Temperature-controlled in vivo ocular exposure to 1090-nm radiation suggests that near-infrared radiation cataract is thermally induced

Abstract

The damage mechanism for near-infrared radiation (IRR) induced cataract is unclear. Both a photochemical and a thermal mechanism were suggested. The current paper aims to elucidate a photochemical effect based on investigation of irradiance-exposure time reciprocity. Groups of 20 rats were unilaterally exposed to 96-W/cm(2) IRR at 1090 nm within the dilated pupil accumulating 57, 103, 198, and 344 kJ/cm(2), respectively. Temperature was recorded at the limbus of the exposed eye. Seven days after exposure, the lenses were macroscopically imaged and light scattering was quantitatively measured. The average maximum temperature increases for exposure times of 10, 18, 33, and 60 min were expressed as 7.0 ± 1.1, 6.8 ± 1.1, 7.6 ± 1.3, and 7.4 ± 1.1 °C [CI (0.95)] at the limbus of the exposed eye. The difference of light scattering in the lenses between exposed and contralateral not-exposed eyes was 0.00 ± 0.02, 0.01 ± 0.03, -0.01 ± 0.02, and -0.01 ± 0.03 transformed equivalent diazepam concentration (tEDC), respectively, and no apparent morphological changes in the lens were observed. An exposure to 96-W/cm(2) 1090-nm IRR projected on the cornea within the dilated pupil accumulating radiant exposures up to 344 kJ/cm(2) does not induce cataract if the temperature rise at the limbus is <8 °C. This is consistent with a thermal damage mechanism for IRR-induced cataract.