UV Radiation in the Setting of Immune Compromise
Habitual tanning bed use has been recognized as a psychologic addiction.3,4 After exposure to UV radiation, damaged DNA upregulates pro-opiomelanocortin, which posttranslationally generates β-endorphins to elevate mood.3,5
Tanning beds deliver a higher dose of UVA radiation than UVB radiation and cause darkening of pigmentation by oxidation of preformed melanin and redistribution of melanosomes.3 UVA radiation (320–400 nm) emitted from a tanning bed is 10- to 15-times higher than the radiation emitted by the midday sun and causes DNA damage through generation of reactive oxygen species. UVA penetrates the dermis; its harmful effect on DNA contributes to the pathogenesis of melanoma.
UVB radiation (290–320 nm) is mainly restricted to the epidermis and is largely responsible for erythema of the skin. UVB specifically causes direct damage to DNA by forming pyrimidine dimers, superficially causing sunburn. Excessive exposure to UVB radiation increases the risk for nonmelanoma skin cancer.6
Severe starvation and chronic malnutrition, as seen in anorexia nervosa, also are known to lead to immunosuppression.7 Exposure to UV radiation has been shown to impair the function of antigen-presenting cells, cytokines, and suppressor T cells, and is classified as a Group 1 carcinogen by the World Health Organization.3,8 Combining a compromised immune system in anorexia with DNA damage from frequent indoor tanning provides a dangerous milieu for carcinogenesis.8 Without immune surveillance, as occurs with adequate nutrition, treatment of cutaneous SCC is, at best, challenging.
Primary care physicians, dermatologists, psychiatrists, nutritionists, and public health officials should educate high-risk patients to prevent TANS syndrome.