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Photokeratitis
Photokeratitis
Photokeratitis
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Photokeratitis
SpecialtyOphthalmology Edit this on Wikidata

Photokeratitis or ultraviolet keratitis is a painful eye condition caused by exposure of insufficiently protected eyes to the ultraviolet (UV) rays from either natural (e.g. intense direct or reflected sunlight) or artificial (e.g. the electric arc during welding) sources. Photokeratitis is akin to a sunburn of the cornea and conjunctiva.

The injury may be prevented by wearing eye protection that blocks most of the ultraviolet radiation, such as welding goggles with the proper filters, a welder's helmet, sunglasses rated for sufficient UV protection, or appropriate snow goggles. The condition is usually managed by removal from the source of ultraviolet radiation, covering the corneas, and administration of pain relief. Photokeratitis is known by a number of different terms, including snow blindness, arc eye, welder's flash, sand eyes, bake eyes, corneal flash burns, flash burns, niphablepsia, or keratoconjunctivitis photoelectrica.

Signs and symptoms

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Common symptoms include pain, intense tears, eyelid twitching, discomfort from bright light,[1] and constricted pupils.

Cause

[edit]

Any intense exposure to UV light can lead to photokeratitis.[2] In 2010, the Department of Optometry at the Dublin Institute of Technology published that the threshold for photokeratitis is 0.12 J/m2.[3] (Prior to this, in 1975, the Division of Biological Effects at the US Bureau of Radiological Health had published that the human threshold for photokeratitis is 50 J/m2.[4]) Common causes include welding with failure to use adequate eye protection such as an appropriate welding helmet or welding goggles. This is termed arc eye, while photokeratitis caused by exposure to sunlight reflected from ice and snow, particularly at elevation, is commonly called snow blindness.[5] It can also occur due to using tanning beds without proper eyewear. Natural sources include bright sunlight reflected from snow or ice or, less commonly, from sea or sand.[6] Fresh snow reflects about 80% of the UV radiation compared to a dry, sandy beach (15%) or sea foam (25%). This is especially a problem in polar regions and at high altitudes,[5] as with about every 300 m (980 ft) of elevation (above sea level), the intensity of ultraviolet rays increases by four percent.[7]

Diagnosis

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Fluorescein dye staining will reveal damage to the cornea under ultraviolet light.[8]

Prevention

[edit]
Snow goggles traditionally used by the Inuit

Photokeratitis can be prevented by using sunglasses or eye protection that transmits 5–10% of visible light and absorbs almost all UV rays. Additionally, these glasses should have large lenses and side shields to avoid incidental light exposure. Sunglasses should always be worn, even when the sky is overcast, as UV rays can pass through clouds.[9]

Inuit, Yupik, and other circumpolar peoples have carved snow goggles from materials such as driftwood or antlers of caribou to help prevent snow blindness for millennia.[10] Curved to fit the user's face with a large groove cut in the back to allow for the nose, the goggles allow in a small amount of light through a long thin slit cut along their length. The goggles are held to the head by a cord made of caribou sinew.[11]

Polar bear cub with sun goggles, possibly to prevent snow blindness

In the event of missing sunglass lenses, emergency lenses can be made by cutting slits in dark fabric or tape folded back onto itself.[12] The SAS Survival Guide recommends blackening the skin underneath the eyes with charcoal (as the ancient Egyptians did) to avoid any further reflection.[13][14]

Arctic and Antarctic explorers

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Explorers of the polar regions employed various methods and materials to protect their eyes from the harsh glare in snowy environments. Edward Evans noted the popularity of yellow and orange-tinted glasses among explorers, though some showed a preference for green.[15] Despite the availability of blue and purple glasses, Edward L. Atkinson advised that all glasses, regardless of colour, should undergo spectroscope testing to ensure effectiveness.

Robert Falcon Scott favoured a more rudimentary approach, opting for goggles crafted from leather or wood with narrow slits, which prevented the accumulation of frost. A similar design principle was also applied in emergency situations, such as when the Swedish expedition, after being shipwrecked, fashioned makeshift goggles from wood or wire frames covered with fabric from a Swedish flag.

The Royal Geographical Society's guidance for travellers included a technique used by indigenous peoples of high-altitude regions, which involved darkening the skin around the eyes and nose to mitigate the risk of snow blindness. This method was adopted by the Terra Nova northern party in the absence of traditional goggles.

