- Email: [email protected]
The Spectra, Classification, and Rationale of Ultraviolet-Protective Intraocular Lenses
The Spectra, Classification, and Rationale of Ultraviolet-Protective Intraocular Lenses Martin A. Mainster, M.D.
I measured the spectral transmittance of 16 implantable intraocular lenses from 12 manufacturers and examined the rationale for using ultraviolet-absorptive intraocular lenses to protect pseudophakic individuals from photic retinopathy. Each ultraviolet-protective lens was classified by the wavelength at which its spectral transmittance fell to 10% in the blue or ultraviolet region of the spectrum. Current ultraviolet-protective intraocular lenses differ in the effectiveness of their protection against photic retinopathy, and product descriptions may be misleading. OPHTHALMIC LORE ascribes the origin of polymethylmethacrylate intraocular lenses to clinical observations of the low reactivity of intraocular polymethylmethacrylate fragments from shattered World War II Spitfire fighter canopies.' Had wartime economies permitted the use of ultraviolet filtering polymethylmethacrylate in fighter canopies, the issue of whether or not to use ultraviolet-protective chromophores in intraocular lenses may never have arisen. Just as the Spitfire canopy, intraocular lenses were initially manufactured without ultraviolet-absorbing chromophores. Unlike the native crystalline lens, however, a clear polymethylmethacrylate intraocular lens transmits near-ultraviolet and deep blue radiation. Unfortunately, these parts of the spectrum are likely to produce photic retinopathy. This study provides measurements and a classification of the spectral transmittance of contemporary ultraviolet-protective intraocular lenses and reexamines the rationale for their use.
Accepted for publication Sept. 10, 1986. From the Department of Ophthalmology, Kansas University Medical Center, Kansas City, Kansas. This study was supported in part by Research to Prevent Blindness, Inc., and Kansas Lions Sight Foundation, Inc. Reprint requests to Martin A. Mainster, M.D., Department of Ophthalmology, Kansas University Medical Center, 39th and Rainbow Blvd., Kansas City, KS 66103.
Material and Methods I used a diode array single-beam, microprocessor-controlled, ultraviolet-visible spectrophotometer to measure the spectral transmittance of 16 intraocular lenses from 12 lens manufacturers. Its radiation source is a plasma discharge in low pressure deuterium gas contained in a quartz envelope. An ellipsoidal mirror focuses radiation (ultraviolet, visible, or infrared) light onto a sample cell containing the lens holder and the intraocular lens to be tested. Transmitted light is reflected onto a holographic grating by a second ellipsoidal mirror. The grating disperses transmitted light onto 328 individual photodiodes, permitting transmittance measurements in 2-nm increments between 190 and 820 nm. I removed each of the 16 intraocular lenses from its factory-sealed packaging, recorded its manufacturer and style, and mounted it in the lens holder. The lens holder and intraocular lens were placed in the sample cell and aligned. Transmittance was measured in 2-nm intervals between 300 and 500 nm and was documented numerically and graphically. After all transmittance measurements were completed, the entire process was repeated twice. Reported transmittances are the average of three independent measurements. Transmittance measurements were typically within 0.5% of each other. The spectral transmittances of ultraviolet-protective intraocular lenses are shown in the Figure and Table 1. For comparison, transmittance measurements are given for two clear polymethylmethacrylate intraocular lenses: one made of Perspex CQ (Imperial Chemical Industries) polymethylmethacrylate (lens 15), and one made of Plexiglas (Rohm and Haas Corporation) polymethylmethacrylate (lens 16). The spectral transmittance of the crystalline lens of a 53-year-old individual is also shown." Table 1 shows the wavelength at which lens transmittance falls to 10% in the blue or ultravi-
©AMERICAN JOURNAL OF OPHTHALMOLOGY 102:727-732, DECEMBER, 1986
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Figure (Mainster). Spectral transmittance of ultravioletprotective and clear polymethylmethacrylate intraocular lenses for three ultraviolet-protective intraocular lenses: a class 1 lens (lens 7), a class 3 lens (lens 10), and a class 5 lens (lens 6). Lenses and their classification are presented in Tables 1 and 2, respectively. For comparison, the spectral transmittance is shown for clear polymethylmethacrylate intraocular lenses made of Perspex CQ (lens 15) and Plexiglas (lens 16). Also shown is the spectral transmittance of the crystalline lens of a 53year-old individual (H).2
WAVELENGTH (nm) olet part of the electromagnetic spectrum, W(10%). Larger values of W(10%) indicate more effective ultraviolet and deep blue protection. Table 1 also shows the percent transmittance at 400 nm, %T(400 nm). Smaller values of
%T(400nm) indicate more effective protection at 400 nm, the lower limit of visible radiation for the phakic eye. Since these two measurements vary with lens power, only 20 D, posterior chamber intraocular lenses were examined.
