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Black and white human skin differences Klaus E. Andersen, M.D.,* and Howard I. Maibach, M.D. San Francisco, CA This review of black and white human skin differences emphasizes the alleged importance of factors other than the obvious, i.e., skin color. Physicochemical differences and differences in susceptibility to irritants and allergens suggest a more resistant black than white skin. Differences appear to exist in the frequency of which several skin diseases occur among blacks and whites. A striking feature in this literature is the disagreement between authors. Common for much of this information is difficulty of interpretation, because of socioeconomic influences and other environmental factors. (J AM ACAD DERMATOL 1:276-282, 1979.)

Knowledge about differences between black and white skin is scattered. The literature reveals limited clinical and experimental data offering problematic interpretation. The subject has been filled with emotion, misinformation, and misconception, presumably for use in racial discrimination politics. 1 Three important reviews appear in textbooks. 2-4 This paper presents an update; the reader is referred to these reviews for further explanation and interpretations. SKIN DISEASES

At least three mechanisms are involved in explaining the apparent differences in skin disease manifestations in blacks versus whites. 2 First, socioeconomic factors such as income, occupation, diet, hygiene, and health care provide bias in collecting patient data from ethnic groups. Disease prevalence and clinical picture reflect socioeconomic factors. Statistics based on outpatient From the Departmentof Dermatology,Universityof California Medical School. Reprint requests to: Dr. Howard I. Maibach, University of California Scbt~o!of Medicine, Department of Dermatology, San Francisco, CA 94143. *Assisted by Nicholas Laboratories, Liv Bryhns Fond, Knud H~jgaards Fond, C. Carl Petersens Fond, PharmaMediea Fonden, and a Fulbrlght-HaysTravel Grant.

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data give a different perspective than statistics based on population at risk. Second, the clinical presentation of skin diseases in blacks may be modified by environment and the biologic characteristics peculiar to black skin (Table I). The difficulty in recognizing and quantitating erythema in black skin must be remembered. Third, pseudofolliculitjs barbae, 5 acne keloid (dermatosis pillaris capillitii), ~ dermatosis papulosa nigra, ~ and perifolliculitis capitis abscedens et suffodienss are skin diseases related to blacks and infrequently seen in whites. The curved black hair follicle and a peculiar connective tissue response to injury might explain the difference in their occurrence in blacks and whites. ~ Psoriasis is uncommon in American and West African blacks, while the disease is more common among East African blacks, 9-1~ though a little less so than in whites. Prevalence data from African studies are difficult to interpret when up to 79% of black patients were seen for nonsyphilitic infectious diseases versus an incidence of nonsyphilitic infectious diseases of 10% to 40% in African whites, about 9% in American whites, and 3% in English whites. 2 The incidence of systemic lupus erythematosus 0190-9622/79/030276+07500,70/0 9 1979 Am Acad Dermatol

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(SLE) was higher in blacks than in whites in an epidemiologic study in New York. 12 The differences were independent of poor housing, overcrowding, and migration, but were associated with racial differences in the gamma globulin levels. Dubois la refuted the idea of racial differences in the occurrence of lupus erythematosus, suggesting that the differences might be sampling errors. Generalized scleroderma occurs without racial predisposition, 14 but Masi and D'Angelo 1'~found a significantly poorer prognosis in blacks than in whites, and a markedly increased mortality rate for affected black females. Photosensitivities such as drug photosensitivity, allergic photocontact dermatitis, polymorphous light eruption, and persistent light eruption are not infrequent in blacks, while chronic clinically obvious actinic damage, such as solar keratoses, basal cell carcinomas, and keratoacanthomas,t6' t7 occurs uncommonly in blacks. They are subject to squamous cell carcinoma in covered, irritated, infected, or injured areas of the skin; the sites of election differ from those in fair-complexioned people to whom ultraviolet light is the most important predisposing factor.'S' ~9 Oluwasanmi et al2~ found 67% of skin cancers in Nigeria to be squamous cell carcinomas, 24% malignant melanomas, 5% basal cell carcinomas, and 4% Kaposi sarcomas. Malignant melanomas showed predilection for the sole. ~s' 2~ Shah and Goldsmith 22 reported plantar melanoma in 44% of black melanoma patients, while this location contained a malignant melanoma in 6.5% of white patients. The explanation for the differences in location of melanomas is still pending. Obviously, sun exposure plays no part in the development of plantar melanomas. They might arise from preexisting nevi. ~3 Trauma might play a less important role than previously thought. ~s Gellin et a124 compared Caucasian melanoma patients with a matched control group and revealed significant differences with respect to complexion, eye and hair color, and amount of outdoor exposure. The prevalence on the arms of vascular lesions in elderly blacks and nevocytic nevi in young blacks is less than in whites, z.~,z~ Dermatofibrosarcoma protuberans and keloids are more common in Afri-

