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A.M. Noury, J. Marshall; Risks from Infrared Devices: An In-Vitro Study of Photochemical IR Damage in the Lens . Invest. Ophthalmol. Vis. Sci. 2003;44(13):294.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: IR cataractogenesis is thought to occur by thermal mechanisms but some evidence suggests that IR, absorbed directly by the lens, may result in photochemical damage. This exhibits reciprocity and implies that chronic, repetitive, low irradiance exposures of IR may lead to cumulative damage. The recent explosion in IR remote devices demands the clarification of such potential damage mechanisms as current codes of practice are based solely on high irradiance, laboratory, thermal models. We therefore aimed to determine the potential for sub acute, photochemical, infrared lenticular damage using a whole lens in vitro model. Methods: Expt A: 48 aseptically dissected porcine lenses were placed in wells containing HBSS (Sigma) and randomly assigned to a control group or one of three IR exposure groups. Irradiation was from a 1310nm diode laser source at 72Jcm-2 (Carl Zeiss Meditec Inc), focussed on the centre of the anterior lens surface. Exposures were of 1s, 10s and 100s to enable a dose-response profile to be established. All lenses were subsequently cultured in clear EMEM (Sigma) for 10 days at 37°C to allow maximum time for photochemical changes to develop. Lens damage was assessed with anterior surface photographs at day 0,1,4,7 and 10, using a digital camera mounted on an inverted microscope (x20). Photographs were randomly presented to a single, blinded examiner and the features classified using predetermined criteria. Expt B: The experiment was repeated with a further 44 lenses using identical exposure times but maximum irradiance (200Jcm-2) and cultured at 40C to accelerate any photochemical damage Note: The model had been previously calibrated with UVB (302nm) as a positive control for photochemical effects, resulting in clear dose dependent damage. 40°C had been established as the maximum permissible temperature of the system that would accelerate UV photochemical damage but not cause thermal damage per se. Results: No damage features were specific to IR exposed lenses. There was no significant difference between control and exposed groups for any damage feature (minimum p=0.635 using Fisher's exact test). No dose dependent damage pattern was obtained for IR exposure in either experiment . Conclusions: IR at 1310nm does not cause lens damage in this non-thermal exposure scenario. This has implications for our understanding of clinical cataractogenesis and the development and use of new IR remote control and scanning devices.
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