What question did this study set out to answer?

To investigate whether low doses of ultraviolet radiation (UVR) cause DNA damage in individuals with Fitzpatrick skin types I-III.

July 1, 2026

The burning question: Does exposure to low dose and low irradiance ultraviolet radiation lead to cutaneous DNA damage in people with skin types I– III ?

Key Points

To investigate whether low doses of ultraviolet radiation (UVR) cause DNA damage in individuals with Fitzpatrick skin types I-III.
Participants with skin types I-III (N=58) were exposed to solar-simulated UVR at two irradiance levels over four days.
Skin biopsies were taken at different time points for analysis of DNA damage markers, including CPD and P53 expression.
Immunofluorescent staining assessed the damage in epidermal cells.
Exposure to 1.6 SED led to significantly higher CPD-positive cells compared to 0.7 SED (3.67% vs. 0.89%, p < 0.0001).
P53 expression increased 2.5- to 3-fold at 72 h after exposure to 1.6 SED compared to 0.7 SED.
8-oxodG levels showed minimal nonsignificant changes over the observation periods.

Abstract

Exposing the skin to low (non-burning) doses of ultraviolet radiation (UVR) can avoid vitamin D deficiency, but whether delivering these doses at naturally occurring UVR indices causes DNA damage in humans is unknown. Participants (Fitzpatrick skin type I-III; N = 58) received solar-simulated UVR (0.7 and 1.6 standard erythemal doses, SED) on the lower back on four consecutive days. Doses were delivered at either UVI 2.8 or UVI 8.0. Skin biopsies were collected at baseline, and from exposed sites at 15 min, 24, and 72 h. Immunofluorescent staining assessed the induction of cyclobutane pyrimidine dimers (CPD), P53 expression, and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) damage in epidermal cells. Exposure to 1.6 SED caused a significantly greater increase in the percentage of CPD-positive cells compared with 0.7 SED (e.g., UVI 8: 15 min 3.67% vs. 0.89%, p < 0.0001). Similarly, exposure to the 1.6 SED dose caused greater P53 expression than the 0.7 SED dose; at 72 h there was a 2.5- to 3-fold higher P53 expression in the samples exposed to 1.6 SED. UVR irradiance did not affect CPD or P53 responses. 8-oxodG showed minimal, nonsignificant changes over time. UVR delivered at doses that can maintain adequate vitamin D status, and at naturally occurring irradiance, leads to measurable DNA damage.

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