Quantifying Direct DNA Damage in the Basal Layer of Skin Exposed to UV Radiation from Sunbeds

Abstract

Nonmelanoma and melanoma skin cancers are attributable to DNA damage caused by ultraviolet (UV) radiation exposure. One DNA photoproduct, the cyclobutane pyrimidine dimer (CPD), is believed to lead to DNA mutations caused by UV radiation. Using radiative transfer simulations, we compare the number of CPDs directly induced by UV irradiation from artificial and natural UV sources (a standard sunbed and the midday summer Mediterranean sun) for skin types I and II on the Fitzpatrick scale. We use Monte Carlo radiative transfer (MCRT) modeling to track the progression of UV photons through a multilayered three dimensional (3D) grid that simulates the upper layers of the skin. By recording the energy deposited in the DNA-containing cells of the basal layer, the number of CPDs formed can be quantified. The aim of this work was to compare the number of CPDs formed in the basal layer of the skin and by implication the risk of developing cancer, as a consequence of irradiation by artificial and natural sources. Our simulations show that the number of CPDs formed per second during sunbed irradiation is almost three times that formed during solar irradiation.

Further evidence that far‐UVC for disinfection is unlikely to cause erythema or pre‐mutagenic DNA lesions in skin

“…2,5 To determine the depth penetration of UVC in Fitzpatrick Skin Type I and the associated direct CPD formation, we employ Monte Carlo radiation transfer (MCRT) codes previously used to study ultraviolet radiation transport in skin. 7,8 The MCRT simulation initiates UV power packets from the spectrum of the source, that diffusely irradiate the skin, and follows their subsequent random walk through a three-dimensional grid comprising 10 6 cubic voxels representing a 0.4 mm thick 5-layer skin model. 7 The wavelength-dependent ab- Careful filtering of UVC spectral emissions, to remove unwanted longer wavelengths, has been shown not to induce tissue inflammation or increase pre-mutagenic DNA lesions in both mammalian skin and an in vitro human skin model.…”

“…7,8 The MCRT simulation initiates UV power packets from the spectrum of the source, that diffusely irradiate the skin, and follows their subsequent random walk through a three-dimensional grid comprising 10 6 cubic voxels representing a 0.4 mm thick 5-layer skin model. 7 The wavelength-dependent ab- Careful filtering of UVC spectral emissions, to remove unwanted longer wavelengths, has been shown not to induce tissue inflammation or increase pre-mutagenic DNA lesions in both mammalian skin and an in vitro human skin model. 2,5,11 Whilst initially this would appear to contradict our results, CPD formation in the upper and mid-layers of the epidermis, from wavelengths below 230 nm, is of minimal contribution to overall simulated CPD (6.4% and 0.3% for each layer, respectively).…”

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“…Prolonged exposure to UVA damages the epidermal connective tissues and thereby can potentially lead to skin cancer, whereas UVB impacts include tans and sunburns. The amount of UV radiation to which skin is exposed and the status of skin pigmentation determines the acuteness of photo-aging 44 .…”

Could psoralen plus ultraviolet A1 (‘ PUVA 1’) work? Depth penetration achieved by phototherapy lamps

“…MCRT methods are widely used and rely on published optical properties of the tissue. Using a modified version of a previously published five‐layered MCRT skin model, irradiation by several phototherapy light sources [metal halide UVA1, fluorescent lamp UVA1, broadband UVA (‘PUVA tubes’) and narrowband UVB (a standard phototherapy)] was simulated. Four simulations were performed, one for each light source, and each simulation was run with 100 million photon packets, to achieve statistically significant results.…”