The 0.8% ultraviolet B content of an ultraviolet A sunlamp induces 75% of cyclobutane pyrimidine dimers in human keratinocytes in vitro

Tanning lamps, emitting predominantly ultraviolet (UV) A, are used widely throughout the U.K. and other countries, but little is known about the long-term risks associated with their use, especially with respect to skin cancer. We have exposed normal human epidermal keratinocytes to a commercial tanning lamp and used the comet assay in association with DNA repair enzymes T4 endonuclease V and endonuclease III to investigate the relative yields of directly formed cyclobutane pyrimidine dimers (CPDs) and indirectly formed types of oxidative DNA damage. To put the risk of using tanning lamps into perspective, the sunbed used in this study (five Philips Performance 80W-R UVA tubes at a distance of 35 cm) was found to be approximately 0.7 times as potent at inducing CPDs as U.K. natural sunlight around noon on a fine summer day. This compares with a relative risk for CPD induction and erythema of 0.8 and 0.7 times, respectively, calculated from the relevant action spectra of tanning lamps and British noontime sunlight. To determine the relative contribution of UVB and UVA to the induction of CPDs and oxidative DNA damage, we modified the spectral output of the tanning lamps with a series of Schott WG UVB filters. The induction of CPDs was more dependent on the UVB component of the sunbed than oxidative types of damage. Schott WG UVB filters with 50% transmission at 305 nm reduced the yield of T4 endonuclease V sites by 42% while there was only a 17% decrease in the yield of endonuclease III sites. CPD induction was not completely abolished after irradiation through WG335 and WG345 nm filters despite there being no detectable UVB. From these data, it was estimated that, although the tanning lamps emitted only 0.8% of their total output in the UVB range, these wavelengths were responsible for the induction of over 75% of CPDs and 50% of the oxidative damage to DNA.     

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.     

Topical riboflavin attenuates ultraviolet B‐ and ultraviolet A‐induced immunosuppression in humans

Background: Riboflavin (vitamin B₂) plays a key role in cellular energy metabolism. We have observed previously that nicotinamide (vitamin B₃), which is also centrally involved in cellular energy restoration after UV irradiation, is highly immune protective in humans. We thus hypothesized that riboflavin might also confer immune protection. Methods: We irradiated healthy, nickel‐allergic volunteers with narrowband UVA (385 nm) and UVB (300 nm) at separate sites on the lower back. These areas were treated with riboflavin solution or vehicle at 24 h and again at 30 min before UV exposure. Forty‐eight hours after irradiation, volunteers were patch tested with nickel‐containing Finn chambers, at both irradiated and nonirradiated sites, with and without prior riboflavin treatment. The resulting contact hypersensitivity reactions at each site were then measured 72 h later with a reflectance erythema meter in order to determine and compare the immune suppressive effects of each intervention. Results: We observed that low doses of both UVB and longwave UVA1 were immune suppressive in humans. Topical riboflavin conferred immune protection against both wavebands. Conclusions: Riboflavin is immune protective in humans, and this may reflect the role of the B group vitamins in cellular energy restoration after UV exposure.     

Immunoprotective haem oxygenase induction by ultraviolet A (320-400 nm) radiation in the mouse is inhibited in interferon-gamma null mice

BACKGROUND: A protective role for the ultraviolet (UV) A waveband against immunosuppression induced by UVB (280-320 nm) radiation has been identified. The mechanism for UVA immunoprotection was found to involve two apparently unrelated mediators, the T-helper-1-associated proinflammatory cytokine interferon (IFN)-gamma and the UVA-induced redox-regulated stress protein, haem oxygenase (HO). OBJECTIVES: To identify a relationship between these two immune regulators. METHODS: The HO response to UVA radiation in the skin and liver was examined in mice with a targeted disruption of the IFN-gamma gene, known to be unresponsive to UVA photoimmunoprotection. Results IFN-gamma null mice did not respond to UVA irradiation with the normal upregulation of HO activity in either the irradiated skin or the liver. Injection of these mice with recombinant IFN-gamma previously shown to restore the UVA-photoimmunoprotective effect, here partially and dose-responsively restored their ability for induction of HO activity in both skin and liver following UVA irradiation. CONCLUSIONS: IFN-gamma appears to be a prerequisite for the immunoprotective induction of HO, although other mediators may also be involved. The UVA responsiveness of HO in an internal organ such as the liver suggests the existence of a soluble UVA-induced mediator from the skin, which may be IFN-gamma.     

