Minimal Erythema Doses Of UVB Research Articles

Application of 233\xa0nm far-UVC LEDs for eradication of MRSA and MSSA and risk assessment on skin models

A newly developed UVC LED source with an emission wavelength of 233 nm was proved on bactericidal efficacy and skin tolerability. The bactericidal efficacy was qualitatively analysed using blood agar test. Subsequently, quantitative analyses were performed on germ carrier tests using the MRSA strain DSM11822, the MSSA strain DSM799, S. epidermidis DSM1798 with various soil loads. Additionally, the compatibility of the germicidal radiation doses on excised human skin and reconstructed human epidermis was proved. Cell viability, DNA damage and production of radicals were assessed in comparison to typical UVC radiation from discharge lamps (222 nm, 254 nm) and UVB (280–380 nm) radiation for clinical assessment. At a dose of 40 mJ/cm2, the 233 nm light source reduced the viable microorganisms by a log10 reduction (LR) of 5 log10 levels if no soil load was present. Mucin and protein containing soil loads diminished the effect to an LR of 1.5–3.3. A salt solution representing artificial sweat (pH 8.4) had only minor effects on the reduction. The viability of the skin models was not reduced and the DNA damage was far below the damage evoked by 0.1 UVB minimal erythema dose, which can be regarded as safe. Furthermore, the induced damage vanished after 24 h. Irradiation on four consecutive days also did not evoke DNA damage. The radical formation was far lower than 20 min outdoor visible light would cause, which is classified as low radical load and can be compensated by the antioxidant defence system.

Diurnal Preference Contributes to Maximal UVB Sensitivity by the Hour of the Day in Human Skin In Vivo

Diurnal Preference Contributes to Maximal UVB Sensitivity by the Hour of the Day in Human Skin In Vivo

Evaluation of the minimal erythema dose for UVB and UVA in context of skin phototype and nature of photodermatosis.

Phototesting is part of the standard procedure for the evaluation of patients with photosensitivity disorders. The response of patients to targeted UVB or UVA radiation helps to find out more about the nature of photodermatosis. Nevertheless, there are no default values of the minimal erythema dose (MED). This study evaluated data of 203 patients (131 female, 72 male, mean age 52years) who were referred for phototesting to the University Hospital Zurich between 2012 and 2017. We retrospectively analyzed the demographic data, medical history, skin phototype, reaction to UVB and UVA radiation, and, if present, the diagnosis of photodermatosis. In patients who did not develop erythema at the highest tested UV doses, the next logical increment was taken for analysis. In case of UVA, the two periphery doses could not be evaluated due to technical issues, so the closest reliable UVA doses were used. The MED-UVB correlated with the skin type and increased with a higher phototype. No such correlation could be seen for MED-UVA. However, the MED-UVA was significantly reduced in patients with photodermatosis without significant differences between the subgroups of photodermatosis. More than half of the patients did not show a reduced MED despite a diagnosed photodermatosis. We showed, how different skin types with and without photodermatosis react to UV radiation. Based on the results, we suggested threshold doses that can be chosen for phototesting, presented which doses can be considered pathologic and showed the probability of a pathologic MED in correlation with a diagnosed photodermatosis.

Photobiological responses in patients with chronic actinic dermatitis and their relationship with the melanocortin-1 receptor gene Arg163Gln variant: a preliminary study

Objective To explore differences in phototest and photopatch test results, and in skin color-related parameters between healthy subjects and patients with chronic actinic dermatitis (CAD), and to examine their relationship with the melanocortin-1 receptor gene (MC1R) Arg163Gln variant. Methods Phototests were performed by using a sun simulator SUN1000, and skin color was analyzed by using Hexameter MX18 in 25 patients with CAD and 25 healthy subjects. The MC1R genotype at position -163 was determined by PCR. Photopatch tests were performed on 25 patients with CAD and 5 healthy subjects using a standard series of photoallergens (RuiMin) and an ultraviolet (UV) phototherapy equipment, SS-03A. Results Regarding phototest results, both UVA-minimal persistent pigment darkening dose (MPPD) and UVB-minimal erythema dose (MED) were significantly lower in CAD patients compared with healthy controls (both P 0.05), but that of the CAA genotype differed significantly between the two groups (P < 0.01). UVA-MPPD and UVB-MED were both significantly lower in CAD patients with the CAA genotype at position-163 in the MC1R gene than in those without the genotype (P = 0.055, 0.325, respectively). Conclusions Skin photobiological testing plays a critical role in the diagnosis of CAD. Further studies are needed to clarify the role of the CAA genotype at position-163 in the MC1R gene in the diagnosis, prevention and treatment of CAD. Key words: Photosensitivity disorders; Pigmentation; Genes, Arg163Gln; Chronic actinic dermatitis; Photopatch tests

