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The significance of ultraviolet radiation for eye diseases
Copyright
Ophthal. Q 1995 Elsevier
Physid. Opt. Vol. 15, No. 2, pp. 83-91, 1995 Science Ltd for British College of Optometrists Printed in Great Britain. All rights reserved
0275-5408195 $lO.OO+O.OO
significance diseases
of ultraviolet
A review with comments contact lenses J. F. 6. Bergmanson’” ’ Ana,:omy and TX 77204-6052,
Pathology USA;
and
radiation
on the efficacy
for eye
of UV-blocking
P. G. S6derberg2
Laboratory, College of Optometry, and 2S:t Eriks tjgonsjukhus, 112
82
University Stockholm,
of Houston, Sweden
Houston,
Summary Acute and cumulative ultraviolet radiation (UVR) exposure has been proposed as an important causative factor in the development of a whole spectrum of eye diseases. The present review examines the scientific evidence for and against such an association, with special emphasis on recent additions to the literature. The sun is the main UVR source on earth, and it is beyond scientific doubt that the cornea can be harmed by both acute and cumulative ambient exposures. There is also powerful epidemiological support for an association between chronic UVR exposure and rhe formation of cataracts and pterygia. The evidence in support of UVR linkage to pingLecula, ocular neoplasms and retinal changes is weaker-in part because there are fewer studies reported in the literature. It is concluded that UVR-blocking hydrogel contact lenses and spec;acles are two equally effective preventive measures in minimizing unnecessary suffering and health costs, especially for people who spend a significant time outdoors and for those who ,ive in more UV intense environments. UVR-blocking contact lenses and spectacles must not, ‘lowever, be substitutes in situations that require UVR-blocking safety goggles. Ophihal.
Pbysiol.
Opt.
1995,
15,
83-91
The Turnan eye is exposed daily to ultraviolet radiation (UVR). The main UVR source is the sun. The UVR dose received on a sunny day while skiing or sailing with unproteizted eyes is sufficient to causeacute photokeratitis. A spectrumof other ophthalmic diseasesin addition to keratitis is believed to have an associationwith UVR. The purpose of the present review is to evaluate the scientific evidence for azzdagainst UVR as a factor in developing theseocular anomalies. The focus is to assessthe impact that more recent laboratory and epidemiological studies have had on our current understandingof the significance of UVR in eye disease. In recent years, contact lenseswith UV filtering capabilities have been introduced as an option for protection from toxic radiation. The usefulnessof suchdevices for the purpose of UV protection is also examined.
Ultraviolet radiation Ultraviolet radiation (UVR) is electromagnetic radiation in the waveband lOO-400nm. It is subdivided into three bands’.‘: UVA (315400nm), UVB (280-315 nm) and UVC (loo-280 nm). The amount of UVR that falls on a unit area of surface is called irrudiarzce (unit of measurement: W mm2).The dose of UVR (J m-‘) is the irradiance times the exposure time. The threshold dose indicates the least radiant energy that is needed to cause a defined biological effect.
Tissue
interaction
spectrum
According to ‘Draper’s law’, only the fraction of energy that is absorbed by a tissue can change or damage it. Therefore, the absorption curve for a tissue will show the waveband to which it is vulnerable. The composition of the optics of the eye has been described3as ‘a consecutive
*FBCO Receir rdc 16 January 1995 Revised ,f&m: 2 February 1995
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series of spectral filters with each component absorbing exclusive wavelengths within the incident light and thus preventing them from impinging on the next tissue or media in the pathlength’. There appears to be agreement between authorities as to the wavebands absorbed by the cornea, lens and retina, respectively4-6. The cornea absorbs UVC and UVB with a peak absorption at 270 nm. The crystalline lens absorbs UVB primarily between 295 and 3 15 nm, but with age the absorption increases to include UVA and even visible light. No UVC or UVB and very little UVA (< 1%) reach the retina5. The retina seems to be most readily traumatized by blue light7. The vitreous is basically transparent to UV light and does not appear to have a role in absorbing harmful radiation. Therefore, in the aphakic eye, the vitreous, and incidentally also the aqueous, contribute little to the protection of the retina5. The conjunctival action spectrum is very similar to that of the cornea*, and the action spectrum usually corresponds to the absorption curve. Damage mechanism Excellent reviews of the current state of knowledge on the mechanism of radiation-induced damage are available in the literature’.“. Low level UV radiant exposure (dose) damages the ocular tissues photochemically, e.g. by changing the chemical structure or composition of biomolecules. Every biomolecule has a specific spectral sensitivity for absorption and damage. In contrast, higher level UV radiant doses as well as high level visible light exposure may provoke thermal damage. The mechanisms for acute and chronic UVR damage may not be identical for a tissue and this is one of the dilemmas in correlating results from laboratory experiments on the acute response with the chronic response evaluated in epidemiological studies. Sources of ultraviolet
radiation
The sun is quantitatively the most important source of UVR. The irradiance of UVR in different wavebands reaching the surface of the earth is largely dictated by the temperature of the sun, its distance from the earth and the composition of the atmosphere. Where on the earth the exposure occurs is important because latitude and altitude affect the irradiance level. For instance, the closer to the equator and the higher the altitude of an individual, the greater the irradiance of UVR. Further information on the effect of geographic location on the level of solar spectral irradiance is available in the literature6. The atmosphere filters out almost all UVR below 290nm and 70-90% of UVB. The filtering depends on the length of the beam path through the atmosphere. For this reason, around 70% of biologically weighted UVR reaches the surface of the earth between 10:OOam and 2:OOpm. A large fraction of the total UVR is scattered and consideration of the ambient UVR is crucial for the total
dose received”. The reflectance from newly fallen snow is 80% while that from grass is only 1%. For the general population, the second largest potential source of UVR is nonfiltered high temperature lamps. These lamps have become popular as workplace illumination and for exhibition displays. Ocular exposure geometry Deep within the orbit behind the eyebrows, the eye is protected from overhead UVR by the eyelids and the eyelashes. In bright light, the exposure to the ocular surface is further reduced by squinting. No information is currently available on how much of the overhead irradiance truly reaches the ocular surface. However the eye is more vulnerable to UVR reflected from flat surfaces such as snow-fields, bodies of water and beaches. These conditions are probably the most common settings for acute photokeratitis. Almost all UVR incident to the eye is scattered. In addition, a large fraction of UVR incident to the cornea is reflected by the tear film-air interface according to the Fresnel law of reflection. UVR-absorbing sunglasses efficiently block UVR incident along the optical axis but allow a considerable dose of UVR to pass around the frame and reach the eye. The dark lenses in sunglasses reduce the behavioural aversion reflex and squinting and may, therefore, in reality increase the effective dose of UVR to the eye. The irradiance at different interfaces in the eye depends on the transmittance to that interface. UVR is attenuated in the eye through absorption and scattering but the refractive apparatus of the eye also concentrates directly transmitted UVR on the retina. Effects
of ultraviolet
radiation
on the cornea
Although earlier cultures may have been painfully aware of the need to avoid photokeratitis, it was only 100 years ago first scientifically demonstrated that that Widmark’2,‘3 ambient UVR causes a severe and painful cornea1 response, known as photokeratitis or snow blindness. Since this discovery, the literature has been enriched with numerous reports on the cornea1 response to UVR in clinical populations and in animal experiments. Acute exposure to direct or reflected intense solar radiation may cause a photokeratitis in as short a time as 30 seconds14. This response is seen particularly often in surroundings covered by snow, hence the term ‘snow blindness’. The human vulnerability to snow blindness is best explained by the fact that fresh snow is the surface with the highest known non-specular reflectance factor for UVR” and that the cornea is less well protected from reflected UVR than overhead UVR. In addition to the sun, acute exposures from artificial sources such as tanning lights and welder’s arcs can induce photokeratitis in the unprotected eye’5.‘6. Tanning parlours use sources that emit predominantly UVA and very little
Significance
of ultraviolet
radiation
