Ann Dermatol.  2014 Jun;26(3):349-356.

A Multicenter Collaborative Study by the Korean Society of Vitiligo about Patients' Occupations and the Provoking Factors of Vitiligo

• Jeon IK
• Park CJ
• Lee MH
• Lee DY
• Kang HY
• Hann SK
• Choi GS
• Lee HJ
• Kim TH
• Lee AY
• Oh SH

Abstract

BACKGROUND
It was previously thought that persons with genetic predispositions to vitiligo develop the condition after exposure to various precipitating environmental factors. However, in many cases, the aggravating factors of vitiligo have not been clearly identified.
OBJECTIVE
To identify the aggravating factors of vitiligo in the working environment and daily life.
METHODS
A total of 489 vitiligo patients were recruited from 10 institutions in South Korea; patients were provided with a questionnaire about environmental factors and behavior patterns in the workplace and in daily life, and their association with vitiligo.
RESULTS
Ninety-five of the 470 enrolled patients (20.2%) answered that environmental risk factors in daily life and in the workplace affected the development of vitiligo. The most frequently attributed causes were trauma and burn (13.6%), followed by sunlight (12.8%), stress (12.8%), cleaning products/disinfectant/chemicals (4.9%), and hair dye (2.1%).
CONCLUSION
Vitiligo of the hand and foot was associated with frequent exposure to aggravating materials and overexposure to sunlight, along with frequent trauma of these areas, all of which could be considered important risk factors of vitiligo. The development of vitiligo could potentially be controlled through the early detection of aggravating factors.

Keyword

Environment; Occupations; Provoking factor; Risk factors; Vitiligo

MeSH Terms

Burns
Foot
Genetic Predisposition to Disease
Hair
Hand
Humans
Korea
Occupations*
Risk Factors
Sunlight
Vitiligo*
Surveys and Questionnaires

Figure

• 

  Fig. 1 Occupations of patients with vitiligo. The most frequent occupation was housewife, followed by office job, working in production, and student.

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  Fig. 2 Frequent exposure to materials and their influence on the development of vitiligo. (A) The materials to which patients were most frequently exposed in the home and workplace were cleaning products (30.0%), followed by cosmetics (17.0%), hair dye (11.4%), nickel (11.2%), rubber (7.3%) and clothing (5.5%). (B) Ninety-five patients (20.2%) reported that frequent exposure to certain materials and environments in daily life affected the development of their vitiligo.

• 

  Fig. 3 Most frequently reported causes associated with the occurrence of vitiligo. The most frequently reported causes associated with vitiligo occurrence were trauma and burn (13.6%), followed by sunlight (12.8%), stress (12.8%), cleaning products/disinfectant/chemicals (4.9%), and hair dye (2.1%).

Reference

1. Jin Y, Mailloux CM, Gowan K, Riccardi SL, LaBerge G, Bennett DC, et al. NALP1 in vitiligo-associated multiple autoimmune disease. N Engl J Med. 2007; 356:1216–1225.

2. Kemp EH, Waterman EA, Weetman AP. Autoimmune aspects of vitiligo. Autoimmunity. 2001; 34:65–77.

3. Dell'anna ML, Picardo M. A review and a new hypothesis for non-immunological pathogenetic mechanisms in vitiligo. Pigment Cell Res. 2006; 19:406–411.

4. Haycock JW, Rowe SJ, Cartledge S, Wyatt A, Ghanem G, Morandini R, et al. Alpha-melanocyte-stimulating hormone reduces impact of proinflammatory cytokine and peroxide-generated oxidative stress on keratinocyte and melanoma cell lines. J Biol Chem. 2000; 275:15629–15636.

5. Lee AY, Kim NH, Choi WI, Youm YH. Less keratinocyte-derived factors related to more keratinocyte apoptosis in depigmented than normally pigmented suction-blistered epidermis may cause passive melanocyte death in vitiligo. J Invest Dermatol. 2005; 124:976–983.

6. Le Poole IC, Das PK, van den Wijngaard RM, Bos JD, Westerhof W. Review of the etiopathomechanism of vitiligo: a convergence theory. Exp Dermatol. 1993; 2:145–153.