The impact of snow blindness extended to animals as well; the expedition’s horses suffered from the condition. Lawrence Oates proposed dyeing the horses’ forelocks as a preventative measure, and they were also equipped with tassels over their eyes for protection. Similarly, mules were provided with canvas snow goggles, demonstrating the breadth of strategies developed to combat this pervasive issue during polar exploration.[16]

Treatment

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The pain may be temporarily alleviated with anaesthetic eye drops for the examination; however, they are not used for continued treatment,[17] as anaesthesia of the eye interferes with corneal healing, and may lead to corneal ulceration and even loss of the eye.[18] In the 1900s polar explorers treated snow blindness by dripping cocaine into the eye.[19] Cool, wet compresses over the eyes and artificial tears may help local symptoms when the feeling returns. Nonsteroidal anti-inflammatory drug (NSAID) eyedrops are widely used to lessen inflammation and eye pain, but have not been proven in rigorous trials. Systemic (oral) pain medication is given if discomfort is severe. Healing is usually rapid (24–72 hours) if the injury source is removed. Further injury should be avoided by isolation in a dark room, removing contact lenses, not rubbing the eyes, and wearing sunglasses until the symptoms improve.[5]

In animals

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See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Photokeratitis

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from Grokipedia
Photokeratitis, also known as or snow blindness, is a painful, acute and damage to the resulting from excessive exposure to (UV) radiation, often likened to a sunburn of the eye. This condition typically develops 3 to 12 hours after exposure and affects both eyes, presenting as a self-limiting superficial keratopathy without long-term damage in most cases. It is most commonly caused by UV-B (280–315 nm) and UV-C (100–280 nm) wavelengths from natural sources like reflected off , , or sand, or artificial sources such as arcs, lasers, tanning lamps, germicidal UV lights, or metal halide bulbs. The hallmark symptoms of photokeratitis include severe eye pain, redness, excessive tearing, a gritty or foreign body sensation, photophobia (extreme light sensitivity), blurred vision, and sometimes eyelid swelling or conjunctival injection. These manifestations arise from UV-induced apoptosis of corneal epithelial cells, leading to punctate erosions visible under slit-lamp examination with fluorescein staining. While generally resolving within 24 to 48 hours as the epithelium regenerates, severe cases can lead to secondary bacterial infection if untreated, and it is considered an ophthalmic emergency requiring prompt evaluation. Treatment focuses on symptom relief and prevention of complications, including oral analgesics like ibuprofen or acetaminophen for , topical lubricants or cycloplegic drops to reduce discomfort and , and prophylactic eye drops or ointments to guard against . Patients are advised to avoid rubbing the eyes, wear dark , and rest in a darkened room until recovery. Prevention is straightforward and critical, involving the use of protective that blocks 100% of UV-A and UV-B rays, such as wraparound , ski goggles, or welding helmets, particularly in high-risk settings like snowy environments, beaches, or industrial sites. Outbreaks have been reported in contexts like recreational events, salons, or during increased UV lamp use, underscoring the need for awareness and adherence to safety guidelines.

Overview

Definition

Photokeratitis is an acute, painful of the , and sometimes the , caused by exposure to (UV) radiation, resulting in superficial damage to the epithelial layer. This condition represents a phototoxic reaction, where high-intensity UV rays trigger immediate photochemical injury to ocular surface cells without involving infectious agents. It is known by several alternative names, including ultraviolet , snow blindness, welder's flash, arc-eye, and corneal flash burns. Unlike chronic UV exposure effects such as or cataracts, which develop gradually from cumulative damage, photokeratitis is a transient response limited to the superficial . Symptoms typically emerge 6-12 hours post-exposure, reach peak intensity around 24 hours, and resolve spontaneously within 24-72 hours, with full epithelial regeneration and no scarring in uncomplicated cases. The primary culprit is UVB radiation (280-315 nm), though details of its mechanism are addressed elsewhere.

