Impact of Long‐Wavelength Ultraviolet A1 and Visible Light on Light‐Skinned Individuals

Abstract

Solar radiation is known to be a major contributor to the development of skin cancer. Most sunscreen formulations, including those with broad spectrum, offer minimal protection in long‐wavelength ultraviolet A1 (UVA1; 370–400 nm) and visible light (VL; 400–700 nm) domain. There is limited information regarding the impact of this broad waveband (VL + UVA1, 370–700 nm) on those with light skin. In this study, ten healthy adult subjects with Fitzpatrick skin phototypes I–III were enrolled. On day 0, subjects' lower back was exposed to a VL + UVA1 dose of 480 J cm−2. A statistically significant increase in erythema immediately after irradiation compared with subjects' baseline nonirradiated skin was observed. Clinically perceptible erythema with VL + UVA1 is a novel finding since the erythemogenic spectrum of sunlight has primarily been attributed to ultraviolet B and short‐wavelength ultraviolet A (320–340 nm). The results emphasize the need for protection against this part of the solar spectra and warrant further investigation.

Impact of Iron-Oxide Containing Formulations Against Visible Light-Induced Skin Pigmentation in Skin of Color Individuals

“…17 Combining LUVA1 and VIS cause an immediate erythema response in skin phototype I-III, while inducing inflammation and immediate pigment darkening in skin phototype IV-VI. [6][7][8] VIS alone or in combination with IR generates ROS, increases collagen degradation, and indirectly leads to DNA damage. 18,19 Since VIS and IR makeup a great proportion of solar radiation and due to the lack of sunscreens offering protection beyond UV, it is crucial that novel means of photoprotection against these longer wavelengths be developed and tested.…”

“…[3][4][5] It has been shown that long wavelength UVA1 (LUVA1) combined with VIS can result in erythema in skin phototype I-III, plus darker, persistent pigmentation and inflammation in subjects with skin phototype IV-VI. [6][7][8] Various protocols consisting of single or multiple exposures have been published to investigate the mechanism of VIS-induced skin darkening. [3][4][5][6][7][8][9] Growing evidence indicates that pigment formed at earlier time points after VIS irradiation is photo-oxidized melanin while, at later time points, new pigments are synthesized through neo-melanogenesis.…”

“…[6][7][8] Various protocols consisting of single or multiple exposures have been published to investigate the mechanism of VIS-induced skin darkening. [3][4][5][6][7][8][9] Growing evidence indicates that pigment formed at earlier time points after VIS irradiation is photo-oxidized melanin while, at later time points, new pigments are synthesized through neo-melanogenesis. 5 The proposed molecular mechanism for VIS-induced skin pigmentation is through the activation of Opsin 3, a photo-receptor, which mediates the expression and activity of the rate-limiting enzyme, tyrosinase, in melanocytes.…”

Impact of ultraviolet radiation and exposome on rosacea: Key role of photoprotection in optimizing treatment

“…We have not found studies on the role of VL in this dermatosis, although VL has been linked to diverse photoaggravated disorders such as melasma, postinflammatory hyperpigmentation, cutaneous porphyrias, and solar urticaria 14 . Furthermore, VL can trigger immediate erythema in light‐skinned individuals, through a synergistic effect with UVA1 15 …”

“…Regarding the impact of nutrition on rosacea, patients report certain foods as triggers such as spicy food (capsaicin), fatty food, those containing cinnamaldehyde (chocolate tomatoes and citrus 15 ), alcohol, and hot beverages 18 as triggers 19 . Capsaicin and cinnamaldehyde can trigger TRP and promote vasodilation and flushing 11 .…”