You are on page 1of 4

COli tact Derlllatitis. 1999. 41.

3 11- 314 Copyright CI Mu" ksgaard 1999


Prill/ed ill Delllllark , All rights reserved
CONTACT DERMATITIS
ISSN 0105·1873

Review Article

How irritant is water? An overview


TSEN-FANG TSAI 1•2 AND HOWARD I. MAIBACH 1
IDepartment of Dermatology, University of California, San Francisco, California and
2Na tional Taiwan University Hospital, Taipei, Taiwan, ROC

Water is a skin irritant which deserves attention because of its ubiqujty. During the Vietnam
war, soldiers suffered from painful swollen feet, so-called tropical immersion foot. In occupational
dermatology, the importance of water as a skin irritant is especially appreciated. The irritancy of
water has been demonstrated by occlusion experiments; occlusion with either closed chambers or
water-soaked patches has been shown to produce clinical and histopathological inflammation .
Functional damage, as revealed by increased transepidermal water loss, bas also been shown.
Repeated water exposure without occlusion caused an increase in blood flow on irritated skin;
however, clinical evaluation did not show a difference in dryness or scaling. Several mechanisms
such as osmolarity, pH, hardness and temperature might account for the irritancy of water. Extrac-
tion or dilution of natural moisturizing factors in the stratum corneum is another po sible expla-
nation. Occlusion per se also changes the physiology of skin and may trigger the activation of
potentially active substances. However, much remains to be done to clarify the risk factors and
mechanisms of water-induced irritation .
Key lVords: water; cumulative irritation; occlusion; irritant contact dermatitis; tropical immersion
foot; occupational; wet work; natural moisturizing factors ; stratum corneum. © Munk gaard.
1999.
Accepted for publication 2 June 1999

When and how is water detrimental to skin? Pro- perimental data on water irritancy. Willis demon-
longed warm water immersion resulted in painful strated the development of clinical and patholog-
swollen feet, so-called tropical-immersion-foot, in ical effects after closed water cup occlusion for 72-
Vietnam (1). Repeated water immersion with 144 h. Buffered water (4 ml/4.0 cm 2 at pH 7.5
periods of drying in between was implicated as a showed stronger reaction as compared to water at
cause of juvenile plantar dermatosis (2). Frequent pH 3.5. Empty cups were u ed as a control, and
or prolonged bathing and showering, even without showed milder changes (14). Kligman occluded
the use of soap, i often discouraged for the care normal skin with water-soaked patche (volume
of dry and senile skin (3). Wet workers such as not provided) of unwoven cloth, for up to 2 weeks
hairdre er, hospital cleaners, cannery workers with changes every 2 days, and induced "hydration
and bartenders have an increased incidence of dermatitis" characterized by vasodilation periven-
hand eczema (4-7). Water may be an irritant in ular lymphocytic infiltration, edema, mast cell
patients with hand eczema, especially in atopic pa- degradation and fibroblast proliferation. Damage
tient (8, 9). Rarely, water may produce pruritus to epidermal cell occurred quickly and wa fully
(la, 11) or urticaria (12, 13). In view of the ap- developed by 2 days. Occlusion with a water-per-
parent potential detrimental effect of water, the ir- meable membrane or a water-ab orbent dre ing
ritancy of tepid water has been tudied , but much for 3 weeks was, however, relati ely innocuous
remain to be elucidated in terms of risk factors (15).
and mechanism . Agner & Serup (16) tudied kin reaction after
Occlu ive studie have produced most of the ex- clo ed patche and showed tran ient water damage
312 TSAI & MAIBACH

as demonstrated by increased transepidermal ecological environment and support the over-


