Tutorial
Introduction
Natural Protection from Light Toxicity
Clinical Manifestations of Disease
Summary
References
Corneal and External Disease from Light Injury
P. Kumar Rao, MD · Justis P. Ehlers, BS
Although ocular exposure to light is an obvious necessity for sight, it has been implicated as a causative element in a host of disorders of the human eye, involving structures including the cornea and ocular surface, crystalline lens, and retina. The cornea, conjunctiva, and ocular adnexa are at high risk because they are directly exposed to incident light that has not been modified in any of its physical characteristics. Although several factors combine to reduce that exposure (see Natural Protection section), a number of corneal and external disease entities are associated with light toxicity: photokeratoconjunctivitis, climatic droplet keratopathy, pterygium, pingueculum, and ocular or adnexal tumors such as basal cell carcinoma and squamous metaplasia/carcinoma.1,2
Natural Protection from Light Toxicity
The human body is equipped with several mechanisms that seem designed to avoid injury from excessive light exposure. These mechanisms include squinting, shading from eyebrows and head positioning, and natural aversion to harmful levels of visible light. For example, squinting effectively shields a significant portion of the ocular surface, reducing the area of cornea and conjunctiva at risk. Additionally, there is an "inherent geometry" to the exposure to natural light, which when combined with the human facial physiognomy and body habitus, results in valuable protection from harm. The most damaging wavelengths from the sun including ultraviolet (UV) and blue visible light are nearly 10 times greater in intensity at noon than a few hours before or after. But at noon, the sun is "directly overhead," which decreases the chances of ocular exposure to these rays. Instead, the eye may be shaded by the brow or by slight reflexive downward tilting of the face. The rays also may be reflected rather the absorbed due to the high angle of incidence on the ocular surface. As the day progresses, the natural scattering of light by the atmosphere reduces the intensity, creating another protective mechanism. Near sunset, for example, though the sun is at a low angle producing a greater chance of direct ocular exposure, the earth's atmosphere scatters most of the UV and blue light, thereby significantly increasing the exposure time required to cause toxicity. The scatter also produces the red appearance at sunset, which is an additional, esthetic benefit.
Natural protection fails when the incident light rays become parallel to the visual axis. This eliminates the possibility of reflecting the harmful rays and greatly increases the absorption and potential for injury. Obviously, staring at the sun is the most dangerous example of such a change in the geometry of light exposure, but reflected light from water or snow (especially the latter) can produce a similarly risky scenario. In fact, a field of fresh snow can reflect more than 80% of the harmful UV and blue wavelengths compared with the 1% reflection from a grassy field in summertime. Special care to protect from ocular injury must be taken by people who place themselves in high-risk environments either for occupational or recreational purposes.1
Clinical Manifestations of Disease
Photokeratoconjunctivitis
Photokeratoconjunctivitis is also known as "welder's flash burn" or "snow blindness." It typically results from exposure to UV light, particularly below 315 nm.1 The clinical features include rapid, though not immediate, onset; significant pain; and decreased visual acuity. The symptoms most often develop 6-12 hours after exposure to the UV light. The exact reason for this is unclear, although it has been proposed that it may be due to decreased sensitivity of the cornea immediately following exposure.2,3 Others postulate that the epithelial sloughing starts after a few hours, resulting in exposure of corneal nerve endings and the onset of pain. Patients most commonly seen with this disorder are welders and tanning enthusiasts, although it may be seen in any person with the appropriate exposure, including "innocent bystanders" who are within approximately 12 feet of welders.
