In contrast mass-related evaporative cooling and sweating efficiency are highest in prepubertal humans [22]. These findings illustrate the different needs of age groups in terms of thermoregulative support by clothing. Although sweat gland activity is directly controlled by the central nervous system controlling the core body temperature, sweat glands can also be influenced by local cutaneous thermal conditions. It might be considered that improper clothing can support the phenotypic realization of focal (axillary or plantar) hyperhidrosis. Local temperatures above 32°C predominantly affect neurotransmitter release [23]. On the other hand, there are also gender- and gene-related differences in thermoregulation of humans [24]. The sweating rate is higher in males [25]. In women after the menopause, changes in reproductive hormone levels substantially alter the thermoregulatory control of skin blood flow as illustrated by the occurrence of hot flashes. Pre-existent pathological conditions alter the thermoregulative response as well. In type 2 diabetics the ability of skin blood vessels to dilate is impaired [26]. Compared to normal males hypertensive males develop higher skin temperatures in the heat. Water ingestions recommended for normal men during exercise may cause abnormal cardiac workload in hypertensive individuals [27]. Functional textiles may support patients to ensure a quite normal body temperature without cardiac overload by water ingestion.

Cold stress can quickly overwhelm human thermoregulation leading to impaired performance or even death. Convective heat loss is the most important factor. Cold exposure induces both vasoconstriction and thermogenesis [28]. Several layers of textiles with thermoinsulative qualities and a wet-protective outer surface are capable of allowing to stay in the cold and an unfriendly environment.

Clothing at its best is an interactive barrier ensuring thermal balance despite changes in ambient temperature and humidity, metabolic heat production, gender and age differences, and intended use [29, 30]. In such a way clothing can serve a protective function by reducing radiant heat gain and thermal stress. Clothing construction affects these functions [31].

During exercise in moderate heat, a clothing fabric that promotes sweat evaporation did not affect mean body temperature, rectal temperature (as a measure of core temperature), mean skin temperature, heart rate or comfort sensation responses compared to a traditional cotton fabric [32]. The more intense the exercise and/or the more extreme the environment, the higher is the impact of clothing on thermoregulation [33]. Intermittent regional microclimate cooling is more than twice as efficient in reducing exercise heat strain than constant microclimate cooling [34]. Adoptive functions of textiles should be capable of supporting microclimate changes. Major items of interaction of clothing with the human body and the environment are thermal and water vapour resistance, mass transfer, directed fluid transport (e.g. of sweat), evaporation, thermal load, air gaps and contact layers. Perception of clothing comfort is positively related to warmth and negatively to dampness [35].

Clothing and the Skin-Associated Antimicrobial Defence System

The skin-associated immune system comprises specific and non-specific defence mechanisms. The non-specific ones will be discussed in detail, since they seem to represent the base for human body homeostasis. The specific part is composed of antigen-presenting cells (i.e. Langerhans cells and epidermal keratinocytes) and lymphocytes (B, T and NK types).

The prototype of a specific immune reaction to clothing, completely unwanted but fortunately quite rare, is (allergic) contact dermatitis. The induction of an allergic contact dermatitis has been recognized since the 19th century. This type of an allergic contact dermatitis needs an intense contact with the skin surface. Areas with a high sweat gland density are at special risk such as the intertriginous skin. The most common allergens are textile dyes such as disperse dyes [36, 37]. Rarely other components like fibre additives, finishing or contaminants may be responsible for textile-related allergies. For a more

Fig. 2. Acute contact dermatitis due to clothing and sweating. Sweat is a critical component in interactions between human skin and textiles. Sweat may dissolve dyes and other components from clothing and increase the skin permeability for hydrophilic compounds.

detailed discussion we would like to refer to the excellent review by Hatch and Maibach [36] and Le Coz [37] (fig. 2). The matter needs a re-evaluation with development and usage of smart, hybrid and interactive or electronic textiles in the market [38-40]. However, even more important is the possible interference of textiles with non-specific defence mechanisms of the skin.

The non-specific immune function of skin involved in antimicrobial defence is of even greater importance, provides the base for resistance to microbial threat and may interact in several ways with the specific immune function whenever necessary.

