V S T Centre for Glaucoma Services, L. V. Prasad Eye Institute, Hyderabad, India
Allen Foster Research Center for Community Eye Health, L. V. Prasad Eye Institute, Hyderabad, India ; International Center for Advancement of Rural Eye Care, L. V. Prasad Eye Institute, Hyderabad, India
Allen Foster Research Centre for Community Eye Health, International Centre for Advancement of Rural Eye Care, L. V. Prasad Eye Institute, Hyderabad, India
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Refer this article as: Kumar Addepalli, U., Damage of the ultraviolet on the lens, Points de Vue, International Review of Ophthalmic Optics, N67, Autumn, 2012

Damage of the ultraviolet on the lens

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The human lens

The lens is a key refractive element of the eye which, with the cornea, focuses images of the visual world onto the retina. This is achieved by its biconvex shape, high refractive index, almost perfect transparency.[1] Lens transparency is due to the three dimensional arrangement of the lens proteins and these proteins are prone to aggregation by heating, which increases the optical density.[2]

The lens is clear for the first 3 years of life and then gradually develops yellow pigments (3-hydroxy kynurenine and its glucoside). This is a protective pigment, which absorbs UV radiation and safely dissipates its energy.[3] The crystalline lens filters UV and its total transmission of visible light decreases with age as the color becomes yellower.[1] An aged lens absorbs a great part of the short wavelength region of the visible light as it contains chromophores that help absorbing the radiation.[3] The crystalline lens readily absorbs UV –A and the remaining 2% of the UV-B not absorbed by the cornea and aqueous humour.[4] It is important to protect the crystalline lens against the potential hazards of UV exposure.

As the crystalline lens ages, a process known as brunescence occurs. The lens becomes denser and more opaque, allowing less light, especially at shorter wavelengths, to reach the retina.[5]

Lens transparency

The transparency of the crystalline lens depends on its avascularity, paucity of organelles, narrow inter-fibre spaces and the regular organization of its cells and proteins. At the cellular level, there is
limited light-scattering by cellular organelles, which are relatively sparse in the central epithelium and displaced to the equator in the fibres, away from the light path.[1]

In the lens cortex, transparency is enhanced by the high spatial order of the fibre architecture and the narrow intercellular spaces. This compensates for light-scattering caused by fluctuations of the refractive index between membranes and cytoplasm.[1] 

Lens growth

Lens growth is achieved by the addition of new fibres to the surface of the fibre mass over the lifespan. At a certain depth, the superficial, active, nucleated fibres lose their organelles and become transcriptionally incompetent, relatively inactive metabolically and lacking in synthetic capability.[1]

Aside from the skin, the eye is the organ most susceptible to sunlight and artificial lighting–induced damage. Solar radiation exposes the eye to ultraviolet-B (UV-B; 280–315 nm), UV-A (315–380 nm), and visible light (380–780 nm).[3]

Description of ultraviolet radiation

The eye dependent on the visible light energy and can be damaged by the contiguous ultraviolet and infrared wavelengths. The conditions in which sunlight is implicated in the pathogenesis is termed the “ophthalmohelioses”, for example, pterygium and cataract formation.[6] Exposure to UV radiation from the sun is one of the widespread risk factors for the development if cataract and various skin diseases.

The spectrum of nonionizing radiation ranges from short wavelength UV RADIATION (wavelength 100 nm) through to far infrared radiation (1 mm or 1 000 000 nm). The visible spectrum lies between 380 nm to 780 nm. Above the visible spectrum is infrared radiation, and below the visible spectrum are the shorter wavelengths of nonionizing radiation called UV radiation. Wavelengths below 290 nm are totally absorbed by the ozone layer in the stratosphere, and longer wavelengths are absorbed to a lesser extent. Thus, in nature, one does not encounter UV radiation below 290 nm, although the physical spectrum of UV radiation ranges from 100 nm to 380 nm.[7]

Although UV radiation is only 5% of the sun's energy, it is the most hazardous portion encountered by man. UV radiation has been subdivided into three bands:

UV-A or near UV (315-380 nm): Produces sun tanning (the browning of the skin due to an increase in the skin content of melanin), as well as photosensitivity reactions.

UV-B (280-315 nm): It is the sunburn spectrum and causes sunburn and tissue damage (blistering) and also associated with skin cancer.

UV-C (100-280 nm): It is germicidal and may also cause skin cancer.

UV-C, or far UV, is not commonly encountered on the earth's surface and comes entirely from artificial sources such as germicidal UV lamps or arc welding. Furthermore, UV-B is much more biologically active than UV-A.[7, 8]

The temporal side of the eye is most vulnerable to solar UV radiation, focusing the light on the nasal part of the cornea and lens.[9] The intensity of the light, the age of the recipient, the wavelength emitted and received by ocular tissues determines the damage to the eye due to UV radiation. However, the human lens is continuously exposed to small quantities of UV exposure every day, but, if this exposure exceeds a certain level, the lens may become irreversibly damaged.[10]

Exposure to UVB and UVA radiation is associated with photochemical damage to cellular systems. UV radiation can generate free radicals including oxygen-derived species, which are known to cause lipid peroxydation of cellular membranes. It has also been shown that UV can damage DNA directly, decrease mitochondrial function, and induce apoptosis. Oblique rays entering the eye from the temporal side, can reach the equatorial (germinative) area of the lens. The intraocular filters effectively filter different parts of the UV spectrum and only allow 1% or less to reach the retina.[11]

The eye is largely shielded from this by the eyelids and brow ridges. Thus, for the eye, reflection (for example, off grass, sand, or snow) and scattering (for example, from patchy cloud cover) are important sources of UV exposure, with the dose and location of the incident UV radiation. Fig. 1 

Fig. 1: Showing the oblique rays reaching the equatorial (germinative) area of the lens.[12] Authorised reproduction.

