Abstract
Experimental investigations of microwave cataractogenesis, as well as the application of theoretical methods, suggest the involvement of thermal damage. Time-intensity cataract thresholds for acute exposures of rabbits indicate dose reciprocity. The induction of lens opacification following repeated exposure at intensities below the threshold for single-dose exposures suggests a cumulative component of lens damage and the existence of repair mechanisms. Repair mechanisms are also indicated, in experimental biochemical studies of microwave effects on rabbit lens epithelial cells with a 10-20-day cellular recovery period. Experimental studies have revealed a relationship between the site of ocular damage and radiation wavelength. Cataract induction has also been reported in humans accidentally overexposed to microwave radiation. Although dosimetric data is not adequate to specify exposure thresholds, acute lens opacification in humans appears to involve thermally induced lens damage that occurs at exposure intensities of 100 mW/cm2or greater. Epidemiological studies of workers have in some instances suggested that occupational microwave exposure may result in lens alterations but there is no evidence that such effects are associated with visual impairment or cataract formation.

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