The stratum corneum is the essential structure for non-specific resistance supported by skin gland secretions. There is a close relationship between horny layer barrier function and the risk of skin infection [41]. In recent years research has identified several families of antimicrobial peptides in vertebrates including humans [42, 43]. Many of these peptides are multifunctional. They are not only natural antibiotics but chemotaxins as well. The human cathelicidin LL-37 is chemotactic for neutrophils, monocytes, mast cells and T lymphocytes, causes mast cell degranulation and supports vascularization and re-epithelialization of wounds [44].

In human skin appendages genes like DCD and CAMP are expressed encoding antimicrobial peptides cathelicidin LL-37 and dermicidin. By the action of serine proteases, new antimicrobials are produced with their own antimicrobial profile [45, 46]. (32-Defensin has been identified in lamellar bodies of the human skin [47]. There seems to be some antimicrobial activity of the lipid phase in the stratum corneum. In addition, such substances are secreted together with the sweat and spread on the skin surface [46, 48].

In newborns there is a 10- to 100-fold increase in the expression of cathe-licidin LL-37 and (32-defensin compared with adult skin [49]. This can be viewed as a compensatory mechanism of a still immature immune system in adapting to postuterine life. The antimicrobial peptides are concentrated in the vernix caseosa. Both a1- to a3-defensin and cathelicidin LL-37 have been detected there [50].

During the recovery of barrier function after wounding or inflammatory disease (eczema, psoriasis) there is a close interaction between growth factors and antimicrobial peptides [51]. The microbial settlement induces antimicrobial control mechanisms: for instance, the saprophytic yeast Malassezia furfur, but bacteria as well, induces the expression of p2-defensin in human epidermal ker-atinocytes [52, 53].

Clothing may impair the antimicrobial defence of skin by mechanical alteration of the barrier function but also by its effects on skin wetness and local blood flow. Athletes are prone to develop tinea pedis, 'athletes' feet', due to the humidity in socks and sports shoes. Viral plantar warts are not uncommon and their spread can be facilitated by plantar hyperhidrosis [54].

On the other hand, textiles can support the non-specific cutaneous defence. In the most simplistic way, clothing provides a mechanical barrier against infestation, insect bites, protozoa and microbes, e.g. the mosquito net or the protective textiles in an operation room.

The use of textile materials to support and deliver active chemicals is as old as the application of an ointment to a fabric for covering a wound. What may not be so obvious is the potential volume and number of textile products which could benefit from this technology. Medical products are perhaps the largest application of this kind of technology. In health-related professions, protection from pathogens is a growing concern, and textiles with antimicrobial properties are desirable. Fungi, bacteria and associated insects are responsible for significant infections and allergy problems. Less obvious applications for antimicrobial textiles include air filters (indoor air quality), carpets, draperies, wall coverings etc., particularly in environments where the sick, elderly and other susceptible individuals live.

Until recently, biocidal textiles have not been widely available in the market, in spite of the obvious commercial potential. Even with the recent announcements of new products, their efficacy and safety are not readily compared. There is a reasonable array of chemicals which can act as biocides, including chemical oxidants, photo-oxidants, membrane disrupters, heavy metals, organic protein denaturants and chemicals which mimic biochemical intermediates but which function improperly in the micro-organism. Protein denaturants and biochemical metabolites are likely to require release from the biocidal fibre and diffusion through the cell wall before being effective. Membrane disrupters may work acceptably from outside the microbe and may not require release from the fibre, at least until the microbe is in close proximity [55].

General oxidants and some membrane disrupters appear to be the least objectionable and offer the greatest potential as biocidal agents in textiles. The more specific materials which inhibit micro-organisms by malfunctioning in a metabolic pathway are more elegant, but are more likely to induce immunity in the organism. Induced immunity is a problem which has just been reported for the latest, widely used antimicrobial agent for consumer goods.

The scientific and technological approaches are complex. Biocidal particles have to be attached to the fibre surface or alternatively incorporated into the fibre. Conventional chemical reactions are evaluated to attach molecules and particles covalently to the fibre surface, but also copolymerization of biocidal monomers into the fibre-forming polymer - followed by fibre extrusion, surface grafting of a biocidal monomer covalently to the fibre surface with ultraviolet or peroxide initiation, and incorporation of an antimicrobial agent into fibre during extrusion.

Finally, the molecular mechanics modelling approaches are under investigation. They have to address each of the issues such as the number of reactive groups which can be stored on the surface, the kinetics of ionic release and the mobility of the surface-grafted molecules.

