Most of the cutaneous damage resulting from radiation exposure occurs from the UV band. The shortest of the UV rays, UVC (100-280 nm), fail to penetrate the earth’s ozone layer and thus exert little damage. UVB (290-320 nm) is responsible for most of the cutaneous changes induced by exposure to the sun. Known biochemical changes induced by UVB include alterations in DNA, RNA, and protein synthesis, induction of cyclobutyl pyrimidine dimers, and production of various cytokines (27,28).
In the past, UVA was believed to play less of a role in the pathogenesis of skin cancer and sun damage. The longer wavelengths of UVA (320-400 nm) allow deeper penetration into the skin. UVA induces an immediate pigment-darkening reaction and new melanin pigment formation (29). Earlier sun protection focused primarily on eliminating UVB exposure to the skin. UVA is now known to contribute to skin cancers by inducting DNA mutations directly as well as by augmenting damage incurred by UVB (30). Human skin exposed to UVA has altered expression of the p53 tumor suppressor protein (31). These mutations can be reduced by using UVA sunscreens, demonstrating that there is less p53 accumulation with better UVA protection (32).