Abstract

BackgroundChildhood is a high risk time for ultraviolet induced skin damage as this age group has more time and opportunity to be outdoors in the sun. Children in Africa with the inherited condition oculocutaneous albinism (OCA) are especially vulnerable due to their lack of protective melanin. They are highly susceptible to developing skin lesions that have both cosmetic and health complications, with a high risk of developing skin cancers. The study aimed to explore the adequacy of sun protection strategies of children with albinism in order to inform future provision.MethodsCommunity based participatory research methods were employed to investigate sun protection strategies in 90 pupils with OCA (40 female and 50 male) boarding at a special school educating pupils with visual impairment in a rural area of northern South Africa. Hats worn and sunscreen preparations used were examined during semi-structured face to face interviews conducted in small peer groups. The resident nurse interpreted if necessary and provided additional information on monitoring and treatment of skin lesions.ResultsParticipants with albinism in this study were exposed to high levels of ultraviolet radiation throughout the year and showed skin damage despite wearing protective head gear. All except one pupil possessed at least one hat, with a mean brim width of 5.4 cm. Gender differences in sun avoidance behaviour were documented, with females seeking shade during recreational periods and males playing soccer outside. Although 38% of pupils were using a sunscreen with a sun protection factor (SPF) rating, only 12% had government sponsored tubes of SPF15 cream. Government sponsored sunscreen preparations were only provided if actively sought, involving time consuming trips to regional hospitals, with inadequate availability and insufficient supply.ConclusionChildren with albinism living away from home in rural areas appear to have inadequate sun protection strategies. Changes in health policy could address these deficiencies. We recommend providing more detailed health care information, giving advice on appropriate styles of hat to wear and how to assess commercial SPF products. Health promotional material should also be evaluated to determine its effectiveness among user groups.

Highlights

  • Childhood is a high risk time for ultraviolet induced skin damage as this age group has more time and opportunity to be outdoors in the sun

  • Setting The participants attended a special school for visually impaired children in a rural area of Limpopo Province in South Africa, located close to the Tropic of Capricorn at a high altitude (1230 m) with an average 8.5 hours of sunshine a day

  • Pupils possessed sufficient hats, but the brim widths were largely insufficient to protect the lower face and neck; Uptake of free government SPF15 sunscreen Tubes of generic sun protection factor (SPF) 15 cream were available free of charge through local regional hospitals but only six Pupils using commercial or SPF preparations provided by regional hospitals*

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Summary

Introduction

Childhood is a high risk time for ultraviolet induced skin damage as this age group has more time and opportunity to be outdoors in the sun. Children in Africa with the inherited condition oculocutaneous albinism (OCA) are especially vulnerable due to their lack of protective melanin. They are highly susceptible to developing skin lesions that have both cosmetic and health complications, with a high risk of developing skin cancers. The distinctive phenotype of those affected with their pale, chalky, de-pigmented skin, sandy coloured hair and blue to hazel eyes marks them as 'different' in this population group, leading to problems of social integration and ostracism [1]. OCA2, the form of albinism found in Africa, is inherited as an autosomal recessive disorder In this type of OCA tyrosinase, the key enzyme for synthesising melanin, is present and functional, as the gene encoding this enzyme is not mutated. The defect in OCA2 is in the P gene coding for a membrane protein of the melanosome, leading to malfunction of the melanin synthesis pathway [2]

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