TABLE 1 TRANSMITTANCE AND CLASSIFICATION OF ULTRAVIOLET-PROTECTIVE INTRAOCULAR LENSES LENS
MANUFACTURER'
TYPE
WAVELENGTH' (%T
10 11 12 13 14
American Medical Optics CllCO Coburn CooperVision Copeland Intermedics IOlAS IOlAS IOPTEX Optical Radiation Precision Cosmet Surgidev Surgidev Vision Care/3M
15 16
CllCO IOlAS
2
3 4 5 6 7 8 9
~
10%)
Ultraviolet Protective 401 PC-15lS SK21lRU 388 68UV 389 823-01 388 405 MODJ U37SC 378 412 U706S 400 G708G 384 UV301-01 UV31K 396 409 489 329 20-15 UV20-20 387 380 34lE Clear Polymethylmethacrylate 263 SK21 329 103Q
*IOlAS and Surgidev advertise more than one type of ultraviolet-protective intraocular lens. 'Wavelength at which percent transmittance (%T) falls to 10%.
TRANSMITTANCE
CLASS
(%T at 400 nm)
8.20
2
71.00 41.00 73.00 0.87 85.00 0.15 9.40 62.00 19.00 0.23 87.00 72.00 86.00
4 4 4 2 5 1 2 4 3 2 N 4 4
89.00 86.00
Ultraviolet-Protective Intraocular Lenses
Vol. 102, No.6
TABLE 2 CLASSIFICATION OF ULTRAVIOLET-PROTECTIVE INTRAOCULAR LENSES BASED ON W(10%)* W(10%)
CLASS
1 2 3 4 5
N'
410 400 390 380
nm and higher to 409 nm to 399 nm to 389 nm
370 to 379 nm Below 370
LENSES IN TABLE 1
7 1,5,8,11 10 2,3,4,9, 13, 14
729
methacrylate, without ultraviolet-absorbing chromophores. With this lens potentially hazardous ultraviolet radiation between 330 and 400 nm is transmitted to the retina. The term "natural" apparently refers to the absence of ultraviolet-protective chromophores, even though there is nothing "natural" about clear polymethylmethacrylate or the absence of near-ultraviolet protection.
6 12
'Wavelength at which %T (percent transmittance) falls to 10%. 'N, non-ultraviolet-protective. All intraocular lenses with ultraviolet-absorbing chromophores had a W(10%) above 370 nm.
For comparison of ultraviolet-protective intraocular lenses, I grouped intraocular lenses into six classes based on their W(10%) values. These classes are defined in Table 2.
Results Several conclusions can be drawn from the data. First, despite similar claims by manufacturers, there is a wide disparity in the ultraviolet protection offered by ultraviolet-protective intraocular lenses, ranging from excellent protection (classes 1 and 2), to poor protection (classes 4 and 5), to protection no better than clear polymethylmethacrylate (class N). Second, intraocular lens advertising can be misleading. For example, lens 5 is promoted as an ultraviolet-absorbing lens, even though its current advertised transmittance spectrum is that of a clear polymethylmethacrylate intraocular lens with a W(10%) of 335 nm and a %T(400 nm) of 98%. The actual lens 5 currently sold to clinicians is one of the most effective ultraviolet-protective intraocular lenses, however, suggesting that either the manufacturer is unaware of changes in the polymethylmethacrylate provided by its supplier, or does not feel it necessary to change promotional literature or prescribing information enclosed with the actual implantable lens when it changes the polymethylmethacrylate in its intraocular lenses. Another example of misleading advertising is lens 12, promoted as composed of "natural ultraviolet absorbing polymethylmethacrylate." This lens is made of clear polymethyl-
Discussion Light can damage ocular tissues in three ways: through its ionizing effects, thermal effects, and photochemical effects. Ionizing effects are produced by Q-switched Nd:YAG lasers with brief exposures, typically nanoseconds (10- 9 seconds) to picoseconds (10- 12 ) in duration. These effects occur when a focused laser beam produces an irradiance high enough to strip electrons from molecules in the target tissue, producing a collection of ions and electrons called a "plasma." Rapid plasma expansion combined with latent tissue stress incises target tissues, as in an Nd:YAG laser discission for an opacified posterior capsule." Thermal effects are produced with longer light exposures, typically between 0.1 and 0.5 seconds. They occur when a focused laser beam heats target tissues to a temperature high enough to produce a local inflammatory response. Coagulation and scarring are the desired therapeutic end points, as in panretinal photocoagulation for proliferative diabetic retinopathy or laser trabeculoplasty for chronic open-angle glaucoma. 4 Photochemical effects are produced with even longer exposures, typically greater than 10 seconds in duration. They occur when light produces chemical reactions in target tissues, at light levels and temperature increases far below those needed for photocoagulation. Photochemical effects can be deliberate, as in laser exposure of tissues sensitized with a lightsensitive chromophore such as HpD derivative," or they can be inadvertent, as in photic retinopathy from solar observation." welding arc exposure, ;,8 or operating microscope exposure.P-" Photochemical effects were first documented in 1966. 11 The retina has two lines of defense against light damage. The outer segments of rod and cone photoreceptors shed photopigmentcontaining disks, thereby eliminating struc-
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AMERICAN JOURNAL OF OPHTHALMOLOGY