Penetration of UV radiation to various structures of the eye

UV radiation incident on the eye is largely absorbed by the tear film, the cornea and the lens. The cornea is transparent to visible light but absorbs a significant portion of the UV-B radiation and a very small amount of UV-A radiation. The anterior layers of the cornea (epithelium and Bowman layer) are believed to be up to twice as effective at absorbing UV-B radiation as the more posterior layers.

Ultraviolet wavelengths from 295 to 317 nm are absorbed in the aqueous humor, due to the presence of ascorbic acid. It also provides antioxidant protection from UV-induced damage to the lens surface.

The UV radiation transmission also varies from the tear film to the retina. The figure below shows the percentage of light transmitted through each ocular tissue.[8] Fig. 2

Fig. 2: Showing the percentage of light transmittance through ocular media.[8, 13] Authorised reproduction

The incidence of cataract is high in countries with excessive sunlight. Yellow to brown coloration of cataracts were noted in countries with higher solar intensities due to photooxidation of proteins such as tryptophan moieties, when compared to people living in higher latitudes.

High incidence of cataracts in countries with excessive light could be because of the photochemical generation of reactive oxygen species (ROS), including superoxide and its derivatization to other potent entities such as hydrogen peroxide, hydroxyl radicals, and singlet oxygen, in the aqueous and the lens resulting oxidative damage.[14]

The inferonasal localization of early cortical cataract has been confirmed in various epidemiological and animal model studies. The germinative zone of the crystalline lens is located equatorially, this
region is more sensitive to UV radiation than other parts of the crystalline lens. It is for this reason, the resultant cataract is predominantly spoke shaped.[6]

Damage to the ocular tissue by UV irradiation occurs by many mechanisms such as protein cross-linking, dysfunction of enzymes, ion pump inhibition, genetic mutations, and membrane damage. Short term complaints of UV exposure include excessive blinking, swelling, or difficulty looking at strong light. UV exposure can also cause acute photokeratopathy, such as snow blindness or welders’ flash burns.

It is estimated that in Australia, where UV levels are consistently high, almost half cases of pterygium treated annually are caused by sun exposure and 10% of cataracts are potentially caused by UV radiation exposure. By the year 2050, assuming 5% to 20% ozone depletion, there will be 167,000 to 830,000 more cases of cataracts.[4]

UV exposure is based on environmental conditions (altitude, geography, cloud cover, ground reflection) and factors like extent of outdoor activities.[4]

Ground reflectance (ρ) will determine if photokeratitis will result from spending time in outdoor daylight. The “global” (whole sky) reflection, and the typical, effective actinic UV reflectance is approximately 20%. Thus walking on a concrete pavement produces nearly 10-fold more UV-effective dose to the cornea than walking over green grass. Sunlight reflection from water gives the highest natural UV exposure. It has been found in various animal models that oral administration of vitamin E had a protective action against UV radiation-induced cataract.[15]

Previous epidemiological studies have shown a significant frequency of cataracts in populations that have a high annual exposure to sunlight and UV radiation.[16] Higher odds ratios for cortical cataract were found in people who spend more than 4 hours outside in the daytime during their 20s to 30s and their 40s to 50s in comparison with people who spend hardly any time outside during the day. No
similar relationship was found for nuclear cataract, although smoking was found to increase the risk of nuclear opacification.[17-20]

The mechanism of light damage to the eye due to UV radiation is eithe due to inflammatory response or due to photooxidation.

In inflammatory response, acute exposure to intense radiation causes a burn in the eye similar to sunburn that can damage the cornea, lens, and retina. The eye is immune privileged, which means that under ordinary stress its immune response is suppressed. In the presence of very intense UV and visible light (for instance, emitted from lasers), this suppression is overwhelmed. There is a release of interleukin-1, a T-cell and macrophage invasion at the site of irritation and a subsequent release of superoxide and peroxides and other reactive oxygen species, which eventually damage the ocular tissues.[3]

In photooxidation, chronic exposure to less intense radiation damages the eye through a phototoxidation reaction. In this, a pigment in the eye absorbs light, produces reactive oxygen species such as singlet oxygen and superoxide, and these damage ocular tissues.[3]