Molecular effects of UVA1 in human skin in vivo

The carcinogenic potential of UVA1 (340–400nm) is increasingly being recognised as evidence accumulates of its ability to induce cyclobutane pyrimidine dimers (CPD) ex vivo and in vivo in human beings which if unrepaired may lead to skin cancer. Despite widespread use in phototherapy, tanning lamps and its abundance in terrestrial UVR (ultraviolet radiation), we lack data on its effects on gene expression in human skin. 12 volunteers with skin type I/II were tested for UVR sensitivity: five were given 1 minimal erythema dose (MED) of UVA1 and biopsy samples taken at 6 h and 24 h; an unirradiated control sample was also taken. A further four participants were given 1 MED of UVB and UVA1 and biopsy samples taken at 6 h and 24 h, RNA extracted, converted to cRNA, and hybridised to agilent 44K oligomicroarray plates. After rosetta resolver software analysis, the data were analysed using GeneGo metacore v7 and DAVID.UVA1 upregulated 301 genes at 6 h and 264 genes at 24 h (p<0·05, ≥2 fold change). At 6 h, key gene expression pathways upregulated were inflammation (p=3·46×10−17), apoptosis (p=2·148×10−8), and response to oxidative stress (p=6·457×10−7). CD83 was also dramatically upregulated (positively regulates interleukin 10). At 24 h the top pathway enriched was extracellular matrix remodelling (p=5·549×10−7). A pathway analysis demonstrated that UVB induced the same pathways at 6 h and 24 h as did UVA1; however, functional studies shows that UVB induces a greater upregulation of apoptotic proteins and in terms of genes, similar levels of immunomodulatory genes (CD83, IL10) upregulated.Erythemally equivalent doses of UVA1 induce less apoptosis than UVB but there are similar levels of immunosuppression. Our data suggest that UVA1 might be inducing less of a photoprotective response in vivo in human beings than UVB, which might explain the mechanism of some of our other new findings—that UVA1 CPDs are slower to be repaired at the basal epidermis than UVB CPDs. These findings are important for our understanding of skin cancer. FundingUK Medical Research Council, La Roche- Posay, and Biomedical Research Council.

Systemic photosensitivity due to Goji berries

Systemic photosensitivity due to the intake of plants or herbal compounds is a rare phenomenon. Goji berries are widely used as a well-being and anti-aging remedy. In spite of this, only a few adverse reactions and no cases of photosensitivity have been reported to date. A 53-year-old male consulted due to a pruriginous eruption located on sun-exposed areas of 2 weeks of duration. He had been taking Goji berries and infusions of cat's claw herb for 5 and 3 months, respectively. Minimal erythema dose for UVB (MED-UVB) was diminished when the patient was taking these products, and became normal when they were withdrawn. Photoprovocation tests with Goji berries and cat's claw were performed. MED-UVB decreased after the intake of Goji berries, and was normal with cat's claw. We report the first case of systemic photosensitivity due to Goji berries.

