Two hundred twenty-two nanometers ultraviolet (UV) light produced by a krypton–chlorine excimer lamp is harmful to bacterial cells but not skin. However, the effects of 222-nm UV light exposure to the eye are not fully known. We evaluated acute corneal damage induced by 222- and 254-nm UV light in albino rats. Under deep anesthesia, 6-week-old Sprague-Dawley albino rats were exposed to UV light. The exposure levels of corneal radiation were 30, 150, and 600 mJ/cm². Epithelial defects were detected by staining with fluorescein. Superficial punctate keratitis developed in corneas exposed to more than 50 mJ/cm² of UV light, and erosion was observed in corneas exposed to 600 mJ/cm² of UV light. Hematoxylin and eosin staining also showed corneal epithelial defects in eyes exposed to 254-nm UV light. However, no damage developed in corneas exposed to 222-nm UV light. Cyclobutane pyrimidine dimer-positive cells were observed only in normal corneas and those exposed to 254-nm UV light. Although some epithelial cells were stained weakly in normal corneas, squamous epithelial cells were stained moderately, and the epithelial layer that was detached from the cornea exposed to 600 mJ/cm² of light was stained intensely in corneas exposed to 254-nm UV light. In the current study, no corneal damage was induced by 222-nm UV light, which suggested that 222-nm UV light may not harm rat eyes within the energy range and may be useful for sterilizing or preventing infection in the future.

Corneal damage‐induced various wavelength UV (311, 254, 235, 222 and 207 nm) was evaluated in rats. For 207 and 222‐UV‐C, the threshold radiant exposure was between 10 000 and 15 000 mJ cm⁻² at 207 nm and between 3500 and 5000 mJ cm⁻² at 222 nm. Penetrate depth to the cornea indicated by cyclobutene pyrimidine dimer (CPD) localization immediately after irradiation was dependent on the wavelength. 311 and 254 nm UV penetrate to corneal endothelium, 235 nm UVC to the intermediate part of corneal stroma, 222 and 207 nm UVC only to the most outer layer of corneal epithelium. CPD observed in corneal epithelium irradiated by 222 nm UVC disappeared until 12 h after. The minimum dose to induce corneal damage of short‐wavelength UV‐C was considerably higher than the threshold limit value (TLV^®) promulgated by American Conference of Governmental Industrial Hygienists (ACGIH). The property that explains why UV‐C radiation at 207 and 222 nm is extremely less hazardous than longer UV wavelengths is the fact that this radiation only penetrates to the outermost layer of the corneal epithelium. These cells typically peel off within 24 h during the physiological turnover cycle. Hence, short‐wavelength UV‐C might be less hazardous to the cornea than previously considered until today.

Two krypton‐chloride germicidal excimer lamp units (Care222 TRT‐104C11‐UI‐U3, USHIO Inc.) were installed in the examination room of an ophthalmology department. The irradiation dose was set not to exceed the former (i.e., before 2022) threshold limit value (TLV) (22 mJ cm⁻²/8 h) recommended by the ACGIH. Section 1: The eyes and lids of the six ophthalmologists (5 wore glasses for myopic correction) who worked in the room for a mean stay of 6.7 h week⁻¹ were prospectively observed for 12 months. Slitlamp examinations revealed neither acute adverse events such as corneal erosion, conjunctival hyperemia, and lid skin erythema nor chronic adverse events such as pterygium, cataract, or lid tumor. The visual acuity, refractive error, and corneal endothelial cell density remained unchanged during the study. Section 2: The irradiation of samples placed on the table or floor using the same fixtures in the room (5–7.5 mJ cm⁻²) was associated with >99% inhibition of φX174 phage and >90% inhibition of Staphylococcus aureus. In conclusion, no acute or chronic health effects in human participants was observed in a clinical setting of full‐room ultraviolet germicidal irradiation by 222‐nm lamp units, and high efficacy in deactivation of microorganisms was determined in the same setting.

We examined the cytoprotective effect of quercetin via activator protein (AP-1) and the heat shock protein 70 (Hsp70) pathway against light-induced retinal degeneration in rats. Quercetin was administered intraperitoneally to Sprague-Dawley rats for seven days before light exposure to intense white fluorescent light (3000 lux) for 24 h. Light-induced retinal damage was determined by the number of rows of photoreceptor cell nuclei, the microstructures of the rod outer segments and retinal pigment epithelium, and terminal deoxynucleotidyl transferase (TdT)-mediated 2′-Deoxyuridine-5′-triphosphate (dUTP) nick end labeling. To elucidate the cytoprotective mechanism of quercetin, expression levels were measured in the rat retinas of 8-hydroxy-deoxyguanosine (8-OHdG), a marker of oxidative stress; Hsp70; and transcription factor AP-1 transcription activity. Pretreatment with quercetin inhibited light-induced photoreceptor cellular apoptosis and subsequent retinal degeneration in rats. 8-OHdG and Hsp70 protein expressions were up-regulated markedly by light exposure and suppressed by quercetin pretreatment. The results of an electrophoretic mobility shift assay showed that AP-1-binding activity was activated by light exposure, and binding of c-Fos and c-Jun, but not JunB, mediated the binding activity. Intraperitoneal administration of quercetin decreases photooxidative damage in the retina and mediates cytoprotection against light-induced photoreceptor cell degeneration in rats. Suppression of the heterodimeric combination of c-Jun and c-Fos proteins at the AP-1 binding site is highly involved in quercetin-mediated cytoprotection.

Basal cells in the corneal limbus play an important role in the turnover cycle because they are the source of all cells that constitute the corneal epithelium. We examined the penetration depth of ultraviolet (UV) light in the corneal limbus and assessed the safety of Far‐UV‐C on stem cells in the basal area of the corneal limbus. Rats were irradiated with UV at peaks of 207, 222, 235, 254 and 311 nm while under anesthesia. The UV penetration depth in the rat corneal limbal epithelium was wavelength dependent: 311 nm UV‐B and 254 nm UV‐C reached the basal cells of the epithelium, and 235 nm radiation reached the middle area; however, 207 and 222 nm UV‐C reached only the superficial layer of the epithelium. Porcine cornea, which is similar to the human eye in size and structure, were irradiated with 222 and 254 nm UV‐C. As in rats, 222 nm UV‐C reached only the superficial layer of the porcine corneal limbal epithelium. These results indicate that Far‐UV‐C, such as radiation of wavelengths of 207 and 222 nm, could not reach corneal epithelial stem cells, i.e. the cells remained intact. It is unlikely that the turnover of the corneal epithelium is obstructed or disrupted by exposure to Far‐UV‐C.