窄波UVB诱导正常皮肤色素斑的研究

目的 观测窄波UVB诱导正常人腹部皮肤色素沉着斑的颜色变化指标。方法 采用窄波UVB治疗仪，以1.5倍的最小红斑量照射30例志愿者的腹部皮肤，形成人工色素沉着斑。在照射前、照射后1，2，4，6，8周，分别用 CM-2600d分光光度计测量局部皮肤的L*、a*、b*、△L、△a、△b、 △E值，以SIAscopy仪检测色素斑处血红蛋白、胶原蛋白、黑素总量，并捕获相应图像。同时，用数码相机拍摄志愿者腹部照片。结果 照射后局部皮肤呈淡灰色，4 h后出现局部潮红，1周后色素沉着最明显，2例受试者照射部位出现细小脱屑，所有受试者均无水疱发生。CM-2600d分光光度计测量照射部皮肤，结果显示，照射后1周，L*下降到最低，a*值升至最高，b*变化不明显。1周后L*值开始升高，而a*值下降，直到照射后8周，各自接近照射前水平。SIAscopy仪检测提示，照射后1周，皮肤血红蛋白增加最明显，以后迅速下降，低于照射前水平。而总黑素含量和胶原蛋白照射后持续缓慢增加，第6周达最高。结论 窄波UVB可诱导正常皮肤色素斑形成，通过观察皮肤色素的变化规律，客观地评估美白产品的功效。     

皮肤颜色客观评估方法的比较

目的:通过比较皮肤科学和化妆品研究领域常用的两种皮肤颜色仪器测量方法,为临床和科研提供实际应用指导。方法:应用三刺激值色度计(MinoltaChromameterCR200)和窄谱反射分光光度计(MexameterMX16及MX18)先定量测定标准色板和志愿者皮肤颜色,然后再比较这些仪器在体内外测定的重复性、敏感性以及相关性。结果:这3种仪器在体内外都表现出重复性高(CV=0.01%～3.32%)、敏感性好。MexameterMX16及MX18在体外及人体都有显著相关性(P<0.01)。两种型号的Mexameter与ChromameterCR200间也显著相关(P<0.01)。结论:3种仪器都能准确地表现皮肤颜色。L*、b*、MI适合色素沉着测定,而a*、EI则更适合测定皮肤的红斑。     

UVA与UVB治疗寻常型银屑病临床对照研究

目的：评价煤焦油软膏外用联合UVA＋UVB照射治疗寻常型银屑病的疗效及安全性。方法：91例寻常型银屑病患者外用煤焦油软膏联合UVA＋UVB照射，并与53例寻常型银屑病患者外用煤焦油软膏联合UVA、51例联合UVB照射进行对比观察。结果：治疗8周后UVA＋UVB组痊愈率为63．74％，总有效率为98．90％，明显高于UVA组和UVB组；治疗2周、4周、6周和8周后PASI评分均较治疗前明显下降，UVA＋UVB组与UVA组、UVB组对比有显著性差异；1年内复发率UVA＋UVB组27．66％，明显低于UVA组或UVB组。结论：外用煤焦油软膏联合UVA＋UVB照射治疗寻常型银屑病较单纯联合UVA或UVB照射疗效高、复发率低。     

两种皮肤颜色测量仪器间测量参数的相关性研究

目的探讨自主研发的皮肤颜色数字图像计算机分析系统PLPSC-CDIA与窄谱反射分光光度计Mexameter MX18检测皮肤颜色结果的相关性。方法应用PLPSC-CDIA系统和Mexameter MX18测定30位色素性和血管性皮肤病患者面部相同位点,共150个位点,然后比较这两种仪器检测结果的相关性。结果 PLPSC-CDIA系统的L值与Mexameter MX18黑素指数（MI）呈明显的负相关。皮肤颜色数字图像分析检测系统的a值与Mexameter MX18红斑指数（EI）呈高度相关性。其它区域与正常部位的MI差值△MI与黑素色差△Mel呈明显相关性,EI差值△EI与血红素色差△Hb呈明显相关性。结论基于偏振光数码摄影技术的皮肤颜色数字图像计算机分析系统可以更为直观性、客观性、准确地表达皮肤颜色,可为色素性和血管性皮肤病的临床观察和疗效判断提供可靠的客观依据。     