Treatment of progressive macular hypomelanosis with narrow-band ultraviolet B phototherapy

Treatment for progressive macular hypomelanosis (PMH) has been disappointing. Recently, Propionibacterium acnes had been postulated as the causative agent and narrow-band ultraviolet B (NBUVB) had been shown to stimulate melanogenesis and has antibacterial properties. The aim of this study was to evaluate the effectiveness of NBUVB in the treatment of PMH. A retrospective analysis of PMH cases diagnosed and treated with NBUVB treatment from 1 January 2007 to 30 April 2009 at the National Skin Centre (NSC) was conducted. The diagnosis of PMH was clinical. Treatment with NBUVB (311 nm) was given twice to thrice weekly. The initial treatment dose was determined as 70% of the patients' individual 311 nm UVB minimal erythema dose. The dose was increased by 10-20% if previous treatment had caused no or slight erythema. Percentage repigmentation from baseline was assessed at each follow-up. A total of six patients diagnosed with PMH were treated with NBUVB in NSC in the past 2 years. Three patients had good improvement and the remainder had moderate improvement. Recurrence did occur. No adverse events were documented. The success of NBUVB as a monotherapy provides a viable and relatively safe, albeit temporary relief, for these individuals.

Prevention of Polymorphic Light Eruption with a Sunscreen of Very High Protection Level Against UVB and UVA Radiation Under Standardized Photodiagnostic Conditions

Polymorphic light eruption (PLE), with an overall prevalence of 10-20%, is mainly provoked by ultraviolet A (UVA) (320-400 nm) and to a lesser degree by UVB (280-320 nm). The most effective prophylaxis of PLE, application of UV protection clothing, is not feasible for all sun-exposed areas of the skin and UV-hardening is time-consuming and may be associated with side-effects. Most sunscreens protect predominantly against UVB and therefore fail to prevent PLE. The protection level of potent UVA-protective filters remains unresolved. This single-centre, open, placebo-controlled, intra-individual, comparative study, analysed the efficacy of a sunscreen of very high protection level against UVB and UVA, containing methylene bis-benzotriazolyl tetramethylbutylphenol (Tinosorb M), bis-ethylhexyloxyphenol methoxyphenyl triazine (Tinosorb S) and butyl methoxydibenzoylmethane as UVA absorbing filters, in the prevention of PLE under standardized photodiagnostic conditions. After determination of the minimal erythema dose at day 0, photoprovocation was performed in 12 patients with a clinical history of PLE, on days 1, 2 and 3 with 100 J/cm2 UVA and variable doses of UVB, starting with the 1.5-fold minimal erythema dose of UVB. Prior to irradiation, placebo was applied to the right and sunscreen to the left dorsal forearm under COLIPA (European Cosmetic, Toiletry and Perfumery Association) conditions. In 10 patients PLE could be provoked at the placebo site, with positive reactions in 90% of the UVA, 40% of the UVB and 90% of the UVA/UVB irradiated fields. At the site with the active treatment none of these patients developed PLE. These data demonstrate that a sunscreen with effective filters against UVA and UVB can successfully prevent the development of PLE. Further studies are needed to examine whether regular application of sunscreen under everyday conditions, especially in doses less than the tested COLIPA-norm, could be an equivalent alternative to UV-hardening therapy.

Investigation of the Anti-Inflammatory Potential of Aloe vera Gel (97.5%) in the Ultraviolet Erythema Test

Background:Aloe vera is a natural product that is frequently used in soothing skin care products such as aftersun lotions. In the present study we aimed to explore the anti-inflammatory potential of a highly concentrated A. vera gel in the UV erythema test in vivo. Methods: 40 volunteers with skin types II and III were included in the randomized, double-blind, placebo-controlled, phase III monocenter study. Test areas on the back were irradiated with the 1.5-fold minimal erythema dose of UVB. Subsequently, the test areas were treated occlusively on 2 subsequent days with A. vera gel (97.5%), the positive controls (0.25% prednicarbate, 1% hydrocortisone in placebo gel and 1% hydrocortisone cream) and a placebo gel. Erythema values were determined photometrically after 24 and 48 h. Results:A. vera gel (97.5%) significantly reduced UV-induced erythema after 48 h, being superior to 1% hydrocortisone in placebo gel. In contrast, 1% hydrocortisone in cream was more efficient than A. vera gel. Conclusions: In this study after 48 h the A. vera gel (97.5%) displayed some anti-inflammatory effects superior to those of 1% hydrocortisone in placebo gel. The A. vera gel tested here might be useful in the topical treatment of inflammatory skin conditions such as UV-induced erythema.