UVB light. Therefore, a cornea1 response to the exposure from these sources is usually not experienced by tanners using no protection. However, this lack of symptomology should be no excuse for not using filters since UVA is absorbed by the crystalline lens and possibly also the retina. Chronic low dose exposure to UVR appears also to affect the cornea. Karai et ~1.‘~ compared 118 welders with an average of 17 years of employment with 8.5 controls who had no welding experience, and found increased cornea1 endorhelial polymegethism and a decrease in the proportion of hexagonal cells among the welders. They believed this effec; to be the result of UVR from the welder’s arc, but they (did not discuss what kind of UV protection the welders had been using. Good and Schoessler’8 obtained similar resull:s when studying outdoor workers compared with a control group. They found a correlation between chronic ambient UVR exposure and increased pleomorphism and polyrnegethism. Chronic exposure to UVR has been suggested as a significanl. factor in the development of climatic droplet keratopath) . This permanent cornea1 pathology, also referred to as spheroid degeneration, is associated with people subjected to long-term environmental UVR exposure’9m25. One of the more recent and perhaps most comprehensive of these studies25 involved 838 subjects and concluded that there is ‘a clear association between a high personal UVR exposure and an increased risk of climatic droplet keratopathy’. Individual case reports and epidemiological studies share a common shortcoming in that there is little opportunity to control other factors that may contribute to or influence the manifestations of the response evaluated. Therefore, wellcontrolled animal studies are invaluable in identifying causative factors when studying specific conditions. It should also be remembered that the epidemiological study generally assesses the chronic, low dose exposure conditioq, while the laboratory study usually examines the acute response to high dose exposures. As mentioned above, these two study conditions are dissimilar and we are not free to assume that the two variant experimental settings necessarily trigger the same damage or repair mechanism. The action spectrum for UVR-induced keratitis has been studied in rabbits4.26. Early studies described cornea1 epith.elial cell changes and cell death27z3’. Clarke et ~1.~~ offered a quantification of cellular exfoliation and recovery following a suprathreshold exposure to UVR. However, the cornea1 epithelium regenerates quickly (within 5 days )33.34and therefore this painful condition was generally not regarded as a serious threat to cornea1 health. However, more recent studies have shown that the damage goes deeper than the epithelium. In fact, the response involves the full cornea1 thickness35-38,40-43. UVR can induce significant damage and cell death among keratocytes and endothelial cells35-38 while cornea1 nerves appear structurally intact38.39. This deeper cornea1 damage
on
the
eye:
J. P. G. Bergmanson
and
P. G. Sdderberg
85
in photokeratitis was shown in both primates and rabbits. As a consequence, it may be assumed that the mammalian cornea is unlikely to vary significantly in its vulnerability to UVR. The threshold to cornea1 damage for 300 nm UVB appears to be37,400.03-0.08 Jcm-*. It is expected that the structural trauma caused by suprathreshold UVR has functional consequences. Studies monitoring the cornea1 thickness after UVR exposure have consistently found that irradiation leads to a thickening of the cornea40m43.Increases in cornea1 thickness is caused by a fluid imbalance and this abnormal cornea1 hydration strongly implicates endothelial dysfunction, especially when lasting more than 5 days. Initially epithelial damage with a subsequent inability to control fluid movement from an anterior direction could camouflage or be confused with an endothelial involvement. However, the quoted studies by Cullen et uZ.~‘, Riley et ~1.~‘) and Doughty and Cullen4’,” all had adequate control to identify an endothelial cause for the cornea1 oedema measured. The inhibition of the endothelium may be caused by increased permeability (deturgescence) or a reduced fluid pump function. Indeed, Doughty and Cullen showed that the UVB-induced cornea1 swelling is explained by deficiencies in both these aspects with most of the thickening explained by the reduction in fluid pumping. There is a rapid and large decrease in cornea1 sensitivity following a UVR overdose but a complete recovery occurs within 4 hours44. The explanation for this prompt recovery appears to lie in the structural integrity of cornea1 nerve fibres following suprathreshold UVR exposures38,39. The initial inhibition of the nerve fibre impulses, however, is likely to have a physiological rather than a structural basis. Lattimore4s.46 examined the effect of UVR on cornea1 biochemistry. Following exposure he found a decrease in cornea1 oxygen uptake, a reduction in phosphocreatine, an increase in glucose and an elevation in glycogen. These findings suggest that UVR is capable of severe disruption of cornea1 metabolism. The cumulative effect of epidemiological and experimental evidence found in the literature for a relationship between UVR and cornea1 damage is very strong and suggests that all cornea1 structures are vulnerable to UVR. The trauma induced by UVR exposure involves vital cornea1 structures and functions, but the epithelial basement membrane, posterior limiting lamina (Descemet’s membrane) and the nerve fibres are spared. Effects
of ultraviolet
radiation
on the conjunctiva
In a number of studies, UVR has been linked to conjunctival changes. But the evidence is to a great extent indirect, since this literature is almost exclusively based on epidemiological data. One recent study explored the conjunctival action spectrum and found it similar to the cornea1 epithelium8. Therefore, in acute photokeratitis there will
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also be a conjunctival response. Pinguecula and pterygium are the conditions most commonly thought to have an association with chronic exposure to UVR. Pinguecula A pinguecula is a fibro-fatty degenerative change in the bulbar conjunctiva within the palpebral aperture. In assessing pinguecula in people from Labrador it was found that the size correlated with the severity of climatic droplet keratopathy24. In another study, Taylor et a1.25 found a weak association between pinguecula formation and UVA and UVB exposure in fishermen from Chesapeake Bay, Maryland, USA. They calculated the risk of developing pinguecula to be less than for climatic droplet keratopathy or pterygium. Norn47 reported a high prevalence of pinguecula among Arabs in the Red Sea region. Karai et a1.17 found that, unlike pterygium, there was no difference between welders and a control group with regard to the incidence of pinguecula. The evidence for a correlation between pinguecula and UVR exposure is indirect and based on a small number of epidemiological studies. It must, therefore, be concluded that, although a relationship between UVR exposure and pinguecula may exist, it has yet to be established. Pteiygium A pterygium is a hyperplasia of the bulbar conjunctiva. The pterygium may grow over the cornea and, on rare occasions, cause blindness. Two such cases are reported involving an Eskimo and an Australian aborigine48X49. These victims lived an outdoor life facing significant exposure to UVR during their lifetimes. A historical example is Lord Nelson who spent his life at sea and suffered from bilateral pterygia; incidentally, he added, as a helpful measure, a green eye shade to his admiral’s cocked hat”. Well-designed epidemiological studies suggest a correlation between UVR and pterygia developments. Hollows and Moran” found in an Australian study that the incidence of pterygium was related to the time spent outdoors. In a study from the northern hemisphere, Taylor et aZ.25x52 found a similar relationship. In fact, in this study on fishermen in Chesapeake Bay, it was concluded that there is a ‘clear association between a high personal exposure to UVR and an increased risk for both pterygium and climatic droplet keratopathy (CDK)‘. Mackenzie et a1.53 in their study of Australians, also found that time spent outdoors and pterygium development were linked. It appears that artificial sources containing larger energies of UVR are also capable of causing the development of pterygium. Karai et al. ” evaluated 191 Japanese welders and found that they had an increased risk of developing pterygium the longer they worked as a welder. Histopathological evidence supports the link between
UVR and pterygium formation. Austin et a1.54 found that an important component of both pinguecula and pterygium is abnormal synthesis and secondary degeneration of elastic fibres. This response shares similarities with sun-induced skin changes. Coroneo et a1.j5 offered an explanation for the specific location and shape of the pterygium. According to their hypothesis, peripherally incident light (or UVR) is refracted to foci at the nasal limbus, which is the most common site for pterygia. They also suggested that peripheral light (or UVR) may also be focused on the nasal aspect of the crystalline lens which may explain some cortical cataracts. Coroneo et al.” also proposed that individual variations in common environments may be the result of varying degrees of limbal focusing, which depends on cornea1 shape and the depth of the anterior chamber. Other factors apart from environmental or artificial UVR exposure may contribute to the formation of pterygium. In particular, sandy and dusty environments have been suggested as contributing or alternative factors54.S6. According to this hypothesis, it is believed that particular matter causes ocular irritation or microtrauma to the bulbar conjunctiva leading to the stimulus to pterygium growth. This notion is obviously not supported by the study on the fishermen in Chesapeake Bay, where the climatic conditions would not be described as dusty, hot or dry. Therefore, the evidence currently available clearly points to UVR as a significant factor in causing pterygium. Effects
of ultraviolet
radiation
on the lens
