Ultraviolet Keratitis (Snow Blindness, Electric Ophthalmia)

Key Points at a Glance

Key Points of This Disease

• Ultraviolet keratitis is an acute corneal epithelial disorder caused by ultraviolet radiation damaging the DNA and proteins of corneal epithelial cells.
• It is broadly classified into two types: electric ophthalmia (UVC from welding or germicidal lamps) and snow ophthalmia (solar UVB, commonly known as “snow blindness”).
• The most characteristic feature is the latent period (30 minutes to 24 hours). A typical course is severe pain at night after daytime exposure, leading to an emergency visit.
• Many patients have severe eye pain and difficulty opening the eyes voluntarily, and it often occurs bilaterally.
• Diagnosis is made by slit-lamp microscopy with fluorescein staining, revealing widespread superficial punctate keratitis (SPK) and corneal erosion.
• It usually heals spontaneously within 24 to 48 hours. Symptomatic treatment includes antibiotic eye drops, NSAID eye drops, and therapeutic soft contact lenses.
• Wearing protective glasses or goggles is the most effective preventive measure.

1. What is Ultraviolet Keratitis (Snow Blindness, Electric Ophthalmia)?

Ultraviolet keratitis is a disease in which ultraviolet radiation is absorbed by nucleic acids and aromatic amino acids in living organisms, denaturing genes and proteins, and causing damage to the corneal epithelium. It occurs as an acute corneal epithelial disorder, and chronic exposure can induce cataracts, pinguecula, pterygium, squamous metaplasia, and squamous cell carcinoma.

Classification into Two Types

Ultraviolet keratitis is divided into two types based on the wavelength of the causative ultraviolet radiation and the exposure source.

Disease Name	Cause	Main UV Type	Characteristics
Electric ophthalmia	Electric welding, acetylene welding, germicidal lamps, mercury lamps	UVC (100–280 nm)	Severe symptoms. Rapid onset.
Snow blindness	Sun exposure at ski resorts or high altitudes	UVB (280–315 nm)	Relatively mild symptoms. Longer time to onset.

Wavelength classification of ultraviolet radiation

Wavelength band	Wavelength range	Main effects on the eye
UVA (long-wave ultraviolet)	315–400 nm	Relatively few acute eye disorders. Mainly affects the skin.
UVB (medium-wavelength ultraviolet)	280–315 nm	Main cause of snow blindness and sunburn. Absorbed by the cornea and lens.
UVC (short-wavelength ultraviolet)	100–280 nm	Most harmful. Not present in sunlight. Emitted by artificial light sources.

UVC is not present in sunlight, but is emitted by artificial light sources such as electric welding, acetylene welding, germicidal lamps, and mercury lamps. Therefore, electric ophthalmia caused by UVC is important as an occupational injury in welders.

Epidemiology and onset

Electric ophthalmia occurs when a person looks directly at an artificial light source without wearing protective glasses. Snow blindness develops when tourists at ski resorts or high mountains go outside for long periods without wearing goggles or sunglasses. A typical course is that after daytime welding or skiing, severe eye pain occurs at night, leading to an emergency visit. It often affects both eyes ¹².

In a prospective study of outdoor workers, the incidence of snow blindness among participants under UV exposure was 0.06%, and 87% of those affected were not wearing sunglasses ². The higher the altitude, the less UV attenuation by the atmosphere; at 5,000 m above sea level, UV levels are about 40% higher than at sea level, increasing the risk of snow blindness for climbers ².

Q What is the difference between electric ophthalmia and snow blindness?

A

The main difference is the wavelength and source of the ultraviolet radiation. Electric ophthalmia is caused by exposure to artificial light sources (welding, germicidal lamps) that include UVC, resulting in more severe symptoms and faster onset. Snow blindness is caused by UVB from sunlight, with relatively milder symptoms and longer time to onset. Ultraviolet radiation in sunlight has longer wavelengths than artificial sources, so it is relatively less harmful to living tissue.