小剂量长波紫外线多次照射对人体皮肤的影响

目的:研究小剂量长波紫外线(UVA)辐射对人体皮肤的累积效应.方法:以10名志愿者的臀部作为受试部位,共分为3个区域:阴性对照区域,不进行照射;小剂量照射区域和阳性对照区域分别进行UVA照射,每周照射3次,连续13周,共39次.其中小剂量照射区域的累积剂量为50 J/cm2:阳性对照区域的累积剂量为1 000 J/cm2:照射前后测定皮肤角质层含水量、经皮水分丢失(transepidermal water loss,TEWL)、pH值、皮肤颜色的L*a*b*值和M、E值.取照射区皮肤组织进行苏木精-伊红染色、弹性纤维染色和免疫组化染色.观察表皮、角质层厚度、胶原纤维、弹性纤维的变化、基质金属蛋白酶(MMP)-1和人类长寿基因SIRT1的蛋白表达产物在UVA照射后的变化.结果:小剂量照射区域角质层含水量有下降趋势,TEWL有增加趋势,L*值下降,M、a*、E值升高,pH值无明显变化.皮肤的角质层和表皮厚度增加,真皮中的胶原纤维细碎、淡染,弹性纤维片断化.MMP-1和SIRT1的表达增加.结论:小剂量UVA照射可以引起皮肤光老化.     

日常暴露日光改变表皮通透屏障功能稳态动力学及角质层的致密性

日晒导致皮肤的变化主要由UVA和UVB所致.通常UVA主要导致真皮的改变,而UVB主要引起表皮的改变.由UVB所致的表皮改变包括:晒斑、晒伤、色素增加、皮肤肿瘤等.角质层的功能也可由UVB照射而发生改变.动物试验显示,UVB照射降低角质层含水量[1],红斑量UVB照射降低表皮通透屏障功能[2],亚红斑量UVB促进表皮屏障功能的恢复[3].日常直接日光暴露对表皮通透屏障功能及角质层的致密性是否有影响,尚未见相关的报道.了解这些对于我们日常生活中更好地预防UVB对皮肤的损害具有指导意义.为此,我们在大连地区测量日常直接日光暴露时间长短不同的群体的表皮通透屏障功能及角质层的致密性.基金项日:2008中华医学会-薇姿皮肤医学研究基金(080923ACD1472328)     

慢性光线性皮炎患者光生物试验和Arg163Gln初步研究

目的：探讨慢性光线性皮炎（CAD）患者与健康志愿者光试验、光斑贴试验、皮肤颜色相关参数的差异以及与Arg163Gln基因型特征分布关系。方法用日光模拟仪SUN1000、瑞敏牌光斑贴抗原、紫外线光疗仪SS?03A和窄波反射分光光度仪对25例CAD患者和25例健康志愿者进行光试验、皮肤色素测定，同时用PCR法行Arg163Gln基因型检测。其中25例CAD患者和5例健康志愿者进行光斑贴试验。结果光试验：CAD患者UVA最小持续性黑化量和UVB最小红斑量均显著低于健康志愿者（P<0.05），其中UVB最小红斑量更明显（P<0.01）。光斑贴试验出现阳性反应16例（64%），其中光变态反应13例（52%）。对于4处不同皮肤颜色相关参数的检测，CAD患者面颊部、前额、上臂内侧、手背皮肤的血红蛋白含量均显著高于健康志愿者，而面颊、前额、上臂内侧皮肤的黑素含量差异无统计学意义，仅手背皮肤黑素含量显著高于健康志愿者（P<0.01），CAD患者曝光部位皮肤黑素和血红蛋白含量均显著高于上臂内侧（P<0.05）。CAD在Arg163Gln位点突变为CGA比例与健康志愿者相比，差异无统计学意义（P>0.05）；CAD在Arg163Gln位点突变为CAA比例与健康志愿者相比，差异有统计学意义（P<0.01）。比较Arg163Gln突变为CAA阳性者和CAA阴性者对UVA和UVB的反应性差异，发现Arg163Gln突变为CAA阳性者的UVA最小持续性黑化量（P=0.055）和UVB最小红斑量（P=0.325）均明显低于CAA阴性者。结论皮肤光生物学检查方法在CAD的诊断中具有一定价值。Arg163Gln突变为CAA基因型特征在CAD诊断和防治中有一定的提示作用。     

