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

Background: Concurrent impact of repeated low-level summer sunlight exposures on vitamin D production and cutaneous DNA damage, potentially leading to mutagenesis/skin cancer, is unknown. Objectives: Experimental study (i) determining dual impact of repeated low-level sunlight exposures on vitamin D status and DNA damage/repair (via both skin and urinary biomarkers) in light-skin adults (ii) comparing outcomes following same exposures in brown-skin adults. Methods: Ten white Caucasians (phototype II) and six South Asians (V), 23–59y, received 6-weeks’ simulated summer sunlight exposures (95% UVA/5% UVB, 1.3SED x3 weekly) wearing summer clothing exposing ~35% surface. Assessments made were: circulating 25(OH)D; immunohistochemistry for cyclobutane pyrimidine dimer (CPD)-positive nuclei in skin: (i) unexposed, (ii) immediately-post single UVR, (iii) immediately-post and (iv) 24h-post x18 UVR-exposures; urinary biomarkers of direct and oxidative (8-oxo-dG) DNA damage. Results: Serum 25(OH)D rose from mean 36.5 (SD13.0) to 54.3 (10.5) nmol/L [14.6 (5.2) to 21.7 (4.2) ng/mL] in phototype II versus 17.2 (6.3) to 25.5 (9.5) nmol/L [6.9 (2.5) to 10.2 (3.8) ng/mL] in V (p<0.05). Phototype II skin showed CPD-positive nuclei immediately post-course, mean 44% (range 27-84) cleared after 24h, contrasting with minimal DNA damage and full-clearance in V (p<0.0001); findings did not differ from following single UVR-exposure. Urinary CPD remained <detection threshold in both groups; 8-oxodG was higher in II than V (p=0.002), but unaffected by UVR. Conclusions: Low-dose summer sunlight exposures confer vitamin D sufficiency in light-skin people concurrent with low-level, non-accumulating DNA damage. The same exposures produce minimal DNA damage but less vitamin D in brown-skin people. This informs tailoring of sun-exposure policies.