An Intraindividual Study of the Characteristics of Erythema Induced by Bath and Oral Methoxsalen Photochemotherapy and Narrowband Ultraviolet B¶

We compared the characteristics of psoralen and ultraviolet A (PUVA) erythema in skin photosensitized by bath or oral methoxsalen in 20 subjects. Erythema was assessed visually and with a reflectance instrument at 24 h intervals for 7 days. In addition, narrowband ultraviolet B (TL-01 UVB) erythema was examined in 19 of these subjects at 4, 8, 12, 24, 48 and 72 h and in another nine subjects at 12, 15, 18, 21 and 24 h. Both bath and oral PUVA exhibited broad erythemal peaks beyond 72 h. For topical PUVA the lowest minimal phototoxic dose (MPD) occurred at 120 and 144 h (P = 0.01 and 0.03 compared with 72 h). Oral PUVA erythema peaked earlier at 96 h: the MPD was significantly lower at 96, 120 and 144 h compared with 72 h (P = 0.001, 0.01 and 0.02, respectively). At 120 h, bath PUVA had a significantly steeper slope compared with oral PUVA. The TL-01 UVB minimal erythema dose was significantly lower at 12 h compared with 24 h (P = 0.019). The majority of subjects were at maximal erythema at 12 h (22 of 28) and 15 h (eight of nine). Our results suggest that peak erythema for bath PUVA, oral PUVA and TL-01 UVB occurs at 120, 96 and 12-15 h, respectively.

Chloroquine treatment reduces the number of cutaneous HLA-DR+ and CD1a+ cells in patients with systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can be exacerbated by exposure to ultraviolet radiation (UVR). The number and phenotype of antigen presenting cells in the skin play a role in cutaneous immune response generation. Although antimalarials are widely used in SLE treatment, their mode of action is not completely elucidated. The aim of our study was to determine the effect of chloroquine treatment on HLA-DR+ and CD1a+ cell number in locally irradiated (three minimal erythema doses of UVB) and normal appearing skin in SLE patients and healthy subjects. A significantly higher number of HLA-DR+ and CD1a+ cells were found in both locations in SLE patients compared with controls. Following three months of daily chloroquine treatment (250 mg), the HLA-DR+ and CD1a+ cell counts were significantly reduced in both irradiated and unirradiated sites of SLE patients, although still higher than in controls. Chloroquine treatment reduces the number of antigen presenting cells in the skin of SLE patients, and this effect may explain the antimalarials beneficial immunoregulatory and anti-inflammatory properties.

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.

In Vivo UVA-1 and UVB Irradiation Differentially Perturbs the Antigen-Presenting Function of Human Epidermal Langerhans Cells

Ultraviolet B (UVB, 290-320 nm) radiation is known to suppress the immune function of epidermal Langerhans cells. We have recently described that in vitro UVB irradiation perturbs the antigen-presenting cell function of Langerhans cells by inhibiting their expression of functional B7 costimulatory molecules (B7-1, B7-2). The aim of this study was to determine wavelength-specific UV effects on Langerhans cells function in vivo, specifically UVB and UVA-1. To address this issue, volunteers were irradiated on the sun protected volar aspects of their forearms with 3 x minimal erythema dose of UVB (Philips TL-12) and UVA-1 (UVASUN 5000 Mutzhaas). Langerhans cells were isolated from suction blister roofs immediately following irradiation. Langerhans cells isolated from UVB- but not from UVA-1-irradiated skin failed to activate naïve resting allogeneic T cells (mixed epidermal cell leukocyte reaction) or primed tetanus toxoid reactive autologous T cells. Langerhans cells isolated from sham-irradiated or UVA-1-irradiated skin strongly upregulated B7-2 molecules during short-term tissue culture. By contrast, Langerhans cells from UVB-irradiated skin did not upregulate B7-2 molecules. Furthermore, exogenous stimulation of the B7 pathway by anti-CD28 stimulatory monoclonal antibodies restored the capacity of UVB-irradiated Langerhans cells to activate both alloreactive and tetanus toxoid-reactive T cells, implying suppressed antigen-presenting cell activities and perturbed B7 expression of Langerhans cells isolated from UVB-irradiated skin are related. Those studies demonstrate that in vivo UVB, but not UVA-1, interferes with the activation-dependent upregulation of B7 molecules on Langerhans cells, which in turn is of functional relevance for the perturbed antigen-presenting cell function of Langerhans cells within UVB- but not UVA-1-irradiated skin.