Although it would seem that the number of reactive species that could be stored by simply grafting a 'storage polymer' to the surface of the fibre could increase without bound, available data argue against this. When the radius of gyration of the storage polymer is equal to one half the average distance between graft sites, the maximum storage potential is achieved. For smaller molecules, the surface has many bare spots which do not store any reactive species. When the storage polymer is larger than optimum, it blocks adjacent graft sites, thus preventing attachment of additional storage polymers, again resulting in bare fibre surface. Recent investigations try to optimize the effect of polydispersity, both in the storage polymer and in the graft site density on the surface, on storage efficiency.

Most polymers (except cellulose) have very few reactive sites on their surfaces. Therefore, it is impractical to store a large amount of reactive species on their surfaces unless an amplification system is used. Although plasma treating can be used, it is too expensive for most applications. Another approach is to graft to the surface a polymeric material that contains groups to which the reactive species can be grafted, e.g. poly(acrylic acid), poly(vinyl alcohol), poly(vinyl amine) or copolymers containing these groups [55]. There are several issues that need to be dealt with: (a) What is the maximum number of reactive groups that can be stored on the surface? (b) How can they be released? (c) How does the mobility of the surface-grafted polymer affect the delivery of the reactive species?

The durability or rechargeability of the fabric is a practical problem. Recharging would reduce waste products. Can it be realized in situ or does it need repeated processing of the fabric? More important for textile-skin interaction are fundamentals of safety and toxicity. Under these circumstances the release of active chemicals from the fabric bears a greater potential risk than biocidals that remain attached either by covalent binding or physical attachment to the textile. Novel approaches include inclusion of biocidal compounds into silica matrices using the sol-gel technique. Moreover, silica coatings with embedded nanoparticular silver combined with organic biocidal compounds effectively decreased the survival rates of different bacteria on textiles and medical catheters [56].

To enhance the protective efficiency against insects, clothing has been impregnated with repellents. As shown in a French study in Côte d'Ivoire on military health service personnel, permethrin impregnation of uniforms improved protection against mosquito bites but not enough to reduce significantly the incidence of malaria among non-immune troops [57].

Copper and silver ions exert antibacterial, fungicide and nematocide activities. They are not skin sensitizing. Their use in mattresses, antifungal socks, anti-dust-mite mattress covers or antibacterial fabrics is under investigation [58, 59]. Silver-nylon fibres were effective in vitro against Staphylococcus aureus, Pseudomonas aeruginosa and Candida albicans. In vivo silver-nylon cloth prevented colonization of burn wounds [58]. Silver-coated textiles have been shown to reduce colonization of skin by S. aureus in atopic dermatitis within a couple of days [60]. The S. aureus cell wall compononents peptidoglycan and liptotei-choic acids have been identified to activate human keratinocytes by activation of toll-like receptor 2 pathways [61]. In the clinical study reduction of skin colonization was accompanied by clinical improvement of atopic dermatitis [60].

A combination of polyhexamethylene biguanidine, quaternary ammonium silane organic-based compounds and silver was developed for uniform bacteria mitigation on the military battle field. After 24 h a 100% effectiveness was obtained against Gram-positive bacteria on nylon-based fabrics [62]. Heavy metals and protein denaturants are effective, but toxicity problems are a concern [63].

Silver is used as a topical agent in wound dressings for burns, diabetic ulcers and other chronic open wounds. Absorption can lead to deposition within the wound and internal organs such as the liver and kidney. Despite this, the risk of lasting tissue damage or functional disorders has been estimated to be low [64].

Very recently, de novo synthesis of biomimetic polymers and oligomers that mimic the structure and biological activity of natural antimicrobial peptides such as margainins and creopins has become reality. It remains to be seen whether such compounds will offer new options and safety in finished textiles.

The resident skin flora represents a balanced ecosystem, where resident germs play an important physiological role. One of the main benefits that humans derive from resident flora is protection from infection. Any change in the microbiological equilibrium can carry negative consequences [65]. In preterm infants, coagulase-negative staphylococci are the most common species on the skin representing about 80% of the neonate's flora, numerous strains with antibiotic resistance or multiresistance [66]. Later on there is a great interindividual and intra-individual variation of resident microflora. With increasing age, streptococci disappear and corynebacteria occur. Anaerobic propioni-bacteria are more frequent in youngsters when sebum production is increased. Micrococci, Gram-negative germs like Acinetobacter and yeasts like Malassezia spp. are also components of the resident flora [67].