遗传过敏性湿疹的长波和中波紫外线联合照射疗法

许多遗传过敏性湿疹病人在夏季皮肤改善,日光浴2～3周后可完全消退。作者用长波(UVA)和中波紫外线(UVB)联合照射治疗23例遗传过敏性湿疹病人。另一组33例单用UVB治疗作为对照。两组平均年龄基本相同。每周治疗5天,并外用1%氢化可的松软膏,每天一次,照射剂量根据每个病人情况给予亚红斑量照射。结果33例接受UVB治疗病人仅9例(占27.3%)皮损完全消退,19例(57.6%)显效,2例(6%)有效、3例(9.1%)无效。UVB和UVA联合治疗23例中11例(47.8%)完全消退,11例(47.8%)显效,1例(3.6%)有效,证明UVB和UVA联合治疗遗传过敏性湿疹比单用     

皮肤生物物理参数与UVB皮肤反应的相互影响

紫外线（UV）对皮肤的作用和影响因皮肤类型的不同而差异很大。中波紫外线（UVB）对皮肤所产生的反应则更明显，它是皮肤日光型分类中的主要依据，也是预防UV对皮肤损害的重要波段。研究在同一皮肤类型（或东方人种）皮肤对UVB的反应情况和部分皮肤生理参数对UVB反应的影响是预防UVB对东方人皮肤损害的基础。笔者通过黑素指数（melaninindex，MI）、皮肤红斑指数（erythemaindex，EI）和经表皮失水率（transepidermalwaterloss，TEWL）等不同皮肤生理参数对UVB反应的影响和他们在UVB反应后的改变情况进行了初步探讨。１材料与方…     

红景天苷对UVA/UVB辐射的成纤维细胞中 TNF-α和 IL-1β mRNA表达的影响

目的：测定红景天苷对经UVA/UVB辐射后人皮肤成纤维细胞凋亡过程中TNF-α和IL-1β mRNA表达的影响。方法：在进行UVA/UVB辐射的体外培养人皮肤成纤维细胞实验组中加入红景天苷，应用RT-PCR法检测TNF-α和IL-1β mRNA的表达。结果： UVA/UVB辐射体外培养的成纤维细胞后，TNF-α和 IL-1β mRNA 的表达增加(0.48±0.01/0.47±0.03和0.54±0.04/0.47±0.03)；加入红景天苷后，TNF-α和IL-1β mRNA的表达降低(0.24±0.02/0.26±0.03和0.22±0.03/0.22±0.04)。结论：经UVA/UVB辐射后，体外培养人皮肤成纤维细胞中TNF-α和IL-1β mRNA的表达增高，加入红景天苷后TNF-α和IL-1β mRNA的表达降低，延缓成纤维细胞的凋亡过程。     

The pattern of fibrinolytic activity in human skin following exposure to middle-wavelength ultraviolet light or psoralen and long-wave ultraviolet light.

