Sunscreen Photoprotection and Vitamin D Status

T. Passeron; R. Bouillon; V. Callender; T. Cestari; T.L. Diepgen; A.C. Green; J.C. van der Pols; B.A. Bernard; F. Ly; F. Bernerd; L. Marrot; M. Nielsen; M. Verschoore; N.G. Jablonski; A.R. Young

Disclosures

The British Journal of Dermatology. 2019;181(5):916-931. 

In This Article

Abstract and Introduction

Abstract

Background: Global concern about vitamin D deficiency has fuelled debates on photoprotection and the importance of solar exposure to meet vitamin D requirements.

Objectives: To review the published evidence to reach a consensus on the influence of photoprotection by sunscreens on vitamin D status, considering other relevant factors.

Methods: An international panel of 13 experts in endocrinology, dermatology, photobiology, epidemiology and biological anthropology reviewed the literature prior to a 1-day meeting in June 2017, during which the evidence was discussed. Methods of assessment and determining factors of vitamin D status, and public health perspectives were examined and consequences of sun exposure and the effects of photoprotection were assessed.

Results: A serum level of ≥ 50 nmol L−1 25(OH)D is a target for all individuals. Broad-spectrum sunscreens that prevent erythema are unlikely to compromise vitamin D status in healthy populations. Vitamin D screening should be restricted to those at risk of hypovitaminosis, such as patients with photosensitivity disorders, who require rigorous photoprotection. Screening and supplementation are advised for this group.

Conclusions: Sunscreen use for daily and recreational photoprotection does not compromise vitamin D synthesis, even when applied under optimal conditions.

Introduction

The prevention of rickets and osteoporosis by vitamin D has long been established. More recently, vitamin D has been implicated in many metabolic and immunological disorders as well as many cancers. Its pleiotropic activity may be mediated by modulation of ~1000 genes via the vitamin D receptor (VDR),[1,2] which is expressed by at least 60 human cell types.[3] The VDR controls many cellular functions including growth, differentiation and apoptosis. However, the role of vitamin D in the prevention of nonskeletal diseases remains highly controversial.[4–8]

Terrestrial ultraviolet radiation (UVR) is the main determinant of vitamin D status. Stratospheric ozone absorbs all solar UVC (100–280 nm), attenuates UVB (280–315 nm) but not UVA (315–400 nm). The sun's height determines the UVR pathlength through the ozone layer. Thus, UVB intensity (irradiance) depends mainly on latitude, season and time of day. The ratio of UVA to UVB also varies with the sun's height because of the differential effect of the ozone layer. Thus, terrestrial UVR typically contains ≤ 5% UVB (~295–315 nm) and ≥ 95% UVA.

The minor UVB component is responsible for vitamin D synthesis,[9] the initiating event of which is the isomerization of the epidermal chromophore (a UVR-absorbing molecule) 7-dehydrocholesterol (7-DHC) into pre-vitamin D3, which is thermally converted into cholecalciferol (vitamin D3).[10] Pre-vitamin D3 increases linearly as a function of time of exposure to UVR (i.e. dose) over a period of 30 min.[11] Vitamin D3 enters the circulation via the vitamin D binding protein (DBP) and is hydroxylated into 25-hydroxyvitamin D3 [25(OH)D3] in the liver [by vitamin D3-25-hydroxylase (CYP2R1)], and then in the kidney [by 25(OH)D3-1α-hydroxylase (CYP27B1)] to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], the active form of vitamin D (calcitriol), which in fact is a hormone. However, many tissues including the skin[12] also contain both hydroxylases for the synthesis of calcitriol.

Multiple intrinsic and extrinsic factors modulate vitamin D synthesis and overall status, including genetic polymorphisms, age, geographical location, sun exposure behaviour, UVB dose, clothing, body surface area (BSA) exposed.[13] These are summarized in Figure 1[14] and Appendix S1 (see Supporting Information). Vitamin D3 may also be obtained from supplementation and/or animal-based foods (e.g. oily fish) and undergoes the same hydroxylations. Alternatively, vitamin D2 from nonanimal dietary uptake (e.g. mushrooms), is hydroxylated into 25(OH)D2 and then converted into 1,25(OH)2D2 (ergocalciferol). However, in general, intake from diet is low. For example, food intake in the U.S.A. between 2005 and 2006 in 19–30-year-old males and females was 204 IU ± 12 (5·1 μg) and 144 IU ± 12 (3·6 μg), respectively, which represents 34% and 24% of the recommended dietary allowance (RDA).[15]

Figure 1.

Factors that affect the synthesis of vitamin D3. Many factors determine vitamin D3 production. The most important external factor is UVB dose, which is the product of UVB intensity (irradiance) and exposure time. Cutaneous pre-vitamin D3 is synthesized from 7-dehydrocholesterol after UVB exposure. Thermally converted into vitamin D3, it then binds to vitamin D binding protein (DBP) in the blood to be activated sequentially by the liver and kidney. Cytochrome P450 (CYP) enzymes are crucial for the synthesis of biologically active vitamin D3 (calcitriol), which binds to intracellular vitamin D receptor (VDR) in most cells in the body. Adapted from Jolliffe et al.14 More details of these factors are given in the Supporting Information. BSA, body surface area; RXR, retinoid X receptor; VDRE, vitamin D response element.

Solar UVR has many adverse effects, the most obvious of which is sunburn (erythema). The World Health Organization has defined the global solar UV index (UVI) (http://www.who.int/uv/publications/en/UVIGuide.pdf) to allow comparisons of erythemal potential at various geographical locations (latitudes), seasons and times of day.[16] This is a numerical index of the erythemally weighted irradiance of terrestrial UVR. It is divided into five bands: 'low' (1–2), 'moderate' (3–5), 'high' (6–7), 'very high' (8–10) and 'extreme' (≥ 11). The UVI is primarily an index of UVB irradiance because this spectral region is the main cause of erythema (see Conclusions and recommendations: Spectral considerations: Ultraviolet B, below) and sun protection is advised when the UVI is ≥ 3.[17]

Global concern about vitamin D deficiency has fuelled debates on the importance of solar exposure to meet vitamin D requirements.[18–21] The acute and chronic health benefits of using sunscreens are established[22] but there has been concern about their possible impact on vitamin D status. An international panel was tasked to review the published evidence to reach a consensus on the influence of photoprotection by sunscreens on vitamin D status, considering other relevant factors.

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