UVA tanning devices interact with solar-simulated UV radiation in skin tumor development in hairless mice

Summary The carcinogenic effect of three UVA tanning sources was studied in lightly pigmented hairless mice. The three tanning sources (Bellarium-S SA-1-12, Philips TL 09R and Philips TL 10R) have different emission spectra, and emit different amounts of UVB. Radiation from the tanning sources was administered for 20 min/day, 5 day/week in daily doses equivalent to those used in suntan salons. The radiation was given alone or after 12 weeks of exposure to solar-simulated UV radiation (SOLAR UV) (10min/day, 4 day/week; daily dose, 19.5 kJ/m² UVA and 3.9 kJ/m² UVB). Irradiation with Bellarium-S SA-1-12 for 47 weeks and Philips TL 09R for 74 weeks induced skin tumours in 20/20 and 13/20 of the animals, respectively. When irradiation with Bellarium-S SA-1-12 and Philips TL 09R was administered after 12 weeks of SOLAR-UV exposure, a strong enhancement of SOLAR-UV-induced photocarcinogenesis was observed (p<0.001). Irradiation with Philips TL 10R was only slightly carcinogenic, and during 85 weeks of irradiation only one skin tumor appeared in a group of 20 mice. However, when irradiation with Philips TL 10R was administered after 12 weeks of exposure to SOLAR UV, an enhancement of SOLAR-UV-induced carcinogenesis was observed (p<0.001). Our results suggest that the hazards of exposure to commercial tanning devices are increased when they are used after a period of natural sun exposure. Even tanning sources with a low carcinogenic potential are able to increase SOLAR-UV-induced carcinogenesis significantly.     

紫外线所致皮肤鳞状细胞癌小鼠模型的建立

目的 应用日光模拟器模拟日光照射SKH-1无毛小鼠,建立皮肤鳞状细胞癌（鳞癌）动物模型,探讨其生物学特性。方法 将91只SKH-1无毛小鼠随机分成7个实验组（每组10只）和7个对照组（每组3只）。实验组每天给予红斑量日光紫外线照射,对照组不做任何处理;在第4、8、12、16、20、24、28周分别处死小鼠行病理检查。实验过程中观察小鼠一般状态和照射区域皮肤变化,分析各期小鼠皮损特点及组织学变化。结果 10周后实验组部分小鼠陆续出现直径≥1 mm的丘疹,紫外线照射20周开始实验组剩余小鼠中39.3%出现肿瘤（11/28）,照射28周后成瘤率达100%（10/10）,累计UVB剂量约为26.99 J/cm2,UVA剂量约为242.91 J/cm2。对照组未见肿瘤形成。照射各时期组病理显示,12周30%、16周33.3%、20周60%、24周87%、28周100%的小鼠具有鳞癌特征。结论 紫外线照射可诱导SKH-1无毛小鼠皮肤组织增生,并随照射时间延长产生皮肤鳞癌。     

Effect of a new narrow-band UVB lamp on photocarcinogenesis in mice.

Thirty lightly pigmented hairless (Hr/Hr) mice were irradiated 5 days per week for 30 weeks to assess the photocarcinogenicity of a new Philips TL 01 narrow-band (311 nm +/- 2) UVB lamp. All mice were found to be tumour-bearing after 16 weeks and histologically, 83% of these had definite squamous cell carcinomas. Compared with our previous study where conventional broad-band Philips TL 12 UVB irradiation was used, tumours appeared earlier with the TL 01 lamp. The total irradiation dose was, however, several times greater in the TL 01 assay while the total MED dose was considerably less.     

A polychromatic action spectrum for photosensitivity to orally administered 8-methoxypsoralen in humans

The action spectrum for producing minimal phototoxic erythema after oral administration of 8-methoxypsoralen (8-MOP) was determined in the range of 312-368 nm in 12 human volunteers using six different UV radiation sources. The peak sensitivity was found to be at 343 nm. The 8-MOP photosensitivity was at a high level (1.75 of maximum) between 336 and 355 nm. Conventional UVA radiation sources, like the Philips TL/09R tube, have a high energy output within 335 and 355 nm, and are therefore highly recommended in oral psoralen plus UVA radiation treatment.     

