Concurrent beneficial (vitamin D production) and hazardous (cutaneous DNA damage) impact of repeated low-level summer sunlight exposures

Background The concurrent impact of repeated low-level summer sunlight exposures on vitamin D production and cutaneous DNA damage, potentially leading to mutagenesis and skin cancer, is unknown. Objectives This is an experimental study (i) to determine the dual impact of repeated low-level sunlight exposures on vitamin D status and DNA damage/repair (via both skin and urinary biomarkers) in light-skinned adults; and (ii) to compare outcomes following the same exposures in brown-skinned adults. Methods Ten white (phototype II) and six South Asian volunteers (phototype V), aged 23-59 years, received 6 weeks' simulated summer sunlight exposures (95% ultraviolet A/5% ultraviolet B, 1.3 standard erythemal doses three times weekly) wearing summer clothing exposing similar to 35% body surface area. Assessments made were circulating 25-hydroxyvitamin D [25(OH) D], immunohistochemistry for cyclobutane pyrimidine dimer (CPD)-positive nuclei and urinary biomarkers of direct and oxidative (8-oxo-deoxyguanosine) DNA damage. Results Serum 25(OH) D rose from mean 36.5 +/- 13.0 to 54.3 +/- 10.5 nmol L-1 (14.6 +/- 5.2 to 21.7 +/- 4.2 ng mL(-1)) in phototype II vs. 17.2 +/- 6.3 to 25.5 +/- 9.5 nmol L-1 (6.9 +/- 2.5 to 10.2 +/- 3.8 ng mL(-1)) in phototype V (P < 0.05). Phototype II skin showed CPD-positive nuclei immediately post-course, mean 44% (range 27-84) cleared after 24 h, contrasting with minimal DNA damage and full clearance in phototype V (P < 0.001). The findings did not differ from those following single ultraviolet radiation (UVR) exposure. Urinary CPDs remained below the detection threshold in both groups; 8-oxo-deoxyguanosine was higher in phototype II than V (P = 0.002), but was unaffected by UVR. Conclusions Low-dose summer sunlight exposures confer vitamin D sufficiency in light-skinned people concurrently with low-level, nonaccumulating DNA damage. The same exposures produce minimal DNA damage but less vitamin D in brown-skinned people. This informs tailoring of sun-exposure policies.