Total body heliotherapy.

Sunlight has long been known to be beneficial for a variety of skin diseases. Patients with psoriasis and eczema frequently employ ambient heliotherapy to control their conditions. However, social norms do not permit a person to expose the entire body in public, thus placing severe restrictions on the utility of this modality for the treatment of generalized psoriasis, for example. Tan-Thru bathing suits, designed to attract those who wish to tan without an accentuated "tan line", are reported to absorb ultraviolet (UV) rays up to a maximum equivalent of a sun protection factor (SPF) 10 sunblock, thus offering approximately 89% protection while in use, according to their manufacturer. If so, this bathing suit may allow patients with UV-responsive skin dermatoses to achieve full body exposure in a socially acceptable manner. The objective of this study was to verify the SPF and to determine the actual transmittance to skin covered by a Tan-Thru bathing suit. Ten healthy adult subjects were recruited for this investigation. UVB minimal erythema dose (MED) was determined on unaffected gluteal or lower back skin, once with and once without the swimsuit on. Our results showed that the mean SPF afforded by the bathing suit was in fact 4.9 (range 4.5-5.6). In conclusion, theoretically, the Tan-Thru bathing suits could allow enough UVB penetration under ambient conditions to be beneficial for patients with UVB responsive conditions.

Prediction of minimal erythema dose with a reflectance melanin meter

The relationship between skin pigmentation and sensitivity to ultraviolet (UV) radiation-induced erythema was investigated in 60 healthy subjects of sun-reactive skin types I-V. Using a portable reflectance spectrometer, skin pigmentation was measured as the 'melanin index' (MI) in all subjects. A solar-simulated array of filtered UVA and UVB-emitting fluorescent lamps was then used to determine the UVB minimal erythema dose (MED) of each subject. MI readings and MED testing were both performed on the subjects' mid to upper backs. Using this technique, we found a close correlation between MI and MED. Comparison of the mean MI or MED of subjects with different skin types revealed progressive differences in MI and MED between all five skin types. Erythema dose-response curves, which provide further information about UV sensitivity, were also calculated for 43 subjects. A significant negative correlation was found between the gradients of these curves and both MI and MED, indicating that paler subjects respond more strongly to increments of UV above the MED than subjects with greater pigmentation. Our results indicate that although traditional, subjective means of predicting UV sensitivity to erythema are not without some value, MED correlates particularly strongly with objective measures of skin pigmentation. We therefore conclude that the reflectance spectrometer can rapidly and accurately predict UVB sensitivity, and should prove clinically useful for planning and optimizing UVB phototherapy.

Prevention of UVB-induced immunosuppression in humans by a high sun protection factor sunscreen

<h3>Background and Design:</h3> To date, studies of the effectiveness of sunscreens in preventing UVB-induced suppression of contact hypersensitivity in humans have not been published. Several studies in mice of the protection afforded by sunscreens from UVB-induced suppression of contact hypersensitivity and rejection of transplanted skin cancers have yielded dissimilar results, ranging from ''no'' to ''complete'' protection. We sought to determine whether the effect of preapplication of a sun protection factor (SPF) 29 sunscreen (containing octyl methoxycinnamate, oxybenzone, and octyl salicylate) could prevent local UVB-induced suppression of contact hypersensitivity to dinitrochlorobenzene (DNCB). Nineteen subjects received either three minimal erythema doses of UVB daily on three consecutive days (UVB group) or sunscreen followed by this same dose of UVB irradiation (sunscreen plus UVB group) to a 16-cm²area of the buttock. One day after completion of irradiation, DNCB was applied to this buttock site, and 2 weeks later, forearm challenge with four different concentrations of DNCB was performed. A control group of 10 subjects underwent DNCB testing as above, but with no prior exposure to UVB (no-UVB group). <h3>Results:</h3> The UVB group had a reduced response rate to all challenge doses of DNCB (3.125, 6.25, and 8.8 μg), except for the highest dose (12.5 μg) compared with the no-UVB control group (Fisher's Exact test, P≤.008), and compared with the sunscreen plus UVB group (P≤.02). The no-UVB and sunscreen plus UVB groups showed no significant differences in response rates to any of the doses of DNCB tested (P≥.53). <h3>Conclusions:</h3> These results indicate that application of a sunscreen with over ninefold greater protection than that needed to prevent erythema prior to localized UVB radiation prevents localized UVB-induced suppression of contact hypersensitivity. Further studies are needed to determine whether sunscreens providing less protection, yet still preventing erythema, adequately prevent suppression of contact hypersensitivity, a possible surrogate marker for skin cancer tumor antigen recognition and rejection. (Arch Dermatol. 1995;131:1128-1133)