This experiment was carried out in order to investigate the time sequence of tissue fibrinolytic activity in human skin following UVB or UVA after topically applicated psoralen using Todd's technique of fibrinolytic autography. Tissue fibrinolytic activity increased in the upper dermis for one to six hours after exposure to psoralen and subseqent UVA, when erythema responses were absent. The return to a normal pattern of fibrinolysis occured in the upper dermis 12–18 hours after treatment with psoralen and UVA, and then psoralen-UVA-induced erythema responses began. These responses were maximal 96 hours after treatment with psoralen and UVA, although no fibrinolytic activity was found in the upper dermis. Little change was observed in the lower dermal activity throughout the course of these responses. After UVB irradiation, a transient increase in fibrinolytic activity occured, with a normal pattern of lysis returning in the lower dermis at 12–18 hours. In the lower dermis an increase was observed at one to 6 hours although the activity in the upper dermis had already decreased. UVB erythema responses appeared within this period, were maximal at 6–12 hours, and declined gradually after 12 hours concomitantly with the activity in the upper and lower dermis. The upper dermal activity disappeared at 18 hours, while the lower dermal activity was not found after 72 hours.     

Change of biophysical properties of the skin caused by ultraviolet radiation-induced photodamage in Koreans.

BACKGROUND/PURPOSE: Ultraviolet (UV) irradiation affects the function and complexion of the skin by inducing changes in physical properties through formation of erythema, proliferation of epithelial cells, DNA damage, activation or inactivation of various enzymes and proteins, and free radical formation. In this study, the authors intended to observe the overall course of changes in barrier function and reflectance of the skin induced by photodamage, and healing reaction in the course of time, and alteration of the skin complexion. METHODS: The subjects were chosen from 15 healthy Korean men 20-35 in age, that fall into the category of Fitzpatrick's skin types II, III, and IV without history of recent exposure to sunlight, photosensitivity, or having taken any drugs that induce phototoxicity or photoallergic reactions. The subjects were artificially exposed to suberythemogenic dose [0.5 minimal erythemal dose (MED), 0.75 MED], 1 MED and high dose (2.5 MED) by solar simulator, and changes in skin barrier function and skin reflectance were assessed with a Tewameter, a Corneometer, and a Colorimeter for 4 weeks. RESULTS: Transepidermal water loss (TEWL) increased abruptly at Day 1 of single solar UV (SSUV) exposure, and slowly returned to the original level from Day 2/Day 3. In the case of exposure with 0.75 MED, it returned to the original level at Day 4 of exposure, and at Days 7 and 28 in the cases of 1 MED and 2.5 MED exposure, respectively. Water-holding capacity sharply declined at Day 1 of exposure, hitting the lowest point at Day 2, and then slowly recovered starting on Day 3. In the case of exposure with 0.75 MED and 1 MED, it returned to the original level at Days 7 and 28 in the case of 2.5 MED exposure. The a(*) values abruptly increased and reached the peak at Day 1 and slowly returned to the original level at Day 2, while the b(*) values slowly increased at Day 3, peaking at Day 7 and slowly returning to the original level thereafter. The L(*) values abruptly declined at Day 1, maintaining plateau through Day 7 and slowly returning to the baseline level thereafter. The individual typology angle (ITA degrees ) were compatible with L(*) values change. The erythema index increased abruptly at Day 1 of SSUV exposure, peaking at Day 2 and slowly returned to the original level starting at Day 3. Melanin index slowly started to increase on Day 3 of SSUV exposure, peaking at Day 7 and gradually returned to the original level thereafter. However, L(*), a(*), b(*), erythema index, and melanin index did not return to the original level during the 28-day course of this study. CONCLUSION: This study shows that in the skin of Korean subjects, changes in skin barrier function and delayed melanization do occur even in exposure to a suberythemogenic dose of SSUV. Also, given the fact that restoration of barrier function occurs as the process of melanization begins, melanization is considered to be a useful predictive indicator of the restoration of the skin barrier function after sunburn.     