Cataract is a clinical syndrome involving an opacification of the crystalline lens that causes reduced vision. Experimental induction of cataracts with UVR is today a wellestablished model. There are numerous epidemiological studies concluding that exposure to UVR is an important risk factor for cataracts. Again, it should be reiterated that epidemiological studies cannot control all possible factors such as genes, diet, social behaviour, etc. Lately, cataract morbidity has been correlated with estimated individual dose. In the beginning of the 198Os, the solar dose of UVR for different populations was associated with the prevalence of cataract. There are numerous observational reports of a high prevalence of cataract in sunny areas compared to areas with little sun. Studying fishermen in Hong Kong57, it was found that the risk for cortical cataract among men aged 40-50 years who spent 5 or more hours per day outdoors, was increased compared with that for men who spent less time outdoors. In India, outdoor occupations were found to have an elevated risk for cataract compared with indoor occupations”. In a study from Italy, an excess of pure cortical and mixed cataracts was found among workers in sun-intense locationss9. Further, an increased incidence of cortical and mixed cataract was associated with leisure time spent in the
Significance
of ultraviolet
radiation
sunlight. Posterior subcapsular cataracts were associated with UVB exposure in a study from Maryland on cataract patients6’ and a study on fishermen in Chesapeake Bay, Maryland53, found an association between UVB and cortical cataracts. In Nepa16’, a correlation was found between the prevalence of cataracts and the average hours of sur:light when comparing different zones of the country. Another study, in rural areas of China62, demonstrated that ‘he prevalence of cataracts was correlated with annual direct total solar radiation. When evaluating the prevalence of cataract in different parts of Australia, it was found that cataract is more common in areas with a high average daily dose of UVB52,63. Hollows and Morar?’ studied an Australian population, the Aborigines, who spent most of their time outdoors and who followed a relatiT;ely uniform social pattern. It was found that the closer to the equator members of this population lived, the eerlier they would acquire cataracts. A North American study revealed that the solar dose of UVB is associated with cortical cataracts64. In an earlie- study of the same data a correlation between average solar dose of UVB and prevalence of cataract was reported65,66. Further, there have been observational studies since the end of the nineteenth century that reporl an increased prevalence of cataract in sunny area?‘. Thus, epidemiological studies strongly support UVR as a risk factor for cataract. Although the epidemiological studies have aimed at elucidating a possible dose-response relationship, a causal association cannot be established epidemiologically. Hoyvever, cataract was experimentally induced with UVR as early as the end of the nineteenth century6’. Since then, a number of studies on experimental induction of cataract have 3een published. Modern experimental studies have confirmed that UVB induces anterior cortical opacities and later posterior cortical opacil:ies4. Microscopically, the cortical opacities correspond 1.0swelling of lens epithelial cells and cortical fibres, until they rupture and thus cause vacuolization of the cortical area7”-83. The swelling has been associated with a transient increase of lens water74 which is related to a sodium-potassium shift75. The energy-dependent Na+-K+ ATPase that is responsible for maintenance of the Na+-I(+ balance over lens cell membranes, has been found to become impaired after exposure to UVR76. Extended low dose exposure to UVR has been found to induce changes in lens proteins”,‘*. The experimental studies discussed in the present report provide strong evidence for a causal relationship between exposure to UVR and the development of cataract. The major criticism regarding these experiments is that nonhuman species are studied and that a relatively high dose is given during a short time. Long-term, low intensity studies would be welcome.
on
the
eye:
Effects
J. P. G. Bergmanson
of ultraviolet
and
radiation
P. G. Sijderberg
87
on the retina
Extremely small amounts of UVR reach the retina”. The transmittance of UVR is highest in the newborn and decreases with age. Cruickshanks et al. *’ found an association between late stage age-related macular degeneration and summer leisure time outdoors. A study on fishermen in Maryland, showed that individuals with established age-related macular degeneration had significantly higher exposure to visible light from the sun during the previous 20 years8’.8’. More studies are needed to clarify the role of UVR for age-related macular degeneration. Experimental studies on primates have shown that high intensity light may cause acute photochemical damage”. The photochemical damage is strongly wavelength dependent84. The action spectrum for UVR-induced damage to the retina changes dramatically in aphakia’” with increased sensitivity at short wavelengths. Experimental exposure of primate eyes to 325 nm from a HeCd laser demonstrated retinal damage at doses below cornea1 thresholds5. An interesting observation was made by Yanuzzi et a1.86 who reported an elevated incidence of solar retinitis in areasof ozone depletion. It was found that the visual acuity was reduced to between 20140 and 20180 in affected individuals, but within 3-9 months, the visual acuity had returned to between 20/20 and 20130. Additional clinical manifestations reported were small central scotomasand permanent fovea1 lesions. Ultraviolet radiation-induced ocular malignancy Cornea1neoplasmsare extremely rare and when they occur they are usually connected to a limbal or conjunctival growth. These neoplasms are intraepithelial. Recently, three caseswere reported where the age range was 3 1 to 38 years and all caseshad a history of soft contact lens wear and exposureto high intensity UVR”. Templetong reported a high incidence of conjunctival squamouscell carcinoma in an African population living in Uganda near the equator. A recent epidemiological study, involving 60 caseswith ocular surface epithelial dysplasia, examined risk factors in developing cornea1 and conjunctival epithelial dysplasia, carcinoma in situ and squamouscell carcinomagy. It was concluded that cumulative UVR exposure is an important risk factor in developing these diseases.Other factors of significance were fair skin, pale iris, propensity to sunburn and a history of previous cancers. In summary, the evidencefor an associationbetweenUVR exposureand ocular surfaceneoplasmis scantbut mounting. Contact lenses and spectacles as ultraviolet filters
radiation
Contact lenses can be designed to be effective UVR
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1995
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absorbers” but contact lenses without a UVR blocker transmit 90% of the UVR spectrum”. A number of studies have clearly demonstratedthat when placed on the eye, a UVR filtering contact lens offers good protection of the cornea and presumably also the internal eye38.92393. However, it should be recognized that a soft contact lens offers more protection than a rigid gas permeable (RGP) contact lens becausethe former covers the entire cornea while the latter only covers a portion of the cornea. A second fundamental difference between soft and rigid contact lensesis the way that the latter provides no limbal or conjunctival coverage when fitted in its customary size, smaller than the cornea1diameter. In contrast, a well-fitted hydrogel lens covers limbal cornea and much, if not all, of the conjunctival palisadesof Vogt. This is of considerable significance since this is the location of a large number of the epithelial stem cells that continuously, in health and in disease, provide new cells to the cornea1 epithelium94. Cornea1 clarity is compromised when these cells are injured. An effective UV-blocking hydrogel contact lens would protect thesevital cells and their function from UVR damage. Effective UV-blocking spectacle lenses are available commercially and they provide a good general protection95.However, spectacleswith such lensesdo not provide complete protection since radiation may reach the cornea and conjunctiva without passingthrough the lenses.It may be argued that the well-fitted hydrogel lens is providing comparable or possibly better protection than a spectacle prescription, and, therefore, is an equally appropriate preventive measure.It must be stressedthat in UV intense environments, such as welding, neither spectacles nor contact lenses should be substituted for recommended safety goggles. The question whether the wearing of contact lenses makesthe cornea more vulnerable to UV trauma has been raised93.96.97 but this possibility has not yet been confirmed nor ruled out beyond doubt. Further researchon this issue is desirable. Concluding comments There is no evidence that exposure of the eye to UVR is essentialfor the human body or beneficial to vision itself. However, there is today conclusive evidence that an acute overdose of UVR from the suncausesacute photokeratitis. There is very strong epidemiological support for an association between long-term exposure to the sun and the development of both pterygium and cataract. Furthermore, there is experimental and epidemiological evidence suggesting that UVR reaches the retina and may ultimately cause macular
degeneration79-85.
Considering
the above-
cited data, there is no scientific basis for denying the eye UVR protection. Both
contact
lenses
and spectacles
offer
an excellent
opportunity
to decrease
the load of UVR
on the eye. A
number of studieshave shown that a contact lens can be an efficient UVR filter if the appropriate absorbing chromophore is included in the contact lens materia137~38~90~9’~93~98~99 but without such material formulation, the lens offers no protection. A wide-brimmed hat is a helpful adjunct to UV filtering ophthalmic devices. The use of UVR-blocking contact lenses or spectacles does not preclude the need to
use UVR-filtering safety goggles or sunglasseswith side protection
in environments
with
high intensity
of UVR.