Hepatocyte growth factor establishes autocrine and paracrine feedback loops for the protection of skin cells after UV irradiation

Hepatocyte growth factor (HGF) is a multifunctional cytokine, which, among various other activities, acts as a growth factor for melanocytes and has recently been implicated in the pathogenesis of malignant melanoma. In the skin, the main source for HGF is dermal fibroblasts (FB). Here, we have investigated the regulation of HGF production and secretion by cytokines derived from UV-irradiated keratinocytes (KC) and by direct UV irradiation. We demonstrate that supernatants of ultraviolet (UV)B-irradiated KC strongly induce HGF production in FB, and that this effect was mediated primarily by IL-1alpha. Direct irradiation of FB with UVB had no effect on HGF expression. In contrast, irradiation with UVA1 strongly upregulated HGF mRNA production and secretion of the functional protein. Addition of neutralizing anti-HGF antibodies after UVA1 irradiation, as well as transfection of FB with HGF small-interfering RNA (siRNA); which completely abrogated HGF secretion led to a dramatic rise of FB apoptosis demonstrating that autocrine HGF efficiently protected FB from UVA1-induced apoptosis. Our data suggest that upregulation of HGF plays a role in skin homeostasis after UV irradiation. However, a negative side effect of UV-induced HGF secretion by dermal FB might represent a decisive factor for induction and/or progression of melanoma.     

不同波长紫外线照射后皮肤颜色的变化

目的 观察不同波长紫外线照射皮肤后，颜色变化的过程。方法 用双倍剂量最小持续性黑化量和最小红斑量对10例Ⅲ型受试者皮肤进行照射，通过临床评分、扫描反射比分光光度仪和窄谱反射分光光度计三种方法对照射后的皮肤进行14天的评价和测定。结果 UVB照射后，a*值和红斑指数（EI值）在照射后6 h急剧增加，照射后2天达到高峰；L*值在照射后1天出现急剧降低；ITA°在第7天显著降低；黑素指数（MI值）在照射后2天内有逆向的降低趋势，直到照射后7天才有显著增高。在UVA照射下，a*值和EI值改变不明显；L*值在照射后6 h出现显著降低；ITA°在第14天达到最低值； MI值仅照射后1天有显著增高。结论 UVA和UVB照射后的皮肤颜色改变在时间动力学和反应程度方面有明显区别。a*值和EI值是评价照射后日晒伤较为敏感而准确的参数，而ITA°和MI值是评价晒斑较好的参数。     

Provocation testing in polymorphic light eruption using fluorescent ultraviolet (UV) A and UVB lamps

BACKGROUND: Provocation testing is frequently performed during investigation of patients with suspected polymorphic light eruption (PLE). Techniques are not standardized between centres. OBJECTIVES: We sought to evaluate the efficacy of different fluorescent ultraviolet (UV) radiation lamps for provocation testing in PLE. METHODS: We analysed results in 68 patients referred consecutively for phototesting in whom a diagnosis of PLE seemed likely based on clinical history. Patients' case notes were reviewed and responses recorded to provocation testing on forearm skin over three consecutive days using broadband UVA, narrowband and broadband UVB lamps. RESULTS: A positive papular response to broadband UVA exposure was seen in 38 patients [56%, estimated 95% population confidence interval (CI) 43-67.9]. Thirty-four patients (50%) had a positive papular response to narrowband UVB exposure (95% CI 37.6-62.4). The probability of a positive provocation test following irradiation with both lamps was 80.9% (95% CI 69.5-89.4). From April 1999, 34 patients also had provocation testing with broadband UVB. Although six patients (18%) had a positive papular response, they all showed a positive response to one or both of the other lamp types. CONCLUSIONS: Provocation testing with fluorescent UVA and UVB lamps is a cheap and readily available method that can be used as a diagnostic aid to investigate patients with suspected PLE. Using both broadband UVA and narrowband UVB lamps for testing increases the likelihood of confirming the diagnosis than if either lamp is used alone.     