water loss after occlusion for 24 h. However, the growth of pathological organisms on the skin (36-
irritancy of water under occlusion can result from 38).
water per se or from retention of sweat, which is Extraction of water-soluble substances, or
more irritant than the water per se (17). Notwith- natural moisturizing factors (NMFs), from the
standing, after prolonged occlusion, anhidrosis re- skin is another mechanism. NMFs are a group
sults (18- 20). Occlusion modifies reactive events in of water-extractable substances, including sodium
Langerhans cells (21, 22), and has a profound ef- pyrrolidone carboxylic acid, sodium calcium lac-
fect on cytokine production (23). Not all physio- tate, amino acids, urea and a sugar-protein com-
logical changes from occlusion are damaging to plex. These substances can bind 3 to 4 x their
the skin. Occlusive dressings alone have been used own weight of water (39). Water is the main plas-
as effective adjuvant therapy (24-26). The alleged ticizing factor of the horny layer (40), and the
healing power of silicon gel sheet on keloids is con- presence of water in the stratum corneum de-
sidered to be through its occlusiveness (27) and oc- pends on an intercellular bilayer membrane that
clusion has also been used to treat psoriasis (28) encloses the NMFs as in an envelope. Water con-
and periungual verrucae (29). tent of the stratum corneum decreases when the
To separate the influence of occlusion from the NMFs are reduced, and superficial cracks may
influence of water, Ramsing & Agner (30) studied develop. The amino acid content of senile skin is
the effect of water on experimentally irritated skin decreased, and frequent showering combined with
in healthy volunteers, to evaluate water as a cumu- a delay in the replenishment of NMF may
lative irritant. Volunteers exposed one hand to further aggravate this situation (4 1, 42). How-
water IS min 2Xdaily for 2 weeks, while the other ever, intercellular lipids have been identified as
hand served as control. Water did not significantly the major factors in maintaining water content of
influence transepidermal water loss, but caused a the stratum corneum, and the significa nce of
significant increase in skin blood flow, as evaluated NMFs is not indisputable (43).
by laser Doppler flowmetry. However, clinical The irritancy of water could theoretically also
evaluation did not show a difference in .dryness or result from the neutral pH 7.0, which is alkaline
scaling (30), and erythema alone does not equate compared to normal skin pH (4.2 to 6.0). The
to irritancy. neutralization capacity of lesional skin in hand ec-
An irritant is any agent, physical or chemical, zema appears to be defective (44). However, since
capable of producing cell damage if applied for water has no buffering capacity, the irritancy of
sufficient time and in sufficient concentration. Im- water pH is somewhat doubtful. Besides, the sig-
munological processes are not involved. Strong ir- nificance of skin surface acidity is under dispute
ritants will induce a clinical reaction witb a single (4S). Hypotonicity of pure water may be irritant
application, whereas with less potent irritants, the on abraded skin (46), and change of water pressure
response may be subclinical and require repeated gradient acro s the stratum corneum, which may
or prolonged application (31). Weaker irritants in- trigger the release of cytokines (47, 48), may also
duce damage by gradually exhausting the horny playa role in the irritancy of water. Kligman sug-
layer, denaturing the keratin, removing stratum gested that the skin may also contain several po-
corneum lipids and altering the water-holding ca- tentially active substance that may become active
pacity of the skin (32). Such damage results in a when hydrated (49). Clearly, contam inants and
drier, less pliable surface, which might result in hardness of water (SO), as well as osmolarity (SI)
cracks and fissures. Water is considered a weak ir- and temperature (S2), are also important to the
ritant. Theoretically, water can exert detrimental irritancy of water.
effects on the skin through several mechanisms. In conclusion, water can be an irritant and the
Hydration of the stratum corneum may facilitate dictum of Kligman that "almost any substance
the penetration of foreign substances, and contrib- can be an irritant under some circumstances"
ute to the development of allergic and irritant con- (S3) also applie to plain water. Water exposure
tact dermatitis (33). The same principle is also can modify physiologic functions of the skin and
used in occlusive dressing therapy to enhance the produces skin disease. But most of the reported
therapeutic effects of topical preparations such as irritancy of water may result mainly from oc-
corticosteroids (34). Brief wash ing enhances re- clusion or from occlusion as an additive fa ctor.
sponse to some non-immunologic contact urt- However, ince water expo ure is ubiquitous,
icants and some other materials. This phenom- more studies are warranted to elucidate the
enon is relevant to the use of soap and water in mechanisms of its irritancy. Patient care should
routine cosmetic skin care (3S). Persistent hy- improve when we know better the biology of
dration of the skin surface may also change the water and kin.
THE IRRITANCY OF WATER 313