The antibacterial activity of biocide-finished textile products containing silver, zinc, ammonium zeolite and chitosan was evaluated under wet and dry conditions. The antibacterial activity was limited to wet conditions. Addition of organic matter decreased the antibacterial activity. In any case antibacterial effects required several hours of incubation. Some bacteria species and strains were not affected. The authors concluded that antibacterial properties of biocide-finished textiles in the clinical setting may be of limited value [68].

The body odour is a product of sweat gland activity, bacterial contamination (in particular corynebacteria) and steroidal metabolism. Diseases (like diabetes, cancer or Fish odour disease) interfere with body odour just as nutrition or medication and the use of cosmetics and hygiene products as well. Body odour may be a signal of sexual attraction and a non-verbal communicator of emotions [69, 70]. Malodour of the axillary and pubic region has been associated with Corynebacterium spp. which are capable of generating several odorous compounds derived from androgens [71]. Reduction of malodour can be achieved by antimicrobial measures and reduction of sweat gland activity. Textiles with a high rate of directed vapour transport may thereby reduce the odour in a non-specific way. Antimicrobial activity is used to diminish the bacterial load. The antibacterials should be fixed to the textile fibres to avoid contact sensitization and disturbances of non-specific microbial defence by the resident microflora. Development of bacterial resistance has to be considered as a serious problem [72, 73].

Prevention of odour and discoloration of the textile material are significant, if less critical reasons to use antimicrobials. Consumers are showing increasing interest in antimicrobial products, particularly those products like carpets which are suspected of harbouring microbes. The applications will result in products which will become pervasive throughout the medical services, filtration industries, home furnishings and selected apparel items (like socks). Indeed, several product introductions in this area have been made.

Triclosan-incorporated polymers are on the market for hospital use as fabric seat covers, chairs and clothing. Testing antibacterial activity on the other hand was found to be discouraging. In light of recent studies that have shown specific interactions of triclosan with the bacterial lipid synthesis pathway, triclosan-incorporated polymers may provide an ideal setting for resistant strains of bacteria to grow and thus should not be used in a broad range but only in selected hospital settings [74]. Safety concerns have been addressed on the other hand because of a possible interaction with the normal skin flora, percutaneous absorption and systemic toxicity [73]. Human studies suggest that percutaneous absorption of heavy metals through intact skin is poor [64].

The situation is somewhat different for triclosan. After in vivo topical application of a 64.5-mM alcoholic solution of [3H]triclosan to rat skin, 12% radioactivity was recovered in the faeces, 8% in the carcass, 1% in the urine, 30% in the stratum corneum and 26% was rinsed from the skin surface 24 h after application. Free triclosan and the glucuronide and sulfate conjugates of triclosan were found in urine and faeces. Triclosan penetrated rat skin more rapidly and extensively than human skin in vitro. Twenty-three percent of the dose had penetrated completely through rat skin into the receptor fluid by 24 h, whereas penetration through human skin was only 6.3% of the dose. Chromatographic analysis of the receptor solutions showed that triclosan was metabolized to the glucuronide, and to a lesser extent to the sulphate, during passage through the skin. Triclosan glu-curonide appeared rapidly in the receptor fluid whereas triclosan sulphate remained in the skin. Although the major site of metabolism was the liver, conjugation of triclosan in skin was also demonstrated in vitro and in vivo, particularly to the glucuronide conjugate which was more readily removed from the skin. By extrapolation of the comparative in vitro data for human and rat skin it is reasonable to deduce that dermal absorption in humans of triclosan applied at the same dose is about one third of that in the rat in vivo [75].

Charcoal-containing textiles are in use as wound dressings for the malodorous wound. Creating an enlargement of the adsorptive surface by charcoal, physical binding of debris and bacteria is supported. The health hazards on intact skin are not known. In open wounds carbon may be deposited within the phagocytic cells without further medical problems [64].

Charcoal-containing devices can also be used to improve body odour or to reduce flatus odour when worn inside underwear. Here they are quite efficient to bind sulphide gases when used in construction of briefs made of activated charcoal fibres. Pads were much less effective under this view [76].