In vivo estimation of pigmentation in ultraviolet-exposed hairless mice

A new in vivo method of visual scoring of pigmentation in hairless hr/hr mice with a C3H/Tif background is described. The mice were placed under a bank of 6 Philips TL08 fluorescent ultraviolet A (UVA) tubes in a dark room, and the pigmentation of the skin was compared with a Kodak Gray Scale with 20 different shades from white to black. The radiation from the tubes changed both the color of the back of the mouse and the gray scale into purple hues. The purple color of the back of each mouse could then be classified as one of 20 shades on the gray scale. An experiment was conducted exposing 3 groups of 20 mice to different doses of UV radiation from Philips TL01 tubes. One group of 20 mice was not irradiated and served as control. The pigmentation of each mouse was scored by one investigator every 2–3 weeks. After a few weeks of exposure a clear distinction between the groups was seen. To evaluate the inter- and intrapersonal variation of the method, 30 mice with various degrees of pigmentation were scored independently and blindly by two investigators. This was done twice during the study with a few days' interval. No interpersonal difference was found, but one investigator scored differently the first and second time by only 0.5 points. The described method provides a reproducible in vivo method, with very good discrimination, for estimation of pigmentation in hairless mice.     

UVA-induced tumours in pigmented hairless mice and the carcinogenic risks of tanning with UVA

Summary An animal experiment is presented in which two groups of pigmented hairless mice were exposed daily to suberythemal doses of UVA to study tumourigenesis. The aim of the study was to estimate the carcinogenic risks of tanning by UVA. The pigmented hairless mice, Skh-hr2, were separated by selective breeding into two groups, the browns and the blacks. Both groups were exposed daily to UVA from fluorescent UVA lamps (Philips TL40W/09) purified by rigorously filtering out the shorter wavelengths. No acute actinic damage was observed after any exposure. However, in most UVA exposed animals, especially in the blacks, a marked scratching preceded the development of tumours. Hyperkeratosis was also observed. All animals developed tumours. Histopathologically at least 60% of the tumours were squamous cell carcinomas. Depositions of melanophages were observed, but no melanomas. It is beyond any doubt that UVA is carcinogenic in laboratory animals. The present state of knowledge justifies no preference for tanning with UVA over tanning with UVB.     

Contrasting effects of an ultraviolet B and an ultraviolet A tanning lamp on interleukin-6, tumour necrosis factor-α and intercellular adhesion molecule-1 expression

BACKGROUND: Recent studies have demonstrated that a tanning lamp emitting predominantly ultraviolet (UV) A induces significant yields of the type of potentially mutagenic DNA damage that are associated with the onset of skin cancer (i.e. cyclobutane pyrimidine dimers). UV-induced immunosuppression is also an important event leading to skin cancer. OBJECTIVES: To the modulation of key immunological molecules following exposure to a broad-spectrum UVB lamp and a predominantly UVA-emitting tanning lamp using model in vitro systems. METHODS: We compared secretion and mRNA expression of interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha in normal human epidermal keratinocytes, and interferon (IFN)-gamma-induced intracellular adhesion molecule (ICAM)-1 in normal human fibroblasts irradiated in vitro with a broad-spectrum UVB lamp or with a Philips 'Performance' tanning lamp. RESULTS: With broad-spectrum UVB irradiation, upregulation of IL-6 and TNF-alpha mRNA was detected 6 h after irradiation, and a dose-dependent increase of cytokines in the supernatants of irradiated cells was found 24 h after irradiation. In contrast, there was no cytokine secretion and little evidence for mRNA upregulation following exposure to a tanning lamp. When cells were exposed first to broad-spectrum UVB, then the tanning lamp, UVB-induced cytokine secretion was inhibited, although mRNA levels were upregulated to a level close to that observed with UVB alone. By using a Schott WG 320 nm filter to attenuate the level of UVB relative to UVA emitted by the tanning lamp, the inhibition of cytokine secretion was shown to be associated with UVA exposure. Both UV sources inhibited IFN-gamma-induced ICAM-1 mRNA expression in a dose-dependent fashion. By using a Schott WG 335 nm filter, inhibition of ICAM-1 mRNA expression by the tanning lamp was shown to be associated with UVB exposure. CONCLUSIONS: These results suggest that UV sources emitting different levels of UVA and UVB have differential effects on the modulation of different immunoregulatory molecules, and indicate that there are potential interactions between these wavelengths.     