C, Feingold K R. Occlusion lowers cytokine mRNA


References levels in essential fatty acid-deficient and normal mouse
I. Allen A M. Taplin D. Tropical immersion foot. Lancef epidermis, but not after acute barrier disruption. J [/II'eST
1973: 2: 1185- 1189. Dermatol 1994: 103: 834-838.
2. Steck W D. Juvenile plantar dermatosis: the " wet a nd dry 24. Berardesca E, Maibach H r. Skin occlusion: treatment or
foot syndrome". Cleveland Clinic Quarterly 1983: 50: drug-like device? Skin Pharmacol 1988: 1: 207- 215.
145 149. 25. Witkowski J A, Parish L C. Occlusive therapy in histori-
3. Hogstel M O. Skin care for the aged. J Gerontol Nursing cal perspective. lIlT J Derlllatol 1998: 37: 555- 558.
1983: 9: 431-443. 436-437. 26. Broby-Johansen U, Kristensen J K. Antipsoriatic effect
4. Rustemcyer T. Frosch P 1. Occupational skin diseases in of semi-occlusive treatment- 02-consumption, blood flow
dcntal laboratory technicians (T). Clinical picture and and temperature measurement compared to clinical par-
causative factors. COl/fact Derll1atitis 1996: 34: 125- 133. ameters. Clin Exp Dermarol 1989: 14: 286-288.
5. Meding B. Swanbeck G. Occupational hand eczema in an 27. Sawada Y, Sone K. Hydration and occlusion treatment
industrial city. Conflict Dermafifis 1990: 22: 13- 23. for hypertrophic scars and keloids. Br J Plasf Surg 1992:
6. Nilsson E. Individual and environmental risk factors for 45: 599- 603.
hand eczcma in hospital workers. ACfll Derll/ato-venereol- 28. Baxter D L, Stoughton R B. Mitotic index of p oriatic
ogica 1986: 128 (sllppl): I 63. lesions treated with anthralin, glucocortico teriod and oc-
7. Nilsson E. Mikaelsson B. Andersson S. Atopy, occu- clu ion only. J Invest Dermatol 1970: 54: 410-412.
pation and domestic work as risk factors for hand ec- 29. Lilt J Z. Don 't excise-exorci e. Treatment for subu ngu a l
zcma in hospital workers. COl/tact Derlllatitis 1985: 13: and periungual warts. Cutis 1978: 22: 673 676.
216 223. 30. Ramsing D W, Agner T. Effect of water on experimen-
8. Forsbeck M. Skog E, Asbrink E. Atopic hand dermatitis: tally irritated human skin. Br J Dermarol 1997: 136: 364-
a comparison with atopic dcrmatitis without hand in- 367.
volvement, especially with respect to influence of work 31. Wilkinson J D, Rycroft R J G. Contact dermatitis. Tn:
and development of contact sensitization. Acta Dermato- Champion R H, Burton J L , Ebling F J G. (eds): Text-
vel/ereologica 1983: 63: 9- 13. book of derlllafology. 5th edition. Oxford: Blackwell
9. Lammintausta K. Kalimo K. Atopy and hand dermatitis Scientific, 1992: 616.
in hospital wet work. COlllact Derlllatifis 1981: 7: 301 - 32. Fulmer W A. Kramer G 1. Stratum corneum lipid abnor-
308. malities in surfactant induced dry scaly skin. J Invest
10. Potasman I. Heinrich I. Bassan H M. Aquagenic pru- Dermatol 1986: 86: 598- 802.
ritus: prevalence and clinical characteristics. lsI' J Med 33. Van dcr Valk P G , Maibach H I. Post-application oc-
Sci 1990: 26: 499- 503. clusion substantially increases the irritant response of the
II . Bircher A J, Meier-Ruge W. Aquagenic pruritus. Water- skin to repeated short-term sodium lauryl sulfate (SLS)
induced activation of acetylcholinesterase. Arch Dennatol exposure. ConracT DermatiTis 1989: 21: 335 338.
1988: 124: 84-89. 34. Saucr G C. Sulzberger on ACTH , corticosteroids, and
12. Medeiros M Jr. Aquagenic urticaria . J II/vest AI/ergol occlusive dre sing therapy. lilt J DermaTo/ 1977: 16: 362-
C/in 1II11l111noi 1996: 6: 63- 64. 364.
13. Czarnetzki B M, Breetholt K H, Traupe H . Evidence 35. Lahti A , Pylviinen V. Hannuksela M . Immediate irritant
that water acts as a carrier for an epidermal antigen in reactions to benzoic acid are enhanced in washed skin
aquagenic urticaria . J AI1I Acad Dermatol 1986: 15: 623- areas. Contact Dermatitis 1995: 33: 177 182.
627. 36. Faergemann J, Aly R, Wilson D R , Maibach H I. Skin
14. Willis I. The effects of prolonged water cxposure on hu- occlusion: effect on Pityrosporum orbiculare, skin PC0 2 ,
man skin. J II/I'es f Dermafol 1973 : 60: 166- 171. pH , transepidermal water loss, and water content. Arch
15. Kligman AM . Hydration injury to the skin. In: van der Dermatol Res 1983: 275: 383- 387.
Valk P G M, Maibach H I (eds) The irritant contact der- 37. Aly R, Shirley C, Cunico B, Maibach H I. Effect of pro-
maTiTis sYl/drome. Boca Raton , Florida: CRC Press, 1996: longed occlusion on the microbial flora, pH, carbon diox-
187 194. ide and transepidermal water loss on human skin. J 1n-
16. Agner T. Serup J. Time course of occlusive effects on vest Dermatol 1978: 71: 378- 381.
skin evaluated by mea urement of transepidermal water 38. Rajka G , Aly R , Bayles C, Tang Y, Maibach H . The ef-
loss (TEWL). COl/taCT DermaTitis 1993: 28: 6- 9. fect of short-term occlusion on the cutaneous flora in
17. Hu H . Sweat-related dermatoses: old concept and new atopic dermatitis and psoria is. Acta Demlato-veflereolog-
scenario. DermaT%gica 1991 : 182: 73- 76. ica 1981: 61: 150-153 .
18. Gordon B I. Maibach H I. On the mechanism of the in- 39. Jacobi 0 K. About the mechanism of moisture regulation
active eccrine human sweat gland. Arch Dermato/ 1968: in the horny layer of the skin. Proc Sci Section of tire
97: 66 68. Toilet Goods Association 1959: 31 : 22- 24.
19. Sulzberger M B. Harri DR . Miliaria and anhidrosis. 3. 40. Bank I H . Factors which influence the water content of
MUltiple mall patche and the effects of different periods the stratum corneum. J Inl'est Dermarol 1952: 18: 433-
of occlu ion. Arch Derl1latol 1972: 105: 845- 850. 440.
20. Papa C M. Mechanisms of eccrine anidrosis. 3. Scanning 41. Jacobson T M, Yliksel K U, Geesin J C, Gordon J S,
electron microscopic study of poral occlusion. J Invest Lane A T, Gracy R W. Effects of aging and xerosis on
Dermotol 1972: 59: 295- 298. the amino acid compo ition of human skin . J IIJI'est
21. Mikulowska A . Reactive changes in human epidcrmis fol- Demlatol 1990: 95: 296-300.
lowing imple occlu ion with water. ContaCT Dermatitis 42. Tezuka T, Qing J, Saheki M , Kusuda ,Takaha hi M .
1992: 26: 224-227. Terminal differentiation of facial epidermi of the aged:
22. Mikulowska A . Reactive change in the Langerhans' cclls immunohistochemical studies. Dermatology 1994: 188:
of human kin caused by occlusion with water and so- 21 24.
dium lauryl sulphate. ACTa Derl/1aTo-venereologica 1990: 43 . Tmokawa G. Kuno H , Kawai M . Stratum corneum lipids
70: 468-473. serve as a bound-water modulator. J blveST Dermatol
23. Wood L lias P M. Sequeira-Martin S M , Grunfeld 1991 : 96: 845 851.
314 TSAl & MAl BACH