On examination, the initial signs will usually be bilateral and include superficial punctuate keratopathy, conjunctival chemosis, blepharospasm, and epiphora. In severe cases, total desquamation of the corneal epithelium may occur. Treatment includes topical antibiotic drops or ointment and oral analgesics. Topical anti-inflammatory drops, either steroids or nonsteroidal anti-inflammatory drugs (NSAIDs) can also be added. Resolution tends to be fast, with reepithelialization complete between 36 and 72 hours after injury in most patients. Typically there are no long-term complications.2
The mechanisms of this injury are likely photochemical and not thermal. The wavelength that most frequently causes photokeratoconjunctivitis is 270 nm, which is a wavelength well absorbed by ozone in the atmosphere. Thus, the most common causes are artificial light sources, such as a welding arc or skin tanning lamps. Similar injuries can be seen resulting from natural light exposures, particularly in situations that increase the intensity of the 270-nm wavelength. These would include areas where the ozone has been depleted, high altitudes where there is less atmospheric filtering, snow fields, and during solar eclipses. 2
Damage occurs in all levels of the corneal tissue. The epithelium shows nuclear fragmentation, decreased mitotic activity, and loosening of the epithelial cells. A rabbit model for photokeratoconjunctivitis has shown reversible damage to the keratocytes of the stroma.2,4 A study of welders also demonstrated increased pleomorphism in the cells of the endothelium. No clearly defined functional or visual deficit was associated with the endothelial changes.2,5
Chronic Solar Toxicity
Chronic exposure to visible and ultraviolet light has been implicated as a possible causative element in the development of several ocular disease entities. The injury in these conditions results from extended exposure to solar rays, in contrast to the acute exposure and time course of photokeratoconjunctivitis. Chronic solar exposure include climatic droplet keratopathy, pterygium, pingueculum, and ocular or adnexal tumors such as basal cell carcinoma and squamous metaplasia/carcinoma are associated with chronic solar exposure.2
Climatic droplet keratopathy (CDK), also known as Labrador keratopathy, has a broad clinical presentation, with symptoms ranging from none at all to functional blindness. On examination, small gray "droplets" are observed in the superficial cornea, at the level of Bowman's membrane. If these droplets are small and scattered, there may be only minimal, if any, effect on vision. However, if these droplets are extensive in nature, they may produce light scatter and reduced acuity. Subepithelial scarring may develop and may lead to visual loss and even blindness if the scarring is axial. CDK is seen in its most severe forms in locales with extreme climatic conditions, such as the higher latitudes, and when the cornea is exposed. A predominance of CDK is seen in men2; however, whether higher risk in men is a result of genetic predisposition or socioeconomic factors has not been determined.
The mechanism of injury in CDK is believed to be related to exposure to short wavelength light, including UVA and UVB. Studies have shown a significant association between chronic sun exposure and CDK. Additionally, a dose response association between duration of exposure and CDK has been demonstrated.2,6
Statistically significant evidence exists of the linkage between chronic ultraviolet light exposure and development of squamous cell carcinoma and basal cell carcinoma of the skin, including the eyelids. Most ophthalmologists also believe that chronic exposure to sunlight leads to ocular surface squamous metaplasia/carcinoma, but to date, the data are not compelling. Logistic regression analysis in one study failed to find a significant association between exposure and squamous metaplasia or carcinoma. On the other hand, the analysis showed definitive linkage between UV light exposure and the development of pterygium, CDK, and pingueculum.2
Endothelium
Clinically observed changes in the corneal endothelium have not been clearly implicated as being a result of light injury. However, experimental evidence has raised the possibility of endothelial involvement, particularly in cases that involve photosensitizing compounds. For example, in vitro studies have shown functional effects from chlorpromazine and light exposure, but this has yet to be observed in humans.
Also, protoporphyrin IX has been shown in rabbits to be photosensitizing and lead to endothelial damage. This phenomenon has not yet been shown to occur in humans, but may be relevant in cases of hyphema.2
Light has the potential to damage the cornea, ocular surface, and adnexa. It is undoubtedly not by chance that the inherent mechanisms of the design of the human body and its methods of interacting with the surrounding environment provide sufficient protection from natural light sources in most situations. However, when under certain high-exposure conditions, such as fresh snow or high altitude, extra precaution should be taken to protect the ocular surface from excessive radiation. A considerable amount of research on light toxicity and its role in corneal and external diseases must be done, but enough evidence of its causative effects in certain entities such as photokeratoconjunctivitis, climatic droplet keratopathy and pterygium already exists. As research continues, it is likely that excessive light exposure will be an important element in other diseases of the ocular surface and other components of the eye, such as the lens and retina.
- Sliney D. Ocular injury due to light toxicity. Int Ophthalmol Clin. 1988;23(3):246-250.
- Schein O. Phototoxicity and the cornea. JAMA. 1992;l84(7): 579-583.
- Millodot M, Earlam R. Sensitivity of the cornea after exposure to ultraviolet light. Ophthalmic Research. 1984;16(6):325-328.
- Ringvold A and Davanger M. Changes in the rabbit corneal stroma caused by UV-radiation. Acta Ophthalmologica. 1985;63(5):601-606.
- Karai I, Matsumura S, Takise S, Horguchi S, Matsuda M. Morphological change in the corneal endothelium due to ultraviolet radiation in welders. Br J Ophthalmol. 1984;68(8):544- 548.
- Taylor H, West S, Rosenthal F, Munoz B, Newland H, Emmet E. Corneal changes associated with chronic UV irradiation. Arch Ophthalmol. 1989;107(10):1481-1484.