Epidemiology

Photokeratitis exhibits limited global incidence data primarily due to underreporting and its often self-limiting nature, though it is recognized as one of the most common corneal conditions . Estimates suggest higher occurrence in regions with elevated (UV) radiation, such as sunny equatorial areas where solar UV intensity is greater due to proximity to the , and among travelers to high-UV destinations. For instance, during the 2017 in , the adjusted incidence rate reached 21 cases per 100,000 eyes in the following two months, highlighting event-related spikes in otherwise low-prevalence settings. Similarly, the 2024 was associated with comparable rates of 14 per 100,000 eyes. At the population level, key risk factors include occupational and recreational demographics such as welders, outdoor workers, and high-altitude climbers, with seasonal peaks in summer from direct solar exposure and winter from reflection amplifying UV doses. Among welders, particularly in informal or outdoor settings, prevalence can be notably high, with studies reporting up to 84% experiencing photokeratitis complaints linked to excessive UV exposure. Recent trends during the (2020-2021) showed increased cases from improper use of UV germicidal lamps in salons and homes, contributing to a surge in domestic exposures. High-altitude studies from 2011 documented an incidence of 0.06% among exposed groups on or water terrain. Notable outbreaks underscore episodic risks, including a 2015 theater production where UV lights affected four pediatric attendees aged 9-13 years, and a 2018 indoor event in where 72-80% of participants developed bilateral photokeratitis from faulty UV-emitting lamps. A 2024 outdoor recreational UV display event led to eight confirmed cases, with symptoms emerging after an average 3-hour exposure. Geographic variations are pronounced in polar regions, where snow blindness—a form of photokeratitis—has historically afflicted explorers and populations due to intense UV reflection off ice, prompting traditional protective innovations like , though exact prevalence remains undocumented in modern cohorts. Urban areas with prevalent or tanning bed use also report elevated rates.

Pathophysiology

Etiology and Risk Factors

Photokeratitis is primarily caused by acute exposure to ultraviolet B (UVB, 280-315 nm) and ultraviolet C (UVC, 100-280 nm) radiation, which is absorbed by the cornea and leads to epithelial damage. Natural sources include direct sunlight and its reflection from surfaces such as snow, water, and sand, with snow blindness being a classic example from intense reflected UVB on snowy terrains. Artificial sources encompass high-intensity UV emissions from welding arcs, lasers, tanning beds, germicidal lamps, and blacklights, where unprotected eyes can receive damaging doses during occupational or recreational use. Environmental factors significantly modulate UV exposure risk. At high altitudes, the thinner atmosphere reduces UV filtration, increasing irradiance by up to 10-12% per 1,000 meters gain. Reflective surfaces like fresh can amplify UV exposure by reflecting 80% or more of incident rays, effectively doubling the dose to the eyes from both direct and indirect paths. UV intensity peaks around solar noon (10 a.m. to 4 p.m.), when the sun's angle minimizes atmospheric scattering, and overcast conditions attenuate but do not eliminate exposure, as diffuse UV can penetrate clouds. Individual risk factors heighten susceptibility to photokeratitis from equivalent UV doses. The absence of protective eyewear, such as UV-blocking , is the most direct risk, leaving the fully exposed during high-UV activities. Photosensitizing medications, including tetracyclines and sulfonamides, can lower the threshold for UV-induced damage by generating in ocular tissues. Pre-existing conditions like or wear without UV filtration may exacerbate vulnerability, as reduced tear film or lens absorption alters corneal protection. Occupational exposures are prominent among welders and outdoor workers like lifeguards, who face repeated intense UV without consistent protection, while recreational pursuits such as or beachgoing increase risk through prolonged unprotected time in reflective environments. The condition follows a dose-response relationship, with a threshold effective dose for UVB-induced photokeratitis estimated at 0.5-6 mJ/cm², depending on wavelength (peaking near 288 nm), exposed ocular surface area, and exposure duration; doses below this typically cause no symptoms, while exceeding it triggers inflammation.