tures that may be damaged by high light and oxygen concentrations." The retinal pigment epithelium removes this outer segment debris, and is therefore subject to the damaging effects of lipid debris in a high oxygen environment. 13.1 4 The retinal pigment epithelium is protected against these toxic factors by melanin and a battery of antioxidants including superoxide dismutase, peroxidase, catalase, and vitamin £.13.1 4 With age, retinal pigment epithelium lipofuscin increases.I'-" and melanin" and probably other retinal pigment epithelium defense mechanisms decline. Photochemical light damage can affect the retinal pigment epitheliurn." the photoreceptors;" or both the retinal pigment epithelium and neurosensory retina. 19.20 The damage may be additive." and depends on species and the exposure history (duration, intensity and source spectrum, and the location and extent of exposed retina). One of the most striking features of photic retinopathy is that damage susceptibility increases with decreasing wavelength, so that blue light and ultraviolet radiation pose the greatest potential risk. 17-19 The electromagnetic spectrum spans a continuous range of wavelengths, including visible light between 400 and 700 nm, and ultraviolet radiation at shorter wavelengths. In a normal human eye, the cornea, opaque to ultraviolet light below 300 nm, shields internal ocular components from potential harm from light below 300 nm. In the near-ultraviolet region between 300 and 400 nm, however, the cornea is effectively transparent. In this region, the crystalline lens absorbs near-ultraviolet radiation and shields the retina from potential harm. When the crystalline lens is removed in cataract surgery, however, the retina's near-ultraviolet light protection is also removed. Replacing the crystalline lens with a clear polymethylmethacrylate intraocular lens provides little protection because clear polymethylmethacrylate allows most of the near-ultraviolet light to reach the retina. 21,22 There has been a marked increase in reported cases of photic retinopathy from operating microscopes in the past few years,23-27 complementing previous reports of photochemical retinal damage from solar and welding arc observation, and emphasizing the clinical significance of photic retinopathy. Photic retinopathy probably comprises a continuum of related hazards, the nature of biochemical events being determined by the exposure history and
December, 1986
the effectiveness of individual retinal defense mechanisms. Because experimental studies show that mild photochemical retinal damage may not be visible by ophthalmoscopy.A'" clinical reports probably represent only the most severe injuries. The long-term effects of photic retinopathy may not be distinguishable from normal aging changes, such as geographic aging macular degeneration. Furthermore, it is unclear if severe erythropsia'<" produces permanent effects that are not initially apparent by ophthalmoscopy, or if this condition is the clinical analog of blue-sensitive cone photochemical damage observed in primates at very low light levels." The aphakic and nonultraviolet protected retina are exposed and sensitive to nearultraviolet radiation. 30 These patients should be cautioned to wear ultraviolet-protective spectacles in bright environments, such as ski slopes or seashores. 22,31 In view of mounting evidence that the pseudophakic retina needs effective ultraviolet protection, the variability in spectral transmittance of intraocular lenses marketed as ultravioletprotective is disturbing. As shown in Table I, classes 4, 5, and N lenses offer only limited ultraviolet protection, and pseudophakic individuals with those lenses should still be cautioned to wear ultraviolet-protective spectacles in bright enviroriments.P:" Misleading advertisements like those noted earlier are also disturbing. New labeling requirements from the Food and Drug Administration should eliminate some uncertainty, but clinicians should be wary of the performance of the intraocular lenses they implant. In 1978, I reported the increased risk of the pseudophakic individual to thermal" and photochemical retinal damage.F and suggested a possible role for cumulative photochemical retinal damage in aging macular degeneration." If cumulative photochemical damage does contribute to macular degeneration, it may be difficult to prove the efficacy of ultravioletprotective intraocular lenses because the long-term effects of subclinical photic retinopathy may be indistinguishable from normal retinal aging. It would require a large patient population to demonstrate a difference in the incidence of aging macular degeneration between pseudophakic individuals with clear and with ultraviolet-protective intraocular lenses. Since 1978, most intraocular lens manufacturers have introduced ultraviolet-protective lens-
Vol. 102, No.6
Ultraviolet-Protective Intraocular Lenses
es, and over 60% of all new implanted intraocular lenses are ultraviolet-protective (Intraocular Lens Market Survey, North Branch, NJ: Health Products Research, Inc., 1985). Ultravioletprotective intraocular lenses have been shown to reduce the risk of photic retinopathy in experimental animals." Additionally, it has been found that ultraviolet-protective intraocular lenses reduce the risk of postoperative angiographically apparent cystoid macular edema, even though this effect does not have shortterm visual consequences." While it is important to consider the longterm toxicity of ultraviolet-absorbing chromophores in intraocular lenses;" photic retinopathy is a demonstrable clinical syndrome. If clear polymethylmethacrylate intraocular lenses are used, the aged retinae of typical cataract patients are deprived of effective ultraviolet protection at a time when their defenses against photic retinopathy are waning. 15,35 An ideal ultraviolet-absorbing intraocular lens should provide effective protection against potentially harmful radiation below 400 nm that contributes nothing to vision (other than erythropsia, glare, and chromatic aberration), but it should not alter the normal photopic or scotopic spectral sensitivity for the patient's age group. Additionally, chromophore photodegradation and leachability should be minimized. 34,36,37 Blue light is also potentially hazardOUS,17.19,22,31 as demonstrated by solar retinitis," welder's maculopathv.t" and operating microscope damage" in phakic eyes with natural crystalline lens protection. Thus, the ideal value for W(10%), the short-wavelength cut-off for ultraviolet-protective intraocular lenses, is probably between 410 nrn and 430 nm. Some authors have advocated cut-offs as long as 450 nrri." Careful psychophysical studies are needed to determine the longest wavelength cut-off (greatest protection) that does not impair photopic or scotopic vision.
