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Chapter 6 – Light Damage to the Eye

Chapter 6 – Light Damage to the Eye

DAVID MILLER
CLIFFORD A. SCOTT

DEFINITION
• Structural or functional damage to the external or internal eye from thermal or photochemical effects of the absorption of light.

KEY FEATURES
• With age, many of the photoprotective mechanisms of the eye degrade.
• Cataract development and the risk of macular degeneration are accelerated by cumulative or excessive exposure to UV radiation.

ASSOCIATED FEATURES
• Reduction of environmental exposure and the use of absorptive lenses diminish the risk of light damage to the eye.
• Intake of antioxidant foods or dietary supplements may slow the development of cataracts and macular degeneration.

ULTRAVIOLET FILTRATION
The oxygen holocaust, a term invented by Margulis and Sagan,[1] describes that period in the evolution of life on Earth when the atmospheric oxygen content rose from 0.0001% to 21%. The source of such an atmospheric change was the evolution of photosynthesis by ancient green and purple bacteria, which seems to have started about 2 billion years ago. Of course, the change in environment destroyed most of the anaerobic microbes on Earth. Newly evolved resistant bacteria multiplied and ultimately developed the reactions of aerobic metabolism that prevail in life today.
A secondary effect of this “newly formed oxygen” was that as it rose into the upper reaches of the Earth’s atmosphere, it reacted with incoming ultraviolet (UV) light from the sun and formed the ozone layer near the top of the atmosphere, about 30 miles (48.3?km) up. The ozone layer is important in two ways[2] ( Fig. 6-1 ). First, it helps to stabilize the atmospheric oxygen level at 21% (excess oxygen is used to make more ozone); it has been suggested that many living organisms would not tolerate levels of atmospheric oxygen a few percent higher than 21%. However, it is the second effect of the ozone layer that is discussed in this chapter.
The ozone layer, only about 2–3?mm in thickness, is produced in the stratosphere by a photochemical reaction fueled by UV-C radiation and/or lightning and spread by the stratospheric winds. This is ironic, because the ozone layer then filters out most of the potentially destructive UV light that arrives from the sun. Research that started in 1980 noted a 3–6% per decade decay in the ozone layer, notably in the Northern Hemisphere. This depletion of the ozone layer, thought to be caused by chlorine from industrial pollutants, leads to an approximate 1% increase in UV-B radiation that reaches the Earth’s surface for every 1% reduction in ozone.[3]

Figure 6-1 Spectral composition of sunlight. Before reaching ozone layer and after passing through the ozone layer. (Adapted from MacCracken M, Change J. Preliminary study of the potential chemical and climate effects of atmospheric nuclear explosion. UCRL 51653. San Francisco: Lawrence Livermore Laboratory, 1975 April 25:48.)
Ultraviolet Profile
Of all the light energy that rains down on Earth, <10% may be considered to be UV radiation in the range 280–400?nm.[4] The UV spectrum has been subdivided into the following categories:
• UV-A, 400–320?nm (90% of UV radiation from the sun)
• UV-B, 320–280?nm
• UV-C, 280?nm and below
Although UV radiation with this profile has fallen on Earth from the time the ozone layer was established, forms of life still remain that can be damaged by UV radiation. Of course, the specific wavelength and dosage determine the specific organism's response. Thus bacteria may survive under the fluorescent light of the operating room (which has very small amounts of UV) but are destroyed by germicidal lamps (high amounts of short-wavelength UV radiation). Planck's equation states that the energy content (eV) of radiation of a certain wavelength is 1240/wavelength (nm). Normal human skin maintains health under average light conditions but can experience sunburn that is damage caused by prolonged exposure to high doses of UV radiation.
ULTRAVIOLET VULNERABILITY
UV radiation can be potentially damaging if a certain balance is upset. Groups vulnerable to ocular UV radiation damage are discussed in this chapter.

