Blue Light Hazard

Visual function depends on two types of photoreceptors within the retina: rods and cones. Required for scotopic vision,rod vision lacks color information and is characterized by high sensitivity but low resolution. Highly concentrated in the center of the macula, cones enable both sharp image resolution and color detection. 

Rods and cones in the retina initiate the visual process when visual pigments absorb photon energy and convert it into neural signals. Th is biological conversion of light to electrical signals is supported by an enzyme-mediated process called the “visual cycle” that allows effi cient reuse of key chemicals in the reaction.

 The visual pigments that initiate the process are made up of an opsin combined with the chromophore 11-cis-retinal. The important photochemical reaction is the conversion of the 11-cis-retinal to all-trans-retinal, caused by photon energy striking the pigment. This changes the shape of the retinal molecule, breaking its connection with opsin and leaving the opsin free to initiate a series of reactions that leads to a neural signal and ultimately to vision. 

In the meantime, the all-trans-retinal is converted to all-trans-retinol and transported to the retinal pigment epithelium (RPE) where it is either stored or reconverted to the 11-cis-retinal form for transport back to the photoreceptors. Th ere it can recombine with opsin to complete the visual cycle (Figure 3).

Figure 3. The visual cycle

 The visual cycle takes place within the outer segment of the rods and cones and in the RPE cells. The RPE cells are not photoreceptive, but they are essential to the regeneration of visual pigments and also play a critical role in the survival  and normal function of photoreceptors. With microvilli on their apical surfaces interdigitating with the outer segments of photoreceptors, the RPE cells supply the photoreceptors with nutrients and oxygen. They also help maintain the homeostasis of photoreceptors by phagocytosis and digestion of oxidized photoreceptor outer segments.

The Blue-light hazard

The most certain impact on retinal  health and vision from exposure to higher-energy visible (indigo and blue) light is acute phototoxicity, as seen in humans who stare directly at an arc lamp or the sun. It is established that this damage is photochemical, not thermal, and studies in primates have made it possible to de- fi ne the action spectrum for this type of damage, which peaks around 440 nm.2 It is certainly reasonable to suppose that over the long term, and especially as aging changes erode cellular defense mechanisms, retinal exposure to high-energy light could have a damaging effect. Many in vitro studies, including those detailed in this report, have helped us to understand the photochemical and cellular mechanisms by which this damage occurs. Visual pigment, retinoids, and bisretinoids (in particular A2E, a major photosensitive component of lipofuscin) have been implicated in photochemical damage to the outer retinal layers, and additional not-yet-identifi ed chromophores may also act in this way. High energy visible light exposure also induces oxidative damage, to which retinal cells are especially vulnerable.