References 1. Ridley, H.: Intra-ocular acrylic lenses. Trans Ophthalmol. Soc. U.K. 71:617, 1951.
2. Boettner, E. A., and Wolter, J. R.: Transmission of the ocular media. Invest. Ophthalmol. Vis. Sci. 1:776, 1962.
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3. Mainster, M. A., Sliney, D. H., Belcher, C. D., III, and Buzney, S. M.: Laser photodisruptors. Damage mechanisms, instrument design and safety. Ophthalmology 90:973, 1983. 4. Mainster, M. A.: Finding your way in the photoforest. Laser effects for clinicians. Ophthalmology 91:886, 1984. 5. L'Esperance. F. A., Jr.: Ophthalmic Lasers. St. Louis, C. V. Mosby Co., 1983, pp. 340-350. 6. White, T. J., Mainster, M. A., Wilson, P. W., and Tips, J. H.: Chorioretinal temperature increases from solar observation. Bull. Math. Biophys. 33:1, 1971.
7. Naidoff, M. A., and Sliney, D. H.: Retinal injury from a welding arc. Am. J. Ophthalmol. 77:663,
1974.
8. Rornanchuk, K. G., Pollak, V., and Schneider, R. J.: Retinal burn from a welding arc. Can. J. Ophthalmol. 13:120, 1978. 9. Calkins, J. L., and Hochheimer, B. F.: Retinal light exposure from operation microscopes. Arch. Ophthalmol. 97:2362, 1979. 10. Robertson, D. M., and Feldman, R. B.: Photic retinopathy from the operating room microscope. Am. J. Ophthalmol. 101:561, 1986. 11. Noell, W. K., Walker, V. S., Kang, B. S., and Berman, S.: Retinal damage by light in rats. Invest. Ophthalmol. Vis. Sci. 5:450, 1966. 12. Young, R. W.: Visual cells and the concept of renewal. Invest. Ophthalmol. Vis. Sci. 15:700, 1976. 13. Feeney, L., and Berman, E. R.: Oxygen toxicity. Membrane damage by free radicals. Invest. Ophthalmol. Vis. Sci. 15:789, 1976. 14. Marshall, J.: Radiation and the aging eye. Ophthalmol. Physiol. Opt. 5:241, 1985. 15. Feeney-Burns, L., Hilderbrand, E. S., and Eldridge, S.: Aging human RPE. Morphometric analysis of macular equatorial and peripheral cells. Invest. Ophthalmol. Vis. Sci. 25:195, 1984. 16. Wing, G. L., Blanchard, G. c.. and Weiter, J. J.: The topography and age relationship of lipofuscin concentration in the retinal pigment epithelium. Invest. Ophthalmol. Vis. Sci. 17:601, 1978. 17. Ham, W. T., [r., Mueller, H. A., and Sliney, D. H.: Retinal sensitivity to damage from short wavelength light. Nature 260:153, 1976. 18. Sperling, H. G., Johnson, C.; and Harwerth, R. S.: Differential spectral photic damage to primate cones. Vision Res. 20:1117, 1980. 19. Lawwill, T.: Three major pathologic processes caused by light in the primate retina. A search for mechanisms. Trans. Am. Ophthalmol. Soc. 80:517, 1982. 20. Noell, W. K.: Possible mechanisms of photore-
ceptor damage by light in mammalian eyes. Vision Res. 20:1163, 1980. 21. Mainster, M. A.: Spectral transmittance of intraocular lenses and retinal damage from intense light sources. Am. J. Ophthalmol. 85:167, 1978. 22. - - - : Solar retinitis, photic maculopathy and
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the pseudophakic eye. Am. Intra-Ocular Implant Soc. J. 4:84, 1978. 23. Parver, L. M., Auker, C. R., and Fine, B. S.: Observations on monkey eyes exposed to light from an operating microscope. Ophthalmology 90:964, 1983. 24. Irvine, A. R., Wood, 1., and Morris, B. W.: Retinal damage from the illumination of the operating microscope. An experimental study in pseudophakic monkeys. Arch. Ophthalmol. 102:1358, 1984. 25. McDonald, H. R., and Irvine, A. R.: Lightinduced maculopathy from the operating microscope in extracapsular cataract extraction and intraocuLar lens implantation. Ophthalmology 90:945, 1983. 26. Ross, W. H.: Light-induced maculopathy. Am. J. Ophthalmol. 98:488, 1984. 27. Brod, R. D., Barron, B. A., Suelflow, J. A., Franklin, R. M., and Packer, A. J.: Phototoxic retinal damage during refractive surgery. Am. J. Ophthalmol. 102:121, 1986. 28. Kamel, 1. D.,' and Parker, J. A.: Protection from ultraviolet exposure in aphakic erythropsia. Can. J. Ophthalmol. 8:563, 1973. 29. Saraux, H., Manent, J.-P., and Laroche, L.: Erythropsie chez un porteur d'implant. Etude physiologique et electrophysiologique. J. Fr. Ophtalmol. 7:557, 1984. 30. Werner, J. S., and Hardenbergh, F. E.: Spec-