Psoralen-containing sunscreen is tumorigenic in hairless mice

Sunscreens containing 5-methoxypsoralen (5-MOP) are currently being marketed to promote tanning by inducing psoralen-mediated ultraviolet (UV) A (320-400 nm) melanogenesis. The rationale is that this may prevent UVB (290-320 nm) radiation-induced skin damage. However, mouse studies have shown that 5-MOP has the same cutaneous photocarcinogenic potential as 8-methoxypsoralen. In addition, the 5-MOP--containing sunscreen Sun System III (SS III), when combined with UVA, induces epidermal ornithine decarboxylase activity, an enzyme associated with tumor promotion. Therefore, we investigated whether SS III had sufficient psoralen concentration to be tumorigenic in hairless mice exposed to chronic, intermittent UVA radiation. SS III was applied to hairless mice 5 days per week for 20 weeks. After each application the mice were exposed to 2.5 to 10 joules/cm2 UVA radiation. All test groups developed atypical squamous papillomas in direct proportion to the dosage of UVA radiation received. A shorter latency period for tumor development was seen with larger UVA doses. Test animals followed up to 1 year developed invasive squamous cell tumors. Control groups (SS III without UVA and UVA without SS III) remained free of tumors. Animals receiving SS III plus UVA developed persistent skin thickening and increased dermal cyst formation similar to that reported with chronic exposure to UVB, a known carcinogenic wavelength. Over-the-counter sunscreens containing 5-MOP do contain sufficient psoralen concentrations to cause cutaneous phototoxicity and photocarcinogenicity in mice, and their use in humans should be discouraged in the interest of preventing further UV-induced skin damage and skin cancer.     

A comparison of erythema efficacy of ultraviolet B irradiation from Philips TL12 and TL01 lamps

The erythema efficacy of UVB irradiation from Philips TL12 and TL01 lamps has been evaluated and compared. Thirty-seven healthy Thai volunteers were irradiated on the previously unexposed lower back with TL12 and TL01 lamps in doses ranging 100 to 550 mJ/cm² and 360 to 2020 mJ/cm², respectively. Erythema was evaluated clinically and measured by a narrow-band spectrophotometer before exposure and 24 h after exposure. The threshold doses of UVB that induced barely perceptible erythema (MED_b) with well-defined border erythema (MED_w) and the steepness of the dose-response curves for erythema (DRAE) were compared. We found that MED_b and MED_w of the TL01 lamps were 4.19 and 4.52 times those of TL12 lamps, which were similar to those calculated from the CIE erythema action spectrum (4.2). However, the DRAE of the two lamps were quite similar. Because the initial dosage of UVB phototherapy is usually given as a percentage of a patient's MED, the initial exposure of TL01-UVB phototherapy should be about 4.2 times that of TL12-UVB.     

In vitro effects of ultraviolet A on histamine release from human basophils

BACKGROUND: As long-wave ultraviolet (UV) radiation penetrates the dermis, connective tissue cellular components and circulating blood cells can be possible targets for solar UVA. Basophils, involved in the effector phase of the inflammatory response, play a part in skin diseases such as chronic urticaria, psoriasis, atopic dermatitis, fixed drug eruption, allergic contact dermatitis, urticaria pigmentosa, systemic sclerosis and bullous pemphigoid. OBJECTIVE: The evaluation of the in vitro effect of UVA on histamine release from human basophils. METHODS: Basophils from healthy human volunteers were irradiated, respectively, with UVA at doses of 2.5, 5, 7.5, 10, 20 and 50 J/cm2 and then incubated with an anti-IgE serum. A fluorimetric technique was employed to determine histamine release from samples: (i) incubated with 2% HClO4 (complete lysis of basophils); (ii) irradiated with increasing doses of UVA; and (iii) unirradiated (controls). RESULTS: Histamine release was: 100% for HClO4 incubated basophils, 30% for unirradiated and anti-IgE incubated cells (controls) and 27%, 24%, 34%, 41%, 60% and 70% for basophils irradiated with UVA doses, respectively, of 2.5, 5, 7.5, 10, 20 and 50 J/cm2 and incubated with anti-IgE. Histamine releasability from irradiated samples was statistically significant (P < 0.05), in comparison with controls, at UVA doses equal to 5, 10, 20 and 50 J/cm2. CONCLUSIONS: UVA exerts, at least in vitro, a biphasic dose-dependent action on histamine release from human basophils incubated with an anti-IgE serum: at the lowest irradiation doses (< 5 J/cm2) it exerts an inhibitory effect and at the highest doses (> or = 10 J/cm2) histamine release increases significantly.     