Some naturally occurring polymers like chitosan, alginates or kapok fibres offer antimicrobial activity and biocompatibility [77]. Supramolecular structures fixed to textile fibres like cyclodextrins allow to reduce bacterial contamination of sweat-gland-rich body parts like the axillary region or the feet [77]. The importance of laundering in the prevention of skin infections has been discussed in detail elsewhere [78].


Antimicrobial-finished textiles have just entered the market. Antimicrobial-finished textiles for special purposes such as the operation room or the military battlefield seem to offer advantages. Many of the currently available products interfere more intensely with skin-derived microbes on the textile than with the skin-associated microbial ecosystem. The use of soluble or volatile antimicrobials in clothing can be associated with problems such as intolerance of the human body, allergies or disturbances of the human skin resident flora. The development of new technologies and products should seriously consider the delicate balance of the skin microflora and take it into account for the selection of compounds and techniques. Other important areas of interference of textiles with human skin physiology are barrier function of skin and thermoregulation. If the skin is seen as a complex and adaptive organ, textiles and clothing can be created that will support body function and allow keeping homeostasis even in the most unfriendly environment.


1 Loomis CA, Birge MB: Foetal skin development; in Eichenfield LF, Frieden IJ, Esterly NB (eds): Textbook of Neonatal Dermatology. Philadelphia, Saunders, 2001, pp 1-17.

2 Elias PM: Epidermal lipids, barrier function, and desquamation. J Invest Dermatol 1993;80 (suppl):44S-49S.

3 Feingold KR: The regulation and role of epidermal lipid synthesis. Adv Lipid Res 1991;24:57-82.

4 Forslind B: A domain mosaic model of the skin barrier. Acta Derm Venereol 1999;74:72-77.

5 Behne MJ, Barry NP, Hanson KM, Aronchik I, Clegg RW, Gratton E, Feingold K, Molleran WM, Elias PM, Mauro TM: Neonatal development of the stratum corneum pH gradient: localization and mechanisms leading to emergence of optimal barrier function. J Invest Dermatol 2003;120: 998-1006.

6 Fluhr JW, Behne MJ, Brown BE, Moskowitz DG, Selden C, Mao-Qiang M, Mauro TM, Elias PM, Feingold KR: Stratum corneum acidification in neonatal skin: secretory phospholipase A2 and the sodium/hydrogen antiporter-1 acidify neonatal rat stratum corneum. J Invest Dermatol 2004;122: 320-329.

7 Chapman SJ, Walsh A: Membrane-coating granules are acidic organelles which possess proton pumps. J Invest Dermatol 1989;93:466-470.

8 Hachem JP, Crumrine D, Fluhr J, Brown BE, Feingold KR, Elias PM: pH directly regulates epidermal barrier homeostasis, and stratum corneum integrity/cohesion. J Invest Dermatol 2003;121: 345-353.

9 Yoipovitch G: Dry skin and impairment of barrier function associated with itch - New insights. Int J Cosmet Sci 2004;26:1-7.

10 Hildebrandt D, Ziegler K, Wollina U: Electrical impedance and transepidermal water loss of healthy human skin under different conditions. Skin Res Technol 1998;4:130-134.

11 Kligman AM: Hydration injury to human skin: a view from the horny layer; in Kanerva L, Elsner P, Wahlberg JE, Maibach HI (eds): Handbook of Occupational Contact Dermatitis. Berlin, Springer, 2000, pp 76-80.

12 Wollina U: Der diabetische Fuss - Eine Übersicht für Dermatologen. Z Hautkrankh 1999;74: 265-270.

13 Tronnier H: Wirkungen von Textilien an der menschlichen Haut. Dermatol Beruf Umwelt/Occup Environ Dermatol 2002;50:5-10.

14 Grubauer G, Elias PM, Feingold KR: Trans-epidermal water loss: the signal for recovery of barrier structure and function. J Lipid Res 1989;30:323-333.

15 Fisher AA: Non-allergic 'itch' and 'prickly' sensation to wool fibres in atopic and non-atopic persons. Cutis 1996;58:323-324.

16 Williams JR, Burr ML, Williams HC: Factors influencing atopic dermatitis - A questionnaire survey of schoolchildren's perceptions. Br J Dermatol 2004;150:1154-1161.