December, 1986
tral sensitivity and the pseudophakic eye. Arch. Ophthalmol. 101:758, 1983. 31. Mainster, M. A., Ham, W. T., Jr., and Delori, F. c.: Potential retinal hazards. Instrument and environmental light sources. Ophthalmology 90:927, 1983. 32. Peyman, G. A., Zak, R., and Sloane, H.: Ultraviolet-absorbing pseudophakos. An efficacy study. Am. Intra-Ocular Implant Soc. J. 9:161, 1983. 33. Kraf£, M. c., Sanders, D. R., Iampol, L. M., and Lieberman, H. L.: Effect of an ultravioletfiltering intraocular lens on cystoid macular edema. Ophthalmology 92:366, 1985. 34. Clayman, H. M.: Ultraviolet-absorbing intraocular lenses. Am. Intra-Ocular Implant Soc. J. 10:429, 1984. 35. Yew, D. T., Tsang, D. S. c.. and Chan, Y. W.: Photic responses of the retina at different ages. A comparative study using histochemical and biochemical methods. Acta Anal. 123:34, 1985. 36. Lindstrom, R. L., and Doddi, N.: Ultraviolet light absorption in intraocular lenses. J. Cataract Refract. Surg. 12:285, 1986. 37. Gupta, A.: Long-term aging behavior of ultravioletabsorbing intraocular lenses. Am. Intra-Ocular Implant Soc. J. 10:309, 1984. 38. Zigman, S.: Ultraviolet-absorbing intraocular lenses. Am. Intra-Ocular Implant Soc. J. 11:386, 1985.
I measured the spectral transmittance of 16 implantable intraocular lenses from 12 manufacturers and examined the rationale for using ultraviolet-absorptive intraocular lenses to protect pseudophakic individuals from photic retinopathy. Each ultraviolet-protective lens was classified by the wavelength at which its spectral transmittance fell to 10% in the blue or ultraviolet region of the spectrum. Current ultraviolet-protective intraocular lenses differ in the effectiveness of their protection against photic retinopathy, and product descriptions may be misleading. OPHTHALMIC LORE ascribes the origin of polymethylmethacrylate intraocular lenses to clinical observations of the low reactivity of intraocular polymethylmethacrylate fragments from shattered World War II Spitfire fighter canopies.' Had wartime economies permitted the use of ultraviolet filtering polymethylmethacrylate in fighter canopies, the issue of whether or not to use ultraviolet-protective chromophores in intraocular lenses may never have arisen. Just as the Spitfire canopy, intraocular lenses were initially manufactured without ultraviolet-absorbing chromophores. Unlike the native crystalline lens, however, a clear polymethylmethacrylate intraocular lens transmits near-ultraviolet and deep blue radiation. Unfortunately, these parts of the spectrum are likely to produce photic retinopathy. This study provides measurements and a classification of the spectral transmittance of contemporary ultraviolet-protective intraocular lenses and reexamines the rationale for their use.
Accepted for publication Sept. 10, 1986. From the Department of Ophthalmology, Kansas University Medical Center, Kansas City, Kansas. This study was supported in part by Research to Prevent Blindness, Inc., and Kansas Lions Sight Foundation, Inc. Reprint requests to Martin A. Mainster, M.D., Department of Ophthalmology, Kansas University Medical Center, 39th and Rainbow Blvd., Kansas City, KS 66103.
