retinal detachments resulting from trauma or disease. Small lesions are produced by laser or arc-lamp photocoagulators to produce scarring which ''welds” the retina to the adjacent tissues. It has been shown (3, 4) that momentary heat rise in excess of 10°C at the lesion site is necessary to produce a minimum thermal burn. This is impossible to achieve with unconcentrated sunlight on earth (5, 6). Since no element of the SPS contemplates concave, specular reflecting surfaces, it appears reasonable to dismiss the thermal retinal burn as a potential hazard. The second class of retinal damage from light is called the photochemical lesion. This lesion appears after 24 hours, is less obvious by ophthalmoscopy, but may appear as a granularity of the fundus. Histology of the retina displays primary damage to the pigment epithelium, largely involving denuding and clumping of melanin granules, swelling and pyknosis of epithelial cells, and secondary damage to photoreceptors. Functionally, this results in partial or complete loss of vision over the effected area, although there is at least partial recovery in a matter of weeks or months. The photochemical lesion's action spectrum has been determined (7). It is produced by short wavelength visible light, with peak activity at approximately 440 mm in the blue. It's threshold (the minimum energy which produces the lesion half the time) has been determined (7) on monkey retina -2 2 3 as 3 X 10 W/cm for a 2 mm X pupil and 10 seconds exposure. It can definitely be produced by unconcentrated noon sunlight on earth which could exceed this threshold energy in a very brief exposure, depending upon the path through the atmosphere. In fact, Ham (8, 9) points out that these experimental photochemical lesions closely resembles solar retinitis, such as produced by watching eclipses of the sun. Tso (10) has produced nearly identical pathology in human eyes voluntarily exposed to the unattenuated solar disc. It is, therefore, very important that we
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