Although ultraviolet radiation has long been recognized as a factor in the development of cutaneous cancer, aging of the skin, and mutagenic changes, it is only within the last decade or less that ultraviolet radiation has been universally recognized as a causative factor in ocular pathogenesis.
In humans, the eye has evolved into a sophisticated organ having neurophysiologic responses to photons in a certain portion of the electromagnetic spectrum, that provides a constant detailed map of the immediate environment. The action spectrum for these responses lie primarily within the 400-700 nm wavelength range, which has been labeled the visible spectrum or "light."
The maximum of the eye's spectral response corresponds roughly to the maximum of solar spectral irradiance. Because solar UV radiation is present during most of the daylight hours, the eye may be exposed daily to some amount of solar ultraviolet radiation throughout life. Wavelengths shorter than approximately 290 NM or UV-C are partially or completely absorbed within the cornea and conjunctival. The acute effects of exposure to these wavelengths are primarily those of conjunctivitis and a corneal inflammation reaction known as photokeratitis. The inflammatory reaction of the outermost layer of the eye to UV-C and UV-B radiation can be similar to that of the skin in some respects.
The clinical progress or picture of photokeratitis follows a characteristic course. For example, after exposure, there is a period of latency which varies somewhat inversely with the amount of exposure. The latent period may be as short as 30 minutes or as long as 24 hours but it is typically 6 to 12 hours.
Conjunctivitis, which is often accompanied by an erythema of the skin surrounding the eyelids, is associated with the sensation of a foreign body or "sand" in the eyes, varying degress of photophobia (intolerance to light), lacrimation (tearing), and blepharospasm (spasm of lid muscles). Corneal pain can be very severe, and the individual is usually incapacitated for some period of time. These acute symptoms usually last from 6 to 24 hours, and almost all discomfort disappears within 48 hours. Very rarely does conjunctivitis causing exposure result in permanent damage.
However, unlike the skin, the ocular system does not develop tolerance to repeated ultraviolet exposure. Swelling or shrinking of groups of corneal epithelial cells leads to visibly recognizable stippling or irregular mosaic granulation of the corneal surface. With UV doses greater than the threshold for photokeratitis, surface epithelial cells show nuclear fragmentation, mid-epithelial cells show vacuole formation, basal cells show inhibition of mitosis and clouding of the corneal stroma occurs. Inflammation is also present in the conjunctival where vasodilation, edema, and inflammatory cell infiltrate is followed by desquamation.
Because wavelengths longer than 290 nm are largely transmitted by the cornea, the underlying lens and iris are exposed to UV-A. The lens absorbs essentially all of the UV-A striking it and is therefore the ocular tissue especially susceptible to alteration by UV-A exposure of the eye. The possible production of lenticular cataracts in humans by UV-A exposure is therefore a cause of major concern.
Any alterations of the lens or its capsule that result in apparent decreased transmission or increased scattering of visible light may be called a cataract. Minimal alterations, although detectable by careful biomicroscopic examination, cause no change in routine visual acuity, but more marked alterations of light transmission may impair or eliminate vision. The term cataract is often reserved for this symptomatic decrease in vision.