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Figure 6-2 Increasing yellow to brown coloration in human lenses. A, 6 months. B, 8 years. C, 12 years. D, 25 years. E, 47 years. F, 60 years. (Reproduced with permission from Lerman S. Phototoxicity: clinical considerations. Focal Points. San Francisco: American Academy of Ophthalmology. 1987;1–22.)
Older Individuals
Light damage to tissue ultimately depends on a series of photochemical reactions. The body, in turn, has a series of protective molecules that either filter out the harmful wavelengths or scavenge the harmful photometabolites. With increased age, it has been suggested that the concentration of some of these protective molecules decreases. As discussed later, age-related macular degeneration and cataract formation may be related to a combination of cumulative light exposure and a coincident decrease in protective biochemicals.
Lightly Pigmented Individuals
Studies have shown that patients whose irises are blue (lighter-pigmented eyes) have a significantly higher incidence of age-related macular degeneration than a control series of patients who have brown irises.[5] Also, age-related macular degeneration is almost unknown in the black African patient.
Aphakia
Results from the Framingham study suggested that nuclear sclerosis in the elderly protects the retina from age-related degeneration.[6] Lerman[7] [8] has shown that the aging crystalline lens is an efficient filter against UV radiation and blue light ( Fig. 6-2 ). Ham et al.[9] may have brought together the above information when they were able to produce retinal injury in aphakic monkeys using short-wavelength visible light.
Use of Photosensitizing Drugs
Chemical compounds with multiple cyclic rings ( Fig. 6-3 ) that contain alternating double bonds are often photosensitizing agents. These agents are able to absorb UV radiation and short-wavelength visible light and then generate free radicals, which damage tissue. Compounds that fall into this group include phenothiazines, 8-methoxypsoralen (used in that treatment of psoriasis), allopurinol, tetracyclines, and hematoporphyrins used for phototherapy. When these compounds deposit in the lens or retina, the tissues become more vulnerable to light damage.
Outer Segment Turnover
It appears that nature copes with the anticipated light damage to the discs that contain photopigment through the daily retinal pigment epithelium digestion of a portion of the outer segment. If a malfunction occurs in this digestive system as a result of genetics, malnutrition, or injury, then a buildup of photoreceptor disc metabolites results. Such a buildup may be related to drusen deposition and clinical age-related macular degeneration. Thus, some form of faulty, radiation-damage defensive system may be partially responsible for age-related macular degeneration. [10]
BIOCHEMICAL MECHANISM OF UV RADIATION DAMAGE
For photodamage to occur, tissue must contain a molecule that absorbs light. Tissue damage may occur in two ways: molecular fragmentation and free radical generation.
Molecular Fragmentation
Proteins, enzymes, and nucleic acids contain alternating double bonds. Such molecular configurations efficiently resonate with radiation of UV wavelength. An analogy is that of opera singers who break wineglasses by striking certain notes; they tap the glass to establish its resonating frequency and sing loudly in that frequency. The resonating frequency may be thought of as fitting snugly into the glass structure. The increased intensity of UV radiation, like a dynamite charge placed snugly in a rock crevice, breaks the molecular bonds. The new molecules may induce inflammation or neoplasm, or affect the immune system.