2. Main symptoms and clinical findings

Latent period and onset pattern

If a person looks directly at an artificial light source without protective glasses, or stays at a ski resort for 1.5 to 2 hours or more on a sunny day without goggles or sunglasses, symptoms appear after a latent period of 30 minutes to 24 hours. This latent period is a characteristic clinical feature of ultraviolet keratitis, and patients may not be aware of the exposure.

Subjective Symptoms

Symptoms reflect corneal epithelial damage.

• Eye pain: Marked. Many patients cannot open their eyes voluntarily.
• Foreign body sensation: Strong sensation like sand in the eye.
• Tearing: Reflexive secretion of large amounts of tears.
• Photophobia (light sensitivity): Hypersensitivity to bright light.
• Conjunctival injection and chemosis: Redness and swelling of the bulbar conjunctiva.
• Blepharospasm: Involuntary eyelid contraction due to pain and photophobia.
• Decreased vision: Due to extensive corneal epithelial damage.
• Sometimes accompanied by iritis, eyelid redness, and swelling.

Electric ophthalmia tends to be more severe and has a shorter onset time compared to snow ophthalmia.

Comparison of Clinical Findings

Electric Ophthalmia

Cause: UVC (welding, germicidal lamps, mercury lamps)

Symptom severity: Severe

Onset speed: Relatively fast (within hours of exposure)

Ocular findings: Widespread SPK and corneal erosion. May be accompanied by iritis.

Snow blindness (snow ophthalmia)

Cause: UVB (sunlight, ski slopes, high altitudes)

Symptom severity: Relatively mild

Onset speed: Somewhat slower (longer incubation period)

Ocular findings: SPK and corneal erosion are relatively mild. Symptoms are milder than arc eye.

Slit-lamp microscopy findings

The corneal pathology in arc eye and snow blindness is widespread superficial punctate keratopathy (SPK) and corneal erosion, which are corneal epithelial disorders. Fluorescein staining reveals green punctate or diffuse staining.

Q Why do symptoms appear several hours after exposure, not immediately?

A

Ultraviolet radiation damages the DNA and proteins of corneal epithelial cells immediately after exposure, but there is a time delay before cell degeneration progresses and the inflammatory cascade is activated. This time lag between cell degeneration and activation of the inflammatory response manifests as an incubation period of 30 minutes to 24 hours. This is why symptoms are not felt during welding or skiing but appear suddenly several hours later.

3. Causes and risk factors

Causes of arc eye

• Electric welding / acetylene welding: Arc welding emits strong UVC. It occurs when proper welding goggles are not used ¹
• Germicidal lamps (UV-C lamps): Ultraviolet germicidal lamps used in medical, food, and water treatment facilities. Direct eye exposure can occur due to mishandling or improper use. A report from a Korean chicken processing plant described that 26 out of 41 people (63.4%) developed corneal epitheliopathy due to a failure of the automatic shut-off of germicidal lamps ³
• Mercury vapor lamps: Used in factories and outdoor lighting
• In recent years, with the spread of household UV-C disinfection products, accidental exposure cases at home have been increasing⁴

Causes of Snow Blindness

• Ski slopes and ski resorts: Snow reflects UVB at a high rate. At high altitudes, atmospheric UV attenuation is low, resulting in several times more UV radiation than at ground level
• High-altitude mountaineering: The higher the altitude, the thinner the atmosphere, and the less UVB attenuation
• Sandy beaches and snowfields: Environments with high UVB reflectivity

Risk Factors

• Not wearing protective glasses, goggles, or sunglasses
• Prolonged, close-range direct exposure to artificial light sources
• Prolonged outdoor activity at ski resorts or high altitudes (continuous exposure of 1.5 to 2 hours or more)
• Improper equipment operation (e.g., staying in a room while a germicidal lamp is in use)

Prevention Tips

• Always wear appropriate welding protective masks or goggles with the correct shade when welding.
• Use UV400-compliant goggles or sunglasses for skiing, snowboarding, and high-altitude mountaineering.
• For household UV-C disinfection lamps, leave the room during use and enter only after use; strictly follow the instruction manual.
• Remember that your eyes can also get sunburned when you are on snow or sand on a sunny day.