As the normal production of antioxidants in the eye decreases with increasing age, increasing the intake of fruits and vegetables has been suggested to replace the missing protection and have been found to retard age-related cataracts and macular degeneration. In addition, supplementation with vitamins and antioxidants, including Vitamin E and lutein, quenches photooxidative damage, whereas N-acetyl
cysteine has been shown to be particularly effective in quenching UV phototoxic damage and inflammation. Other natural products such as green tea, which contains polyphenols (epigallocatechin gallate) and Ashwagandha (root of Withania somnifera) used in traditional Ayurvedic medicine has also been shown to retard light-induced damage to the lens.[3]

Lens epithelial cells are a likely target for UVB damage because they are the first cells in the lens to be exposed to UV radiation. Epithelial cells, which serve key transport functions for the entire lens, are key sites of enzyme systems that protect the lens from oxidative stress. Exposure of cells to UVB radiation induces DNA damage and triggers alterations in the synthesis of specific proteins. Thus, the lens is particularly susceptible to the long-term effects of stressors such as environmental near-UV radiation. UV absorption by human lenses increases substantially with age.[21, 22]

A concentration of cortical cataract in the lower nasal quadrant of the lens was found by many reviewers.[19, 23] The bony configuration of the orbit and the most probable gaze position during peak sunlight hours suggest that the lower nasal lens region receives the greatest dose of UVB. UVB is proved to be an established risk factor for cortical cataract, due to the fact that the differential exposure by region could account for spatial variation in cataract severity.[19]

Age-related cataractous changes originating in the deep equatorial cortex of the lens are most likely exacerbated by UVB exposure through mechanisms such as increased oxidative radical burden and lipid peroxidation. UVB exposure had a variable effect on cataract severity, with little to no effect in the upper nasal regions of the lens and a maximum effect in the lower regions.[24]


Guidance from the World Health Organisation at its Intersun webpage advises people to wear “wrap – around” sunglasses under many conditions.[6, 12]

The use of UV- blocking contact lenses provides safe, effective, and inexpensive protection of the cornea, limbus, and crystalline lens, especially where sunglasses or hats are undesirable or impractical.
Contact lenses can offer UV protection against all angles of incidences.

UV blocking contact lenses are labled as class 1 and class 2, with each of the different classes indicating the level of UV protection.

Class 1 contact lenses must block 90% of UVA (315 to 380 nm wavelengths) and 99% of UVB (280 to 315 nm wavelengths).

Class 2 contact lenses must block at least 70% of UVA and 95% of UVB radiation. Non – UV – blocking contact lenses have been documented to absorb on average, only 10% UV-A and 30% of UVB[4]


Sunlight-induced processes such as oxidative stress in the skin or in the eye would trigger inflammation. A protective effect for weekly consumption of fish, shellfish, drinking tea daily, and a high consumption of vegetables, in particular carrots, cruciferous and leafy vegetables and fruits, and of these in particular citrus fruits was found.[6]

Above all, Public and practitioner awareness is of critical importance in advising a wrap-around sunglasses or contact lenses or a widebrimmed hat in different situations.


01. Michael R, Bron AJ. The ageing lens and cataract: a model of normal and pathological ageing. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 2011; 366:1278-1292.
02. Kessel L, Eskildsen L, Lundeman JH et al. Optical effects of exposing intact human lenses to ultraviolet radiation and visible light. BMC ophthalmology 2011; 11:41.
03. Roberts JE. Ultraviolet radiation as a risk factor for cataract and macular degeneration. Eye & contact lens 2011; 37:246-249.
04. Chandler H. Ultraviolet absorption by contact lenses and the significance on the ocular anterior segment. Eye & contact lens 2011; 37:259-266.
05. Hardy JL, Frederick CM, Kay P, Werner JS. Color naming, lens aging, and grue: what the optics of the aging eye can teach us about color language. Psychological science 2005; 16:321-327.
06. Coroneo M. Ultraviolet radiation and the anterior eye. Eye & contact lens 2011; 37:214-224.
07. Javitt JC, Taylor HR. Cataract and latitude. Documenta ophthalmologica. Advances in ophthalmology 1994; 88:307-325.
08. Lucas RM. An epidemiological perspective of ultraviolet exposure--public health concerns. Eye & contact lens 2011; 37:168-175.
10. Kim ST, Koh JW. Mechanisms of apoptosis on human lens epithelium after ultraviolet light exposure. Korean journal of ophthalmology : KJO 2011; 25:196-201.
11. Youn HY, McCanna DJ, Sivak JG, Jones LW. In vitro ultraviolet-induced damage in human corneal, lens, and retinal pigment epithelial cells. Molecular vision 2011; 17:237-246.


V S T Centre for Glaucoma Services, L. V. Prasad Eye Institute, Hyderabad, India
Allen Foster Research Center for Community Eye Health, L. V. Prasad Eye Institute, Hyderabad, India ; International Center for Advancement of Rural Eye Care, L. V. Prasad Eye Institute, Hyderabad, India
Allen Foster Research Centre for Community Eye Health, International Centre for Advancement of Rural Eye Care, L. V. Prasad Eye Institute, Hyderabad, India
About us


This article has been read 430 times
Share this content

Refer this article as: Kumar Addepalli, U., Damage of the ultraviolet on the lens, Points de Vue, International Review of Ophthalmic Optics, N67, Autumn, 2012

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