17 Kiriyama T, Sugiura H, Uehara M: Residual washing detergent in cotton clothes: a factor of winter deterioration of dry skin in atopic dermatitis. J Dermatol (Tokyo) 2003;30:708-712.

18 Matthies W: Tensidrückstände auf gewerblicher Wäsche und ihre Bedeutung für die dermatologische Verträglichkeitsbewertung. Dermatol Beruf Umwelt/Occup Environ Dermatol 2001;49: 102-107.

19 Asakura H: Foetal and neonatal thermoregulation. J Nippon Med Sch 2004;71:360-370.

20 Cotter JD, Taylor NA: The distribution of cutaneous sudomotor and alliesthesial thermosensitivity in mildly heat-stressed humans: an open-loop approach. J Physiol 2005;565:335-345.

21 Havenith G: Clothing and thermoregulation; in Elsner P, Hatch K, Wigger-Alberti W (eds): Textiles and the Skin. Curr Probl Dermatol. Basel, Karger, 2003, vol 31, pp 35-49.

22 Inbar O, Morris N, Epstein Y, Gass G: Comparison of thermoregulatory responses to exercise in dry heat among pre-pubertal boys, young adults and older males. Exp Physiol 2004;89: 691-700.

23 De Pasquale DM, Buono MJ, Kolkhorst FW: Effect of skin temperature on the cholinergic sensitivity of the human eccrine sweat gland. Jpn J Physiol 2003;53:427-430.

24 Nguyen MH, Tokura H: Sweating and tympanic temperature during warm water immersion compared between Vietnamese and Japanese living in Hanoi. J Hum Ergol (Tokyo) 2003;32: 9-16.

25 Rosene JM, Whitman SA, Fogarty TD: A comparison of thermoregulation with creatine supplementation between the sexes in a thermo-neutral environment. J Athletic Training 2004;39:50-55.

26 Charkoudian N: Skin blood flow in adult thermoregulation: how it works, when it does not, and why. Mayo Clin Proc 2003;78:603-612.

27 Ribeiro GA, Rodrigues LO, Moreira MC, Silami-Garcia E, Pascoa MR, Camargos FF: Thermoregulation in hypertensive men exercising in the heat with water ingestion. Braz J Med Biol Res 2004;37:409-417.

28 Stocks JM, Taylor NA, Tipton MJ, Greenleaf JE: Human physiological responses to cold exposure. Aviat Space Environ Med 2004;75:444-457.

29 Pascoe DD, Shanley LA, Smith EW: Clothing and exercise. I. Biophysics of heat transfer between the individual, clothing and environment. Sports Med 1994;18:38-54.

30 Pascoe DD, Bellingar TA, McCluskey BS: Clothing and exercise. II. Influence of clothing during exercise/work in environmental extremes. Sports Med 1994;18:94-108.

31 Gavin TP: Clothing and thermoregulation during exercise. Sports Med 2003;33:941-947.

32 Gavin TP, Babington JP, Harms CA, Ardelt ME, Tanner DA, Stager JM: Clothing fabric does not affect thermoregulation during exercise in moderate heat. Med Sci Sports Exerc 2001;33:2124-2130.

33 Barker DW, Kini S, Bernard TE: Thermal characteristics of clothing ensembles for use in heat stress analysis. Am Ind Hyg Assoc J 1999;60:32-37.

34 Cheuvront SN, Kolka MA, Cadarette BS, Montain SJ, Sawka MN: Efficacy of intermittent, regional microclimate cooling. J Appl Physiol 2003;94:1841-1848.

35 Li Y: Perceptions of temperature, moisture and comfort in clothing during environmental transients. Ergonomics 2005;48:234-248.

36 Hatch KL, Maibach HI: Textiles; in Kanerva L, Eisner P, Wahlberg JE, Maibach HI (eds): Handbook of Occupational Dermatology. Berlin, Springer, 2000, pp 622-636.

37 Le Coz C-J: Clothing; in Rycroft RJG, Menné T, Frosch PJ, Lepoittevin J-P (eds): Textbook of Contact Dermatitis, ed 2. Berlin, Springer, 2001, pp 725-749.

38 Da Rocha AM: Development of textile-based high-tech products: the new challenge. Stud Health Technol Inform 2004;108:330-334.