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Table I. Skin changes more pronounced in blacks* 1. Pigment lability--frequent hyper- and hypopigmentation 2. Follicular responses and follicular diseases 3. Mesenchymal responses: fibroplastic and granulomatous *Adapted from Bmuner CJ: In Moschella SL, Pi/lsburry DM,.Hurley HJ: Dermatology. Philadelphia, 1975, Wo B, Saunders Co,

cans than in Europeans; this provides some evidence of there being a "fibroplastic diathesis" in Africans . 'S Kenney~r, 58 suggested a higher incidence of atopic dermatitis, seborrheic dermatitis, and pityriasis rosea in blacks than in whites. Regarding acne, variable and conflicting results have been reported indicating a lower or equal incidence in blacks compared to whites. 2 Nodulocystic acne occurred with a prevalence o f 5% among 893 white inmates compared to 0.5% among 753 black inmates. The same regional distribution of lesions was found in the two races .,,9 Examining the prevalence of Propionibacterium aches on the foreheads of black and white children, Matta 3~ found that black individuals carried more P. acnes than did whites; this finding might merely reflect differences in the age of puberty. Some investigators found a higher nasal carriage rate of staphylococci in whites than in similarly exposed blacks, interpreted as differences in genetics. 31 Noble s2 confirmed the statement by finding a carriage state of Staphylococcus aureus of 41% in white children against 30% in black children, The difference was statistically significant; no difference was seen in relation to age or sex. He found throat carriage of beta hemolytic streptococci equal in whites and blacks. In Vietnam, there occurred fewer cutaneous streptococcal infections among black American soldiers than among white American soldiers, ss The same low frequency was found among the Vietnamese troops, indicating greater immunity from frequent childhood infections in blacks and Vietnamese, and not genetic differences. Pseudomonas infections have been recorded more often in blacks than in whites. 34 Many American studies, e.g.,

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Hall et al)5 of bacterial skin infections have been done in centers where the vast majority of the patients are black; this makes interpretation of racial differences difficult. Fungal infections were more common in blacks than in whites according to Kenney, 28 who explained the differences by different climates and sampling techniques for the patients studied. Contrary to this, Allen and Taplin a6 found clinical zoophilic Trichophyton mentagrophytes infections less common in black than in white servicemen in Vietnam; these infections were almost nonexistent in Vietnamese soldiers; again, acquired immunity in childhood was suggested as an explanation. They added the clinical observation that these infections in blacks appeared as areas of psoriasiform scaling and hyperpigmentation rather than as red rashes. Skin color

Naturally, much information about racial skin differences deals with pigmentation itself..In whites, the melanosomes are smaller and dispersed in groups inside keratinocytes, whereas in blacks melanosomes are larger and dispersed individually inside the keratinocytes? 7 Dark black skin has a minimal erythema dose thirtyfold that of white skin--greatest density of pigment and the largest melanosomes, a8 but no differences in the number of melanocytes. The size of melanosomes determines the distribution pattern, but this pattern alone does not correlate with the intensity of pigmentation. 39 Harrison 4~ estimated that environmental factors caused between 27% and 36% of the variance in pigmentation, and the component of genetically fixable variation was between 63% and 72%. Further unexplained racial differences in melanoproteins from pooled hair occur; the manganese and copper content is higher in Caucasian melanoprotein than in Bantu melanoprotein, while the iron content is similar in the two groups, even though the Bantu has a higher dietary iron intake and higher serum iron levels than the Caucasian. 4' Epidermal cell autofluorescence is more intense in black than in white skin; it is a natural autofluorescence appearing green in untreated frozen skin sections viewed under a fluorescent microscope. This autofluorescence should be distin-

