Evidence of Natural Protection against Sunburn in Darker Skin Types

Dr. Lylah Hill has amassed an impressive combination of clinical expertise as well as academic and histological research across Aesthetic Dermatology, Tissue Regeneration & Biological Science of Skin Ageing. Dr Lylah Hill unpacks the science of SPF, revealing how reliance on erythema-based MED testing and fair-skin models skews our idea of protection. Drawing on histology and photobiology, she shows that darker skin still sustains UV induced DNA damage, that melanin can mask redness without preventing CPDs, and that visible light and UVA1 drive photoageing. A sharp case for inclusive, evidence based SPF standards and smarter public guidance, not a one size fits all sunscreen.

Erythema, widely known as sunburn, is skin reddening resulting from increased blood flow and used as a clinical end point in photobiology as an indicator of Ultra Violet Radiation (UVR) sensitivity. Erythema is the best studied response to UVR, however, its studies are limited to fair skin. Clinically, erythema is associated with Sunburn Cells  SBC’s i.e. apoptotic keratinocytes characterised as dyskeratotic and vacuolated keratinocytes following 24 hours of UV radiation/exposure. SBC’s are used as endpoints in photoprotective studies, forming the basis of minimal UVR dose necessary to induce SBC’S in the epidermal layer  considered the Biologically Effective Dose (BED). BED in vitro is equal to the Minimal Erythema Dose (MED) in vivo as SBC’s become apparent at 1 MED. MED signifies the lowest dose of UV irradiation required to generate an observable skin redness 24 hours after exposure to increasing UV doses. Montagna et al performed a histological analysis comparing sun exposed skin between Black (n=19) and White (n=19) females. Black epidermis showed histological features of vacuoles and dyskeratosis present in keratinocytes of the malpighian layer similar to white counterparts, strongly suggestive of sunburn being present in darker skin individuals as a result of sun exposure. 

Skin samples of various constitutive pigmentation were quantified for SBC’s 24 hours after exposure to increased doses of UVR. Statistically significant association was seen between skin colour measured using ITA and BED, with darker skin showing higher values of BED. A study comparing UVB induced MED in all skin types with minimal flux dose (MFD) equivalent to 30% rise in blood flow from baseline, supports the notion of masking by melanin. Furthermore, similar studies have shown 87% coefficient variation (CV) for MED of FPT VI versus only 36% CV for MFD in the same skin type.

Variations in UVR emission spectra during assessment, further adds inaccuracy to quantifying MED. Phan et al found significant correlation between skin colour and MED at UVR 310nm but not 290nm, indicating melanin in the basal layer only has protective capability with wavelengths greater than 290nm. Tadokoro et al studied the relationship between melanin and extent of UVR induced DNA damage in skin of various ethnicities. Although damage was found to be highest in lighter skin, results showed darker skin types were indeed able to repair DNA damage more efficiently than lighter skin types, however even at low level UVR exposure, irradiation induced considerable DNA damage in all skin types, dispelling the dubious claim that darker skin is completely void of DNA photodamage from UVR irradiation. Cyclobutane pyrimidine dimers (CPD) triggers effects such as erythema, photoageing and immunosuppression, which all increase the risk of skin cancer, whilst erythema is associated with vascular dilatation and characterized by the presence of SBC’s. Given the action spectrum for DNA damage, erythema and melanogenesis is similar, and erythema is widely considered a clinical surrogate for DNA damage, this implies DNA is a chromophore for both melanogenesis and erythema. 

Studies in vitro and in vivo evaluated melanin’s ability to inhibit DNA photodamage, with some but not all showing protection. Sheehan et al found more CPD in unprotected skin of darker skin types than for lighter skin, however after 1 week, significant reduction of damage in darker cohorts was seen, suggesting repair in this skin group is more inducible. Another in vitro study saw peaks in P53 expression at 24 hours in darker skin melanocytes with a steady rise of up to 48 hours in lighter skin melanocytes, further suggesting that darker melanocytes may have more efficient repair systems from p53 induced cell cycle arrest.  Other studies however refute melanin’s protective ability against photodamage in darker skin types, finding no difference in degree of DNA repair between various skin types when assessing acute exposure to UVR doses. One study found no correlation between melanin content and removal of CPD at 7 days following MED based UVR exposure. Although darker skin types provide some protection against solar damage than lighter skin, it is not fully recognised by the general public and physicians that complete protection against photodamage from solar spectrum does not exist. Furthermore, Visible light (VL) and UVAI is thought to play a significant role in photoageing in this cohort. 

Studies highlight that the majority of individuals with darker skin consider themselves exempt from sun protective practices. Peltzer et al examined 25 countries comparing lighter and darker skin type photoprotective practices, concluding that the former cohort was associated with persistent use of sunscreen. Analysis of USA health surveys indicates darker skin types do not have accurate perception of skin cancer risk factors or symptoms, and amongst Hispanics, the third most cited reason for sunscreen neglect was belief they were exempt given their darker skin.

Surveys and focus group studies have consistently found darker skin types underestimate risk and prevention of skin cancer. Buster et al analysed data from the Health Information National Trends Survey (HINTS) to find darker skin types were more inclined to believe skin cancer is unpreventable and found compared with caucasians they were less likely to believe they were at risk of skin cancer.