Citation

Zrenner E. Fortschr. Ophthalmol. 1990; 87(Suppl): S41-S51.

Vernacular Title

Lichtinduzierte Schaden am Auge.

Affiliation

Lehrstuhl und Abteilung für Pathophysiologie des Sehens und Neuroophthalmologie, Universitäts-Augenklinik, Tübingen, Bundesrepublik Deutschland.

Copyright

(Copyright © 1990, Holtzbrinck Springer Nature Publishing Group)

DOI

unavailable

PMID

2083911

Abstract

The following review outlines the mechanisms of phototoxicity that are known so far, how they develop, which risk factors are involved, and what the consequences are for ophthalmology. It is necessary to differentiate between photochemical and thermal damage as they differ with regard to etiology and course. Photochemical damage in the lens originates from the absorption of UV-A light; damage caused by oxidation can cause nuclear cataract. Photochemical damage of the retina occurs typically after a longer interval and is mainly due to short-wavelength visible light ("blue light damage"); it entails destruction of membranes of the photoreceptor outer segments and finally photoreceptor death. There are indications that age-related macular degeneration can be accelerated by photochemical light damage. Lipofuscin, photo-sensitizing drugs and prolonged exposure, as well as aphakia and pseudophakia, can increase the risk. Thermal injury is caused mainly by absorption of longer-wavelength light by the retinal pigment epithelium; the effects are usually immediate. The amount of light that can cause threshold damage by common light sources and ophthalmological instruments is given in relation to wavelength, area, and the period of exposure. This information provides the criteria for optimal light-protection glasses. Phototoxic damage can be avoided by awareness, measurement and corresponding action, including the development of better industrial standards for sunglasses and light-emitting devices.

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