44. Schieferstein G, Krich-Hlobil K. Alkali neutralization P B, Wong L F. The influence of hard water (calcium)
and alkali resistance in persons with healthy skin and in and surfactants on irritant contact dermatitis. Contact
eczema patients. Dermatosen in Beruf und Umwelt 1982: Dermatitis 1996: 35: 337- 343.
30: 7- 13. 51. Nangia A, Thieberg M, Berner B, Wester R, Maibach H .
45. Schmid M H, Korting H C. The concept of the acid Mechanism of irritation of ba ic drugs on human skin.
mantle of the skin: its relevance for the choice of skin Pharm Res 1990: 7 (suppl): s 188.
cleansers. Dermatology 1995: 191: 276-280. 52. Ohlenschlaeger J, Friberg J, Ramsing D, Agner T. Tem-
46. Fregert S, Hjorth N. The principal irritants and sensi- perature dependency of skin susceptibility to water and
tizers. Primary irritants-water. In: Rook A, Wilkinson D detergents. Acta Dermato-venereologica 1996: 76: 274-
S, Ebling F J G (eds): Textbook of dermatology. Philadel- 276.
phia, F.A. Davis, 1968: 1874. 53. Kligman A M. Quantitative testing of chemica l irritants.
47. Elias P M, Ansel J C, Woods L D, Feingold K R . Sig- ]n: Sternberg T H, Newcomer V D (eds): The evaluation
naling networks in barrier homeostasis. The mystery of therapeutic agents and cosmetics. New York: McGraw-
widens. Arch Dermalol 1996: 132: 1505- 1506. Hill, 1964: 186-192.
48. Nickoloff B 1. Immunologic reactions triggered during ir-
ritant contact dermatitis. Am J Contact Dermatitis 1998:
9: 107- 110.
49. KJigman A M. Hydration: a confounding factor in patch Address:
testing. International Symposium on irritant Contact Der- Howard I. Maibach
matitis, Proceedings (abstr), Groningen, Holland , 3- 5 Oc- Box 0989, Surge 110
to ber, 1991. UCSF Medical Center
50. Warren R, Ertel K D, Bartolo R G, Levine M J, Bryant CA 94143, USA

You might also like