Epidermal DNA damage, especially to the basal layer, is an established cause of keratinocyte cancers (KCs). Large differences in KC incidence (20- to 60-fold) between white and black populations are largely attributable to epidermal melanin photoprotection in the latter. The cyclobutane pyrimidine dimer (CPD) is the most mutagenic DNA photolesion; however, most studies suggest that melanin photoprotection against CPD is modest and cannot explain the considerable skin color-based differences in KC incidence. Along with melanin quantity, solar-simulated radiation-induced CPD assessed immediately postexposure in the overall epidermis and within 3 epidermal zones was compared in black West Africans and fair Europeans. Melanin in black skin protected against CPD by 8.0-fold in the overall epidermis and by 59.0-, 16.5-, and 5.0-fold in the basal, middle, and upper epidermis, respectively. Protection was related to the distribution of melanin, which was most concentrated in the basal layer of black skin. These results may explain, at least in part, the considerable skin color differences in KC incidence. These data suggest that a DNA protection factor of at least 60 is necessary in sunscreens to reduce white skin KC incidence to a level that is comparable with that of black skin.-Fajuyigbe, D., Lwin, S. M., Diffey, B. L., Baker, R., Tobin, D. J., Sarkany, R. P. E., Young, A. R. Melanin distribution in human epidermis affords localized protection against DNA photodamage and concurs with skin cancer incidence difference in extreme phototypes.

SummaryTerrestrial solar ultraviolet radiation (UVR) exerts both beneficial and adverse effects on human skin. Epidemiological studies show a lower incidence of skin cancer in people with pigmented skins compared to fair skins. This is attributed to photoprotection by epidermal melanin, as is the poorer vitamin D status of those with darker skins. We summarize a wide range of photobiological responses across different skin colours including DNA damage and immunosuppression. Some studies show the generally modest photoprotective properties of melanin, but others show little or no effect. DNA photodamage initiates non‐melanoma skin cancer and is reduced by a factor of about 3 in pigmented skin compared with white skin. This suggests that if such a modest reduction in DNA damage can result in the significantly lower skin cancer incidence in black skin, the use of sunscreen protection might be extremely beneficial for susceptible population. Many contradictory results may be explained by protocol differences, including differences in UVR spectra and exposure protocols. We recommend that skin type comparisons be done with solar‐simulated radiation and standard erythema doses or physical doses (J/m2) rather than those based solely on clinical endpoints such as minimal erythema dose (MED).

Introduction Unlike “light” cylobutane pyrimidine dimers (CPD) formed during ultraviolet radiation (UVR) exposure, dark CPD (dCPD) are formed afterwards. Studies have attributed this to delayed melanin sensitization. There are no data on the role of melanin in dCPD formation in human skin. Methods and Results Volunteers of Fitzpatrick skin types (FST I/II vs. VI) were exposed to erythemally equivalent doses of solar simulated radiation. CPD were assessed by semi‐quantitative immunostaining in whole epidermis and in three epidermal zones, and quantitative HPLC‐MS/MS (whole epidermis) at different times post‐exposure up to 24 hr. A CPD peak that appeared at 1–2 hr post‐exposure in whole epidermis measurements, in all skin types, demonstrated dCPD. However, both dCPD and light CPD were absent in the basal layer of FST VI with the greatest melanin concentration. Modelling the whole epidermis data showed no differences between the repair kinetics of FST I/II and VI. Discussion Melanin may be a sensitizer or “sunscreen” for dCPD depending on its location and concentration. Previous CPD repair studies in human skin have assumed peak CPD immediately after UVR exposure and so have overestimated total repair.

Conflicts of interestO.E.D. has previously been president of the jury for the L'Or eal African Skin and Hair Research Grant and has also previously received research funding from L'Or eal Research and Innovation. Damilola Fajuyigbe is an employee of L'Or eal Research and Innovation. N.G.J. is a member of the scientific advisory board and of the global ethics and diversity board of L'Or eal Group. Data availabilityThe data that support the findings of this study are available in the supplementary material of this article.

Background People with black skin are much less susceptible to sunburn than white‐skinned individuals, yet there are scarce data on self‐reported incidence of sunburn and sun protection measures in people with deeply‐pigmented skin. Method An on‐line survey tool was used to collect self‐assessed data about demographic variables, sunburn incidence, and use of sun protection modalities. Results Two‐thirds of respondents with black skin living in the UK claimed never to have been sunburnt; a much higher proportion than those living in South Africa and Nigeria where 34 and 46%, respectively, reported never experiencing sunburn. Similar results were seen in the reported use of sun protection measures between the countries with two‐thirds of black people living in the UK claiming they never used any form of sun protection compared with about one‐third of Black Africans. Black people living in the UK were more likely to use sunscreen as a form of sun protection, whereas sunscreen was the least popular modality in the two African countries with shade being the most common form of limiting sun exposure. Conclusion The findings provide some insight into the complexities of skin color perception, incidence of sunburn, and sun protection use among people with deeply‐pigmented skin living in three countries with large differences in the solar UV environment.