Is skin color expression of racial differences in skin function ?
Skin color and thus melanin content of the skin are a most striking differences characterizing racial groups. Is skin function related to skin color 7 Is skin color related to modulation of racial differences in skin responses to chemical and environmental agents ?
Racial differences in skin function have been investigated: Weigand et al (1,2) showed increased intracellular cohesion in blacks; Reinertson and Wheatley (3) higher lipid content in black skin; furthermore, blacks have higher electrical skin resistance levels that whites (4,5).
Mechanisms explaining these differences are minimally documented. By measuring some
biophysical parameters of the skin, we have investigated and classified racial differences
in skin reactions after a variety of stimuli with the hypothesis that understanding the
basic skin differences among the races will provide insights into skin function.
As early as 1919 (6) reactions to dichloroethylsulfide were investigated in blacks and whites revealing a decreased susceptibility ot cutaneous irritants in the former group. Weigand and Gaylor (7) measured the minimal perceptible erythema in blacks and whites after application of DNCB reporting the same findings; this difference was not detectable in stripped skin. Hence, the stratum corneum seemed to modulated different racial responses to irritants.
Recently,. we demonstrated different skin responses to chemical irritation in races after exposure to sodium lauryl sulphate (SLS) (8). Irritant reactions were monitored by means of laser Doppler velocimetry (LDV), transepidermal water loss (TEWL) and stratum corneum water content (WC). The tests were performed on untreated skin and skin pre-treated with short term occlusion or pre-delipidized with ethyl acetate.
LDV reveales significant changes in the untreated and pre-occluded white skin (P<
0.05 and < 0.01 respectively). In blacks the values were different only in the
pre-occluded skin. The TEWL and WC responses demonstrated a higher susceptibility of black
skin to SLS and a different modulation of irritant reactions after exposure to different
amounts of irritant.
On the other hand, there was less erythema in black than white skin and significant differences were appreciable only after the pre-treatments. Probably, not only it is more difficult to detect erythema in black skin, but black skin reacts with a decreased blood flow. This could explain the findings of decreased minimal perceptible erythema in blacks (7).
The same experimental design was undertaken to investigate irritant reactions in hispanics (9). TEWL levels after SLS irritation were higher in hispanics. Namely after delipidization. There is a significant linear relationship between the baseline and the degree of response elicited in hispanics; the higher the baseline, the higher the response for 2.02 SLS. This implies that hispanics develop higher TEWL responses when injured with concentrated chemicals; their water barrier modulation is greater than whites. From this point of view hispanic skin is comparable to the black one (8). On the other hand, the erythematous reaction of hispanic and white skin was strikingly similar. We conclude hispanic skin has some functional features comparable to whites (i.e. erythematous reaction) while other characteristics mirror blacks (i.e. water barrier function).
Racial differences in TEWL between blacks and whites are confirmed with an in vitro technique (10) where the data are more homogeneous, since obtained in absence of sweating and other vital functions. The study reveals a remarkable separation between the two groups with absolute TEWL values significantly higher (P < 0.01) in blacks.
The different racial susceptibility to nicotinates was investigated as a model to evaluate transcutaneous penetration (11).
Two different nicotinates were applied to normal skin and to skin hydrated with previous occlusion or delipidized. The comparison between blacks and whites revealed lower values in the black group for the area under the curve reponse in sites pre-occluded or delipidezed (P < 0.04); for initial response and peak response in pre-occluded sites (P < 0.01). No significant differences were recorded in the responses to the two nicotinates.
Skin surface lipids may play a role in modulating the initial penetration of nicotinates. The study confirms the conventional belief that black skin resists the penetration of some chemicals better than white. Differential effects on penetration due to occlusion (hydration of the stratum corneum) and delipidization (barrier modulation) are suggested. Hispanics did not show differences of nicotinate induced vasodilatation when compared to whites (12). The study confirmed partially the findings reported previously by Guy et al (13). Differences between whites and blacks in post-occlusive reactive hyperemia occur (14) after application of topical corticoids.
The data is consistent with a decreased reactivity of blood vessels in blacks during the hyperemic reaction due to either an increased removal of a vasodilator metabolite which accumulates during occlusion time, or to a different viscoelastic response of the arteriolar wall in black race.
The relatively sparse data supports that there are racial differences (between whites and blacks) in some anatomical and physiological functions of the skin and that these differences could be involved in determining racial patterns in skin behavious, namely response to irritant chemicals and penetration of topically applied drugs. Hispanics, although not completely different from whites seem to have a different reaction pattern.
Non invasive bioengineering techniques continue to add relevant data, allowing repeated, reliable and comparable measures of skin properties; non visible changes such as water content of the stratum corneum and transepidermal water loss may be estimated and quantified resulting in improved standardization of racial differences and responses to environmental and or topical agents.
01. Weigand DA, Haygood C, Gaylor JR: Cell layers and density of negro and caucasian
stratum corneum. J Invest Dermatol 62:563-568, 1974.
02. Thomson ML: Relative efficiency of pigment and horny layer thickness in protecting the skin af Europeans and Africans against solar ultraviolet radiation. J Physiol (London) 127:236-246, 1955.
03. Reinertson RP, Wheatley VR: Studies on the chemical composition of human epidermal lipids. J Invest Dermatol 32:49-59, 1959.
04. Johnson LC, Corah NL: Racial differences in skin resistance. Science 139:766-767, 1960.
05. Korol B, Bergfeld GR, Goldman H, Mc Laughlin LJ: Use of the pigmentometer, a new device for measuring skin albedo: relating skin color with a series of physiological measures. Pavlov J Biol Sci 12:19-31, 1977.
06. Marshall EK, Lynch V, Smith HV: Variation in susceptibility of the skin to dichloroethylsulfide. J Pharmacol Exp Ter 12:291, 1919.
07. Weigand DA, Gaylor JR: Irritant reactioni in Negro and Caucasian skin. South Med J 67:548-551, 1974.
08. Berardesca E. Maibach HI: Racial differences in sodium lauryl sulphate induced cutaneous irritation black and white. Contact Dermatitis 17:12-17, 1987.
09. Berardesca E, Maibach EI: Sodium lauryl sulphate induced cutaneous irritation:comparison of white and hispanic subjects. Contact Dermatitis 19:136-140, 1988.
10. Wilson D, Maibach HI. Berardesca E : In vitro transepidermal water loss : black and white human skin differences. Brit J Dermatol 119:647-652, 1988.
11. Berardesca E, Maibach HI: Racial differences of percutaneous penetration of nicotinates in vivo in human skin black and white. Acta Dermato Venereol (Stockholm). In press, 1989.
12. Berardesca E, Maibach HI: Effect of race on percutaneous penetration of nicotinates on human skin comparison of whites and hispanics. Bioeng Skin 4:15-22, 1988.
13. Guy RH, Tur E, Bierke S, Maibach HI : Are there age and racial differences to methyl nicotinate induced vasodilatation in hunan skin 7 J Am Acad Derm 12:1001, 1985.
14. Berardesca E, Maibach HI: Cutaneous reactive hyperemia : racial differences induced by corticoid application. Brit J Dermatol 120;787-794, 1989.
Dept of Dermatology
University of Pavia
IRCCS Policlinico S. Matteo
27100 Pavia, Italy
Dept of Dermatology
University of California
San Francisco, CA, USA