Contrasting effects of ultraviolet A1 and ultraviolet B exposure on the induction of tumour necrosis factor-α in human skin

Ultraviolet B (UVB) irradiation of the skin causes immunosuppression which is relevant to the induction of skin cancer. The mechanism of this immunomodulation is unclear but various regulatory molecules have been implicated, including cis-urocanic acid (cis-UCA) and the cytokines tumour necrosis factor-α (TNF-α) and interleukin 10 (IL-10). Whether ultraviolet A (UVA) induces similar changes has not been investigated fully. We studied the effect of in vivo UVB and long-wave UVA (UVA1) exposure on the induction of TNF-α, IL-10 and cis-UCA in human skin. Volunteers were irradiated with three minimal erythema doses (MED) of UVB or UVA1. At different times after irradiation, suction blisters were raised from irradiated and from non-irradiated (control) skin. The TNF-α and IL-10 protein concentration, and the percentage of cis-UCA in the blister fluid, were then determined. UVB irradiation of human skin led to a rapid and significant increase in TNF-α concentration in suction-blister fluid, with maximal values 6 h after irradiation (n = 6, P < 0.05). In contrast, UVA1 irradiation led to a decrease in TNF-α concentration in the suction-blister fluid compared with non-irradiated skin, with the lowest values 6 h after irradiation (n = 6, P < 0.05). Both UVB and UVA1 exposure of the skin induced a slight increase in IL-10 concentration. However, the increase in IL-10 was only significant after UVB irradiation (UVB, n = 6, P < 0.05; UVA, n = 7, P < 0.1). As previously shown, both UVB and UVA1 result in the photo-isomerization of trans-UCA and an increased percentage of cis-UCA was found in the suction-blister fluid. Thus the results show differential effects of UVB and UVA1 irradiation on the induction of immunoregulatory molecules, which may help to explain the variation in immune responses after UVB and UVA1 exposure of human skin.     

Long-term evaluation of erythema and pigmentation induced by ultraviolet radiations of different wavelengths

BACKGROUNDS/AIMS: Although multiple studies have been reported about the biological effects of ultraviolet (UV) radiations, the comparative and long-term reactions of human skin by several different UV-wavebands were not reported. The aim of this study was to investigate a time course of erythema and pigmentation induced by UVA 1, broad-band UVA (BBUVA), narrow-band UVB (NBUVB) and broad-band UVB (BBUVB). METHODS: Ten volunteers participated in this study for 6 months. Four skin areas, from the back of each subject, were irradiated with two minimal erythema dose (MED) of four different UV wavelengths corresponding to UVA 1, BBUVA, NBUVB and BBUVB. Skin color changes were evaluated by visual scoring and values were converted into the L*a*b color system. RESULTS: For both UVA 1 and BBUVA, erythema and pigmentation were most pronounced immediately and 1 h after exposure. Thereafter, erythema rapidly diminished but pigmentation persisted throughout the study. For both NBUVB and BBUVB, test areas reacted with erythema of maximum intensity at 1 and 2 days, respectively. A maximum tanning was reached at 3-6 days for NBUVB and 4-7 days for BBUVB, and the return toward the original color point was at 1 and 3 months, respectively. No significant difference was found in visual and colorimetric evaluation for the time course of skin color changes. CONCLUSION: Two MED of UVA produced far prolonged erythema and pigmentation than UVB. For UVA, UVA 1 and BBUVA showed similar intensity and time course of skin reaction. For UVB, erythema and pigmentation produced by NBUVB were milder in intensity and shorter in time course than those by BBUVB. These results would provide standard data on time courses and intensity of skin color changes by different UV wavelengths.     

Topical chloroquine applied before irradiation protects against ultraviolet B (UVB)- and UVA-induced erythema but not against immediate pigment darkening.

Seventeen healthy volunteers were phototested with ultraviolet B (UVB) and UVA before and after topical treatment with chloroquine phosphate. The skin areas treated before but not after irradiation showed higher minimal erythema dose values for UVB and UVA than control skin. The effect was clearly spectral with greater protection afforded against UVB than UVA. The immediate pigment darkening after irradiation with UVA, however, was not affected by pretreatment with the drug. The mechanism of action for this protective effect did not seem to be related to merely absorption and screening, inhibition of the inflammatory reaction or a UV-induced effect on the stereo-isomerization of the drug.     