4. Diagnosis and Examination Methods

Medical History

The first step in diagnosis is a detailed history of exposure.

• History of exposure to welding, germicidal lamps, skiing, high-altitude climbing, etc.
• Time from exposure to symptom onset (confirming a latent period of 30 minutes to 24 hours)
• Use of protective glasses or goggles
• Whether it is bilateral (if unilateral, consider other diseases such as foreign body or infection)

Slit Lamp Examination

Slit lamp examination with fluorescein staining is the definitive diagnostic method.

• Fluorescein staining: Observe the entire cornea under cobalt blue light. Widespread punctate superficial keratopathy (SPK) or corneal erosion confirms the diagnosis.
• Diffuse punctate staining is characteristic of ultraviolet injury and shows a different pattern from linear scratches due to simple mechanical trauma or infectious keratitis.

Findings Supporting the Diagnosis

1. History of exposure (welding, skiing)
2. Bilateral onset (if unilateral, consider other diseases)
3. Incubation period of 30 minutes to 24 hours
4. Widespread SPK or corneal erosion (confirmed by fluorescein staining)

Differential Diagnosis

Disease	Key differentiating features
Corneal foreign body	Symptoms are unilateral and localized. Foreign body confirmed by slit lamp.
Infectious keratitis	Accompanied by corneal infiltration and anterior chamber inflammation. Often not bilateral.
Dry eye-related SPK	Chronic course. Predilection for inferior cornea. No incubation period.
Chemical injury (acid/alkali)	Onset immediately after exposure. No incubation period.

5. Standard Treatment

Acute Phase Symptomatic Therapy

Ultraviolet keratitis usually heals spontaneously within 24 to 48 hours¹⁵. The goal of acute treatment is pain management and prevention of secondary infection.

Treatment	Content	Precautions
Topical anesthetics	Oxybuprocaine hydrochloride, etc., used during examination	Repeated use is contraindicated. Repeated use delays epithelial healing and causes corneal toxicity.
Antibiotic eye drops	New quinolones such as levofloxacin (0.5%) 4 to 6 times daily	Aimed at preventing secondary infection. Corneal epithelial defects increase infection risk.
NSAID eye drops	Diclofenac sodium 0.1% or bromfenac sodium 0.1% 2 to 4 times daily	Effective for pain relief. Long-term use may cause corneal epithelial damage.
Therapeutic soft contact lenses	Bandage contact lens wear	Reduces pain and promotes epithelial healing. Used in combination with antibiotic eye drops.
Eye patch and dark room rest	Performed as needed	Useful for patients with severe photophobia and blepharospasm

Precautions in treatment

• Topical anesthetics (e.g., oxybuprocaine) should be used only once during examination. Repeated use significantly delays corneal epithelial healing and may lead to chronic corneal disorders. Do not prescribe topical anesthetics for take-home use.
• NSAID eye drops are effective for pain relief, but long-term use may cause corneal melting; therefore, limit use to a short period (3–5 days).

Expected course of treatment

• Mild (SPK only): epithelial recovery in 12–24 hours
• Moderate (widespread SPK, corneal erosion): spontaneous healing in 24–48 hours
• Severe (deep corneal erosion): may take 48–72 hours. However, serious visual impairment is rare.

Q Does ultraviolet keratitis heal without treatment?

A

Usually, the corneal epithelium regenerates and heals naturally within 24–48 hours. However, leaving it untreated is not advisable. Antibiotic eye drops should be administered due to the risk of secondary infection (bacterial keratitis). Also, pain is often very severe, and symptomatic treatment with NSAID eye drops or therapeutic soft contact lenses is important to alleviate patient discomfort.