guished from the fluorescence of the fluorescein antibody conjugate used in immunofluorescence microscopy because each of them shows different light absorption ranges. The location of auto fluorescence corresponds to the sites of melanin, but the compound responsible for the fluorescence is not known.42 Formaldehyde-treated melanocytes develop a green-yellow fluorescence, stronger in melanocytes stimulated to increased melanin production. However, Agrup et al 4a found no increased formaldehyde-induced fluorescence of black epidermal melanocytes; as an explanation, they suggested a quenching effect of the melanin or smaller accumulations within the black melanocytes of the intermediate catechols that can condense with formaldehyde. Physicochemical data

No differences were found between black and white hair using the following techniques: amino acid analysis, gel electrophoresis, and x-ray diffraction. 44 Nails, however, differed significantly in nitrogen content. This appeared to be a racial, not an economic status difference. 45 Weigand et a146 examined anatomophysical properties of black and white skin, measuring the number of layers in, and the density of, the stratum corneum. Blacks required a significantly greater number of cellophane tape strippings than whites for removal of stratum corneum. Similarly, the stratum corneum layer counts were significantly higher among blacks. Within the black group, the degree of pigmentation did not correlate with the number of strips or stratum corneum layer counts. Whether or not the individual number of strips correlated with the number of cell layers was not proved. However, the average stratum corneum thickness was similar in the two groups, indicating that the black stratum corneum was more compact. These studies were performed during late autumn and winter months, when the lumbar skin area tested had not been recently exposed to sunlight. The results of buoyant density measurements of stratum corneum were not clear. Sucrose deny sity gradient ultracenWifugation determinations by Weigand et al revealed greater density for black stratum corneum. When skin lipid effects were

Volume 1 Number 3 September, 1979 minimized by organic solvent mixtures, the reverse was noted. However, Reinertson and Wheatley47 reported a higher lipid content in black stratum corneum, which would not explain the diminishing density for the latter observed in organic solvents by Weigand. Skin resistance

In psychological research, electrodermal measurements have been reported, and, overall, the results demonstrated racial differences. Blacks have higher skin resistance levels (lower conductance, higher impedance) than whites. 48, 49 Korol et aP ~ reported that race influenced skin resistance more than skin color. Mechanisms explaining the differences are only partially documented. Fowles and Rosenberry5' suggest that hydration effects might be involved. Hydration of the epidermis reduces electrical skin resistance and promotes swelling of the stratum corneum, mechanical blockage of the sweat gland pore, and subsequent inhibition of surface sweating. Skin glands

Regarding sweating, contradictory information is available. Anatomically, blacks and whites have the same number of eccrine glands in various anatomic sites) 2 Functionally, Robinson et al 5a found blacks from Mississippi maintained a lower body temperature than whites and blacks from the North during physical work. They were superior in temperature regulation. During work, whites had higher sweat rate than blacks, associated with greater elevation of rectal and skin temperature. On the other hand, they mentioned that blacks were capable of higher rates of sweating than whites. Hermann et a154examined the quantitative delivery of thermogenic sweat from American blacks and whites, fnding no difference between the groups regarding the onset or quantity of sweating. Using pilocarpine or heavy work stimulation on African blacks and whites, McCance et al a5'~6 reported greatest sweat production in whites. The interpretation of sweat studies is difficult because some studies53,5~ compared American blacks and whites, while others compared African blacks and whites.~, 56 The electrophysiologic experiments48, 49 compared American