Increased expression of Fas on human epidermal cells after in vivo exposure to single-dose ultraviolet (UV) B or long-wave UVA radiation

BACKGROUND: Apoptosis has been proposed to act as an important mechanism for eliminating keratinocytes that have been irreversibly damaged by ultraviolet (UV) irradiation. One way to induce apoptosis in keratinocytes is through activation of the cell surface receptor Fas (CD95), either with the ligand (FasL) or directly with UV radiation. OBJECTIVES: To investigate the regulation of Fas and FasL expression in human skin and the formation of apoptotic cells after in vivo exposure to UVB or long-wave UVA radiation. METHODS: Volunteers were irradiated with either 3 minimal erythema doses (MED) of UVB (n = 6) or 3 MED of long-wave UVA (n = 6) on buttock skin 12, 24 and 72 h before skin punch biopsies were taken. Expression of Fas and FasL was demonstrated by immunohistochemistry on cryostat sections. Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated fluorescein-deoxyuridine triphosphate nick-end labelling reaction. RESULTS: In five of six subjects, exposure to UVB radiation resulted in increased homogeneous expression of Fas on epidermal cells, with greatest expression at 24 and 72 h after irradiation. In all subjects, exposure to long-wave UVA resulted in increased homogeneous expression of Fas on epidermal cells, with greatest expression at 12 h after irradiation. In five of six subjects, exposure to UVB radiation resulted in temporarily decreased expression of FasL, but after 72 h the expression of FasL had returned to the preirradiation level. The expression of FasL on epidermal cells after exposure to long-wave UVA showed considerable variation. UVB irradiation was a stronger inducer of epidermal apoptosis than was UVA irradiation. The number of apoptotic epidermal cells did not correlate with expression of Fas or FasL. CONCLUSIONS: In human skin the expression of Fas on epidermal cells increases after in vivo exposure to UVB or long-wave UVA. Exposure to UVB causes a temporary decrease in the expression of FasL on epidermal cells.     

Can ultraviolet erythema be used to identify the basal cell carcinoma phenotype?

Since a prolonged duration of a strong UBV erythema has been suggested as a marker for propensity to develop skin cancer, we objectively followed the duration and intensity of erythemas induced by UVB and UVA radiation for 28 days in 18 patients with basal cell carcinoma (BCC), and in 15 healthy controls using reflectance spectrophotometry. The erythema index, defined as the difference in redness between UV-exposed skin and normal, adjacent skin on the lower abdomen, did not differ significantly between the two groups at 24 h, when the reaction was maximal, following a dose of 6 MED of UVB. Erythema values after 7 and 14 days were slightly higher in the BCC group, but this difference did not reach statistical significance. At day 7 some patients in the BCC group showed very strong erythemas. At days 21 and 28 the two groups had almost identical erythemal reactions. Following a standard dose of UVA of 100 J/cm², patients with BCC and healthy controls both showed weak erythemal reactions, which declined somewhat over the study period. No significant differences in pigmentary response were noted between the BCC and the control group, neither following UVB nor UVA. Although individual patients with BCC deviate from the normal erythemal curve for UVB, the UVB response is not a suitable predictive instrument in screening patients with the basal cell carcinoma phenotype.     

Acute skin alterations following ultraviolet radiation investigated by optical coherence tomography and histology