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Figure 6-3 Molecular configurations of photosensitizing drugs.
Free Radical Generation
Pigmented molecules absorb visible light and UV radiation of a specific wavelength. This photon absorption ultimately changes the energy level to the unstable triplet state. The molecule then ejects an electron, which usually combines with a neighboring molecule (often oxygen in cases of photodamage). When an oxygen molecule gains an extra electron, it is known as superoxide, one of a family of compounds called free radicals. These are, in truth, super oxidizers. Free radicals may disrupt cell membranes, mitochondrial membranes, and nucleic acids; depolymerize collagen and hyaluronic acid; and destroy tissue.
Free radical light damage to tissue requires three components. A light-absorbing molecule (dye, pigment), oxygen, and short-wavelength radiation. Fortunately, specialized molecules occur in the body to disarm any newly arrived free radical. These scavenger molecules (of which many exist) include the ubiquitous superoxide dismutase, vitamin C, vitamin E, glutathione peroxidase, and carotene. A shortage of these scavengers in the very young (premature infants), the old, or the nutritionally impaired can tip the balance toward greater vulnerability to light damage.
CLINICAL EXAMPLES OF OCULAR LIGHT DAMAGE
Lids
Caucasian skin, including eyelid skin, is subject to a multitude of changes induced by UV radiation.[11] The simple but annoying acute sunburn reaction falls at one end of the spectrum and is essentially a UV-B–induced response. Clouds do not filter out UV radiation and therefore do not prevent sunburn. Since UV radiation is reflected off sand and water, beach umbrellas do not provide full protection from UV damage.
The middle of the spectrum of common skin conditions induced by UV radiation includes epidermal keratoses, age spots, skin dryness, wrinkling, sebaceous hyperplasia, and comedones. On the far side of the spectrum of UV-B–induced damage are the malignant skin changes, which include basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Each of these conditions has an impressive statistical association with UV radiation.[12]
Cornea
UV damage to the cornea is both wavelength and intensity dependent. [13] For example, the most effective range of damaging wavelengths is 260–290?nm, [14] but as a result of absorption by the ozone layer, radiation of these wavelengths rarely penetrates to the Earth's surface. The source of most superficial punctate keratitis is human produced, such as welding flashes, germicidal lamps, and sun lamps. At 270?nm, only 0.005?mJ/cm2 of energy produces a lesion; at 300?nm, about 0.01?mJ/cm2 produces a lesion; and at 320?nm, 10.5?mJ/cm2 (2000 times above the lowest threshold) does so. Thus, for short wavelengths, a very small amount of UV energy may produce a corneal lesion.[15] From a basic science viewpoint, the nucleic acids of the corneal epithelium maximally absorb these wavelengths, as do certain amino acids such as tryptophan. However, the clinician must not forget that the longer wavelength UV-B (320–400?nm) also may produce corneal lesions, if the exposure is long enough. Snow blindness is a result of prolonged exposure to UV-B radiation reflected from the snow; fresh snow can reflect as much as 85% of the incident UV radiation.[16]
Clinically, superficial punctate keratitis appears about 8–12 hours after exposure. Pain probably arrives when the damaged epithelial cells desquamate, which produces the characteristic punctate fluorescein staining.
Chronic exposure to UV radiation is said to produce spheroidal degeneration of the cornea (Labrador keratitis and climatic droplet keratopathy). The incidence of this condition in the Eskimo population is about 14%.[17] Epidemiological evidence also suggests that chronic exposure to UV radiation produces or is associated with pterygium.[18]
Lens
The chemical components of the crystalline lens are particularly vulnerable to different parts of the electromagnetic spectrum. For example, short wavelength ionizing radiation is cataractogenic. The mechanism is probably a combination of the creation of overwhelming numbers of damaging free radicals, as well as molecular bond breakage.[19]
A number of important epidemiological studies show a connection between environmental levels of UV radiation and a higher incidence of cataract (primarily cortical cataract) formation. [20] [21] [22] [23] [24] Basic biochemical research has given further insight into the mechanism behind these changes. For example, lens exposure to UV-A and UV-B radiation results in lens enzyme changes. Specifically, exposure of rat lenses to 5?mW/cm2 of UV radiation (wavelength, 360?nm) almost totally destroys Na+ /K+ -adenosine triphosphatase activity in less than 24 hours. The lens of the gray squirrel is a favorite model because its yellow color is similar to that of the aging human lens. Exposure of such lenses to 1.5–2?mW/cm2 UV radiation (wavelength, 365?nm) produces

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TABLE 6-1 — ONSET OF PRESBYOPIA IN DIFFERENT REGIONS
Age (years)
Place
Latitude (°)
Author
Year Published
47
England
51–54
Ayrshire
1964
43
England
51–54
Turner
1958
45
New York
41–45
Duane
1912
50
Cleveland
38–42
Allen
1961
45
Japan
36–44
Kajiura
1965
43
Japan
36–44
Fukuda
1965
42
Japan
36–44
Ishihara
1919
43
California
32–42
Hamasaki
1956
45
Texas
26–36
Fitch
1971
41
Israel
32
Raphael
1961
40
South Africa
26–29
Coates
1955
37
India
10–30
Rambo
1960
39
Puerto Rico
18–18.5
Miranda
1977
(From Jacques PF, Chylak LT Jr, Hankinson SE, et al. Long-term nutrient intake and early age-related nuclear lens opacities. Arch Ophthalmol. 2001 Jul;119[7]:1009–19.)

