Ultraviolet-induced photochemical damage in ocular tissues.

Exposure to ultraviolet (UV) lasers may result in pathology to either the cornea, lens or retina of the primate eye. The particular combination of exposure parameters (wavelength, peak power, pulsewidth, pulse repetition rate, and total energy delivered) determines the primary target tissue(s) in each instance. The effect may be acute or chronic, and the implicated damage mechanism may be categorized as photochemical, photoablative or thermal. This paper summarizes a number of specific cases where UV laser radiation affected one or more of the ocular tissues, describes the nature of the pathologies, and indicates what is known about the damage mechanism in each case. Ranges of exposure parameters where each ocular tissue is the most sensitive are defined. The cornea is most sensitive via a photochemical damge mechanism in the 260- to 280-nm range, where the threshold dose is approximately 5 mJ cm-2. For near-UV wavelengths (320-400 nm), different target molecules absorb the radiation and are susceptible to less efficient photochemical damage mechanism yielding corneal thresholds in the range of 10-100 J cm-2. However, we report acute cataract induction following exposure to a 337-nm nitrogen laser at 1 J cm-2 when the energy is delivered in a 10-ns pulse. Further, with longer pulsewidths (approximately 1 s) of comparable wavelength, retinal lesions were induced when 0.28 J was delivered to the eye. The data suggest that the acute lens effect is the result of a thermal mechanism, whereas the UV-induced retinal lesions result from a photochemical insult to the photoreceptors. Data presented include the action spectra for far- and near-UV-induced ocular damage, the pulsewidth and total energy dependencies of ocular thresholds, cumulative effects of repeated exposures, and repair or recovery rates.