Mechanism of Injury

Photokeratitis arises from the photochemical absorption of ultraviolet (UV) radiation by chromophores in the corneal epithelium, primarily urocanic acid and tryptophan, which initiates a cascade of oxidative stress. Upon exposure, UV photons excite these molecules, leading to the production of reactive oxygen species (ROS), such as singlet oxygen and superoxide anions, that overwhelm cellular antioxidant defenses. These ROS cause direct damage to DNA through strand breaks and base modifications, denature proteins by oxidizing amino acids, and peroxidize lipids in cell membranes, compromising epithelial cell integrity. The sequence of injury begins with the induction of in superficial epithelial cells, triggered by ROS-mediated activation of and mitochondrial pathways, resulting in punctate erosions on the corneal surface. This initial cell death is followed by an inflammatory cascade, where damaged cells release pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), which recruit neutrophils and promote further ROS production. The cytokines contribute to localized and of corneal nerves, amplifying the inflammatory response without systemic involvement. Unlike deeper thermal injuries from (IR) radiation, which can penetrate the stroma and cause , UV-induced damage in photokeratitis is confined to the , sparing and underlying structures due to the strong absorption of UV wavelengths (below 320 nm) in the superficial layers. This superficial nature accounts for the condition's typical reversibility within 24-48 hours through epithelial regeneration from limbal stem cells. Severity is modulated by wavelength specificity, with UVB (280-315 nm) being more damaging than UVA (315-400 nm) owing to higher absorption and energy per ; exposure dose, where thresholds around 0.5-6 mJ/cm² can induce injury; and individual factors such as corneal thickness, which influences penetration, and content in the limbus, providing partial photoprotection by scavenging free radicals.

Clinical Features

Signs and Symptoms

Photokeratitis typically manifests with a delayed onset of symptoms, appearing 6 to 12 hours after (UV) radiation exposure, rather than immediately. This delay corresponds to the time required for the to undergo damage and slough off, exposing underlying nerves. Symptoms generally progress over the first 24 hours, peaking in intensity before resolving spontaneously within 24 to 48 hours in most cases, though severity increases with the duration and intensity of UV exposure. The condition most commonly presents bilaterally due to symmetric exposure, though unilateral involvement can occur with asymmetric UV sources, such as in occupational settings like . Primary ocular symptoms include severe eye pain or a sensation, often described as feeling like sand in the eyes, accompanied by intense , excessive tearing (lacrimation), (involuntary eyelid closure), and . Conjunctival injection (redness) is a hallmark sign, contributing to the overall discomfort. Associated signs may include eyelid swelling and (conjunctival edema), with temporary reduction in and, in rare instances, transient disturbances. Rubbing the eyes can occasionally lead to secondary bacterial , exacerbating symptoms. Variations in presentation depend on exposure type and dose; milder cases from low-level sources like tanning beds may involve only mild irritation and tearing, while high-reflection scenarios such as snow (causing "snow blindness") or water can result in more severe pain, , and vision impairment due to amplified UV intensity.

Diagnosis

Clinical Evaluation

Diagnosis of photokeratitis begins with a detailed history taking, focusing on recent unprotected exposure to (UV) radiation sources such as outdoor activities in high-altitude or reflective environments (e.g., or ), without proper , or artificial UV lamps like those in tanning beds. Patients typically report a delayed onset of symptoms, with pain, tearing, and sensation emerging 3 to 12 hours after exposure, which is a hallmark it from immediate-onset conditions. This timeline, combined with bilateral involvement, helps confirm the early. Physical examination includes assessment of , which is often normal or only mildly reduced due to the superficial nature of the injury. Slit-lamp biomicroscopy is essential and reveals characteristic findings such as conjunctival injection, , and diffuse on the with hazy appearance limited to the superficial layers. Fluorescein staining during the exam highlights these epithelial defects as bright green spots under light, confirming the extent of corneal damage without deeper stromal involvement. Ancillary tests are rarely required for straightforward cases but may include fluorescein dye application for precise mapping of erosions if the exam is inconclusive. If the presentation is —such as unilateral involvement or signs of discharge—corneal cultures may be performed to rule out superimposed bacterial or viral . involves distinguishing photokeratitis from conditions with overlapping symptoms like infectious , which typically presents unilaterally with purulent discharge and deeper stromal involvement, unlike the bilateral, superficial, exposure-related pattern here. Chemical burns are differentiated by a history of direct ocular chemical contact rather than UV exposure, often showing more irregular or full-thickness damage. Acute angle-closure is excluded based on the absence of elevated , severe , , and mid-dilated , with photokeratitis lacking these systemic features and showing only anterior segment superficial changes. Other considerations include viral or , which lack the punctate erosions and UV exposure history.