Acknowledgements We gratefully acknowledge the generous assistanceprovided by Mr Todd Sheldon and Mr Doug Wike in the preparation
of this manuscript.
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34 35 36 37
263-273
40 41 42 43
44
(1987)
Bergmanson, J. P. G., Pitts, D. G. and Chu, L.W.-F. The efficacy of a UV-blocking soft contact lens in protecting cornea against UV radiation. Actu Ophthalmol. 65, 279-286
39
89
the pigmented rabbit studied by quantitative scanning electron microscopy. Acta Ophthalmol. 68, 639-650 (1990) McDonald, M. B.; Frantz, J. M.. Klyce, S. D., Beuerman, R. W., Varnell, R., Munnerlyn, C. R., Clapham, T. N., Salmeron, B. and Kaufman, H. E. One year refractive results of central photorefractive keratectomy for myopia in the nonhuman primate cornea. Arch. Ophthalmol. 108, 40-47 (1990) Gartry, D., Kerr, M. M. and Marshall, J. Excimer laser photorefractive keratectomy: 18 month follow-up. Ophthalmology 99, 1209-1219 (1992) Ringvold, A., Davanger, M. and Griinvold-Olsen, E. Changes of the cornea1 endothelium after ultraviolet radiation. Actu Ophthalmol. 60, 41-53 (1982) Ringvold, A., Davanger, M. and Gronvold-Olsen, E. Changes in the rabbit cornea1 stroma caused by UVradiation. Acta Ophthalmol. 63, 601-606 (1985) Pitts, D. G. i Bergmanson, J. P. G., Chu, L.W.-F., Waxier, M. and Hitchins, V. M. Ultrastructural analysis of cornea1 exposure to UV radiation. Acta. Ophthalmol. 65,
38
and P. G. Sdderberg
(1987)
Bergmanson, J. P. G. Cornea1 damage in photokeratitisWhy is it so painful? Optom. Vision Sci. 67, 407-413 (1990) Cullen, A. P., Chou, B. R., Hall, M. G. and Jany, S. E. Ultraviolet-B damages cornea1 endothelium. Am. J. Optom. Physiol. Opt. 61, 473-478 (1984) Riley, M. V., Stanley, S., Peters, M. I. and Schwartz, C. A. The effects of UV-B irradiation on the cornea1 endothelium. Curr. Eye Rex 6, 1021-1033 (1987) Doughty, M. J. and Cullen, A. P. Long-term effects of a single dose of ultraviolet-B on albino rabbit cornea-I. In vivo analysis. Photochem. Photobiol. 49, 185-196 (1989) Doughty, M. J. and Cullen, A. P. Long-term effects of a single dose of ultraviolet-B on albino rabbit cornea-II. Deturgescence and fluid pump assessed in vitro. Photochem. Photobiol. 51, 439-449 (1990) Millodot, M. and Earlam, R. A. Sensitivity of the cornea after exposure to ultraviolet light. Ophthalmic Res. 16, 325-328
(1984)
Lattimore, M. R. Glucose concentration profiles of normal and ultraviolet radiation-exposed rabbit corneas. Exp. Eye Res. 47, 699-704 (1988) 46 Lattimore, M. R. Effects of ultraviolet radiation on the oxygen uptake rate of the rabbit cornea. Optom. Vision Sci. 66, 117-122 (1989) 47 Norn, M. S. Spheroid degeneration, pinguecula, and pterygium among Arabs in the Red Sea Territory, Jordan. Acta Ophthalmol. 60, 949-954 (1982) 48 Taylor, H. R. and Hollows, F. C. Pterygium leading to blindness: a case report. Austral. J. Ophthalmol. 6, 45
155-156
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Fritz, M. H. Blindness from multiple pterygiums in an Alaskan native. Am. J. Ophthalmol. 39, 572 (1955) 50 Pugh, P. D. G. Nelson and his Surgeons, Livingstone, Edinburgh, UK (1968) 51 Hollows, F. and Moran, D. Cataract-the ultraviolet risk factor. Lancet 2, 1249-1250 (1981) 52 Taylor, H. R., West, S. K., Rosenthal, E. S., Munoz, B., Newland, H. S., Abbey, H. and Emmett, E. A. Effect of ultraviolet radiation on cataract formation. New Engl. J. Med. 319, 1429-1433 (1988) 49
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53 Mackenzie, F. D., Hirst, L. W., Battistutta, D. and Green. A. Risk analysis in the development of pterygia. Ophrha(molog~ 99, 1056-1061 (1992) 54 Austin, P., Jakobiec. F. A. and Iwamoto. T. Elastodysplasia and elastodystrophy as the pathologic bases of ocular pterygia and pinguecula. Ophthalmology 90, 966109 (1983) 55 Coroneo. M. T.. Muller-Stolzenburg, N. W. and Ho. A. Peripheral light focussing by the anterior eye and the ophthalmohelioses. Ophthal. Surg. 26, 705-711 (1991) 56 Dhir, S. P., Detels, R. and Alexander, E. R. The role of environmental factors in cataract, pterygium and trachoma. Am. J. Ophthalmol. 64, 128-135 (1967) 57 Wong, L., Ho, S. C.. Coggon, C., Cruddas, A. M., Hwang, C. H., Ho, C. P., Robershaw, A. M. and McDonald. D. M. Sunlight exposure, antioxidant status and cataract in Hong Kong fishermen. J. Epidemiol. Comm. Hlth. 47, 46-49 (1993) 58 Bhatnagar, R., West, K. P., Vitale, S.. Sommer, A., Joshi, S. and Venkataswamy: G. Risk of cataract and history of severe diarrhea1 disease in Southern India. Arch. Ophthahnol. 109, 696-699 (1991) 59 Italian-American Cataract Study Group. Risk factors for age-related cortical, nuclear, and posterior subcapsular cataracts. Am. J. Epidemiol. 133, 541-553 (1991) 60 Barlow, T. W., West, S. K., Azar, A., Munoz, B., Sommer, A. and Taylor, H. R. Ultraviolet light exposure and risk of posterior subcapsular cataracts. Arch. OphthnlmoZ. 107, 369-372 (1989) 61 Brilliant, L. B., Grasset, N. C., Polshrel, R. P., Kolstad; A., Lepkowski, J. M.; Brilliant, G. E., Hawks, W. N. and Pararajasegaram, R. Associations among cataract prevalence, sunlight hours, and altitude in Himalayas. Am. J. Epidemiol. 118, 250-264 (1983) 62 Mao. W. and Hu, T. An epidemiological survey of senile cataract in China. Chinese Med. J. 95, 813-818 (1982) 63 Taylor, H. R. The environment and the lens. Br. J. Ophthalmol. 64, 303-310 (1980) 64 Hiller, R.. Sperduto, R. D. and Ederer, F. Epidemiologic associations with nuclear, cortical and posterior subcapsular cataracts. Am. J. Epidemiol. 124, 916-925 (1986) 65 Hiller, R., Giacometti; L. and Tuen, X. Sunlight and cataract: An epidemiological investigation. Am. J. Epidemiol. 105, 450-459 (1977) 66 Hiller, R.. Sperdrits, R. D. and Ederer, F. Epidemiologic associations with cataract in the 1971-1972 national health and nutrition examination survey. Am. J. Epidemiol. 118, 239-249 (1983) 67 Pitts, D., Cameron. L. L., Jose, J. G. et al. Ch. 2 Optical radiation and cataracts. In Optical Radiation and Visual Heulth (eds M. Waxler and V. M. Hitchins), CRC Press, Boca Raton, FL, USA, pp. 5-41 (1986) 68 Widmark, J. Uber die Durchlassigkeit der Augenmedien fur Ultraviolette Strahlen. BeitrHge. 2. Ophthalmology 460-502 (189 1) 69 SBderberg; P. G. Experimental cataract induced by ultraviolet radiation. Actu Ophthalmol. (Suppl.) 68, 196 (1990) 70 Jose, J. G. and Pitts, D. G. Wavelength dependency of cataracts in albino mice following chronic exposure. Exp. Eye Res. 41, 545-563 (1985) 71 Soderberg, P. G., Bergmanson, J. P. G., Philipson, B. T. and Tengroth, B. M. A new model for in vitro investigation of acute response in the UVR radiation exposed lens. In Hazards of Light, Myths and Realities,
72
73
74 75 76 77
