Age-related macular degeneration (AMD) is a major health problem in the developed world accounting for approximately half of all blind registrations. Current treatment options are unsuitable for the majority of patients and therefore the identification of modifiable risk factors that may inform disease prevention programmes is a priority. This review evaluates the long-held belief that blue light exposure has a role in the pathogenesis of AMD. Laboratory evidence has demonstrated that photochemical reactions in the oxygen-rich environment of the outer retina lead to the liberation of cytotoxic reactive oxygen species (ROS). These ROS cause oxidative stress which is known to contribute to the development of AMD. The precise chromopore that may be involved in the pathogenesis of AMD is unclear but the age pigment lipofuscin is a likely candidate. Its aerobic photoreactivity and adverse effects on antioxidant activity combined with its gradual accumulation over time suggests that its in vivo phototoxicity increases with age despite changes in the absorption characteristics of the crystalline lens. Evidence from animal studies confirms blue light's damaging potential but the results are not directly applicable to macular degeneration in humans. Studies of human macular pigment density and the risk of AMD progression following cataract surgery lend further weight to the hypothesis that blue light exposure has a role in the pathogenesis of AMD but the epidemiological evidence is equivocal. On balance the evidences suggests but does not yet confirm that blue light is a risk factor for AMD. Given the socio-economic impact of this disease and urgent need to identify modifiable risk factors, future work should include a large-scale clinical trial to evaluate the effect of blue blocking filters on AMD progression rates.
Copyright 2004 Elsevier Ltd.