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blacks and whites. The American blacks constitute a more ethnically mixed group than the African blacks. The answer to the controversial information lies perhaps in adaptation as a superior factor to race regarding sweating. Regarding apocrine glands, Hurley and Shelley 57 found blacks to have larger glands, producing greater amounts of apocrine sweat after epinephrine stimulation or emotional stress than whites. On the other hand, Wollard ~8 demonstrated great individual variation in the distribution and size of apocrine glands, invalidating the use of these for purposes of racial differentiation. Similarly conflicting information exists about the sebaceous glands. 2 Irritation

Regarding occupational medicine, the statement that blacks resist chemical and ultraviolet light skin irritation better than light-skinned persons is at least 60 years old, mentioned in Schwartz, Tulipan, and Birmingham's 59 Occupational Dis. eases of the Skin from 1939, and later by Shelley. 6~ The statement is supported by the work of Marshall et a161 as early as 1919: they dropped 1% dichloroethylsulfide in mineral oil on the arms of whites and blacks and found erythema in 15% of the blacks compared to 59% of the whites. Marshal116, 62 repeated the statement but provided no data to support it. Kenney 28 believed the statement is still open to question. Weigand and Mershon 63 noted more resistant black skin by measuring the minimal perceptible erythema (MPE) using quantitative patch test exposures to o-chlorobenzylidene malononitrile, a lacrimator. Weigand and Gaylor ~ determined MPE on black and white volunteers by applying increasing amounts of dinitrochlorobenzene (DNCB) to the skin of the back. They reported that whites tended to have MPEs at lower concentrations of DNCB than did blacks. On stripped skin, reactivity was more homogenous. They read their tests in a room with artificial lighting, arguing that the differences were not due to perceptual error in reading of erythema, because of constant reading conditions, a dose response curve for each subject, and because the differences were not observed on stripped skin. The possible protective effect of

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melanin granules in black skin was discussed, but they concluded that melanin could not be the main protectant, since it is distributed mainly below the removed stratum corneum. Frosch and Kligman ~5 experienced less susceptibility to irritants in blacks than in whites, but no data were presented. Most studies evaluated irritancy using erythema as the end point in equating white versus black responses; this procedure is questionable because erythema is difficult to detect in black skin, so the differences in irritancy response between the two races might be less pronounced than reported. Sensitization

Leyden and Kligman ~6 found no significant difference in allergic contact dermatitis between black and white people when testing a wide spectrum of materials for topical use by the updated maximization procedure. 67 In earlier reports, Kligman found increased sensitization rate in whites compared to blacks; the difference was significant for the weaker allergens such as penicillin and neomycin. 88 Rostenberg and Kanot~9 found blacks less susceptible to experimental sensitization than whites using DNCB and paranitrosodimethylaniline as allergens. Pereutaneous absorption

No marked racial difference was found in in vivo percutaneous absorption of a topical steroid when examined in three whites and three blacks, 70 while Stoughton rl found a greater permeation in vitro through normal-appearing white skin than black skin of amputated legs. Additional information

Anthropologists have contributed to the information about racial skin differences. Hypotheses have been advanced to explain the advantage of dark pigmentation in areas with high intensity of solar radiation. Dark pigmented skin might protect against hypervitaminosis D, enhance resistance to vectors or infections, improve visual acuity in bright light, and protect against carcinogenic effect of ultraviolet light.72 The production of vitamin D in black epidermis is 40% of the production in white epidermis. 7~ A new evolutionary hypothesis suggests that dark skin color might protect