Induction of matrix metalloproteinase-9 secretion from human keratinocytes in culture by ultraviolet B irradiation

BACKGROUND: Matrix metalloproteinases (MMPs) are known as important enzymes involved in tissue metabolism. Among them, MMP-2 and MMP-9 are termed gelatinases, but their specific roles in vivo are still unknown, including their expression patterns following ultraviolet (UV) irradiation. OBJECTIVE: To elucidate the effects of UV irradiation on the skin, we analyzed the expression of MMP-2 and MMP-9 by primary human keratinocytes in culture. METHODS: We evaluated the enzymatic functions of MMP-2 and MMP-9 by gelatin-zymography, and of MMP-9 expression by immunofluorescence, using cultured keratinocytes after UV irradiation. RESULTS: The secretion of MMP-2 (72 kDa) remained at low levels under all conditions examined. Although MMP-9 (92 kDa) secretion was not induced by UVA, it was stimulated by UVB irradiation in a dose-dependent manner. In addition, an enzyme-linked immunosorbent assay showed the tendency to increase for the involucrin expression following UVB exposure. Cell viability was decreased by UVB irradiation in contrast to the induction of MMP-9 and involucrin. CONCLUSION: These results suggest that the induction of MMP-9 secretion is related to the inflammation including apoptosis of keratinocytes resulting from UVB irradiation.     

Photocarcinogenesis in hairless mice induced by ultraviolet A tanning devices with or without subsequent solar-simulated ultraviolet irradiation.

The carcinogenic effect of 3 commercially available ultraviolet A (UVA) tanning sources was studied in lightly pigmented hairless mice. The tanning sources (Bellarium-S SA-1-12 and Philips TL 09R and TL 10R) have different emission spectra and emit different quantities of UVB. The tanning sources were administered either alone, or before irradiation with solar-simulated UV (solar UV). All 3 UVA tanning sources were able to induce skin tumors when administered in daily doses resembling those used in tanning salons (20 min/d, 5 d/week). Irradiation with Bellarium-S during 32 weeks induced skin tumors in all mice; a similar response was seen after 66 weeks of irradiation with Philips TL 09R. Irradiation with Philips TL 10R during 98 weeks induced tumors in 6 of 20 mice. Nine groups of 20 mice were pretreated 20 min/d, 5 d/week during 13 weeks with one of the UVA tanning sources. Three groups were irradiated with Bellarium-S, 3 groups with Philips TL 09R and 3 groups with Philips TL 10R in daily doses ranging from 0.2 to 1.8 minimum erythema doses (MED). The highest daily doses were equivalent to the doses received during one session in a commercial solarium. Subsequently all 9 groups were irradiated with 3.1 MED/d solar UV 10 min/d, 4 d/week until all mice had died. Time to first tumor was compared. All groups pretreated with Bellarium-S and Philips TL 09R showed an enhanced tumor development compared with a group irradiated with solar UV only. Pretreatment with Philips TL 10R did not enhance the carcinogenic effect of solar UV.     

GM-CSF production by epithelial cell line: Upregulation by ultraviolet A

It was demonstrated that UVB increases synthesis and expression of IL-1α and GM-CSF by keratinocytes. Upregulation of GM-CSF by UVB is reported to be mediated by IL-1α. However, regulation of IL-1α and GM-CSF by UVA is not well-known. The purpose of the present study was to evaluate the effects of UVA on IL-1α and GM-CSF production. Here we used a competitive RT-PCR for measuring cytokine gene expression in an epidermal cell line after UVA irradiation. IL-1α and GM-CSF mRNA did not show any change at 1 h and 6 h following exposure to UVA. After UVA irradiation, however, IL-1α mRNA decreased and GM-CSF mRNA increased at 24 h and the level of GM-CSF in culture supernatant increased at 24 h and 48 h. Addition of antihuman IL-1α neutralizing antibody to UVA irradiated cells did not prevent the increase of GM-CSF mRNA expression. These results suggest that UVA radiation may induce GM-CSF production through an IL-1α independent pathway.     

Tanning facility use: are we exceeding Food and Drug Administration limits?

BACKGROUND: The US Food and Drug Administration (FDA) recommends exposure limits for tanning bed use. Tanning patrons may not be following these recommendations and may be overexposed to damaging ultraviolet radiation (UV). OBJECTIVE: This study was conducted to assess tanning patrons' adherence to FDA-recommended exposure limits and to measure the amount of UVA and UVB radiation emitted by tanning beds. METHODS: A community-based survey was administered during routine state inspections of North Carolina tanning facilities (n = 50). At each facility, patron records were randomly selected (n = 483) for a survey of exposure records, and UVA and UVB outputs were measured for each tanning bed. RESULTS: The recommended limits were exceeded by 95% of patrons, and 33% of patrons began tanning at the maximum doses recommended for maintenance tanning. Average tanning bed output was 192.1 W/m(2) UVA and 0.35 W/m(2) erythemally weighted UVB. CONCLUSIONS: Interventions for tanning bed operators and patrons are needed to increase compliance with federally recommended exposure limits.     