Eye and Skin (eds J. Cronly-Dillon. E. S. Rosen and J. Marshall), Pergamon Press, New York, USA, pp. 221-228 (1986) Soderberg, P. G. Acute cataract in the rat after exposure to radiation in the 300nm wavelength region. A study of macro-, micro- and ultrastructure. Actu Ophthulmol. 66, 141-152 (1988) Cullen, A. P. and Monteith-McMaster, C. A. Damage to the rainbow trout (Oncorhyncus mykiss) lens following an acute dose of UVB. Curr. Eye Res. 12, 97-106 (1993) Soderberg, P. G. Mass alteration in the lens after exposure to radiation in the 300nm wavelength region. Acta Ophthalmol. 67, 633-644 (1989) Soderberg. P. G. Na and K in the lens after exposure to radiation in the 300nm wavelength region. J. Photochem. Photobiol. B: Biol. 8, 279-294 (1991) Torriglia, A. and Zigman, S. The effect of near-UVR light on Na-K-ATPase of the rat lens. Curr. Eye Res. 7, 539 (1988) Zigman, S., Schultz, J. and Yule, T. Possible roles of near-UVR light in the cataractous process. Exp. Eye Res. 15, 201-208
(1973)
78 Zigman, S., Griess; G., Yule, T. and Schultz, J. Ocular protein alterations by near-UV light. Exp. Eye Res. 15, 255-264 (1973) 79 Boettner, E. A. and Walter, J. R. Transmission of the ocular media. Invest. Ophthulmol. 1, 776-783 (1962) 80 Cruickshanks, K. J., Klein, R. and Klein, B. E. Sunlight and age-related macular degeneration: The Beaver Dam Eye Study. Arch. Ophthulmol. 111, 514-518 (1993) 81 Taylor. H. R., Munoz, B., West, S. K., Bressler, N. M., Bressler, S. B. and Rosenthal, F. S. Visible light and risk of age-related macular degeneration. Trans. Am. Ophthulmol. Sot. 88, 163-177 (1990) 82 Taylor, H. R., West, S. K., Munoz, B., Rosenthal, F. S., Bressler, S. B. and Bressler, N. M. The long-term effects of visible light on the eye. Arch. Ophthulmol. 110, 99-104 (1992) 83 Ham, W. T., Mueller, H., Ruffolo, J., Guerry, D. and Guerry, R. A. Action spectrum for retinal injury from near-ultraviolet radiation in the aphakic monkey. Am. J. Ophthulmol. 93, 299-306 (1982) 84 Ham. W. T., Ruffolo, J. J. and Mueller, H. A. Histologic analysis of photochemical lesions produced in rhesus retina by short wavelength light. Invest. Ophthalmol. 17, 1029-1035 (1978) 85 Zuclich, J. A. Ultraviolet induced damage in the primate cornea and retina. Curr. Eye Res. 3, 27-34 (1984) 86 Yanuzzi, L. A., Fisher, Y. L., Kreuger, A. and Slakter, J. Solar retinopathy: A photobiological and geophysical analysis. Am. J. Ophthulmol. Sot. LXXXV, 120-158 (1987) 87 Guex-Grosier, Y. and Herbort, C. P. Presumed cornea1 intraepithelial neoplasia associated with contact lens wear and intense ultraviolet light exposure. Br. J. Ophthalmol. 77, 191-192 (1993) 88 Templeton, A. C. Tumours of the eye and adnexa in Africans of Uganda. Cancer 20, 168991698 (1967) 89 Lee, G. A., Williams, G., Hirst, L. and Green, A. C. Risk factors in the development of ocular surface epithelial dysplasia. Ophthalmology 101, 360-364 (1994) 90 Pitts, D. G., Bergmanson, J. P. G. and Chu, L. W.-F. The efficacy of a UV-blocking soft contact lens in protecting cornea against UVR radiation. Acta Ophthalmol. 65, 279-286 (1987)
Significance
of ultraviolet
radiation
91 Chou, B. R., Cullen, A. P. and Egan, D. J. Spectral transmittance of contact lens material. ht. Contact Lens C/in. 11, 106-114 (1984) 92 Bergmanson, J. P. G., Pitts, D. G. and Chu, L. W.-F. Protection from harmful UV radiation by contact lenses. J. A17:. Optom. Assoc. 59, 178-182 (1988) 93 Cullen, A. P., Dumbleton, K. A. and Chou, B. R. Contact lenses and acute exposure to ultraviolet radiation. Optom. Vision sci. 66, 407-411 (1989) 94 Theft, R. A. The XYZ hypothesis of cornea1 epithelial maintenance. Invest. Opktkal. Visual Sci. 24, 1442-1443 (1983) 95 Pitis, D. G. Principles in ocular protection. In Environmental Vi: ior? (eds D. G. Pitts and R. N. Kleinstein), ButterworthHememann, Boston, MA, USA, pp. 259-280 (1993)
on the eye: J. P. G. Bergmanson
and P. G. S&derberg
91
96 Ahmedbhai, N. and Cullen, A. P. The influence of contact lens wear on the cornea1 response to ultraviolet radiation. Opktkal. Pkysiol. Opt. 8, 183-189 (1988) 97 Pitts, D. G., Bergmanson, J. P. G. and Chu, L. W.-F. Does the endothelium of the contact lens wearing cornea require UV protection? J. Br. Contact Lens Assoc. 11, 23-27 (1988) 98 Dumbleton, K. A., Cullen, A. P. and Doughty, M. J. Protection from acute exposure to ultraviolet radiation by ultraviolet-absorbing RGP contact lenses. Opktkal. Pkysiol. Opt. 11, 232-238 (1991) 99 Pitts, D. G. and Lattimore, M. R. Protection against UVR using the Vistakon UV-Bloc soft contact lens. Int. Contact Lens Clin. 14, 22-30 (1987)
Ophthal. Q 1995 Elsevier
Physid. Opt. Vol. 15, No. 2, pp. 83-91, 1995 Science Ltd for British College of Optometrists Printed in Great Britain. All rights reserved
0275-5408195 $lO.OO+O.OO
significance diseases
of ultraviolet
A review with comments contact lenses J. F. 6. Bergmanson’” ’ Ana,:omy and TX 77204-6052,
Pathology USA;
and
radiation
on the efficacy
for eye
of UV-blocking
P. G. S6derberg2
Laboratory, College of Optometry, and 2S:t Eriks tjgonsjukhus, 112
82
University Stockholm,
of Houston, Sweden
Houston,
Summary Acute and cumulative ultraviolet radiation (UVR) exposure has been proposed as an important causative factor in the development of a whole spectrum of eye diseases. The present review examines the scientific evidence for and against such an association, with special emphasis on recent additions to the literature. The sun is the main UVR source on earth, and it is beyond scientific doubt that the cornea can be harmed by both acute and cumulative ambient exposures. There is also powerful epidemiological support for an association between chronic UVR exposure and rhe formation of cataracts and pterygia. The evidence in support of UVR linkage to pingLecula, ocular neoplasms and retinal changes is weaker-in part because there are fewer studies reported in the literature. It is concluded that UVR-blocking hydrogel contact lenses and spec;acles are two equally effective preventive measures in minimizing unnecessary suffering and health costs, especially for people who spend a significant time outdoors and for those who ,ive in more UV intense environments. UVR-blocking contact lenses and spectacles must not, ‘lowever, be substitutes in situations that require UVR-blocking safety goggles. Ophihal.
Pbysiol.
Opt.
1995,
15,
83-91
The Turnan eye is exposed daily to ultraviolet radiation (UVR). The main UVR source is the sun. The UVR dose received on a sunny day while skiing or sailing with unproteizted eyes is sufficient to causeacute photokeratitis. A spectrumof other ophthalmic diseasesin addition to keratitis is believed to have an associationwith UVR. The purpose of the present review is to evaluate the scientific evidence for azzdagainst UVR as a factor in developing theseocular anomalies. The focus is to assessthe impact that more recent laboratory and epidemiological studies have had on our current understandingof the significance of UVR in eye disease. In recent years, contact lenseswith UV filtering capabilities have been introduced as an option for protection from toxic radiation. The usefulnessof suchdevices for the purpose of UV protection is also examined.
