Department of Dermatology, Pediatric Dermatology and Dermatological Oncology, Medical University of Łódź, 90-647, Łódź, Poland.
University of Copenhagen, Bispebjerg Hospital, Department of Dermatological Research, Copenhagen, 2400, Denmark.
Br J Dermatol. 2019 Mar;180(3):604-614. doi: 10.1111/bjd.17277. Epub 2018 Dec 5.
Sun protection factor (SPF) is assessed with sunscreen applied at 2 mg cm . People typically apply around 0·8 mg cm and use sunscreen daily for holidays. Such use results in erythema, which is a risk factor for skin cancer.
To determine (i) whether typical sunscreen use resulted in erythema, epidermal DNA damage and photoimmunosuppression during a sunny holiday, (ii) whether optimal sunscreen use inhibited erythema and (iii) whether erythema is a biomarker for photoimmunosuppression in a laboratory study.
Holidaymakers (n = 22) spent a week in Tenerife (very high ultraviolet index) using their own sunscreens without instruction (typical sunscreen use). Others (n = 40) were given SPF 15 sunscreens with instructions on how to achieve the labelled SPF (sunscreen intervention). Personal ultraviolet radiation (UVR) exposure was monitored electronically as the standard erythemal dose (SED) and erythema was quantified. Epidermal cyclobutane pyrimidine dimers (CPDs) were determined by immunostaining, and immunosuppression was assessed by contact hypersensitivity (CHS) response.
There was no difference between personal UVR exposure in the typical sunscreen use and sunscreen intervention groups (P = 0·08). The former had daily erythema on five UVR-exposed body sites, increased CPDs (P < 0·001) and complete CHS suppression (20 of 22). In comparison, erythema was virtually absent (P < 0·001) when sunscreens were used at ≥ 2 mg cm . A laboratory study showed that 3 SED from three very different spectra suppressed CHS by around ~50%.
Optimal sunscreen use prevents erythema during a sunny holiday. Erythema predicts suppression of CHS (implying a shared action spectrum). Given that erythema and CPDs share action spectra, the data strongly suggest that optimal sunscreen use will also reduce CPD formation and UVR-induced immunosuppression.
防晒因子(SPF)是在涂抹 2mg/cm 的防晒霜的情况下进行评估的。人们通常会涂抹约 0.8mg/cm 的防晒霜,并在假期中每天使用防晒霜。这种使用方式会导致红斑,而红斑是皮肤癌的一个风险因素。
旨在(i)确定在阳光明媚的假期中,典型防晒霜的使用是否会导致红斑、表皮 DNA 损伤和光免疫抑制,(ii)确定最佳防晒霜的使用是否能抑制红斑,以及(iii)在实验室研究中,红斑是否是光免疫抑制的生物标志物。
度假者(n=22)在特内里费岛度过一周(紫外线指数非常高),使用自己的防晒霜但没有指导(典型防晒霜的使用)。其他人(n=40)使用 SPF15 的防晒霜,并接受了关于如何实现标签 SPF 的指导(防晒霜干预)。个人紫外线辐射(UVR)暴露通过电子监测作为标准红斑剂量(SED)进行监测,并对红斑进行量化。通过免疫染色确定表皮环丁烷嘧啶二聚体(CPDs),通过接触过敏反应(CHS)反应评估免疫抑制。
典型防晒霜使用组和防晒霜干预组的个人 UVR 暴露没有差异(P=0.08)。前者在五个 UVR 暴露的身体部位每天出现红斑,CPDs 增加(P<0.001),CHS 完全抑制(22 例中的 20 例)。相比之下,当防晒霜的使用量≥2mg/cm 时,红斑几乎不存在(P<0.001)。一项实验室研究表明,来自三种非常不同光谱的 3SED 抑制 CHS 约 50%。
最佳防晒霜的使用可防止在阳光明媚的假期中出现红斑。红斑预测 CHS 抑制(意味着有共同的作用光谱)。鉴于红斑和 CPDs 具有共同的作用光谱,这些数据强烈表明,最佳防晒霜的使用也将减少 CPD 的形成和 UVR 诱导的免疫抑制。