Prevention of UVB-Induced Immunosuppression in Humans by a High Sun Protection Factor Sunscreen

To date, studies of the effectiveness of sunscreens in preventing UVB-induced suppression of contact hypersensitivity in humans have not been published. Several studies in mice of the protection afforded by sunscreens from UVB-induced suppression of contact hypersensitivity and rejection of transplanted skin cancers have yielded dissimilar results, ranging from "no" to "complete" protection. We sought to determine whether the effect of preapplication of a sun protection factor (SPF) 29 sunscreen (containing octyl methoxycinnamate, oxybenzone, and octyl salicylate) could prevent local UVB-induced suppression of contact hypersensitivity to dinitrochlorobenzene (DNCB). Nineteen subjects received either three minimal erythema doses of UVB daily on three consecutive days (UVB group) or sunscreen followed by this same dose of UVB irradiation (sunscreen plus UVB group) to a 16-cm2 area of the buttock. One day after completion of irradiation, DNCB was applied to this buttock site, and 2 weeks later, forearm challenge with four different concentrations of DNCB was performed. A control group of 10 subjects underwent DNCB testing as above, but with no prior exposure to UVB (no-UVB group). The UVB group had a reduced response rate to all challenge doses of DNCB (3.125, 6.25, and 8.8 micrograms), except for the highest dose (12.5 micrograms) compared with the no-UVB control group (Fisher's Exact test, P < or = .008), and compared with the sunscreen plus UVB group (P < or = .02). The no-UVB and sunscreen plus UVB groups showed no significant differences in response rates to any of the doses of DNCB tested (P > or = .53). These results indicate that application of a sunscreen with over ninefold greater protection than that needed to prevent erythema prior to localized UVB radiation prevents localized UVB-induced suppression of contact hypersensitivity. Further studies are needed to determine whether sunscreens providing less protection, yet still preventing erythema, adequately prevent suppression of contact hypersensitivity, a possible surrogate marker for skin cancer tumor antigen recognition and rejection.

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.

The effect of a clear tar ointment on the minimal erythema dose for UVB

The effect of a clear tar ointment on the minimal erythema dose for UVB

Clothing prevents ultraviolet-B radiation-dependent photosynthesis of vitamin D3.

Photoprotection of the skin is mainly a function of clothing, although the effectiveness of the latter against UV-B solar radiation (wavelengths 290-320 nm) has not been measured in vivo. Since UV-B mediates the cutaneous formation of vitamin D3, we examined the attenuation of that photosynthetic reaction by the commonly used fabrics cotton, wool, and polyester in black and white colors. Direct transmission of UV-B was attenuated the most by black wool (98.6% of incident irradiance) and the least by white cotton (47.7%). None of the fabrics allowed the photoproduction of previtamin D3 from 7-dehydrocholesterol irradiated in vitro with up to 40 min of simulated sunlight or the elevation of serum vitamin D3 after irradiation with approximately one minimal erythema dose (MED) of UV-B in volunteers wearing jogging garments made of these fabrics. Increasing the whole body irradiation dose to six MEDs still failed to produce a serum vitamin D3 response in garment-clad subjects. Regular (seasonal) street clothing also prevented an elevation of the vitamin D3 in response to UV-B radiation. We conclude that clothing prevents or significantly impairs the formation of vitamin D3 after photostimulation with up to six MEDs of UV-B.