Ultraviolet radiation Ultraviolet radiation (UVR) is electromagnetic radiation in the waveband lOO-400nm. It is subdivided into three bands’.‘: UVA (315400nm), UVB (280-315 nm) and UVC (loo-280 nm). The amount of UVR that falls on a unit area of surface is called irrudiarzce (unit of measurement: W mm2).The dose of UVR (J m-‘) is the irradiance times the exposure time. The threshold dose indicates the least radiant energy that is needed to cause a defined biological effect.
Tissue
interaction
spectrum
According to ‘Draper’s law’, only the fraction of energy that is absorbed by a tissue can change or damage it. Therefore, the absorption curve for a tissue will show the waveband to which it is vulnerable. The composition of the optics of the eye has been described3as ‘a consecutive
*FBCO Receir rdc 16 January 1995 Revised ,f&m: 2 February 1995
83
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series of spectral filters with each component absorbing exclusive wavelengths within the incident light and thus preventing them from impinging on the next tissue or media in the pathlength’. There appears to be agreement between authorities as to the wavebands absorbed by the cornea, lens and retina, respectively4-6. The cornea absorbs UVC and UVB with a peak absorption at 270 nm. The crystalline lens absorbs UVB primarily between 295 and 3 15 nm, but with age the absorption increases to include UVA and even visible light. No UVC or UVB and very little UVA (< 1%) reach the retina5. The retina seems to be most readily traumatized by blue light7. The vitreous is basically transparent to UV light and does not appear to have a role in absorbing harmful radiation. Therefore, in the aphakic eye, the vitreous, and incidentally also the aqueous, contribute little to the protection of the retina5. The conjunctival action spectrum is very similar to that of the cornea*, and the action spectrum usually corresponds to the absorption curve. Damage mechanism Excellent reviews of the current state of knowledge on the mechanism of radiation-induced damage are available in the literature’.“. Low level UV radiant exposure (dose) damages the ocular tissues photochemically, e.g. by changing the chemical structure or composition of biomolecules. Every biomolecule has a specific spectral sensitivity for absorption and damage. In contrast, higher level UV radiant doses as well as high level visible light exposure may provoke thermal damage. The mechanisms for acute and chronic UVR damage may not be identical for a tissue and this is one of the dilemmas in correlating results from laboratory experiments on the acute response with the chronic response evaluated in epidemiological studies. Sources of ultraviolet
radiation
The sun is quantitatively the most important source of UVR. The irradiance of UVR in different wavebands reaching the surface of the earth is largely dictated by the temperature of the sun, its distance from the earth and the composition of the atmosphere. Where on the earth the exposure occurs is important because latitude and altitude affect the irradiance level. For instance, the closer to the equator and the higher the altitude of an individual, the greater the irradiance of UVR. Further information on the effect of geographic location on the level of solar spectral irradiance is available in the literature6. The atmosphere filters out almost all UVR below 290nm and 70-90% of UVB. The filtering depends on the length of the beam path through the atmosphere. For this reason, around 70% of biologically weighted UVR reaches the surface of the earth between 10:OOam and 2:OOpm. A large fraction of the total UVR is scattered and consideration of the ambient UVR is crucial for the total
dose received”. The reflectance from newly fallen snow is 80% while that from grass is only 1%. For the general population, the second largest potential source of UVR is nonfiltered high temperature lamps. These lamps have become popular as workplace illumination and for exhibition displays. Ocular exposure geometry Deep within the orbit behind the eyebrows, the eye is protected from overhead UVR by the eyelids and the eyelashes. In bright light, the exposure to the ocular surface is further reduced by squinting. No information is currently available on how much of the overhead irradiance truly reaches the ocular surface. However the eye is more vulnerable to UVR reflected from flat surfaces such as snow-fields, bodies of water and beaches. These conditions are probably the most common settings for acute photokeratitis. Almost all UVR incident to the eye is scattered. In addition, a large fraction of UVR incident to the cornea is reflected by the tear film-air interface according to the Fresnel law of reflection. UVR-absorbing sunglasses efficiently block UVR incident along the optical axis but allow a considerable dose of UVR to pass around the frame and reach the eye. The dark lenses in sunglasses reduce the behavioural aversion reflex and squinting and may, therefore, in reality increase the effective dose of UVR to the eye. The irradiance at different interfaces in the eye depends on the transmittance to that interface. UVR is attenuated in the eye through absorption and scattering but the refractive apparatus of the eye also concentrates directly transmitted UVR on the retina. Effects
of ultraviolet
radiation
on the cornea
Although earlier cultures may have been painfully aware of the need to avoid photokeratitis, it was only 100 years ago first scientifically demonstrated that that Widmark’2,‘3 ambient UVR causes a severe and painful cornea1 response, known as photokeratitis or snow blindness. Since this discovery, the literature has been enriched with numerous reports on the cornea1 response to UVR in clinical populations and in animal experiments. Acute exposure to direct or reflected intense solar radiation may cause a photokeratitis in as short a time as 30 seconds14. This response is seen particularly often in surroundings covered by snow, hence the term ‘snow blindness’. The human vulnerability to snow blindness is best explained by the fact that fresh snow is the surface with the highest known non-specular reflectance factor for UVR” and that the cornea is less well protected from reflected UVR than overhead UVR. In addition to the sun, acute exposures from artificial sources such as tanning lights and welder’s arcs can induce photokeratitis in the unprotected eye’5.‘6. Tanning parlours use sources that emit predominantly UVA and very little
Significance
of ultraviolet
radiation
UVB light. Therefore, a cornea1 response to the exposure from these sources is usually not experienced by tanners using no protection. However, this lack of symptomology should be no excuse for not using filters since UVA is absorbed by the crystalline lens and possibly also the retina. Chronic low dose exposure to UVR appears also to affect the cornea. Karai et ~1.‘~ compared 118 welders with an average of 17 years of employment with 8.5 controls who had no welding experience, and found increased cornea1 endorhelial polymegethism and a decrease in the proportion of hexagonal cells among the welders. They believed this effec; to be the result of UVR from the welder’s arc, but they (did not discuss what kind of UV protection the welders had been using. Good and Schoessler’8 obtained similar resull:s when studying outdoor workers compared with a control group. They found a correlation between chronic ambient UVR exposure and increased pleomorphism and polyrnegethism. Chronic exposure to UVR has been suggested as a significanl. factor in the development of climatic droplet keratopath) . This permanent cornea1 pathology, also referred to as spheroid degeneration, is associated with people subjected to long-term environmental UVR exposure’9m25. One of the more recent and perhaps most comprehensive of these studies25 involved 838 subjects and concluded that there is ‘a clear association between a high personal UVR exposure and an increased risk of climatic droplet keratopathy’. Individual case reports and epidemiological studies share a common shortcoming in that there is little opportunity to control other factors that may contribute to or influence the manifestations of the response evaluated. Therefore, wellcontrolled animal studies are invaluable in identifying causative factors when studying specific conditions. It should also be remembered that the epidemiological study generally assesses the chronic, low dose exposure conditioq, while the laboratory study usually examines the acute response to high dose exposures. As mentioned above, these two study conditions are dissimilar and we are not free to assume that the two variant experimental settings necessarily trigger the same damage or repair mechanism. The action spectrum for UVR-induced keratitis has been studied in rabbits4.26. Early studies described cornea1 epith.elial cell changes and cell death27z3’. Clarke et ~1.~~ offered a quantification of cellular exfoliation and recovery following a suprathreshold exposure to UVR. However, the cornea1 epithelium regenerates quickly (within 5 days )33.34and therefore this painful condition was generally not regarded as a serious threat to cornea1 health. However, more recent studies have shown that the damage goes deeper than the epithelium. In fact, the response involves the full cornea1 thickness35-38,40-43. UVR can induce significant damage and cell death among keratocytes and endothelial cells35-38 while cornea1 nerves appear structurally intact38.39. This deeper cornea1 damage
on
the
eye:
J. P. G. Bergmanson
and
P. G. Sdderberg
85