Prevention

To prevent recurrence and manage occupational/recreational risks, provide the following guidance:

• Welding work: Always wear appropriate protective masks or goggles with proper shade (shade number 10–14).
• Skiing and high-altitude activities: Wear UV400-compliant goggles or sunglasses. Reflected UVB is particularly strong on sunny days with fresh snow.
• Germicidal lamps: Always leave the room while the lamp is in use. Use of a timer is recommended.

6. Pathophysiology and Detailed Mechanisms

Ultraviolet-Induced Cell Damage

Ultraviolet radiation is directly absorbed by nucleic acids and aromatic amino acids in living organisms, causing damage by denaturing genes (DNA) and proteins. The main mechanisms of injury in corneal epithelial cells are as follows:

• DNA damage: UVB and UVC are absorbed by DNA in corneal epithelial cells, forming photoproducts such as thymine dimers (cyclobutane pyrimidine dimers). This damage impairs DNA replication and transcription, inducing cell death.
• Protein denaturation: Aromatic amino acids (tyrosine, phenylalanine, etc.) absorb ultraviolet light, causing denaturation of protein three-dimensional structures. This leads to loss of enzyme and structural protein function.
• Reactive oxygen species (ROS) production: Ultraviolet light indirectly produces ROS, causing lipid peroxidation, protein oxidation, and oxidative DNA damage.

Mechanism of the Latent Period

The latent period of 30 minutes to 24 hours from UV exposure to symptom onset occurs through the following sequence:

1. UV exposure → initiation of DNA damage and protein denaturation
2. Damaged corneal epithelial cells undergo shedding and apoptosis
3. Cell degeneration products induce release of inflammatory mediators (prostaglandins, cytokines, etc.)
4. Activation of inflammatory cascade → symptom manifestation as pain, redness, edema, and blepharospasm

This time delay appears as the latent period. The more advanced the cell degeneration, the more extensive the inflammatory response.

Tissue absorption sites for each wavelength band

• UVC (100–280 nm): Almost entirely absorbed by the corneal epithelium. It is the most harmful to the anterior segment and is the main cause of electric ophthalmia.
• UVB (280–315 nm): Partially penetrates the cornea and reaches the lens. Acute damage includes snow blindness and corneal injury. Long-term chronic exposure increases the risk of cataracts.
• UVA (315–400 nm): Easily reaches the interior of the eye. Acute corneal damage is relatively rare, but long-term effects on the lens and retina are possible.

Pathological changes in the cornea

1. UVB/UVC exposure → DNA damage and protein denaturation in corneal epithelial cells
2. Cell shedding → Corneal epithelial defect. Widespread SPK (superficial punctate keratopathy).
3. SPK progression → Corneal erosion (disruption of epithelial continuity).
4. Inflammatory cascade → Pain, hyperemia, edema, blepharospasm.
5. Spontaneous repair → Regeneration by corneal epithelial stem cells (limbal stem cells) within 24–48 hours.

The corneal epithelium has a high regenerative capacity, and complete repair can be expected within 1–2 days if there is no secondary infection.

Delayed damage from chronic exposure

Repeated ultraviolet exposure not only causes acute keratitis but also increases the risk of the following chronic diseases.

• Cataract: Due to oxidative denaturation of lens proteins (mainly crystallins). UVB is considered the main cause.
• Pterygium: A degenerative disease in which conjunctival tissue invades the cornea from the limbus. Ultraviolet exposure is a major risk factor.
• Pinguecula: A white to yellow nodule on the bulbar conjunctiva near the corneal limbus. Ultraviolet exposure and dryness are triggers.
• Squamous metaplasia and squamous cell carcinoma: Malignant changes in the conjunctival and corneal epithelium. Long-term ultraviolet exposure is involved.