Modest in vivo exposure to solar wavelengths induces a visible absorbing chromophore in Skh-1 mouse epidermis

BACKGROUND/PURPOSE: In the previous work, we correlated epidermal hyperplasia with increased epidermal absorption in the 250-400 nm region. During a recent review of that work, the apparent formation of a chromophore, with absorption slightly longer than 400 nm, in the epidermis of irradiated animals was noted. In this study, we have extended the transmission measurement to include the 250-800 nm region. METHODS: Age-matched Skh-1 hairless mice were separated into three groups. One group was irradiated with 6.3 J/cm(2) (0.9 minimal erythemal dose; MED) of solar simulating ultraviolet radiation (SSUVR) five times/week for 2 weeks, then increased to 1.1 MED (7.1 J/cm(2)) for two additional weeks (20-day group). A second 10-day group, added halfway through the protocol, was irradiated with 0.9 MED five times/week for 2 weeks. The control group received no UV irradiation. Routine H&E staining and epidermal absorption spectral analysis were carried out on biopsy specimens from each animal. RESULTS: This work confirms the development or enhancement of a visible chromophore with a maximum absorption at ca 412 nm. This peak appears to be radiation dose dependent. It can be discerned in both the groups, albeit more prominently in the 20-day animals. The absorption is sufficiently strong to impart a yellow to reddish appearance to skin viewed in full spectrum visible light. CONCLUSIONS: Accumulation of such a chromophore in humans may contribute to the coloration of chronically exposed skin. The absorption strength and wavelength location of the peak is strongly suggestive of a heme-like compound. We are currently conducting experiments to further characterize this chromophore.     

Interactions between tazarotene and ultraviolet light

Tazarotene in combination with phototherapy is being used clinically for the treatment of plaque psoriasis. This study investigates the dose of UVB light required to induce minimal erythema and the dose of UVA light required to induce immediate pigment darkening, with and without pretreatment with tazarotene 0.1% gel. The photostability of tazarotene is also assessed. Pretreatment with tazarotene 0.1% gel 3 times per week for 2 weeks before phototherapy significantly reduced the mean minimal erythema dose (MED) for UVB from 56.25 to 42.50 mJ/cm(2) (P <.01), and significantly reduced the mean UVA exposure required to induce immediate pigment darkening from 20.18 to 18.50 J/cm(2) (P <.05). A thin application of tazarotene gel immediately before phototherapy had no significant effect on the mean MED for UVB, whereas a thick application of the gel increased the MED slightly, from 56.25 to 62.50 mJ/cm(2) (P =.1). Tazarotene remained chemically stable when used in conjunction with UVB or UVA phototherapy. To reduce the patient's potential to burn or tan, we recommend initiating UVB phototherapy at 50% to 75% of the MED when it is used in combination with tazarotene. We also recommend initiating PUVA therapy at slightly lower doses than usual. Lower total doses of UVA or UVB may be needed when patients with psoriasis are treated concomitantly with tazarotene.     

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.     

Epidermal changes caused by chronic low-dose UV irradiation induce wrinkle formation in hairless mouse

To investigate the effects of chronic low-dose UV irradiation on the skin, hairless mice were irradiated with a 1/3 minimal erythemal dose (MED) of UV. We examined the relationship between visible changes and skin damage in the dermis and epidermis. Hairless mice were irradiated with UVB (20 mJ/cm2) and UVA (14 J/cm2) three times a week for 10 weeks, followed by a 24-week non-irradiation period. Visible fine wrinkling was present after 4 weeks of irradiation, and the wrinkling progressively worsened throughout the period of irradiation. The wrinkles remained after irradiation was discontinued. In dermal components, no significant histological changes in the collagen fibers and elastic fibers were found, and the amount of hydroxyproline was also not changed. Thus, in the epidermis, there was a significant increase in the number of stratum corneum layers and the terminal-differentiation marker, filaggrin, positive cells. The intensity of staining for the differentiation marker, keratin 1, was reduced. These changes were accompanied by wrinkle formation, and remained after discontinuance of irradiation. These findings suggested that chronic low-dose UV irradiation induces structural and quantitative changes in the epidermis as a result of keratinization impairment, and that this damage in the epidermis is an important causative factor in wrinkle formation.     

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

BACKGROUND/AIMS: The long-term reactions of human skin by different ultraviolet (UV)-wavebands were not reported. This study was to investigate a time course of erythema and pigmentation induced by UVA-1, broadband UVA (BBUVA), narrowband UVB (NBUVB) and broadband 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. RESULTS: For both UVA-1 and BBUVA, erythema and pigmentation were most pronounced immediately and 1 h after exposure. 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 point was at 1 and 3 months, respectively. 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 a time course than those by BBUVB.     