39 Meinander H, Hinkala M: Potential applications of smart clothing solutions in health care and personal care. Stud Health Technol Inform 2004;108:278-285.

40 Schultze C, Burr S: Market research on garment-based 'wearables' and biophysical monitoring and a new monitoring method. Stud Health Technol Inform 2004;108:111-117.

41 Roth RR, James WD: Microbial ecology of the skin. Annu Rev Microbiol 1988;42:441-464.

42 Nicolas P, Vanhoye D, Amiche M: Molecular strategies in biological evolution of antimicrobial peptides. Peptides 2003;24:1669-1680.

43 Izadpanah A, Gallo RL: Antimicrobial peptides. J Am Acad Dermatol 2005;52:381-390.

44 Zanetti M: Cathelicidins, multifunctional peptides of the innate immunity. J Leukoc Biol 2004;75: 39-48.

45 Mangoni ML, Papo N, Mignogna G, Andreu D, Shai Y, Barra D, Simmaco M: Ranacyclins, a new family of short cyclic antimicrobial peptides: biological function, mode of action, and parameters involved in target specificity. Biochemistry 2003;42:14023-14035.

46 Murakami M, Ohtake T, Dorschner RA, Schittek B, Garbe C, Gallo RL: Cathelicidin anti-microbial peptide expression in sweat, an innate defence system for the skin. J Invest Dermatol 2002;119: 1090-1095.

47 Oren A, Ganz T, Liu L, Meerloo T: In human epidermis, beta-defensin 2 is packed in lamellar bodies. Exp Mol Pathol 2003;74:180-182.

48 Schittek B, Hipfel R, Sauer B, Bauer J, Kallenbacher H, Stevanovic S, Schirle M, Schroeder K, Blin N, Meier F, Rassner G, Garbe C: Dermicidin: a novel human antibiotic peptide secreted by sweat glands. Nat Immunol 2001;2:1133-1137.

49 Dorschner RA, Lin KH, Murakami M, Gallo RL: Neonatal skin in mice and humans expresses increased levels of antimicrobial peptides: innate immunity during development of the adaptive response. Pediatr Res 2003;53:566-572.

50 Yoshio H, Tollin M, Gudmundsson GH, Lagercrantz H, Jornvall H, Marchini G, Agerberth B: Antimicrobial polypeptides of human vernix caseosa and amniotic fluid: implications for newborn innate defense. Pediatr Res 2003;53:211-216.

51 Sorensen OE, Cowland JB, Theilgaard-Mönch K, Liu L, Ganz T, Borregaard N: Wound healing and expression of antimicrobial peptides/polypeptides in human keratinocytes, a consequence of common growth factors. J Immunol 2003;170:5583-5589.

52 Donnarumma G. Paoletti I, Biommino E, Orlando M, Tufano MA, Baroni A: Malassezia furfur induces the expression of beta-defensin-2 in human keratinocytes in a protein C-dependent manner. Arch Dermatol Res 2004;295:474-481.

53 Chung WO, Dale BA: Innate immune response of oral and foreskin keratinocytes: utilization of different signalling pathways by various bacterial species. Infect Immun 2004;72:352-358.

54 Adams BB: Dermatologic disorders of the athlete. Sports Med 2002;32:309-321.

55 Edwards JV Vigo Tl: Bioactive Fibres and Polymers. Weimar/Texas, Culinary and Hospitality Industry Publications Service, 2001.

56 Haufe H, Thron A, Fiedler D, Mahltin B, Böttcher H: Biocidal nanosol coatings. Surf Coatings Int B Coating Trans 2005;88:55-60.

57 Deparis X, Frere B, Lamizana M, N'Guessan R, Leroux F, Lefevre P, Finot L, Hougard JM, Carnevale P, Gillet P, Baudon D: Efficacy of permethrin-treated uniforms in combination with DEET topical repellent for protection of French military troops in Côte d'Ivoire. J Med Entomol 2004;41:914-921.

58 Deitch EA, Marino AA, Malakanok V Albright JA: Silver nylon cloth: in vitro and in vivo evaluation of antimicrobial activity. J Trauma 1987;27:301-304.

59 Borkow G, Gabbay J: Putting copper into action: copper-impregnated products with potent bio-cidal activities. FASEB J 2004;18:1728-1730.