Alterations in human epidermal Langerhans cells by ultraviolet radiation: quantitative and morphological study

BACKGROUND: Ultraviolet (UV) exposure of human skin induces local and systemic immune suppression. This phenomenon has been well documented when UVB radiation (290-320 nm) is used. The mechanism is thought to involve Langerhans cells (LCs), the epidermal dendritic cells that play a crucial role in antigen presentation. A variety of studies have clearly demonstrated that UVB radiation decreases LC density and alters their morphology and immunological function, but little is known about the effects of the entire UV spectrum (ultraviolet solar simulated radiation, UV-SSR or UVB + UVA) or UVA (320-400 nm) radiation alone. OBJECTIVES: The purpose of this study was to analyse and compare the effects of a single exposure of human volunteers to UV-SSR, total UVA or UVA1 (340-400 nm) in the human epidermal LC density and morphology. METHODS: Immunohistochemistry on epidermal sheets with various antibodies and transmission electron microscopy (TEM) were used. RESULTS: Immunostaining for class II antigen revealed that a single UV-SSR exposure, corresponding to twice the minimal erythemal dose (MED), induced a significant reduction in LC density with only slight morphological alterations of remaining cells. After a single UVA exposure, LC density showed a dose-dependent reduction with a significant effect at 60 J cm(-2) (well above the MED). Moreover, the reduction of LC dendricity was also dose-dependent and significant for doses exceeding 30 J cm(-2). UVA1 radiation was as effective as total UVA for the later endpoint. As demonstrated by TEM, the location of Birbeck granules containing epidermal cells was modified in UVA-exposed areas. They were located in the spinous rather than in the suprabasal layer. In addition, the morphology of these cells was altered. We observed a rounding up of the cell body with a reduction of dendricity. Alterations of mitochondrial membrane and ridges were also seen. CONCLUSIONS: A single exposure of human skin in vivo to UV-SSR, UVA or UVA1 radiation results in different alterations of density and/or morphology of LCs. All these alterations may impair the antigen-presenting function of LCs leading to an alteration of immune response.     

Effect of ultraviolet radiation on the expression of pp38MAPK and furin in human keratinocyte-derived cell lines

Background: Ultraviolet radiation (UVR) is known to induce the activation of stress‐inflammation signal transduction pathways, and to induce the activity of many proteases in skin cells. It is unknown whether the activation of proteases such as furin is related to changes in the phosphorylation status of p38MAPK. Methods: The effect of UVR on immortalized keratinocyte (HaCaT) and squamous cell carcinoma (Colo16) cells was investigated with respect to cell survival, phosphorylation of p38MAPK, and the proprotein convertase, furin. The cells were exposed to either a low or a high dose of UVA and/or UVB and the viability was monitored over 48 h, along with changes in the intracellular expression of p38MAPK and furin. Results: Low‐dose UVA (2 kJ/m²) and/or UVB (0.2 kJ/m²) radiation had no effect on cell viability, except in UVA‐irradiated Colo16 cells. High UVA (20 kJ/m²) caused a loss of cell viability in HaCaT cells, but not in Colo16 cells. The opposite effect was seen in cells exposed to a high UVB dose (2 kJ/m²). The viability of both cell cultures decreased when exposed to high‐dose UVA+B radiation. UV irradiation downregulated the expression of phosphorylated p38 (pp38) in HaCaT cells irrespective of the UV dose and type. In Colo16 cells, UV radiation induced pp38 expression in the cells following exposure, with the highest increase in cells exposed to high‐dose UVA. The expression of furin in UV‐irradiated HaCaT cells was similar to that seen for pp38 expression. In Colo16 cells, UV radiation induced furin expression, with the highest increase seen in cells 24 h after exposure to both high‐dose UVB and UVA+B radiation. Conclusion: The results show that there are differences between the effect of UV types and doses on cell function in the keratinocyte‐derived cell lines examined in this study. The level of furin expression in Colo16 cells correlated to changes in pp38 levels in the cells following exposure to UV radiation, but not in HaCaT cells. From an improved understanding of the signalling pathways and their downstream events and how these may differ as a result of tumorigenesis, it may enable the development of inhibitors, which may have therapeutic applications.     