critical metabolites in blood and dermal tissues from photodecomposition by solar ultraviolet radiation. Branda and Eaton 74 showed 30% to 50% loss of folate in human plasma exposed to ultraviolet light; they found abnormally low serum folate concentrations in patients receiving phototherapy for dermatologic disorders. COMMENTS The alleged plethora of differences between black and white skin is impressive, but the contradictory results and statements in many papers alert us. Clinical research aimed at evaluating differences between black and white skin must be carefully planned, and the effect of environmental factors must be considered. Vollum 75 experienced a similar pattern of skin disease in Uganda as in any European clinic, but she noted that most patients waited until the disease was more severe or until there was secondary infection before seeking assistance. Although color is the most striking racial skin difference, it is but one piece of a biologic mosaic. At the moment, we follow the recommendation of Korol et aP ~ by recording not only skin color but also family history of genetic background. American blacks must be considered separately from less racially heterogenous groups such as the African blacks. C. J. McDonald, M.D., kindly reviewed the manuscript. REFERENCES 1. McDonald CJ: Some thoughts on differences in Nack and white skin. Int J Dermatol 15:427-430, 1976. 2. Brauner CJ: Cutaneous disease in the black races, in Moschella SL, Pillsburry DM, Hurley HJ, editors: Dermatology. Philadelphia, 1975, W. B. Saunders Co., pp. 1704-1737. 3. McDonald CJ: In Demis DJ, Dobson RL, McGuire J, editors: Dermatology of black skin.. New York, 1976, Harper & Row Publishers, vol. 4, unit 30-1. 4. McDonaldCJ, Kelly AP: Dermatologyand venereology, in Williams RA, editor: Textbook of black-related diseases. New York, 1975, McGraw-Hill Book Co., pp. 513-591. 5. Strauss J, Kligman AM: Pseudofolliculitisof the beard. Arch Dermatol 74:533-542, 1956. 6. Adamson HG: Dermatitis papillaris capillitii (Kaposi): Acne keloid. Br J Dermatol 26:69-83, 1914. 7. HairstonAM, Reed RJ, Derbes VJ: Dermatosispapulosa nigra. Arch Dermatol 89:655-658, 1964. 8. MoyerDG, Williams RM: Perifolliculitis capitis absce-

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dens et suffodiens. Arch Dermatol 85:118-124, 1962. 9. Farber EM, Craner F, Zamba F: Racial incidence of psoriasis. Cesk Dermatol 40:289-297, 1965. 10. Shrank AB, Harman RRM: The incidence of skin diseases in a Nigerian teaching hospital dermatological clinic. Br J Dermatol 78:235-241, 1966. 11. Verhagen ARHB, Koten J'W: Psoriasis in Kenya, Arch Dermatol 96:39-41, 1967. 12. Siegel M, Seelenfreund M: Racial and social factors in systemic lupus erythematosus. JAMA 191:77-92, 1965. 13. Dubois EL: The clinical picture of systemic lupus erythematosus, in Dubois EL, editor: Lupus erythematosus, ed. 2. Los Angeles, 1974, University of Southern California Press, p. 241. 14. Sackner MA: Scleroderma. New York, 1966, Grune & Stratton, Inc., p. 18. 15. Masi AT, D'Angelo WA: Epidemiology of fatal systemic sclerosis (diffuse scleroderma). Ann Intern Med 66:870-883, 1967. 16. Marshall J: Skin diseases in Africa. Cape Town, 1964, Maskew Miller Ltd, pp. 21 and 77. 17. Belisario JC: Keratoacanthomas. Cutis 16:527-548,1975. 18. Rippey JJ, Schmaman A: Skin tumours of Africans, in Marshall J, editor: Essays on tropical dermatology. Amsterdam, 1972, Excerpta Medica Foundation, vol. 2, pp. 98-115. 19. White JE, Strudwick WJ, Ricketts WN, Sampson C: Cancer of the skin in Negroes. JAMA 178:845-847, 196 l. 20. Oluwasanmi JO, Williams AO, Alli AF: Superficial cancer in Nigeria. Br J Cancer 23:714-728, 1969. 21. Pantoja E, LIobet RE, Roswitt B: Melanomas of the lower extremity among native Puerto Ricans. Cancer 38:1420-1423, 1976. 22. Shah J'P, Goldsmith HS: Malignant melanoma in the North American Negro. Surg Gynecol Obstet 133:437439, 197 i. 23. Lewis MG: Malignant melanoma in Uganda, in Clifford P, Linsell CA, Timms GA, editors: Cancer in Africa. Nairobi, 1968, East African Medical Journal, p. 454. 24. Gellin GA, Kopf AW, Garfinkel L: Malignant melanoma. Arch Dermatol 99:43-48, 1969. 25. Kopf WF, Lazar M, Bont RS, Dubin N, Brombers J: Prevalence of nevocytic nevi on lateral and medial aspects of arm. J Dermatol Surg Oncol 4:153-158, 1978. 26. Tindall JP: Skin changes and lesions in our senior citizens: Incidences. Cutis 18:359-362, 1976. 27. Kenney JA: Management of dermatoses peculiar to Negroes. Arch Dermatol 91: 126-129, 1965. 28. Kenney JA: Dermatoses seen in American Negroes. Int J Dermatol 9:110-113, 1970. 29. Wilkins JW Jr, Voorhees JJ: Prevalence of nodulocystie ache in white and Negro males. Arch Dermatol 102: 631-634, 1970. 30. Matta M: Carriage of Corynebacterium acnes in school children in relation to age and race. Br J Dermatol 91:557-561, 1974. 31. Millian SJ, Baldwin JN, Rheins MS, Weiser HH: Studies on the incidence of coagulase-positive staphylococci in a normal unconfined population. Am J Pub Health 50: 791-798, 1960. 32. NoNe WC: Carriage of Staphylococcus attreus and beta