60 Gauger A, Mempel M, Schekatz A, Schäfer T, Ring J, Abeck D: Silver-coated textiles reduce Staphylococcus aureus colonization in patients with atopic eczema. Dermatology 2003;207: 15-21.

61 Mempel M, Voelcker V Kollisch G, Plank C, Rad R, Gerhard M, Schnopp C, Fraunberger P, Malli AK, Ring J, Abeck D, Ollert M: Toll-like receptor expression in human keratinocytes: nuclear factor kappaB controlled gene activation by Staphylococcus aureus is toll-like receptor 2 but not toll-like receptor 4 or platelet activating factor receptor dependent. J Invest Dermatol 2003;121: 1389-1396.

62 Gavrin AJ, Gonyer RG, Blizard KG, Santos L: Medical textiles for uniform bacteria mitigation. 24th Army Sci Conf Proc, Orlando, 2004, KS-16.

63 BfR - Federal Institute for Risk Assessment: Exercise caution when using disinfectants! Press release 2004.

64 Lansdown AB, Williams A: How safe is silver in wound care? J Wound Care 2004;13:131-136.

65 Meloni GA, Schito GC: Microbial ecosystems as targets of antibiotic actions. J Chemother 1991;3(suppl 1):179-181.

66 Savey A, Fleurette J, Salle BL: An analysis of the microbial flora of premature neonates. J Hosp Infect 1992;21:275-289.

67 Korting HC, Lukacs A, Braun-Falco O: Mikrobielle Flora und Geruch der gesunden menschlichen Haut. Hautarzt 1988;39:564-568.

68 Takai K, Ohtsuka T, Suda Y, Nakao M, Yamamoto K, Matsuoka J, Hirai Y: Antibacterial properties of antimicrobial-finished textile products. Microbial Immunol 2002;46:75-81.

69 Chen D, Haviland-Jones J: Human olfactory communication of emotion. Percept Mot Skills 2000;91:771-781.

70 Rikowski A, Grammer K: Human body odour, symmetry and attractiveness. Proc R Soc Lond B Biol Sci 1999;266:869-874.

71 Austin C, Ellis J: Microbial pathways leading to steroidal malodour in the axilla. J Steroid Biochem Mol Biol 2003;87:105-110.

72 Kalyon BD, Olgun U: Antibacterial efficacy of triclosan-incorporated polymers. Am J Infect Control 2001;29:124-125.

73 Wollina U: Streit um antimikrobiell ausgerüstete Textilien - Geruchskiller in Socken und Höschen: Gefahr für die Haut? (Interview). MMW - Fortschr Med 2004;146:14.

74 Pirot F, Millet J, Kalia YN, Humbert P: In vitro study of percutaneous absorption, cutaneous bioavail-ability and bioequivalence of zinc and copper from five topical formulations. Skin Pharmacol 1996;9:259-269.

75 Moss T, Howes D, Williams FM: Percutaneous and dermal metabolism of triclosan (2,4,4'-trichloro-2'-hydroxydiphenyl ether). Food Chem Toxicol 2000;38:361-370.

76 Ohge H, Furne JK, Springfield J, Ringwala S, Levitt MD: Effectiveness of devices purported to reduce flatus odor. Am J Gastroenterol 2005;100:397-400.

77 Wollina U, Heide M, Müller-Litz W, Obenauf D, Ash J: Functional textiles in prevention of chronic wounds, wound healing and tissue engineering; in Elsner P, Hatch K, Wigger-Alberti W (eds): Textiles and the Skin. Curr Probl Dermatol. Basel, Karger, 2003, vol 31, pp 82-97.

78 Kurz J: Laundering in the prevention of skin infections; in Elsner P, Hatch K, Wigger-Alberti W (eds): Textiles and the Skin. Curr Probl Dermatol. Basel, Karger, 2003, vol 31, pp 64—81.

U. Wollina, MD Head of Department

Department of Dermatology, Hospital Dresden-Friedrichstadt Academic Teaching Hospital of the Technical University of Dresden Friedrichstrasse 41 DE-01067 Dresden (Germany)

Tel. +49 351 480 1210, Fax +49 351 480 1219, E-Mail [email protected]

Interactions between Skin and Biofunctional Metals

Hipler U-C, Elsner P (eds): Biofunctional Textiles and the Skin. Curr Probl Dermatol. Basel, Karger, 2006, vol 33, pp 17-34

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