significant aggregation of insoluble lens proteins. These large protein aggregates of insoluble lens proteins are responsible for the increased light scatter seen in the aging human lens and in human cataracts.[25] The mechanism for these changes is related to the formation of singlet oxygen by the radiation. Specifically, Goosey et al. showed that an inhibitor of singlet oxygen formation (sodium azide) completely prevented protein aggregation in the presence of UV radiation.[26] However, whereas high doses of antioxidant nutrient supplementation does not appear to affect the development or progression of cataracts, dietary intake of antioxidant foods is associated with a lower prevalence of nuclear lens opacities.[27] [28]
Infrared (IR) radiation also has an effect on the lens. The higher frequency (lower wavelengths) of IR radiation closely matches the resonant frequency of water molecules. The development of glassblower's cataract has long been recognized as a clinical example of this relationship, in which lens water absorbs the radiation from the IR source and literally cooks the proteins that surround the lens.
Finally, it is important to mention the relationship between age of onset of presbyopia and geographic latitude ( Table 6-1 ). Note that presbyopia occurs 5 years earlier in the tropics than in northern climates. Increased solar radiation has been suggested as the cause. In particular, the IR rather than the UV portion of the solar spectrum has been implicated because in a specific latitude the onset of presbyopia is earlier in coastal regions (less UV radiation) than in mountain regions.[29]
Retina
There is no doubt that prolonged illumination from the indirect ophthalmoscope, the operating microscope, or the sun can produce a level of light equivalent to the noonday sun at equinox and 40° latitude, which measures 12,800 foot candles (137,700 lux). Light measurements from different operating microscopes are in the range 5,120–28,160 foot candles (55,090–303,000 lux) at the surface of the patient's eye. Clearly, such intensity directed on a dilated pupil for a prolonged period may produce maculopathy. [30] [31] [32] Illumination from the indirect ophthalmoscope with a focusing lens may produce a focal energy on the retina equivalent to that produced by the sun.[33] It is not clear which specific wavelengths that emanate from these instruments produce the damage. This damage may result from a combination of wavelengths, since photochemical damage from short wavelengths is enhanced by an increase in the retinal temperature of 3–4°C.[9]
Age-related macular degeneration has been suggested as a manifestation of light toxicity.[9] Experimental visible wavelengths (primarily blue light) can produce retinal damage to the monkey retina,[9] but these experimental lesions do not resemble age-related macular degeneration in humans in terms of clinical appearance. Bleached visual pigments (which become waste products [i.e., lipofuscin] and may have photocytotoxic effects in the retinal pigment epithelium[34] ) maximally absorb blue and UV-A.[35] Enhanced choroidal pigmentation seems to protect against this degeneration.[36] To complicate matters further, epidemiological studies of age-related macular degeneration in the elderly are difficult to evaluate when cataract is present, since a cataract may filter out light harmful to the retina.
However, it is not known if the increased melanin works its protective effect as a light filter or as a metabolic agent. It seems as if any condition in which bleached visual pigments build up in the retina may promote light damage. The increased choroidal melanin in the African black patient may simply prevent the light reflected off the sclera from striking the vulnerable pigments on a second pass. With so many unanswered questions, further research is required in this area.
Finally, it seems appropriate to address the role of light toxicity in the causation of retinopathy of prematurity (see Chapter 116 , Retinopathy of Prematurity). Certainly, strong evidence associates the use of oxygen therapy with the early development of the disease in the premature infant.[9] As noted above, the combination of oxygen, light, and the appropriate pigmented molecules may incubate damaging free radicals. Therefore light may enhance the damaging potential of oxygen. Interestingly, fluorescent lights were introduced into nurseries at about the same time as oxygen therapy for premature infants. The production of a high concentration of free radicals in an immature retina (perhaps devoid of protective agents [i.e., free radical scavengers]) may lead to the disease. One experimental study seems to support the hypothesis that light damage is involved in retinopathy of prematurity. [37] Again, further research is needed in this area.
In summary, the human eye is quite resistant to light damage. However, age, pigmentation, nutritional status, drugs taken, and genetic and biochemical makeup can make some patients more vulnerable to light damage.[38] [39]
LIGHT PROTECTION
During Surgery
As noted earlier, light from the operating microscope has been shown to produce maculopathy during a prolonged cataract extraction (with or without an implant). [29] [30] [31] [32] Thus a number of methods have been suggested to reduce the concentration of light that strikes the retina during surgery. For example, light can

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TABLE 6-2 — COMMONLY PRESCRIBED LENS TINTS
Lens Tint
Visible Light Transmission (%)
Uses
UV absorbing clear
90
Absorbs almost all UV up to 385?nm
Amber
90
Enhances low light contrast
Light gray
35
Outdoor glare reduction

Uniform color transmission
Standard gray sunglass
15
Uniform color transmission
Mirrored lenses (reflect rather than absorb light)
15
Uniform color transmission