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33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43.

44. 45. 46. 47. 48. 49. 50.

51. 52. 53.

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hemolytic streptococci in relation to race, Acta Derm Venereol 54:403-405, 1974. Allen AM, Taplin D, Twigg L: Cutaneous streptococcal infections in Vietnam. Arch Dermatol 104:271-280, 1971. Hall JH, Callaway JL, Tindall JP, Smith J Graham Jr: Pseudomonas aeruginosa in dermatology. Arch Dermatol 97:312-323, 1964. Hall WD, Blumberg RW, Moody MD: Studies in children with impetigo. Am J Dis Child 125: 800-806, 1973. Allen AM, Taplin D: Epidemic Tricophyton mentagrophytes infections in servicemen. JAMA 226:864-867, 1973. Szabo, G, Gerald AB, Pathak/VIA, Fitzpatrick T: Racial differences in the fate of melanosomes in human epidermis. Nature 222" 1081-1082, 1969. Olson RL, Gaylor J, Everett MA: Skin color melanin and erythema. Arch Dermatol 108:541-544, 1973. Konrad K, Wolff K: Hyperpigmentation, melanosome size, and distribution patterns of melanosomes. Arch Dermatol 107:853-860, 1975. Harrison GA: Differences in human pigmentation: Measurement, geographic variation, and causes. J Invest Dermatol 60:418-426, 1973. Wassermann HP: Ethnic differences in natural melanoproteins. Dermatologica 141:44-48, 1970. Fellner MJ: Green autofluorescenee in human epidermal cells. Arch Dermatol 112:667-670, 1976. Agrup G, Falck B, Olivecrona H, Rorsman H: Formaldehyde-induced fluorescence of epidermal melanocytes of Caucasian and Negro skin. Acta Derm Venereol (Stockh) 51: 350- 352, 1971. Hardy D, Baden HP: Biochemical variation of hair keratins in man and non-human primates. Am J Phys Anthropol 39: 19-24, 1973. Hein K, Cohen MI, McNamara H: Racial differences in nitrogen content of nails among adolescents. Am J Clin Nutr 30:496-498, 1977. Weigand DA, Haygood C, Gaylor JR: Cell layers and density of Negro and Caucasian stratum corneum. J invest Dermatol 62:563-568, 1974. Reinertson RP, Wheattey VR: Studies on the chemical composition of human epidermal lipids. I Invest Dermatol 32:49-59, 1959. Johnson LC, Corah NL: Racial differences in skin resistance. Science 139:766-767, 1960. Janes CL, Worland J, Stern JA: Skin potential and vasomotor responsiveness of black and white children. Psychophysiology 13:523-527, 1976. Korol B, Bergfeld GR, Goldman H, McLaughlin LJ: Use of the pigmentometer, a new device for measuring skin atbedo: Relating skin color with a series of physiological measures. Pavlov J Biol Sci 12:19-31, 1977. Fowles DC, Rosenberry R: Effects of epidermal hydration on skin potential responses and levels. Psyehophysiology 10:601-611, 1973. Montagna W, Parakkal PF: The structure and function of skin, ed. 3. New York, 1974, Academic Press, Inc. Robinson S, Dill DB, Wilson JW, Nielsen M: Adaptations of white men and Negroes to prolonged work in humid heat. Am J Trop Med 21:261-287, 1941.