Prevention and Management

Prevention Strategies

Preventing photokeratitis requires proactive measures to minimize ultraviolet (UV) radiation exposure to the eyes, primarily through the use of appropriate protective equipment and behavioral adjustments. The most effective strategy involves wearing eyewear that blocks 100% of UVA and UVB rays, such as polarized or wraparound sunglasses certified to meet standards like ANSI Z80.3 for UV protection. For activities involving intense artificial UV sources, such as arc welding, the Occupational Safety and Health Administration (OSHA) mandates the use of welding helmets or hand shields equipped with filter lenses of appropriate shade numbers (typically 10 or higher for most operations, based on amperage guidelines) to shield against harmful UV emissions from the welding arc. Behavioral modifications further reduce risk by limiting direct UV exposure, particularly during peak midday hours from 10 a.m. to 4 p.m. when UV intensity is highest. Individuals should avoid unprotected proximity to reflective surfaces like , , or , which can amplify UV rays by up to 80-90% in snowy environments, and instead opt for wide-brimmed hats, umbrellas, or seeking shade. Targeted education campaigns are essential for high-risk populations, including skiers, beachgoers, and outdoor workers, to promote consistent use of protective measures and awareness of environmental UV amplification. In occupational settings, adherence to regulatory guidelines is critical; for instance, OSHA's general industry standard (29 CFR 1910.252) requires employers to provide and ensure the use of appropriate for workers exposed to operations or other sources. Similarly, the U.S. (FDA) issues warnings on devices, which can emit UV radiation 10 to 15 times more intense than midday summer sun, recommending the use of protective eyewear during use to prevent acute eye injuries like photokeratitis. Emerging tools enhance prevention by enabling real-time UV monitoring; mobile applications such as the EPA's SunWise UV Index app provide location-based forecasts and alerts to guide protective actions during high-UV periods. Additionally, applying UV-blocking films to windows or protective shields around germicidal UV lamps in professional or laboratory settings can mitigate stray radiation exposure. Historically, indigenous Arctic peoples, including the , crafted from materials like caribou antler with narrow slits to reduce UV entry and prevent snow blindness, a traditional adaptation that underscores the long-recognized need for eye shielding in reflective environments.

Treatment Approaches

Treatment of photokeratitis is primarily supportive and symptomatic, aimed at alleviating discomfort from symptoms such as and while allowing the to heal naturally. Initial steps include immediately removing any contact lenses to prevent further irritation and potential complications, followed by resting in a dark environment to minimize light exposure. Cold compresses applied to closed eyelids can help reduce swelling and provide soothing relief, typically used for 10-15 minutes several times a day during the first 24-48 hours. Oral analgesics, such as ibuprofen, are commonly recommended to manage pain and inflammation, with dosing typically following standard over-the-counter guidelines (e.g., 400-600 mg every 6-8 hours as needed). Topical lubricants, including , should be applied frequently—ideally hourly while awake—to maintain ocular surface moisture and promote epithelial recovery. In cases of severe ciliary spasm contributing to , short-term use of cycloplegic agents like 1% (1-2 drops 2-3 times daily) may be prescribed to relax the iris and ciliary muscles, though this is not routinely required. Eye patching is generally not recommended for severe cases, as evidence shows it does not improve healing or reduce pain and should only be considered under medical guidance. Antibiotics are rarely indicated, as photokeratitis is typically sterile, but topical agents (e.g., or erythromycin ointment) may be used if secondary bacterial is suspected based on clinical signs. Patients should avoid rubbing the eyes to prevent worsening of the epithelial defect. The condition is self-limiting, with full recovery usually occurring within 1-2 days as the regenerates rapidly without scarring. Follow-up evaluation is advised if symptoms persist beyond 48 hours to exclude complications such as or deeper .

