Ultraviolet (UV) radiation spectrum is classified by its wavelength: UVA (315-380 nm), UV-B (280-315 nm), and UV-C (100-280 nm). While the ozone layer completely filters UV-C and 90% of UV-B from reaching the Earth’s surface, the remaining UV radiation is sufficient to cause damage to the eye, particularly so in the tropics where there is year-long exposure to strong sunlight. And this is further exacerbated by the losses of the stratospheric ozone of about 6% in the southern mid-latitudes and 4% in the northern mid latitudes [1]. A 1% reduction in the ozone layer leads to an increase in radiation of 0.2% to 2% reaching the Earth’s surface.

The cornea absorbs most of the UV-B and all of the UV-C that reaches the eye. While the corneal epithelium and Bowman layer have significantly higher absorption coefficients than that of the stroma, the whole thickness of the corneal stroma absorbs 70-75% of the UV spectra shorter than 310 nm [2].

The threshold for acute UV photokeratitis is found at a peak sensitivity of 270 nm, which is only possible with manmade implements since the ozone layer blocks off UV-C. But it is possible to develop acute UV keratitis under natural sources such as solar eclipse burns [3] and during skiing (commonly referred as “snow blindness”). Welders with acute photokeratitis may present with tearing, pain, photophobia, and is usually not apparent till several hours after exposure. It is akin to sunburn of the cornea and conjunctiva, though it is shown to be phototoxic rather than thermal injury to the corneal epithelium. Signs include superficial punctate keratopathy, conjunctival injection and chemosis. 

Chronic solar exposure has been linked to multiple ocular surface disorders, such as pterygium, pinguecula, climatic droplet keratopathy and ocular surface squamous neoplasia (OSSN). Pterygium commonly occurs in the tropics, and multiple studies have shown an association with increased levels of UV-A and UV-B [4, 5]. However, the mechanism by which UV radiation induces pterygium remains to be investigated.

Climatic droplet keratopathy, also known as Labrador keratopahty, chronic actinic keratopathy, proteinaceous degeneration and keratinoid degeneration, is a spheroidal degeneration of the superficial cornea, found in areas of high UV exposure. A study of Chesapeake Bay watermen found a high odds ratio of 6.36 for average annual UV-B exposure in the upper quartile [5]. Histologically, the hyaline-like deposits are found in the Bowman’s layer and superficial stroma. The source of the deposits remains controversial. Fraunfelder [6] believed that it is secreted by corneal and conjunctival fibroblasts, while others postulated that it is of plasma origin. Clinical findings are characterized by yellow, oily-appearing spherules in the subepithelium, within Bowman’s layer, or in the superficial corneal stroma (Fig.1). These spherules measure 0.1 to 0.4 mm, appearing at the limbus in the interpalpebral region in the early stages.

Fig. 1: Climatic droplet keratopathy. Golden-yellowish subepithelial spherules are seen on the inferior half of the cornea, associated with secondary amyloidosis of the central cornea.

While there is strong association between UV-B exposure and squamous cell carcinoma of the eyelid [7], the etiology and pathogenesis of ocular surface squamous neoplasia is multifactorial, including UVB exposure, cigarette smoking, Human Papilloma Virus infection, exposure to petroleum derivatives and host susceptibility [8]. OSSN invariably involves the cornea at the sun-exposed interpalpebral region. Whether it is due to a greater propensity for malignant change in this zone, or environmental exposure remains unclear. 

Excimer laser of different wavelengths can be produced with a combination of a noble gas and a halogen gas. The 193 nm excimer laser in the range of UV-C is utilized in laser refractive surgery such as photorefractive keratectomy (PRK) and laser in-situ keratomileusis (LASIK) for its precise etching abilities [9]. In vitro tests have shown a risk of carcinogenesis with the excimer laser, but its cell-damaging effects are less for lasers at 193 nm compared to the longer wavelengths. Furthermore, the short exposure of the cornea to the excimer laser mitigates this risk. The exposure of the stromal bed to UV-B during PRK may cause prolonged stromal healing and subepithelial haze formation [10]. It has been suggested that the lower incidence of haze seen in laser-assisted subepithelial keratectomy (LASEK) may be due to less UV radiation causing cellular damage to the corneal stroma with the near intact epithelium [2].

UV radiation has been implicated in the pathogenesis of multiple corneal disorders. Although further studies need to be done to ascertain the casual effect on these conditions, there is sufficient data to suggest such an association. With the depleting ozone layer, there is an increasing exposure of UV radiation, especially in the tropics. And personal protective devices such as hats and sunglasses, and life style changes can help to minimize exposure of UV radiation to the eye.