Material and Methods I used a diode array single-beam, microprocessor-controlled, ultraviolet-visible spectrophotometer to measure the spectral transmittance of 16 intraocular lenses from 12 lens manufacturers. Its radiation source is a plasma discharge in low pressure deuterium gas contained in a quartz envelope. An ellipsoidal mirror focuses radiation (ultraviolet, visible, or infrared) light onto a sample cell containing the lens holder and the intraocular lens to be tested. Transmitted light is reflected onto a holographic grating by a second ellipsoidal mirror. The grating disperses transmitted light onto 328 individual photodiodes, permitting transmittance measurements in 2-nm increments between 190 and 820 nm. I removed each of the 16 intraocular lenses from its factory-sealed packaging, recorded its manufacturer and style, and mounted it in the lens holder. The lens holder and intraocular lens were placed in the sample cell and aligned. Transmittance was measured in 2-nm intervals between 300 and 500 nm and was documented numerically and graphically. After all transmittance measurements were completed, the entire process was repeated twice. Reported transmittances are the average of three independent measurements. Transmittance measurements were typically within 0.5% of each other. The spectral transmittances of ultraviolet-protective intraocular lenses are shown in the Figure and Table 1. For comparison, transmittance measurements are given for two clear polymethylmethacrylate intraocular lenses: one made of Perspex CQ (Imperial Chemical Industries) polymethylmethacrylate (lens 15), and one made of Plexiglas (Rohm and Haas Corporation) polymethylmethacrylate (lens 16). The spectral transmittance of the crystalline lens of a 53-year-old individual is also shown." Table 1 shows the wavelength at which lens transmittance falls to 10% in the blue or ultravi-
©AMERICAN JOURNAL OF OPHTHALMOLOGY 102:727-732, DECEMBER, 1986
727
728
December, 1986
AMERICAN JOURNAL OF OPHTHALMOLOGY
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o
a:
90
Q.
80
W
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~
60
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40
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30
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20
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Figure (Mainster). Spectral transmittance of ultravioletprotective and clear polymethylmethacrylate intraocular lenses for three ultraviolet-protective intraocular lenses: a class 1 lens (lens 7), a class 3 lens (lens 10), and a class 5 lens (lens 6). Lenses and their classification are presented in Tables 1 and 2, respectively. For comparison, the spectral transmittance is shown for clear polymethylmethacrylate intraocular lenses made of Perspex CQ (lens 15) and Plexiglas (lens 16). Also shown is the spectral transmittance of the crystalline lens of a 53year-old individual (H).2
WAVELENGTH (nm) olet part of the electromagnetic spectrum, W(10%). Larger values of W(10%) indicate more effective ultraviolet and deep blue protection. Table 1 also shows the percent transmittance at 400 nm, %T(400 nm). Smaller values of
%T(400nm) indicate more effective protection at 400 nm, the lower limit of visible radiation for the phakic eye. Since these two measurements vary with lens power, only 20 D, posterior chamber intraocular lenses were examined.
TABLE 1 TRANSMITTANCE AND CLASSIFICATION OF ULTRAVIOLET-PROTECTIVE INTRAOCULAR LENSES LENS
MANUFACTURER'
TYPE
WAVELENGTH' (%T
10 11 12 13 14
American Medical Optics CllCO Coburn CooperVision Copeland Intermedics IOlAS IOlAS IOPTEX Optical Radiation Precision Cosmet Surgidev Surgidev Vision Care/3M
15 16
CllCO IOlAS
2
3 4 5 6 7 8 9
~
10%)
Ultraviolet Protective 401 PC-15lS SK21lRU 388 68UV 389 823-01 388 405 MODJ U37SC 378 412 U706S 400 G708G 384 UV301-01 UV31K 396 409 489 329 20-15 UV20-20 387 380 34lE Clear Polymethylmethacrylate 263 SK21 329 103Q
*IOlAS and Surgidev advertise more than one type of ultraviolet-protective intraocular lens. 'Wavelength at which percent transmittance (%T) falls to 10%.
TRANSMITTANCE
CLASS
(%T at 400 nm)
8.20
2
71.00 41.00 73.00 0.87 85.00 0.15 9.40 62.00 19.00 0.23 87.00 72.00 86.00
4 4 4 2 5 1 2 4 3 2 N 4 4
89.00 86.00
Ultraviolet-Protective Intraocular Lenses
Vol. 102, No.6
TABLE 2 CLASSIFICATION OF ULTRAVIOLET-PROTECTIVE INTRAOCULAR LENSES BASED ON W(10%)* W(10%)
CLASS
1 2 3 4 5
N'
410 400 390 380
nm and higher to 409 nm to 399 nm to 389 nm
370 to 379 nm Below 370
LENSES IN TABLE 1
7 1,5,8,11 10 2,3,4,9, 13, 14
729
methacrylate, without ultraviolet-absorbing chromophores. With this lens potentially hazardous ultraviolet radiation between 330 and 400 nm is transmitted to the retina. The term "natural" apparently refers to the absence of ultraviolet-protective chromophores, even though there is nothing "natural" about clear polymethylmethacrylate or the absence of near-ultraviolet protection.
6 12
'Wavelength at which %T (percent transmittance) falls to 10%. 'N, non-ultraviolet-protective. All intraocular lenses with ultraviolet-absorbing chromophores had a W(10%) above 370 nm.
For comparison of ultraviolet-protective intraocular lenses, I grouped intraocular lenses into six classes based on their W(10%) values. These classes are defined in Table 2.