Optical coherence tomography (OCT) appears to be a promising technique to study skin in vivo. As part of an exploratory study to investigate UV induced effects non-invasively we aimed to evaluate the kinetics of acute UVB- as well as UVA1 induced skin alterations by means of OCT, and to correlate the results obtained with routine histology. Twelve healthy subjects received daily 60 J/cm² of UVA1 and 1.5 minimal erythema doses of UVB on their upper back over three consecutive days. One day (24 h) after the last UV exposure, OCT measurements and skin biopsies were performed in four subjects (day 1) on the centre of the irradiated sites and an adjacent non-irradiated control site. The same procedure was performed in four subjects 3 days and 6 days after irradiation, respectively. Prior to OCT assessment two waterproof marks were drawn on the centre of UVB and UVA1 exposed sites and the control site. The OCT scanner, SkinDex 300, was used in the RI1D measurement modus in order to investigate morphological features, epidermal thickness, and scattering coefficients. Immediately after OCT assessment, 4 mm punch biopsies were taken from the previously marked sites. OCT as well as histological examinations performed on day 1, 3, and 6, revealed markedly higher values for epidermal thickness on UVB exposed skin sites, and slightly increased epidermal thickening in UVA1 exposed sites. UVB exposed sites showed disruption of the entrance signal in the B-scan of OCT resulting in a thickened layer with a signal-poor centre corresponding to hyperkeratosis and parakeratosis as confirmed by routine histology. Surprisingly, the mean scattering coefficients of the epidermis were slightly lower on UVA1 exposed sites, as compared to non-irradiated skin. By contrast, the scattering coefficient of the upper dermis of UVA1 irradiated skin was hardly altered. Moreover, the scattering coefficient of the upper dermis assessed on UVB exposed skin on day 1 was clearly smaller than the scattering coefficient observed on non-irradiated and UVA1 exposed skin. Conclusively, it was possible to demonstrate by means of OCT differences of epidermal thickness and pathological features of the stratum corneum following UV exposure. UVA1 induced epidermal pigmentation as well as UVB induced dermal inflammation may affect the light attenuation in the tissue indicated by a decrease of the scattering coefficient. OCT seems to be a useful tool to monitor UV induced effects in vivo.     

Dosimetry of solar ultraviolet radiation. Daily and monthly changes in Paris

The intensity of ultraviolet A and B radiations was measured in Paris (48 degrees North) by means of silicon photoelectric cells (Osram Centra dosimeter) from December, 1984 till February, 1986. The results, which must be regarded as approximate, are expressed as physical units (mW/cm2) and biological units (minimal erythema dose/hour). For sunny days two curves are presented separately for UVB and UVA: daily variations in radiation (hourly measurements) and daily variations at 11 hours (solar time) during one year. Maximum irradiation was observed at noon in early July: UVB 0.15 mW/cm2, UVA 5.4 mW/cm2. Between December and July the amount of UVB radiation was multiplied by 14 and that of UVA radiation by 9. For subjects with clear photo-type and when the sun was at its zenith, an MED per hour was obtained from May 1 onwards. Within a day, 30 p. 100 (summer) and 50 p. 100 (winter) of erythema-producing UV intensity were delivered between 11 and 13 hours (solar time). This kind of study has numerous clinical applications: advice regarding exposure to sun rays, dosing of heliotherapy, epidemiological data concerning photodermatitis (circumstances of exposure, UV threshold dose) and photocarcinogenesis (determination of annual MED doses in relation to areas of uncovered skin and occupational exposure to sun rays). Other studies on the French territory will provide a map of UV irradiation.     

Skin temperature changes induced by ultraviolet A exposure: implications for the mechanism of erythemogenesis

Measurement of the change in skin temperature caused by exposure of the skin to ultraviolet (UV) radiation may give insight into the mechanism responsible for the development of the UV erythema. Under controlled environmental conditions we determined the temperature change of skin areas exposed to UVA, up to 24 h after irradiation. The UVA doses given were 3 or 4 times the minimal erythema dose (MED). The 3-MED and the 4-MED doses resulted in elevation of skin temperature. Delayed UVA erythema was accompanied by skin temperature rise, indicating involvement of arteriolar vessels in the UVA erythema. This arteriolar dilation is best explained if we assume that the delayed erythema is caused by a vasoactive mediator, most likely released in the epidermis, which reaches the dermal blood vessels by diffusion. This result, combined with earlier studies, leads to the conclusion that the erythemas elicited by UVA, UVB and UVC are probably all brought about by diffusing mediators, and not by direct action of the radiation on the blood vessels.