in photokeratitis was shown in both primates and rabbits. As a consequence, it may be assumed that the mammalian cornea is unlikely to vary significantly in its vulnerability to UVR. The threshold to cornea1 damage for 300 nm UVB appears to be37,400.03-0.08 Jcm-*. It is expected that the structural trauma caused by suprathreshold UVR has functional consequences. Studies monitoring the cornea1 thickness after UVR exposure have consistently found that irradiation leads to a thickening of the cornea40m43.Increases in cornea1 thickness is caused by a fluid imbalance and this abnormal cornea1 hydration strongly implicates endothelial dysfunction, especially when lasting more than 5 days. Initially epithelial damage with a subsequent inability to control fluid movement from an anterior direction could camouflage or be confused with an endothelial involvement. However, the quoted studies by Cullen et uZ.~‘, Riley et ~1.~‘) and Doughty and Cullen4’,” all had adequate control to identify an endothelial cause for the cornea1 oedema measured. The inhibition of the endothelium may be caused by increased permeability (deturgescence) or a reduced fluid pump function. Indeed, Doughty and Cullen showed that the UVB-induced cornea1 swelling is explained by deficiencies in both these aspects with most of the thickening explained by the reduction in fluid pumping. There is a rapid and large decrease in cornea1 sensitivity following a UVR overdose but a complete recovery occurs within 4 hours44. The explanation for this prompt recovery appears to lie in the structural integrity of cornea1 nerve fibres following suprathreshold UVR exposures38,39. The initial inhibition of the nerve fibre impulses, however, is likely to have a physiological rather than a structural basis. Lattimore4s.46 examined the effect of UVR on cornea1 biochemistry. Following exposure he found a decrease in cornea1 oxygen uptake, a reduction in phosphocreatine, an increase in glucose and an elevation in glycogen. These findings suggest that UVR is capable of severe disruption of cornea1 metabolism. The cumulative effect of epidemiological and experimental evidence found in the literature for a relationship between UVR and cornea1 damage is very strong and suggests that all cornea1 structures are vulnerable to UVR. The trauma induced by UVR exposure involves vital cornea1 structures and functions, but the epithelial basement membrane, posterior limiting lamina (Descemet’s membrane) and the nerve fibres are spared. Effects
of ultraviolet
radiation
on the conjunctiva
In a number of studies, UVR has been linked to conjunctival changes. But the evidence is to a great extent indirect, since this literature is almost exclusively based on epidemiological data. One recent study explored the conjunctival action spectrum and found it similar to the cornea1 epithelium8. Therefore, in acute photokeratitis there will
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also be a conjunctival response. Pinguecula and pterygium are the conditions most commonly thought to have an association with chronic exposure to UVR. Pinguecula A pinguecula is a fibro-fatty degenerative change in the bulbar conjunctiva within the palpebral aperture. In assessing pinguecula in people from Labrador it was found that the size correlated with the severity of climatic droplet keratopathy24. In another study, Taylor et a1.25 found a weak association between pinguecula formation and UVA and UVB exposure in fishermen from Chesapeake Bay, Maryland, USA. They calculated the risk of developing pinguecula to be less than for climatic droplet keratopathy or pterygium. Norn47 reported a high prevalence of pinguecula among Arabs in the Red Sea region. Karai et a1.17 found that, unlike pterygium, there was no difference between welders and a control group with regard to the incidence of pinguecula. The evidence for a correlation between pinguecula and UVR exposure is indirect and based on a small number of epidemiological studies. It must, therefore, be concluded that, although a relationship between UVR exposure and pinguecula may exist, it has yet to be established. Pteiygium A pterygium is a hyperplasia of the bulbar conjunctiva. The pterygium may grow over the cornea and, on rare occasions, cause blindness. Two such cases are reported involving an Eskimo and an Australian aborigine48X49. These victims lived an outdoor life facing significant exposure to UVR during their lifetimes. A historical example is Lord Nelson who spent his life at sea and suffered from bilateral pterygia; incidentally, he added, as a helpful measure, a green eye shade to his admiral’s cocked hat”. Well-designed epidemiological studies suggest a correlation between UVR and pterygia developments. Hollows and Moran” found in an Australian study that the incidence of pterygium was related to the time spent outdoors. In a study from the northern hemisphere, Taylor et aZ.25x52 found a similar relationship. In fact, in this study on fishermen in Chesapeake Bay, it was concluded that there is a ‘clear association between a high personal exposure to UVR and an increased risk for both pterygium and climatic droplet keratopathy (CDK)‘. Mackenzie et a1.53 in their study of Australians, also found that time spent outdoors and pterygium development were linked. It appears that artificial sources containing larger energies of UVR are also capable of causing the development of pterygium. Karai et al. ” evaluated 191 Japanese welders and found that they had an increased risk of developing pterygium the longer they worked as a welder. Histopathological evidence supports the link between
UVR and pterygium formation. Austin et a1.54 found that an important component of both pinguecula and pterygium is abnormal synthesis and secondary degeneration of elastic fibres. This response shares similarities with sun-induced skin changes. Coroneo et a1.j5 offered an explanation for the specific location and shape of the pterygium. According to their hypothesis, peripherally incident light (or UVR) is refracted to foci at the nasal limbus, which is the most common site for pterygia. They also suggested that peripheral light (or UVR) may also be focused on the nasal aspect of the crystalline lens which may explain some cortical cataracts. Coroneo et al.” also proposed that individual variations in common environments may be the result of varying degrees of limbal focusing, which depends on cornea1 shape and the depth of the anterior chamber. Other factors apart from environmental or artificial UVR exposure may contribute to the formation of pterygium. In particular, sandy and dusty environments have been suggested as contributing or alternative factors54.S6. According to this hypothesis, it is believed that particular matter causes ocular irritation or microtrauma to the bulbar conjunctiva leading to the stimulus to pterygium growth. This notion is obviously not supported by the study on the fishermen in Chesapeake Bay, where the climatic conditions would not be described as dusty, hot or dry. Therefore, the evidence currently available clearly points to UVR as a significant factor in causing pterygium. Effects
of ultraviolet
radiation
on the lens
Cataract is a clinical syndrome involving an opacification of the crystalline lens that causes reduced vision. Experimental induction of cataracts with UVR is today a wellestablished model. There are numerous epidemiological studies concluding that exposure to UVR is an important risk factor for cataracts. Again, it should be reiterated that epidemiological studies cannot control all possible factors such as genes, diet, social behaviour, etc. Lately, cataract morbidity has been correlated with estimated individual dose. In the beginning of the 198Os, the solar dose of UVR for different populations was associated with the prevalence of cataract. There are numerous observational reports of a high prevalence of cataract in sunny areas compared to areas with little sun. Studying fishermen in Hong Kong57, it was found that the risk for cortical cataract among men aged 40-50 years who spent 5 or more hours per day outdoors, was increased compared with that for men who spent less time outdoors. In India, outdoor occupations were found to have an elevated risk for cataract compared with indoor occupations”. In a study from Italy, an excess of pure cortical and mixed cataracts was found among workers in sun-intense locationss9. Further, an increased incidence of cortical and mixed cataract was associated with leisure time spent in the
Significance
of ultraviolet
radiation
sunlight. Posterior subcapsular cataracts were associated with UVB exposure in a study from Maryland on cataract patients6’ and a study on fishermen in Chesapeake Bay, Maryland53, found an association between UVB and cortical cataracts. In Nepa16’, a correlation was found between the prevalence of cataracts and the average hours of sur:light when comparing different zones of the country. Another study, in rural areas of China62, demonstrated that ‘he prevalence of cataracts was correlated with annual direct total solar radiation. When evaluating the prevalence of cataract in different parts of Australia, it was found that cataract is more common in areas with a high average daily dose of UVB52,63. Hollows and Morar?’ studied an Australian population, the Aborigines, who spent most of their time outdoors and who followed a relatiT;ely uniform social pattern. It was found that the closer to the equator members of this population lived, the eerlier they would acquire cataracts. A North American study revealed that the solar dose of UVB is associated with cortical cataracts64. In an earlie- study of the same data a correlation between average solar dose of UVB and prevalence of cataract was reported65,66. Further, there have been observational studies since the end of the nineteenth century that reporl an increased prevalence of cataract in sunny area?‘. Thus, epidemiological studies strongly support UVR as a risk factor for cataract. Although the epidemiological studies have aimed at elucidating a possible dose-response relationship, a causal association cannot be established epidemiologically. Hoyvever, cataract was experimentally induced with UVR as early as the end of the nineteenth century6’. Since then, a number of studies on experimental induction of cataract have 3een published. Modern experimental studies have confirmed that UVB induces anterior cortical opacities and later posterior cortical opacil:ies4. Microscopically, the cortical opacities correspond 1.0swelling of lens epithelial cells and cortical fibres, until they rupture and thus cause vacuolization of the cortical area7”-83. The swelling has been associated with a transient increase of lens water74 which is related to a sodium-potassium shift75. The energy-dependent Na+-K+ ATPase that is responsible for maintenance of the Na+-I(+ balance over lens cell membranes, has been found to become impaired after exposure to UVR76. Extended low dose exposure to UVR has been found to induce changes in lens proteins”,‘*. The experimental studies discussed in the present report provide strong evidence for a causal relationship between exposure to UVR and the development of cataract. The major criticism regarding these experiments is that nonhuman species are studied and that a relatively high dose is given during a short time. Long-term, low intensity studies would be welcome.
