Sun and ski holidays improve vitamin D status, but are associated with high levels of DNA damage.

Skin cancer is caused by solar UVR, which is also essential for vitamin D production. DNA damage (thymine dimers: T-T dimers) and vitamin D (25(OH)D) synthesis are both initiated by solar UVB. We aimed to investigate the simultaneous adverse and beneficial effects of solar UVB exposure in holidaymakers. Sun-seekers and skiers (n=71) were observed over 6 days through on-site monitoring, personal diary entries, and recording of personal UVB exposure doses with electronic dosimeters. Urine and blood samples were analyzed for T-T dimers and 25(OH)D, respectively. The volunteers had a statistically significant increase in vitamin D. There were strong associations between UVB exposure and post-holiday levels of T-T dimers and vitamin D, as well as between post-holiday T-T dimers and vitamin D. We conclude that UVB-induced vitamin D synthesis is associated with considerable DNA damage in the skin. These data, on two major health predictors, provide a basis for further field studies that may result in better understanding of the risks and benefits of "real life" solar exposure. However, vitamin D status can be improved more safely through the use of vitamin D dietary supplements.

UVA1 is skin deep: molecular and clinical implications.

Long wavelength UVA1 (340-400 nm) is the main component of terrestrial UVR and is increasingly used in skin phototherapy. Its damage to critical biomolecules such as DNA has been widely attributed to its ability to generate reactive oxygen species (ROS) via other chromophores. However recent studies in vitro and in vivo have shown that UVA1 has a specific ability to generate cyclobutane pyrimidine dimers (CPD), especially thymine dimers (T<>T), and that this is probably due to direct absorption of UVR. The CPD has been implicated in many aspects of skin cancer. Measuring UVB-induced CPD in the epidermis and dermis in vivo shows that, as expected, the skin attenuates UVB. In contrast, our data show that this is not the case with UVA1: in fact there is more damage with increased skin depth. This suggests that the basal layer, which contains keratinocyte stem cells and melanocytes, is more vulnerable to the carcinogenic effects of UVA1 than would be predicted by mouse models. These data support the continuing trend for better UVA1 protection by sunscreens.