Chemical leukoderma

Contact urticaria, angioedema, and anaphylaxis Penetration of irritants through gloves Others endotoxin reactions, ethylene oxide, chemical leukoderma... 

Gellin 1990), while chemical leukoderma or toxic vitiligo, although not clearly defined, describes a depigmentation caused by the cutaneous exposure to chemicals that have direct, specific melanocytotoxic effects or suppress the capacity of melanocytes to produce melanin (Cummings and Nordlund 1995). 

Chemical leukoderma is a form of cutaneous pigment loss resembling vitiligo and is caused by exposure to a variety of chemicals that act by selective melanocyto-toxicity (Gellin and Maibach 1985). Most cases result from skin contact, but ingestion or inhalation of chemicals may also be factors. Chemical leukoderma has been referred to as occupational vitiligo, but a number of non-occupational cases have also been reported. 

Table 7. Selected chemicals associated with chemical leukoderma. Adapted from Gellin (1987), Ortonne et al. (1983), and Taylor et al. (1993)...

In most studies, there was some degree of spontaneous follicular-based repigmentation after avoidance of the presumed chemical however, depigmentation at times is permanent (Kahn 1970 Malten et al. 1971 Horio 1977). This is in contrast to untreated vitiligo, in which depigmentation is usually permanent (Fisher 1994). Malten et al. (1971) found that the more limited the extent of chemical leukoderma and the shorter its duration before avoidance, the earlier that spontaneous repigmentation was apt to occur. 

Host factors may also be involved to explain the observation that not all workers exposed to depigmenting chemicals will develop chemical leukoderma. This may involve a genetic predisposition, similar to the case of vitiligo. 

Histopathology does not reliably distinguish between chemical leukoderma and vitiligo. On light microscopy, both demonstrate reduced numbers of melanocytes. Vitiligo has been associated, classically, with an increased number of Langerhans cells, compared with a normal number in chemical leukoderma (Zelickson 1985). 

In the workplace, it is important to prevent and minimize exposure to known depigmentating agents through environmental engineering and industrial hygiene measures. These include good work practices, local exhaust ventilation, chemical substitution and, as a last resort, personal protective equipment. Prevention is especially important for those with chemical leukoderma. 

Key diagnostic criteria for chemical leukoderma include documented exposure to a known depigment-ing chemical, pigment loss consistent with such exposure by both history and examination, no evidence of idiopathic vitiligo, and reproduction of the pigment loss by chemical rechallenge - usually a patch test - in the patient or an animal model. 

Cohen SR (1985) Yellow staining caused by 4,4 -methylenedi-aniline exposure. Arch Dermatol 121 1022-1024 Cowan C, Haider R, Grimes P, et al. (1986) Disturbances in vitiligo. J Am Acad Dermatol 15 17-24 Cummings MP, Nordlund JJ (1995) Chemical leukoderma fact or fancy. Am J Contact Dermat 6 122-127 Das M, Tandon A (1988) Occupational vitiligo (1988). Contact Dermatitis 18 184-185... 

Miyamoto L, Taylor JS (2000) Chemical leukoderma chapter 32. In Hann SK, Nordlund JJ (eds) A comprehensive monograph on its clinical and basic science. Blackwell, Oxford, pp 271-282 Mosher D, Fitzpatrick T, Hori Y, et al. (1993) Disorders of pigmentation. In Fitzpatrick T, Eisen A, Wolff K, et al. (eds) Dermatology in generd medicine, 4th edn. McGraw-Hill, New York, pp 903-995... 

Kelly BD, Lundon DJ, McGuinness D, Brady CM. Methylphenidate-induced erections in a prepubertal child. J Pediatr Urol 2013 9(l) el-2. Ghasri P, Gattu S, Saedi N, Ganesan A. Chemical leukoderma following appHcation of transdermal methylphenidate patch. J Am Acad Dermatol 2012 66 e237-8. 

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