on
the
eye:
Effects
J. P. G. Bergmanson
of ultraviolet
and
radiation
P. G. Sijderberg
87
on the retina
Extremely small amounts of UVR reach the retina”. The transmittance of UVR is highest in the newborn and decreases with age. Cruickshanks et al. *’ found an association between late stage age-related macular degeneration and summer leisure time outdoors. A study on fishermen in Maryland, showed that individuals with established age-related macular degeneration had significantly higher exposure to visible light from the sun during the previous 20 years8’.8’. More studies are needed to clarify the role of UVR for age-related macular degeneration. Experimental studies on primates have shown that high intensity light may cause acute photochemical damage”. The photochemical damage is strongly wavelength dependent84. The action spectrum for UVR-induced damage to the retina changes dramatically in aphakia’” with increased sensitivity at short wavelengths. Experimental exposure of primate eyes to 325 nm from a HeCd laser demonstrated retinal damage at doses below cornea1 thresholds5. An interesting observation was made by Yanuzzi et a1.86 who reported an elevated incidence of solar retinitis in areasof ozone depletion. It was found that the visual acuity was reduced to between 20140 and 20180 in affected individuals, but within 3-9 months, the visual acuity had returned to between 20/20 and 20130. Additional clinical manifestations reported were small central scotomasand permanent fovea1 lesions. Ultraviolet radiation-induced ocular malignancy Cornea1neoplasmsare extremely rare and when they occur they are usually connected to a limbal or conjunctival growth. These neoplasms are intraepithelial. Recently, three caseswere reported where the age range was 3 1 to 38 years and all caseshad a history of soft contact lens wear and exposureto high intensity UVR”. Templetong reported a high incidence of conjunctival squamouscell carcinoma in an African population living in Uganda near the equator. A recent epidemiological study, involving 60 caseswith ocular surface epithelial dysplasia, examined risk factors in developing cornea1 and conjunctival epithelial dysplasia, carcinoma in situ and squamouscell carcinomagy. It was concluded that cumulative UVR exposure is an important risk factor in developing these diseases.Other factors of significance were fair skin, pale iris, propensity to sunburn and a history of previous cancers. In summary, the evidencefor an associationbetweenUVR exposureand ocular surfaceneoplasmis scantbut mounting. Contact lenses and spectacles as ultraviolet filters
radiation
Contact lenses can be designed to be effective UVR
88
Ophthal.
Physiol.
Opt.
1995
15: No 2
absorbers” but contact lenses without a UVR blocker transmit 90% of the UVR spectrum”. A number of studies have clearly demonstratedthat when placed on the eye, a UVR filtering contact lens offers good protection of the cornea and presumably also the internal eye38.92393. However, it should be recognized that a soft contact lens offers more protection than a rigid gas permeable (RGP) contact lens becausethe former covers the entire cornea while the latter only covers a portion of the cornea. A second fundamental difference between soft and rigid contact lensesis the way that the latter provides no limbal or conjunctival coverage when fitted in its customary size, smaller than the cornea1diameter. In contrast, a well-fitted hydrogel lens covers limbal cornea and much, if not all, of the conjunctival palisadesof Vogt. This is of considerable significance since this is the location of a large number of the epithelial stem cells that continuously, in health and in disease, provide new cells to the cornea1 epithelium94. Cornea1 clarity is compromised when these cells are injured. An effective UV-blocking hydrogel contact lens would protect thesevital cells and their function from UVR damage. Effective UV-blocking spectacle lenses are available commercially and they provide a good general protection95.However, spectacleswith such lensesdo not provide complete protection since radiation may reach the cornea and conjunctiva without passingthrough the lenses.It may be argued that the well-fitted hydrogel lens is providing comparable or possibly better protection than a spectacle prescription, and, therefore, is an equally appropriate preventive measure.It must be stressedthat in UV intense environments, such as welding, neither spectacles nor contact lenses should be substituted for recommended safety goggles. The question whether the wearing of contact lenses makesthe cornea more vulnerable to UV trauma has been raised93.96.97 but this possibility has not yet been confirmed nor ruled out beyond doubt. Further researchon this issue is desirable. Concluding comments There is no evidence that exposure of the eye to UVR is essentialfor the human body or beneficial to vision itself. However, there is today conclusive evidence that an acute overdose of UVR from the suncausesacute photokeratitis. There is very strong epidemiological support for an association between long-term exposure to the sun and the development of both pterygium and cataract. Furthermore, there is experimental and epidemiological evidence suggesting that UVR reaches the retina and may ultimately cause macular
degeneration79-85.
Considering
the above-
cited data, there is no scientific basis for denying the eye UVR protection. Both
contact
lenses
and spectacles
offer
an excellent
opportunity
to decrease
the load of UVR
on the eye. A
number of studieshave shown that a contact lens can be an efficient UVR filter if the appropriate absorbing chromophore is included in the contact lens materia137~38~90~9’~93~98~99 but without such material formulation, the lens offers no protection. A wide-brimmed hat is a helpful adjunct to UV filtering ophthalmic devices. The use of UVR-blocking contact lenses or spectacles does not preclude the need to
use UVR-filtering safety goggles or sunglasseswith side protection
in environments
with
high intensity
of UVR.
Acknowledgements We gratefully acknowledge the generous assistanceprovided by Mr Todd Sheldon and Mr Doug Wike in the preparation
of this manuscript.
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Significance
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91 Chou, B. R., Cullen, A. P. and Egan, D. J. Spectral transmittance of contact lens material. ht. Contact Lens C/in. 11, 106-114 (1984) 92 Bergmanson, J. P. G., Pitts, D. G. and Chu, L. W.-F. Protection from harmful UV radiation by contact lenses. J. A17:. Optom. Assoc. 59, 178-182 (1988) 93 Cullen, A. P., Dumbleton, K. A. and Chou, B. R. Contact lenses and acute exposure to ultraviolet radiation. Optom. Vision sci. 66, 407-411 (1989) 94 Theft, R. A. The XYZ hypothesis of cornea1 epithelial maintenance. Invest. Opktkal. Visual Sci. 24, 1442-1443 (1983) 95 Pitis, D. G. Principles in ocular protection. In Environmental Vi: ior? (eds D. G. Pitts and R. N. Kleinstein), ButterworthHememann, Boston, MA, USA, pp. 259-280 (1993)
on the eye: J. P. G. Bergmanson
and P. G. S&derberg
91
96 Ahmedbhai, N. and Cullen, A. P. The influence of contact lens wear on the cornea1 response to ultraviolet radiation. Opktkal. Pkysiol. Opt. 8, 183-189 (1988) 97 Pitts, D. G., Bergmanson, J. P. G. and Chu, L. W.-F. Does the endothelium of the contact lens wearing cornea require UV protection? J. Br. Contact Lens Assoc. 11, 23-27 (1988) 98 Dumbleton, K. A., Cullen, A. P. and Doughty, M. J. Protection from acute exposure to ultraviolet radiation by ultraviolet-absorbing RGP contact lenses. Opktkal. Pkysiol. Opt. 11, 232-238 (1991) 99 Pitts, D. G. and Lattimore, M. R. Protection against UVR using the Vistakon UV-Bloc soft contact lens. Int. Contact Lens Clin. 14, 22-30 (1987)