No optical advantage
Dark green
2
Shade 5 Welding goggles

be blocked by a small occluder disc placed on the cornea, directly over the pupil. A bubble of air may also be placed in the anterior chamber, which (optically speaking) neutralizes the corneal focusing power. However, the bubble also enhances the refractive power of the anterior surface of the intraocular lens. The combined neutralization and enhancement effects of the bubble substantially defocus the light that strikes the retina. Certain operating microscopes are equipped with an occluder disc that may be placed in the center of the path of the light that strikes the eye. This system produces an annulus of light with a dark center, which is incident upon the cornea. The most effective protective measure against maculopathy induced by operation light is to shorten the time of surgery.
Ultraviolet Filters in Intraocular Lenses
Currently, most intraocular lens manufacturers produce implants with UV filters. In general, these implants filter out all wavelengths of light <400?nm, which not only protects the plastic of the implant from UV degradation, but appears to prevent decreases in visual function such as color vision and contrast sensitivity. [16] [40]
Absorptive Lenses
In certain high-illumination situations, sunglasses allow better visual function in a number of ways ( Table 6-2 ).
Improvement of Contrast Sensitivity
On a bright sunny day, illuminance from the sun is in the range 10,000–30,000 foot lamberts (34,260–103,000?cd/m2 ). These high light levels tend to saturate the retina and therefore decrease finer levels of contrast sensitivity. The major function of a dark sunglass is to return the retina to a level of maximal contrast sensitivity (i.e., eliminate the “increased noise” of the retina).[41] Most dark sunglasses absorb 70–80% of the incident light of all wavelengths. (Light levels are often described in log[10] units [i.e., 1, 2, 3 or -1, -2, -3; a log10 value of -1 reduces the light level by 90% and is equivalent to a sunglass that absorbs 90% of the incident light; a lens that absorbs 70% is equivalent to a log10 value of -0.84.)
Improvement of Dark Adaptation
Experiments have shown that a full sunny day at the beach (without dark sunglasses) may impair dark adaptation for over 2 days. Thus dark sunglasses (absorption of 70–80% of incident light) are recommended for prolonged periods in bright sun.[42]
Reduction of Glare Sensitivity
A number of sunglass modalities may reduce glare sensitivity. Polaroid sunglasses reduce the intensity of reflected light from

Figure 6-4 The darkening and fading of four popular photochromic lenses. Note that most darken maximally by 2–3 minutes and fade in 5 minutes. (Modified with permission from Young JM. Photochromics: past and present. Opt World. 1993;Feb.)
road surfaces, glass windows, lake and river surfaces, and metal surfaces. Thus dazzle and glare sources are reduced in intensity. Since light reflected from a horizontal surface produces light polarized in the horizontal plane, properly oriented Polaroid sunglasses may eliminate this component. For many activities, such as fishing or driving, reduction in surface glare improves overall visual comfort. However, polarized lenses eliminate the clue of reflection to a pilot scanning the skies for other aircraft. Graded density sunglasses are tinted deeply at the top and gradually become light toward the lens center. They effectively remove dazzle from glare sources above the line of sight (e.g., the sun). Wide temple sunglasses reduce glare from sources at the side.[41]
Improvement of Color Contrast
Orange sunglasses efficiently absorb wavelengths in the purple through blue-green range. All these colors appear as different forms of dark gray to the wearer. On the other hand, the wearer clearly sees the spectrum from green through yellow to orange to red. Colors appear slightly unreal, but color contrast improves. Patients who have conditions such as cataracts or corneal edema, for whom color contrast sensitivity has decreased, report improvements in color contrast using these sunglasses.[43]
Use of Photochromic Lenses
Photochromic lenses are either glass or plastic. When short-wavelength light (300–400?nm or longer) interacts with glass photochromic lenses, they darken ( Fig. 6-4 ). The chemical

