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Ultraviolet radiation exposure and human skin health

Extreme Environmental Physiology conference 2019 Larry Kenney (Penn State University, US) The UVR spectrum is categorized by wavelength as UV-A (320-400 nm), UV-B (290-320 nm), and UV-C (200-290 nm) and the biological effects of UVR vary by wavelength. UV-A constitutes ~95% of UVR that reaches the earth’s surface, with the remainder UV-B. In the skin, UV-A is able to penetrate the dermis and reach the cutaneous circulation but most UV-B is absorbed in the epidermis and upper dermis due to its shorter wavelengths. Overexposure to UVR is associated with multiple health risks including DNA damage, immune suppression, premature skin aging, skin vascular dysfunction, and skin cancers. While regular physical activity is associated with a reduced risk of most cancers, skin cancer is an exception. For malignant melanoma, those in the 90th %ile for physical activity have increased hazard ratios compared to those in the 10th %ile. Those who participate in regular outdoor exercise or sport experience high daily doses of UVR exposure. According to ICNIRP guidelines, maximum biologically effective UVR exposure over an 8-h period should be limited to 30 J.m-2, a dose equivalent to 1.0-1.3 SED for fair skin. High daily UVR exposures have been reported for hikers (2-20 SED), tennis players (2-14 SED), and runners (9-24 SED) during the summer and autumn months, exceeding the recommended UVR exposure limit by up to 8-fold. Multiple studies demonstrate an elevated risk of skin cancer for those who regularly participate in outdoor sports or exercise, highlighting the importance of sun-protection strategies in those populations. Yet fewer than 25% of surveyed athletes report regular use of sunscreen. Exposure to UVR not only reddens the skin but also impairs underlying vascular function. The ability of skin arterioles to dilate via nitric oxide- (NO-) is a marker of vascular health. Adequate 5-methyltetrahydrofolate (5-MTHF; the bioactive metabolite of folate) is essential for full expression of NO-mediated vasodilatation through its role in enzymatic coupling of NO synthase. 5-MTHF is degraded by UVR in vitro and skin UVR exposure depletes bioavailable 5-MTHF in the exposed area, mediated by both direct photodegradation of 5-MTHF and indirectly via the production of reactive oxygen species (ROS). Acute UVR exposure may impair NO-mediated vasodilatation through either or both mechanisms. We recently demonstrated that broad spectrum UVR attenuated NO-mediated cutaneous vasodilatation, a response that was prevented by both SPF-50 sunscreen and by simulated sweat on the skin during exposure. The vitamin D-folate hypothesis has been proposed to explain the evolution of human skin pigmentation. According to this hypothesis, darkened skin pigment was adapted by early human populations living in equatorial Africa to protect against photodegradation of bioavailable folate by UVR. As humans moved away from the equator to more northern latitudes and occupied regions of lower UVR exposure and greater seasonal variation, depigmentation occurred to allow for adequate biosynthesis of vitamin D. Vitamin D and folate are both recognized for their evolutionary importance in healthy pregnancy and early childhood development. Populations with darkened skin pigmentation may be at elevated risk of vascular dysfunction and cardiovascular disease in low UVR environments due to hypovitaminosis D. Conversely, lightly-pigmented populations in high UVR environments may be at risk of deleterious vascular effects of UVR-induced folate degradation. Recent evidence has emerged demonstrating the importance of both vitamin D and folate in vascular health via their effects in reducing cutaneous oxidative stress and improving NO bioavailability. The skin’s ability to produce vitamin D is negatively affected by age, darker skin pigmentation, and several gene variants. Alternately, darker skin pigmentation plays a protective role against photodegradation of 5-MTHF; variations in the 5-MTHF response to UVR exposure may also be explained, at least in part, by genetic variation. In summary, exposure to UVR is associated with both beneficial and deleterious effects on cutaneous vascular health. Both folate and vitamin D play important roles in healthy vascular function, but UVR exposure elicits opposing effects on metabolism and bioavailability of these two compounds. The effects of UVR on folate and vitamin D metabolism appears to be influenced by multiple factors, including skin pigmentation, genetics, geographical location, and age. Beyond the influence of UVR on folate and vitamin D metabolism, UVR exposure may cause oxidative stress and inflammatory responses that impair vascular health in a dose-dependent fashion. The interactions between individual characteristics and environment in modulating vitamin D and folate bioavailability and vascular health are highly complex.