The carcinogenic effect of UVA irradiation

The carcinogenic effect of UVA radiation (from Philips black light tubes filtered through a 2 mm-thick glass plate to eliminate the radiation below 320 nm) was studied in 7 groups of 25 lightly pigmented hairless mice. Irradiation with a moderate daily dose of combined UVB and UVA for 3 months induced a tumor incidence of 0.22 after 58 weeks. When the combined UVB and UVA irradiation was followed by filtered UVA for 2, 4, or 6 months, the tumor incidence was marginally significantly increased to 0.42, 0.48, and 0.50 (p less than 0.05), respectively. However, irradiation with the moderate dose of combined UVB and UVA induced a slight but not significantly lower tumor incidence as compared to UVB alone (0.22 vs 0.30, p greater than 0.1). UVA alone induced no tumors. It thus appears that in hairless mice initially exposed to a combination of UVB and UVA, subsequent continued irradiation with UVA increases tumor incidence. While only marginally statistically significant, tumor incidence in these animals seems to increase with duration and hence total UVA exposure. Furthermore, it is suggested that the photoaugmentative carcinogenic effect of UVA irradiation from unfiltered UVA bulbs can be reduced by attenuating the shorter wavelengths of the radiation.     

Photocarcinogenesis by near-ultraviolet (UVA) radiation in Sencar mice

The carcinogenic effect of long-term exposure to UVA (315-400 nm) radiation was examined in Cr:ORL Sencar mice. Daily exposure to FR40T12 PUVA bulbs, filtered with Mylar to eliminate wavelengths below 315 nm, induced skin tumors with 50% probability of tumor development (T50) occurring after 68 weeks of irradiation. Tumors developed primarily on the dorsa of mice and included squamous cell carcinomas, poorly differentiated (spindle cell) tumors, and benign squamous papillomas. By comparison, thrice-weekly exposure of Sencar mice to unfiltered FS40 sunlamps containing both UVB (280-315 nm) and UVA radiation, induced skin tumors with T50 occurring after 23 weeks of irradiation. Tumors developed primarily on the ears and included squamous cell carcinomas and spindle-cell tumors. A small number of spontaneous mammary adenocarcinomas occurred in mice (both irradiated and unirradiated controls) that were older than 50 weeks. This study demonstrates that UVA radiation, which is the major UV waveband in solar radiation, is carcinogenic in a haired mouse strain, although far less carcinogenic than combined UVB/UVA radiation.     

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.     

Connective tissue alterations in the skin of ultraviolet irradiated hairless mice

Connective tissue alterations were induced in hairless mouse skin by ultraviolet (UV) irradiation. Hairless mice were irradiated three times a week for 10 weeks with sunlamps (UVA and UVB) and the skin was examined using immunochemical and biochemical techniques. Indirect immunofluorescence was performed with antibodies directed against elastin, microfibrillar proteins, and fibronectin. Increased fluorescence was observed in the actinically damaged skin for elastin, microfibrillar proteins, and fibronectin. The elastic fiber components, elastin and microfibrillar proteins, were then isolated and quantified. Control skin contained approximately 0.1% by dry weight of elastic fiber components, whereas actinically damaged skin contained 0.2% by dry weight. These data are consistent with previous observations of elastic fiber hyperplasia in UV irradiated mice. In addition, irradiated mouse skin contained 1.12 mg of extracted fibronectin per gram wet weight as compared with 0.59 mg in control skin. Irradiated mouse skin contained increased quantities of hyaluronic acid and chondroitin sulfate (uronic acid content). These studies further support the validity of the UV irradiated hairless mouse as a model of human dermal photoaging.     

The Relationship among Minimal Erythema Dose,Minimal Delayed Tanning Dose,and Skin Color

The relationship among minimal erythema dose (MED), minimal delayed tanning dose (MDTD), and skin color was examined in 16 healthy volunteers using three different spectra. The subjects were exposed to UVB, UVA+B, and UV+Visible light (UV+Visible) with a xenon arc solar simulator as a light source. The MEDs for UVB and UVA+B were less than the MDTDs, whereas the MED for UV+Visible was higher than the MDTD. There was no significant correlation between the MED and the MDTD for UVB or UVA+B. The MED for UV+Visible was significantly correlated to the MDTD (p<0.01). Skin color significantly correlated with MEDs for UVB and UVA+B (p<0.01), but not for UV+Visible. There was no significant correlation between skin color and the MDTD for any spectra. From these results, it is suggested that the relationship between erythemal and melanogenic responses is dependent on spectral bands of the light source and that skin color is a predictor of UV-induced erythema.