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Figure 6-5 Absorption spectra for crown glass, CR-39, CR-39+, and polycarbonate lenses.
reaction (i.e., the conversion of silver ions into elemental silver) is similar to the reaction that occurs when photographic film is exposed to light. In contrast to the chemical reaction in film sensitive to radiation of these wavelengths, that in photochromic lenses is reversible. With continued exposure to radiation of short wavelengths, the lens continually darkens to absorb about 80% of the incident light, and then lightens when the illumination falls to absorb about 20% of the incident light. These lenses take longer to lighten than to darken, but when darkened they are also excellent ultraviolet absorbers.[44] Plastic photochromic lenses are coated with an organic molecule from the generic molecular group indolinospironaphthoxazine, which changes shape and consequently light-absorptive properties when illuminated.
Ultraviolet Absorbing Lenses
Almost all dark sunglasses absorb most of the incident ultraviolet radiation, which is also true for certain coated, clear-glass lenses and the clear plastic lenses made of CR-39 (a commonly used clear plastic with a special coating) or polycarbonate. A study of the transmission spectra for nine inexpensive clip-on sunglasses showed that all but the blue-colored clip-ons remove over 90% of the UV.[45] Figure 6-5 shows the absorption curve for clear glass, CR-39, and clear polycarbonate.
It has been suggested that certain sunglasses, ironically, may produce light damage to the eye. The argument contends that the pupil dilates behind dark glasses. Thus sunglasses that do not absorb significant amounts of UV radiation actually allow more of it to enter the eye than when no sunglass is worn. Figure 6-6 shows that the pupil enlarges most under scotopic conditions. On a bright sunny day, irradiance is in the range 10,000–30,000 foot lamberts (34,260–103,000?cd/m2 ) and the pupil constricts maximally. A dark sunglass (one that absorbs 80% of the incident light) reduces the level of light that strikes the eye to the range 2000–6000 foot lamberts (6,850–20,600?cd/m2 ). Such levels are about ten times higher than those of an averagely lit room. At such light levels, the pupil is still constricted significantly.

Figure 6-6 Relationship between pupillary diameter and ambient level of illumination. (Modified with permission from Reeves P. Response of the average pupil to various intensities of light. J Opt Soc Am. 1970;4:135–9.)

REFERENCES

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2. MacCracken M, Change J. Preliminary study of the potential chemical and climatic effects of atmospheric nuclear explosion. UCRL 51653. San Francisco: Lawrence Livermore Laboratory, April 25. 1975;48.

3. Frederick JE. Yearly Review: Trends in atmospheric ozone and ultraviolet radiation: mechanisms and observations for the Northern Hemisphere. Photochem Photobiol. 1990;51:757–63.

4. Terrestrial Global Spectral Irradiance Tables for Air Mass 1.5. ASTM Document 138 RI E 44.02, Feb 1981.

5. Hyman LG, Lillienfeld AM, Ferris FL III, Fine SL. Senile macular degeneration. A case controlled study. Am J Epidemiol. 1983;118:350–4.

6. Sperduto TD, Holler R, Seigel D. Lens opacities and senile maculopathy. Am Arch Ophthalmol. 1981;99:1004–9.

7. Lerman S. Phototoxicity: clinical considerations. Focal Points. San Francisco: American Academy of Ophthalmology, 1987;1–22.

8. Lerman S. Radiant energy and the eye. New York: Macmillan; 1980.

9. Ham WT Jr, Mueller HA, Ruffolo JJ Jr, et al. Action spectrum for retinal injury from near ultraviolet radiation in the aphakic monkey. Am J Ophthalmol. 1982;93:299–306.

10. Li W, Yanoff M, Li Y, et al. Artificial senescence of bovine retinal pigment epithelial cells induced by near-ultraviolet in vitro. Mechanisms of Aging. 1999;110:137–55.

11. Bernhard JD. Light induced changes in the skin of the lid. In: Miller D, ed. Clinical light damage to the eye. New York: Springer-Verlag; 1987:127–44.

12. Urbash F. Photocarcinogenesis. In: Regan JD, Parrish JA, eds. The science of photomedicine. New York: Plenum Press; 1982:261–92.

13. Voerhoeff FH, Bell L, Walker CB. The pathological effects of radiant energy on the eye. An experimental investigation with a systemic review of the literature. Proc Am Acad Arts Sci. 1916;51:630–818.

14. Cogan DG, Kinsey VE. Action spectrum of keratitis produced by ultraviolet radiation. Arch Ophthalmol. 1946;35:370–6.

15. Pitts DG, Tredici TJ. The effects of ultraviolet on the eye. Am Ind Hyg Assoc J. 1971;32:235–46.

16. Miller D. Clinical light damage to the eye. New York: Springer-Verlag; 1987.

17. Norn MS. Spheroidal degeneration of cornea and conjunctiva. Prevalence among Eskimos in Greenland and Caucasians in Copenhagen. Acta Ophthalmol. 1978;56(4):551–62.

