Eye Damage From Sun and Ultraviolet Rays Exposure

Photo Credit: encolombia.com

The most common sources of UV radiation, apart from sunlight, are germicidal lamps, high pressure mercury arc lamps, fluorescent lamps and welding arcs.

Of particular concern is the increasing use of sunlamps and sunbeds. UV radiations can act upon the eye by two mechanisms- direct: radiation is absorbed by chromophores within the tissue; and indirect: radiation is absorbed by photosensitizing drugs or other compounds.

Direct effects of UV radiation

Cornea~ photokeratitis

UV radiations are absorbed by the corneal epithelium, which results in a reduction of the cell division in mild cases or, in severe cases, in complete death of the epithelial cells and loss of injured cells. Corneal ulceration may occur in extreme cases. The accumulation of damaged and exfoliated cells on the surface of the cornea can act as an effective filter to limit the total exposure dose and filter specific wavelength of UV radiation.

Unfortunately, the eye cannot build up resistance to UV radiation, like the skin does; exposure has an accumulative effect in a 24-hour period. So, while a single exposure may not be harmful, if repeated the accumulative effect may be above threshold and result in epithelial damage.

Following exposure to UV radiation, there is a latent period of 6-12 hours before any symptoms are noticed. This period varies inversely with the dose of UV radiation exposure. The symptoms experienced are:

1. A sensation of sand in the eyes, due to congestion of the conjunctival and episcleral blood vessels;
2. Lacrimation (watery eye);
3. Photophobia (sensitivity to light);
4. Chemosis (swelling of conjunctival tissues);
5. Erythema (redness) of the lids;
6. Blepharospasm (involuntary, sustained and forceful closure of the eyelids).

The condition is generally self-limiting and almost all the discomfort disappears within 48 hours due to the repair mechanisms of the corneal epithelium. Photokeratitis is common amongst welders, when the condition is referred to as 'arc eye' or 'welder's flash'. The latent period appears to be due to a marked decrease in corneal sensitivity. It has been observed that after exposure to UV radiation from electric arc welder the corneal sensitivity decreased. The sensation of sand and pain in the eyes is experienced as the corneal sensitivity is restored.

Therapy consists of instillation of lubricating ointment and decongestant drops. A local/topical anaesthetic can be given and the eye can be patched if pain is severe and blepharospasm is present. Although the primary short-term effect of acute exposures of UV radiation of the cornea is photokeratitis, damage to the corneal endothelium may also occur. It also appears that chronic UV radiation exposure contributes to increased endothelial polymegethism (greater than normal variation in the size of cornea endothelial cells) seen with age.

Pingecula, pterygium and band-shaped keratopathy

Long-term chronic exposure to UV radiation is thought to be partly responsible for other conditions, namely pingeculae, pterygia and band shaped keratopathies. A significantly high incidence of pingeculae and pterygia is found amongst outdoor workers, such as fishermen and welders, who are exposed to UV radiation.

A nodular band-shaped keratopathy has been noted in people who live in areas of the world with high levels of UV. White or cream opacities occur between the epithelium and Bowman's membrane in the palpebral fissure.

Cataracts

As only the shorter wave lengths are filtered out by the cornea, the lens is constantly exposed to the longer wavelengths throughout life. It has been shown that these wavelengths are responsible for generating fluorescent compounds and for the protein cross-linking associated with lens aging and cataract formation. Chronic cumulative photochemical damage results in increased absorption of UV radiation and some visible light due to photochemically generated chromophores.

The chromophores increase in concentration and number with age and are responsible for the increased yellow color of the lens nucleus and hence enable the lens to act as an effective filter, protecting the retina from cumulative photochemical damage by the second to third decade. Report have shown that 'senile' cataract have occurred at an earlier age (40-50 years) in workers exposed to industrial sources of UV, e.g. printing works, dentistry and medicine. So is there any evidence to suggest that exposure to UV radiation is responsible for cataract formation?

Vitreous shrinkage

The vitreous is normally protected from damage by the cornea and lens, which filter wavelength up to 400nm. However, if the eye is aphakic the vitreous has no protection against wavelengths greater than 295nm. The vitreous gel possesses UV-absorbing chromophores and there is experimental evidence that damage, such as vitreous shrinkage and denaturation of the collagen network, can occur.

Retina

As stated above, the retina is generally protected from UV radiation by the cornea and lens but damage can occur to: aphakes (without crystalline lens) who lack the filtering effect of the lens; fishermen and sailors or employees in industries where UV polymerization is employed.

The aphakic eye is also at risk from retinal detachments due to vitreous shrinkage and denaturation of the collagen network. Aging is known to cause a loss of rod and cone cells and it has been suggested that this is due to a potential cumulative action of light, i.e. a phototoxic effect, which is cumulative in the normal aging process.

Indirect effects of UV radiation

There are reports that UV radiation can be indirectly absorbed by photo-sensitizing drugs and cause damage to the crystalline lens and retina. A treatment for psoriasis (skin disease that causes scaling and inflammation), known as PUVA therapy, consists of the ingestion of a psoralen compound followed by exposure to UV radiation.

Ocular protection must be provided as the UV radiation causes binding of the psoralen compound to lens and retinal proteins in aphakic individuals. This protection must be provided for at least 12-24 hours after ingestion, i.e. until there is no psoralen compound remaining in the lens. The opacities occur in the anterior and posterior cortical layer; some are punctate and others are wedge-shaped. It is believed that the opacification is mainly due to binding of tryptophan and lens proteins, which remain in the lens.