Special Populations

In Animals

Photokeratitis, an acute inflammatory response of the to (UV) radiation, is rare in non-human animals but has been documented in veterinary practice across several species, primarily due to environmental or husbandry-related overexposure. In dogs, particularly those with light-colored or eyes, prolonged outdoor exposure to direct or UV reflection from can induce the condition, often termed snow blindness. Veterinary reports indicate that such cases present after extended time in bright, reflective environments like snowy fields, with symptoms appearing 6-12 hours post-exposure. Similarly, in such as sheep grazing in snowy pastures, UV reflection from ice and heightens risk, though cases may be underreported or confounded with infectious keratoconjunctivitis. In captive reptiles, photokeratitis is more frequently encountered due to artificial UV lighting setups in terrariums. Species like s (Python regius) and blue-tongue s (Tiliqua spp.) are particularly susceptible when exposed to high-intensity or inappropriately spectrumed UVB lamps intended for synthesis. A veterinary pathology report detailed severe bilateral ulcerative keratoconjunctivitis in one and one blue-tongue , with histological evidence of epidermal basal cell , superficial , and corneal damage consistent with UV ; bacterial colonization was secondary to the primary UV . Over 80 cases of photo-kerato-conjunctivitis have been documented in , turtles, and since 2006, linked to excessive UVB output from compact fluorescent lamps lacking proper filtering. Risks are amplified in animals with light pigmentation or suboptimal enclosure designs that fail to provide shade or distance from light sources. Clinical signs in affected animals are analogous to those in humans but vary by species: excessive tearing (epiphora), involuntary blinking or squinting (), photophobia, and transient corneal opacity or . In reptiles, ulcerative lesions may develop, leading to secondary infections. relies on veterinary ophthalmologic evaluation, including slit-lamp biomicroscopy to assess corneal integrity and fluorescein staining to reveal epithelial defects, which typically fluoresce under cobalt blue light. Species differences, such as reptiles' , may influence exam techniques but do not alter the core diagnostic approach. Management focuses on supportive care tailored to the species. Topical lubricants and broad-spectrum antibiotics (e.g., erythromycin or fluoroquinolones) are applied to prevent and promote epithelial regeneration, typically resolving symptoms within 24-48 hours. Pain relief via oral or injectable non-steroidal anti-inflammatories is provided, with reptiles often requiring husbandry adjustments like dimming lights during recovery. Prevention emphasizes controlled UV exposure: for reptiles, using calibrated UVB meters to maintain 10-50 µW/cm² gradients and providing hides or UVB-blocking filters in enclosures; for dogs and , limiting unshaded time in high-UV settings (e.g., sun or snow) and considering protective eyewear like canine goggles for working breeds. In reptile cases, replacing faulty lamps prevented recurrence in reported cohorts.

Occupational and Environmental Cases

Photokeratitis frequently occurs in occupational settings where workers are exposed to intense (UV) radiation without adequate eye protection. Among welders, from arcs is a primary cause, leading to the condition commonly known as "welder's flash" or "arc eye," which manifests as painful inflammation shortly after exposure. Tanning salon users also face risks, as the UV lamps in these facilities can sunburn the cornea if protective eyewear is not worn, resulting in symptoms like redness, tearing, and light sensitivity. During the , mishaps with germicidal UV lamps for home disinfection became more common, with studies reporting a significant rise in photokeratoconjunctivitis cases— from 3.1% pre-pandemic to 10.2% afterward—often due to unsupervised exposure in households. In environmental and exploratory contexts, photokeratitis, often termed snow blindness, has long affected Arctic and Antarctic explorers due to UV reflection off snow and ice. Historical Inuit knowledge emphasized protective measures like snow goggles made from bone or wood to prevent such injuries, a practice adopted by 19th-century expeditions, including Robert Falcon Scott's Terra Nova expedition (1910–1913), where multiple crew members suffered snow blindness despite precautions. The condition's recognition intensified after Johann Wilhelm Ritter's 1801 discovery of UV radiation beyond the visible spectrum, which explained its photochemical basis in polar travel. Early documented cases include those during polar explorations in the late 19th century, highlighting the hazards of prolonged UV exposure in reflective environments. Modern instances persist in and recreational activities. A 2011 study of ultraviolet keratitis among mountaineers and outdoor enthusiasts found that 71% of cases occurred in sunny conditions, underscoring the role of clear weather in amplifying UV reflection from . More recently, in 2024, an outdoor recreational event featuring a UV display led to eight confirmed cases of photokeratitis, with symptoms appearing approximately 8–9 hours after an average exposure of 3 hours. These cases illustrate the need for stringent in high-risk settings, where UV intensity increases by approximately 30-36% at altitudes around 3000 meters due to thinner atmospheric filtering, exacerbating photokeratitis risks for explorers and workers alike.

References

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