18. Cameron EE. Pterygium throughout the world. Springfield: CC Thomas; 1965.

19. Geeraets WJ, Harrel W, Guery D, et al. Aging anomalies and radiation effects on rabbit lens. Acta Ophthalmol. 1965;43:3–10.

20. Giblin FH, Chakrapani B, Reddy VN. High molecular weight aggregates in X-ray induced cataracts. Exp Eye Res. 1978;26:507–15.

21. Hiller R, Sperduto RD, Ederse F. Epidemiologic association with cataract. The 1971–72 natural health and nutrition examination survey. Am J Epidemiol. 1983;118:230–49.

22. Brilliant LB, Grosset NC, Ram PT, et al. Association among cataract prevalence, sunlight hours and altitude. Am J Epidemiol. 1983;118:2350–64.

23. Taylor H. The environment and the lens. Br J Ophthalmol. 1980;64:303–10.

24. Taylor H, West SK, Rosenthal FS, et al. Effect of ultraviolet radiation on cataract formation. N Engl J Med. 1988;319(22):1429–33.

25. Zigman S. Light damage to the lens. In: Miller D, ed. Clinical light damage to the eye. New York: Springer-Verlag; 1987:65–78.

26. Goosey JD, Zigler JS Jr, Kinoshita JH. Cross linking of lens crystalline in a photodynamic system. Science. 1980;208:1278–80.

27. No authors listed. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E and beta carotene for age-related cataract and visual loss: AREDS report no. 9. Arch Ophthalmol. 2001 Oct;119(10):1439–52.

28. Jacques PF, Chylak LT Jr, Hankinson SE, et al. Long-term nutrient intake and early age-related nuclear lens opacities. Arch Ophthalmol. 2001 Jul;119(7):1009–19.

29. Miranda MN. The environmental factor in the onset of presbyopia. In: Stark L, Obrecht G, eds. Presbyopia. Recent research and reviews from the Third International Symposium. New York: Professional Press; 1987.

30. Calkins JL, Hochheimer BF. Retinal light exposure from operation microscopes. Arch Ophthalmol. 1974;97:2363–7.

31. Covard DM. Operating microscope light induced retinal injury. J Am Intraocul Implant Soc. 1984;10:438–43.

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32. Irvine AR, Wood I, Morris BW. Retinal damage from the illumination of the operating microscope. Arch Ophthalmol. 1984;102:1358–64.

33. Dawson WW, Herron WL. Retinal illumination during indirect ophthalmoscopy. Invest Ophthalmol. 1970;9:89–95.

34. Davies S, Elliott MH, Floor E, et al. Photocytotoxicity of lipofuscin in human retinal pigment epithelial cells. Free Radic Biol Med. 2001 Jul 15;31(2):256–65.

35. Reeves P. Response of the average pupil to various intensities of light. J Opt Soc Am. 1970;4:135–9.

36. Weiter JJ, Delori FC, Wing GL, Fitch KA. Relationship of senile macular degeneration to ocular pigmentation. Am J Ophthalmol. 1985;99:185–7.

37. Glass P, Avery G. Effect of bright light in the hospital nursery on the incidence of retinopathy of prematurity. N Engl J Med. 1985;313:401–4.

38. Dillon J. The photophysics and photobiology of the eye. J Photochem Photobiol B. 1991;10:23–40.

39. Taylor H, West S, Munoz B, et al. The long-term effects of visible light on the eye. Arch Ophthalmol. 1992;110:99–104.

40. Waxler M, Hitchins VM. Optical radiation and visual health. Boca Raton, Fla: CRC Press; 1986.

41. Miller D, Benedek GB. Intraocular light scattering. Springfield: CC Thomas; 1973.

42. Clark BA. Color in sunglass lenses. Am J Optom. 1969;46:875–80.

43. Tupper B, Miller D, Miller R. The effect of 550?nm cutoff filter on the vision of cataract patients. Ann Ophthalmol. 1985;17:72–4.

44. Young JM. Photochromics: past and present. Opt World. 1993;Feb.

45. Magnante D, Miller D. Ultraviolet absorption of commonly used clip-on sunglasses. Ann Ophthalmol. 1985;17:614–16.

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