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54. Herrmann F, Prose PH, Sulzberger MB: Studies on sweating, V. J Invest Dermatol 18:71-86, 1952. 55. McCance RA, Purohit G: Ethnic differences in the response of the sweat glands to pilocarpine. Nature 221:378-379, 1969. 56. MeCance RA, Rutishauser IHE, Knight "HC: Response of sweat glands to pilocarpine in the Bantu of Uganda. Lancet 1:663-665, 1968. 57. Hurley HJ, Shelley WB: The human apocrine sweat gland in health and disease. Springfield, IL, 1960, Charles C Thomas, Publisher, pp. 9 and 31. 58. Wollard HH: The cutaneous glands of man. J Anat 64:415-421, 1930. 59. Schwartz L, Tulipan L, Birmingham DJ: Occupational diseases of the skin, ed. 3. Philadelphia, 1957, Lea & Febiger, p. 31. 60. Shelley WB: Newer understanding of ecology in dermatology, in Rees RB~ editor: Dermatoses due to envkonmental and physical factors. Springfield, IL, 1962, Charles C Thomas, Publisher, p. 12. 61. Marshall EK Jr, Lynch V, Smith HW: Variations in susceptibility of the skin to dichloroethylsulfide. J Pharmacol Exp Thor 12:291-301, 1919. 62. Marshall J: New skin diseases in Africa. Trans St John's Hosp Dermatol Soc 56:3-10, 1970. 63. Weigand DA, Mershon MM: The cutaneous irritant reaction to agent o-chlorobenzylidene malononitrile (CS). I. Quantitation and racial influence in human subjects. Edgewood Arsenal Technical Report 4332, Febmary, 1970. 64. Weigand DA, Gaylor JR: Irritant reaction in Negro and Caucasian skin. South Med J 67"548-551, 1974.

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65. Frosch PJ, Kligman AM: The chamber-scarification test for assessing irritancy of topically applied substances, in Drill VA, Lazar P, editors: Cutaneous toxicity. New York, 1977, Academic Press, Inc., p. 150. 66. Leyden JJ, Kligman AM: Allergic contact dermatitis: Sex differences. Contact Dermatitis 3:333-336, 1977. 67. Kligman AM, Epstein W : Updating the maximization test for identifying contact allergens. Contact Dermatitis 1:231-239, 1975. 68. Kligman AM: The identification of contact allergens by human assay. II. Factors influencing the induction and measurement of allergic contact dermatitis. J Invest Dermatol 47:375-392, 1966. 69. Rostenberg A, Kanof NM: Studies in eczematous sensitization. J Invest Dermatol 4:504-516, 1941. 70. Wickrema Sinha WJ, Shaw SR, Weber OJ: Percutaneous absorption and excretion o f tritium-labeled diforasone diacetate, a new topical corticosteroid in the rat, monkey and man. J Invest Dermatol 7:372-377, 1978. 71. Stoughton RB: ln Montagna W, Stoughton RB, Van Scott EJ, editors: Pharmacology of the skin. New York, 1969, Appleton-Century-Crofts, p. 542. 72. Daniels FJ, Post PW, Johnson BE: h~ Riley V, editor: Pigmentation: Its genesis and biological control. New York, 1972, Appleton-Century-Crofts, pp. 13-22. 73. Beadle PC: The epidermal biosynthesis of cholecalciferol (vitamin Da). Photochem Photobiol 25:519-527, 1977. 74. Branda RF, Eaton JW: Skin color and nutrient photolysis: An evolutionary hypothesis. Science 201:625626, 1978. 75. Vollum DI: An impression of dermatology in Uganda. Trans St John's Hosp Dermatol Soc 59: 120- 125, 1973.