Ultraviolet protective performance of photoprotective lipsticks: change of spectral transmittance because of ultraviolet exposure

BACKGROUND: Photoinstability of sunscreens because of ultraviolet (UV) exposure is a well-known and common phenomenon. Recently, it was also shown that sunscreens with complex filter combinations are photoinactivated by UV exposures, which can easily be acquired by solar exposure over several hours. OBJECTIVES: To assess the change of the spectral transmission after UV exposure (UV-challenged protective performance) of 27 commercially available photoprotective lipsticks. METHODS: Quartz slides were covered with a lipstick layer (area density 1.0+/-0.1 mg/cm2) and irradiated with increasing doses of solar-simulated radiation. The spectral transmission (T) was measured spectrophotometrically before and after 5, 12.5, 25, and 50 standard erythema doses (SED) of exposure. We calculated the change in transmission (photoinstability) as the difference between the spectral transmission before and after a defined UV exposure, DeltaT, and the arithmetic mean, for both the UVA (DeltaTA) and UVB (DeltaTB) ranges. A product was labelled as photounstable if the mean photoinstability in the UVA, DeltaTA, or UVB range, DeltaTB, was higher than 5% for an UV exposure of 12.5 SED. RESULTS: Eleven products showed a significant photoinstability in the UVA range (DeltaTA between 6% and 27%), only one product in the UVB range (DeltaTB = 13%), and one product in both the UVA (DeltaTA = 31%) and UVB (DeltaTB = 9%) range. In one product photoinstability became significant in the UVA range at higher UV exposures. CONCLUSIONS: Out of 27 lipsticks only 13 products showed a photostable performance (DeltaTA < 5% and DeltaTB < 5% for 12.5 SED). We propose therefore that only products, which fulfil these UV photostability criteria should be marketed.     

The role of glass as a barrier against the transmission of ultraviolet radiation: an experimental study

Background/Purpose: Excessive exposure of the skin to sunlight may cause many symptoms and skin cancer. The aim was to measure the transmission of ultraviolet (UV) A and UVB radiation through glasses of different types, according to the distance from the light source.
Methods: The baseline radiation from UVA and UVB sources was measured at different distances from the photometers. Next, the radiation from the same sources was measured at the same distances, but transmitted by different types of glass. The baseline values were compared with the results after protection using glass.
Results: Laminated glass totally blocked UVA radiation, while smooth ordinary glass transmitted the highest dose (74.3%). Greater thicknesses of glass implied less radiation transmitted, but without a significant difference. Green glass totally blocked UVA radiation, while blue glass transmitted the highest dose of radiation (56.8%). The presence of a sunlight control film totally blocked UVA radiation. All glasses totally blocked UVB radiation.
Conclusion: The main characteristics of glass that make it a photoprotective agent are its type (especially laminated glass) and color (especially green), which give rise to good performance by this material as a barrier against the transmission of radiation.     

Influence of ultraviolet A on scheduled and unscheduled DNA synthesis by ultraviolet B.

After irradiating mouse epidermis in vivo with ultraviolet radiation (UV), autoradiography using 3H-thymidine was performed to study the effects of UV on scheduled and unscheduled DNA synthesis during a 7 day-period. Suppression of scheduled DNA synthesis by 100 mJ/cm2 of UVB was continued for about 24 h and induction of unscheduled DNA synthesis by 100 mJ/cm2 of UVB for about 6 h after irradiation. It was also confirmed that UVA induced DNA damage if a dose of UVA over 30 J/cm2 was used. When UVA was applied 1 h before UVB irradiation, a significant increase in sparsely labeled cells (SLC) was observed and the numbers of SLC increased in proportion to the total dosage of UV. So it was confirmed that UVA preirradiation enhanced DNA damage by UVB.     

Ultraviolet exposure from indoor tanning devices: a systematic review

Use of indoor tanning devices increases the risk of cutaneous melanoma and nonmelanoma skin cancer. Indoor tanning devices have become important sources of ultraviolet (UV) exposure, both UVB and UVA. This systematic review assessed UV measurements performed in indoor tanning devices related to irradiance level, wavelength distribution and similarities to natural sun. The study was performed in accordance with the MOOSE and PRISMA guidelines. We searched PubMed, Embase and Web of Science from inception to May 2015, and also examined the reference lists of the retrieved studies. Eighteen studies were included. Twelve studies examined the erythema‐weighted UV irradiances of indoor tanning devices, 11 studies examined UVB and 13 studies studied UVA. Compliance with irradiance limits was reported in nine studies. Erythema‐weighted irradiances were highest in the most recent studies. Most studies had mean values higher than from natural sun and with large variations between devices. All studies except two had mean unweighted UVB irradiances lower than from natural summer sun (at latitudes from 37°S to 35°N), while mean unweighted UVA irradiances were, with one exception, substantially higher than from natural sun. The high values of UVA exposure from modern tanning devices are alarming in light of the increased focus on UVA irradiance as a carcinogen, and as UVA exposure confers little protection against subsequent UV exposure.     

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.