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Concurrent beneficial (vitamin D production) and hazardous (cutaneous DNA damage) impact of repeated low‐level summer sunlight exposures
Author(s) -
Felton S.J.,
Cooke M.S.,
Kift R.,
Berry J.L.,
Webb A.R.,
Lam P.M.W.,
Gruijl F.R.,
Vail A.,
Rhodes L.E.
Publication year - 2016
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.14863
Subject(s) - phototype , pyrimidine dimer , sunlight , dna damage , medicine , urinary system , vitamin d and neurology , chemistry , dermatology , dna , biochemistry , physics , astronomy
Summary 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 ~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 postcourse, 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 CPD s 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.