7. Latest Research and Future Perspectives

For patients: Please read this

The following content is currently under research or in clinical trials and is not standard treatment available at general hospitals. It is reference information for professionals regarding future medical developments.

New exposure risks from household UV-C disinfection products

In recent years, triggered by the COVID-19 pandemic, household UV-C disinfection lamps and devices have rapidly become widespread. As UV-C light sources designed for medical and professional use enter general households, cases of accidental eye exposure by users without proper knowledge are increasing. In an observational study in Suzhou, China, ultraviolet keratitis cases surged from 31 before the pandemic (October–December 2019) to 109 after (February–April 2020), and the cause dramatically shifted from welding (68%) to improper use of germicidal lamps (57%)⁴. In addition to traditional occupational exposure (e.g., welding), household accidents now account for a non-negligible proportion of causes of electric ophthalmia.

Expansion of industrial use of UV-C LEDs

Replacing conventional mercury lamp UV-C light sources, UV-C LEDs (wavelength around 260–280 nm) are rapidly expanding in industrial use. While applications in water sterilization, air sterilization, and surface sterilization are advancing, UV-C LEDs are small, lightweight, and easy to install, raising concerns about eye injury risks due to use in inappropriate environments.

Assessment of carcinogenic risk from repeated exposure

Research continues on the association between ultraviolet radiation and squamous cell carcinoma of the cornea and conjunctival epithelium (OSSN: Ocular Surface Squamous Neoplasia). Long-term UV exposure, especially in occupations with high outdoor activity (e.g., agriculture, construction, welding), is thought to increase the incidence of ocular surface tumors, reaffirming the importance of regular eye examinations and light-shielding measures.

Development of corneal protective materials

Development of new light-shielding protective equipment and transparent film materials for ophthalmic protection in UV-C disinfection facilities is underway. Additionally, research is being conducted on the potential UV-protective effect of UV-absorbing contact lens materials for regular soft contact lens wearers.

8. References

Footnotes

1. Willmann G. Ultraviolet Keratitis: From the Pathophysiological Basis to Prevention and Clinical Management. High Alt Med Biol. 2015;16(4):277-282. doi:10.1089/ham.2015.0109. PMID: 26680683. https://pubmed.ncbi.nlm.nih.gov/26680683/ ↩ ↩² ↩³

2. McIntosh SE, Guercio B, Tabin GC, Leemon D, Schimelpfenig T. Ultraviolet keratitis among mountaineers and outdoor recreationalists. Wilderness Environ Med. 2011;22(2):144-147. doi:10.1016/j.wem.2011.01.002. PMID: 21396859. https://pubmed.ncbi.nlm.nih.gov/21396859/ ↩ ↩² ↩³

3. Kwon DH, Moon JD, Park WJ, et al. Case series of keratitis in poultry abattoir workers induced by exposure to the ultraviolet disinfection lamp. Ann Occup Environ Med. 2016;28:3. doi:10.1186/s40557-015-0087-7. PMID: 26779342. https://pubmed.ncbi.nlm.nih.gov/26779342/ ↩

4. Wang Y, Lou J, Ji Y, Wang Z. Increased photokeratitis during the coronavirus disease 2019 pandemic: Clinical and epidemiological features and preventive measures. Medicine (Baltimore). 2021;100(24):e26343. doi:10.1097/MD.0000000000026343. PMID: 34128883. https://pubmed.ncbi.nlm.nih.gov/34128883/ ↩ ↩²

5. Izadi M, Jonaidi-Jafari N, Pourazizi M, Alemzadeh-Ansari MH, Hoseinpourfard MJ. Photokeratitis induced by ultraviolet radiation in travelers: A major health problem. J Postgrad Med. 2018;64(1):40-46. doi:10.4103/jpgm.JPGM_52_17. PMID: 29067921. https://pubmed.ncbi.nlm.nih.gov/29067921/ ↩