Results Several conclusions can be drawn from the data. First, despite similar claims by manufacturers, there is a wide disparity in the ultraviolet protection offered by ultraviolet-protective intraocular lenses, ranging from excellent protection (classes 1 and 2), to poor protection (classes 4 and 5), to protection no better than clear polymethylmethacrylate (class N). Second, intraocular lens advertising can be misleading. For example, lens 5 is promoted as an ultraviolet-absorbing lens, even though its current advertised transmittance spectrum is that of a clear polymethylmethacrylate intraocular lens with a W(10%) of 335 nm and a %T(400 nm) of 98%. The actual lens 5 currently sold to clinicians is one of the most effective ultraviolet-protective intraocular lenses, however, suggesting that either the manufacturer is unaware of changes in the polymethylmethacrylate provided by its supplier, or does not feel it necessary to change promotional literature or prescribing information enclosed with the actual implantable lens when it changes the polymethylmethacrylate in its intraocular lenses. Another example of misleading advertising is lens 12, promoted as composed of "natural ultraviolet absorbing polymethylmethacrylate." This lens is made of clear polymethyl-
Discussion Light can damage ocular tissues in three ways: through its ionizing effects, thermal effects, and photochemical effects. Ionizing effects are produced by Q-switched Nd:YAG lasers with brief exposures, typically nanoseconds (10- 9 seconds) to picoseconds (10- 12 ) in duration. These effects occur when a focused laser beam produces an irradiance high enough to strip electrons from molecules in the target tissue, producing a collection of ions and electrons called a "plasma." Rapid plasma expansion combined with latent tissue stress incises target tissues, as in an Nd:YAG laser discission for an opacified posterior capsule." Thermal effects are produced with longer light exposures, typically between 0.1 and 0.5 seconds. They occur when a focused laser beam heats target tissues to a temperature high enough to produce a local inflammatory response. Coagulation and scarring are the desired therapeutic end points, as in panretinal photocoagulation for proliferative diabetic retinopathy or laser trabeculoplasty for chronic open-angle glaucoma. 4 Photochemical effects are produced with even longer exposures, typically greater than 10 seconds in duration. They occur when light produces chemical reactions in target tissues, at light levels and temperature increases far below those needed for photocoagulation. Photochemical effects can be deliberate, as in laser exposure of tissues sensitized with a lightsensitive chromophore such as HpD derivative," or they can be inadvertent, as in photic retinopathy from solar observation." welding arc exposure, ;,8 or operating microscope exposure.P-" Photochemical effects were first documented in 1966. 11 The retina has two lines of defense against light damage. The outer segments of rod and cone photoreceptors shed photopigmentcontaining disks, thereby eliminating struc-
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tures that may be damaged by high light and oxygen concentrations." The retinal pigment epithelium removes this outer segment debris, and is therefore subject to the damaging effects of lipid debris in a high oxygen environment. 13.1 4 The retinal pigment epithelium is protected against these toxic factors by melanin and a battery of antioxidants including superoxide dismutase, peroxidase, catalase, and vitamin £.13.1 4 With age, retinal pigment epithelium lipofuscin increases.I'-" and melanin" and probably other retinal pigment epithelium defense mechanisms decline. Photochemical light damage can affect the retinal pigment epitheliurn." the photoreceptors;" or both the retinal pigment epithelium and neurosensory retina. 19.20 The damage may be additive." and depends on species and the exposure history (duration, intensity and source spectrum, and the location and extent of exposed retina). One of the most striking features of photic retinopathy is that damage susceptibility increases with decreasing wavelength, so that blue light and ultraviolet radiation pose the greatest potential risk. 17-19 The electromagnetic spectrum spans a continuous range of wavelengths, including visible light between 400 and 700 nm, and ultraviolet radiation at shorter wavelengths. In a normal human eye, the cornea, opaque to ultraviolet light below 300 nm, shields internal ocular components from potential harm from light below 300 nm. In the near-ultraviolet region between 300 and 400 nm, however, the cornea is effectively transparent. In this region, the crystalline lens absorbs near-ultraviolet radiation and shields the retina from potential harm. When the crystalline lens is removed in cataract surgery, however, the retina's near-ultraviolet light protection is also removed. Replacing the crystalline lens with a clear polymethylmethacrylate intraocular lens provides little protection because clear polymethylmethacrylate allows most of the near-ultraviolet light to reach the retina. 21,22 There has been a marked increase in reported cases of photic retinopathy from operating microscopes in the past few years,23-27 complementing previous reports of photochemical retinal damage from solar and welding arc observation, and emphasizing the clinical significance of photic retinopathy. Photic retinopathy probably comprises a continuum of related hazards, the nature of biochemical events being determined by the exposure history and
