Germicidal lamps that emit primarily 254 nm ultraviolet radiation (UV) are routinely utilized for surface sterilization but cannot be used for human skin because they cause genotoxicity. As an alternative, 222‐nm UVC has been reported to exert sterilizing ability comparable to that of 254‐nm UVC without producing cyclobutane pyrimidine dimers (CPDs), the major DNA lesions caused by UV. However, there has been no clear evidence for safety in chronic exposure to skin, particularly with respect to carcinogenesis. We therefore investigated the long‐term effects of 222‐nm UVC on skin using a highly photocarcinogenic phenotype mice that lack xeroderma pigmentosum complementation group A ( Xpa ‐) gene, which is involved in repairing of CPDs. CPDs formation was recognized only uppermost layer of epidermis even with high dose of 222‐nm UVC exposure. No tumors were observed in Xpa ‐knockout mice and wild‐type mice by repetitive irradiation with 222‐nm UVC, using a protocol which had shown to produce tumor in Xpa ‐knockout mice irradiated with broad‐band UVB. Furthermore, erythema and ear swelling were not observed in both genotype mice following 222‐nm UVC exposure. Our data suggest that 222‐nm UVC lamps can be safely used for sterilizing human skin as far as the perspective of skin cancer development.

Biological response and DNA damage following irradiation with shorter wavelengths in the UV‐C range were evaluated to investigate the safety at three wavelengths because of the recent emergence of germicidal equipment emitting short‐wavelength UV‐C for various purposes, including medical uses. To estimate an acceptable safety dose for human skin in the UV‐C range, especially short UV‐C, we studied the biological effects of 207, 222 and 235 nm UV‐C using albino hairless mice and evaluated the inflammatory reactions in the skin. To explore an appropriate indicator to evaluate the biological response, we employed determination of the minimal perceptible response dose (MPRD), by which any subtle cutaneous response; erythema, edema and scale could be observed by visual inspection. Erythema was rarely observed, but edema and scale formation were evident for short UV‐C wavelengths. The MPRD at 207, 222 and 235 nm was determined to be > 15, 15 and 2.0 kJ m−2, respectively. These values could be thresholds and indicators for possible safety assessments. Our data suggest that the current human exposure limits for short UV‐C wavelengths below 254 nm are overly restrictive and should be reconsidered for future disinfection lamps with short UV‐C wavelengths.

Life on earth has constantly coped with the impact of solar radiation, especially solar ultraviolet radiation (solar UV). Various biological mechanisms protect us from solar UV. New devices emitting shorter wavelengths UV-C, i.e. <254 nm emitted by conventional UV germicidal lamps, have emerged. These shorter wavelength UV-C emitting devices are useful for various purposes, including microorganism inactivation. However, as solar UV-C does not reach the earth surface, biological impacts of UV-C has been studied using 254 nm germicidal lamps, and those using shorter wavelength UV-C is rarely known. To balance the utility and risk of UV-C, the biological effect of these new UV-C emitting devices must be investigated. In addition, our knowledge of biological impacts of the wavelength-dependent entire UV (100-400 nm) must be enhanced. In this review, we briefly summarize the biological impacts of shorter wavelength UV-C. Mechanisms of UV-C-induced cellular damage and factors affecting the microorganism inactivation efficiency of UV-C have been discussed. In addition, we theoretically estimate the probable photocarcinogenic action spectrum of shorter wavelength UV-C. We propose that increasing the knowledge on UV-C will facilitate the adoption of shorter wavelength UV-C emitting new devices in an optimal and appropriate manner.

The vascular and inflammatory response in Rosacea is exacerbated by exposure to UV radiation. In this study we hypothesized that the excess LL37 known to be present in Rosacea skin may be responsible for this increased sensitivity to UV. To test this, human keratinocytes (NHEK) expressing LL37 were exposed to UVB (25 mJ/cm 2 ), then extracts from these cells, or control cell extracts of non-irradiated NHEK, were added to dermal microvascular endothelial cells (HDMECs). UV-damaged NHEK, but not controls, activated endothelial cells as seen by increased CXCL10 (4.03 fold, p¼0.03) and CX3CL1 (13.6 fold, p<0.0001). This activation of endothelial cells was due to release of dsRNA from UV exposed NHEK since RNAase treatment of the NHEK extract inhibited the response of HDMECs. HDMECs treated with a synthetic dsRNA (snoU1 RNA) required LL37 for activation, a process we refer to as innate immune vetting. To further understand the significance of this vetting phenomenon in rosacea, RNA-sequencing was performed on HDMECs. 117 unique genes were upregulated only by the combination of dsRNA and LL37. As expected, a GO pathway for type I interferon signaling was seen, but HDMECs also showed gene signatures for cell-cell adhesion. q-RT-PCR then validated induction of ICAM1 (10.74 fold, p¼ 0.0406) and VCAM1 (13.9 fold, p¼ 0.0051) by LL37-dsRNA. The role of dsRNA was confirmed by knock down of TLR3 (VCAM1 inhibited 6.02 fold, p¼ 0.0017). Consistent with induction of VCAM1 by RNA-LL37, we also observed that dsRNA-LL37 increased VCAM protein expression, enhanced monocyte adhesion to HDMECs (76.51 fold, p<0.0001), and increased leukocyte transmigration (5.11 fold, p<0.0001) across HDMECs. In mice, only combined injection of U1 and LL37 enhanced VCAM1 expression. These findings prompted examination of human Rosacea biopsies that also showed VCAM1 to be highly expressed in rosacea skin, a finding not previously known in this disorder. Overall, our results suggest LL37 acts as an innate immune vetting molecule in rosacea that enhances activation of endothelial cells after UV exposure. Premature skin aging evidenced by a rough skin texture and wrinkles is known to be driven by external factors, mainly by sunlight and in particular UV radiation including UVB (280-320 nm) and UVA (320-400 nm). However, recent advance highlighted the role of visible light and especially the blue light part (400-500nm) in skin aging. As the blue light is the highest energetic wavelength of the visible light, it penetrates deeper into the skin and damages the skin by inducing oxidative stress and production of proteases which degrade the extracellular matrix of the dermis. We first investigated the negative effects of the blue light in human dermis through the evaluation of MMP1 by immunostaining and image analysis on living skin biopsies exposed to blue light irradiation (peak at 250 nm-85 J/cm 2 ). We further evaluated the blue light preventive effect of a botanical extract selected for its ability to prevent UVB induced oxidative damages by promoting DNA ...