7. Hochstein P, Cohen G. The cytotoxicity of melanin precursors. Ann N Y Acad Sci. 1963; 100:876–886.

8. Boissy RE, Manga P. On the etiology of contact/occupational vitiligo. Pigment Cell Res. 2004; 17:208–214.

9. Cummings MP, Nordlund JJ. Chemical leukoderma: fact or fancy. Am J Contact Dermat. 1995; 6:122–126.

10. Weiss G, Shemer A, Trau H. The Koebner phenomenon: review of the literature. J Eur Acad Dermatol Venereol. 2002; 16:241–248.

11. Westerhof W, d'Ischia M. Vitiligo puzzle: the pieces fall in place. Pigment Cell Res. 2007; 20:345–359.

12. Toosi S, Orlow SJ, Manga P. Vitiligo-inducing phenols activate the unfolded protein response in melanocytes resulting in upregulation of IL6 and IL8. J Invest Dermatol. 2012; 132:2601–2609.

13. Thörneby-Andersson K, Sterner O, Hansson C. Tyrosinase-mediated formation of a reactive quinone from the depigmenting agents, 4-tert-butylphenol and 4-tert-butylcatechol. Pigment Cell Res. 2000; 13:33–38.

14. Yang F, Sarangarajan R, LePoole IC, Medrano EE, Boissy RE. The cytotoxicity and apoptosis induced by 4-tertiary butylphenol in human melanocytes are independent of tyrosinase activity. J Invest Dermatol. 2000; 114:157–164.

15. Jappe U, Geier J, Hausen BM. Contact vitiligo following a strong patch test reaction to triglycidyl-p-aminophenol in an aircraft industry worker: case report and review of the literature. Contact Dermatitis. 2005; 53:89–92.

16. Silvestre JF, Albares MP, Escutia B, Vergara G, Pascual JC, Botella R. Contact vitiligo appearing after allergic contact dermatitis from aromatic reactive diluents in an epoxy resin system. Contact Dermatitis. 2003; 49:113–114.

17. Bhushan M, Beck MH. Allergic contact dermatitis from primula presenting as vitiligo. Contact Dermatitis. 1999; 41:292–293.

18. Riordan AT, Nahass GT. Occupational vitiligo following allergic contact dermatitis. Contact Dermatitis. 1996; 34:371–372.

19. Silvestre JF, Botella R, Ramón R, Guijarro J, Betlloch I, Morell AM. Periumbilical contact vitiligo appearing after allergic contact dermatitis to nickel. Am J Contact Dermat. 2001; 12:43–44.

20. Trattner A, David M. Hair-dye-induced contact vitiligo treated by phototherapy. Contact Dermatitis. 2007; 56:115–116.

21. Vrijman C, Hosseinpour D, Bakker JG, Wolkerstorfer A, Bos JD, van der Veen JP, et al. Provoking factors, including chemicals, in Dutch patients with vitiligo. Br J Dermatol. 2013; 168:1003–1011.

22. Miller RA. The Koebner phenomenon. Int J Dermatol. 1982; 21:192–197.

23. Gauthier Y, Benzekri L. The Koebner's phenomenon. In : Picardo M, TaÏeb A, editors. Vitiligo. Berlin Heidelberg: Springer-Verlag;2010. p. 167–173.

24. van Geel N, Speeckaert R, De Wolf J, Bracke S, Chevolet I, Brochez L, et al. Clinical significance of Koebner phenomenon in vitiligo. Br J Dermatol. 2012; 167:1017–1024.

25. Gauthier Y, Cario-Andre M, Lepreux S, Pain C, TaÏeb A. Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo. Br J Dermatol. 2003; 148:95–101.

26. Jin Y, Birlea SA, Fain PR, Gowan K, Riccardi SL, Holland PJ, et al. Variant of TYR and autoimmunity susceptibility loci in generalized vitiligo. N Engl J Med. 2010; 362:1686–1697.

27. van Geel N, Speeckaert R, Taieb A, Picardo M, Böhm M, Gawkrodger DJ, et al. VETF members. Koebner's phenomenon in vitiligo: European position paper. Pigment Cell Melanoma Res. 2011; 24:564–573.

28. Ezzedine K, Lim HW, Suzuki T, Katayama I, Hamzavi I, Lan CC, et al. Vitiligo Global Issue Consensus Conference Panelists. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res. 2012; 25:E1–E13.

29. Ghosh S, Mukhopadhyay S. Chemical leucoderma: a clinico-aetiological study of 864 cases in the perspective of a developing country. Br J Dermatol. 2009; 160:40–47.