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the effectiveness of individual retinal defense mechanisms. Because experimental studies show that mild photochemical retinal damage may not be visible by ophthalmoscopy.A'" clinical reports probably represent only the most severe injuries. The long-term effects of photic retinopathy may not be distinguishable from normal aging changes, such as geographic aging macular degeneration. Furthermore, it is unclear if severe erythropsia'<" produces permanent effects that are not initially apparent by ophthalmoscopy, or if this condition is the clinical analog of blue-sensitive cone photochemical damage observed in primates at very low light levels." The aphakic and nonultraviolet protected retina are exposed and sensitive to nearultraviolet radiation. 30 These patients should be cautioned to wear ultraviolet-protective spectacles in bright environments, such as ski slopes or seashores. 22,31 In view of mounting evidence that the pseudophakic retina needs effective ultraviolet protection, the variability in spectral transmittance of intraocular lenses marketed as ultravioletprotective is disturbing. As shown in Table I, classes 4, 5, and N lenses offer only limited ultraviolet protection, and pseudophakic individuals with those lenses should still be cautioned to wear ultraviolet-protective spectacles in bright enviroriments.P:" Misleading advertisements like those noted earlier are also disturbing. New labeling requirements from the Food and Drug Administration should eliminate some uncertainty, but clinicians should be wary of the performance of the intraocular lenses they implant. In 1978, I reported the increased risk of the pseudophakic individual to thermal" and photochemical retinal damage.F and suggested a possible role for cumulative photochemical retinal damage in aging macular degeneration." If cumulative photochemical damage does contribute to macular degeneration, it may be difficult to prove the efficacy of ultravioletprotective intraocular lenses because the long-term effects of subclinical photic retinopathy may be indistinguishable from normal retinal aging. It would require a large patient population to demonstrate a difference in the incidence of aging macular degeneration between pseudophakic individuals with clear and with ultraviolet-protective intraocular lenses. Since 1978, most intraocular lens manufacturers have introduced ultraviolet-protective lens-
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Ultraviolet-Protective Intraocular Lenses
es, and over 60% of all new implanted intraocular lenses are ultraviolet-protective (Intraocular Lens Market Survey, North Branch, NJ: Health Products Research, Inc., 1985). Ultravioletprotective intraocular lenses have been shown to reduce the risk of photic retinopathy in experimental animals." Additionally, it has been found that ultraviolet-protective intraocular lenses reduce the risk of postoperative angiographically apparent cystoid macular edema, even though this effect does not have shortterm visual consequences." While it is important to consider the longterm toxicity of ultraviolet-absorbing chromophores in intraocular lenses;" photic retinopathy is a demonstrable clinical syndrome. If clear polymethylmethacrylate intraocular lenses are used, the aged retinae of typical cataract patients are deprived of effective ultraviolet protection at a time when their defenses against photic retinopathy are waning. 15,35 An ideal ultraviolet-absorbing intraocular lens should provide effective protection against potentially harmful radiation below 400 nm that contributes nothing to vision (other than erythropsia, glare, and chromatic aberration), but it should not alter the normal photopic or scotopic spectral sensitivity for the patient's age group. Additionally, chromophore photodegradation and leachability should be minimized. 34,36,37 Blue light is also potentially hazardOUS,17.19,22,31 as demonstrated by solar retinitis," welder's maculopathv.t" and operating microscope damage" in phakic eyes with natural crystalline lens protection. Thus, the ideal value for W(10%), the short-wavelength cut-off for ultraviolet-protective intraocular lenses, is probably between 410 nrn and 430 nm. Some authors have advocated cut-offs as long as 450 nrri." Careful psychophysical studies are needed to determine the longest wavelength cut-off (greatest protection) that does not impair photopic or scotopic vision.
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the pseudophakic eye. Am. Intra-Ocular Implant Soc. J. 4:84, 1978. 23. Parver, L. M., Auker, C. R., and Fine, B. S.: Observations on monkey eyes exposed to light from an operating microscope. Ophthalmology 90:964, 1983. 24. Irvine, A. R., Wood, 1., and Morris, B. W.: Retinal damage from the illumination of the operating microscope. An experimental study in pseudophakic monkeys. Arch. Ophthalmol. 102:1358, 1984. 25. McDonald, H. R., and Irvine, A. R.: Lightinduced maculopathy from the operating microscope in extracapsular cataract extraction and intraocuLar lens implantation. Ophthalmology 90:945, 1983. 26. Ross, W. H.: Light-induced maculopathy. Am. J. Ophthalmol. 98:488, 1984. 27. Brod, R. D., Barron, B. A., Suelflow, J. A., Franklin, R. M., and Packer, A. J.: Phototoxic retinal damage during refractive surgery. Am. J. Ophthalmol. 102:121, 1986. 28. Kamel, 1. D.,' and Parker, J. A.: Protection from ultraviolet exposure in aphakic erythropsia. Can. J. Ophthalmol. 8:563, 1973. 29. Saraux, H., Manent, J.-P., and Laroche, L.: Erythropsie chez un porteur d'implant. Etude physiologique et electrophysiologique. J. Fr. Ophtalmol. 7:557, 1984. 30. Werner, J. S., and Hardenbergh, F. E.: Spec-
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