While there is evidence that digital devices can increase eyestrain for long-term users, there is currently not enough evidence to say that blue light from digital devices contributes to the development of eye diseases, such as age-related macular degeneration. On the other hand, there are no publications on the effect of long-term exposure to blue light and consequent eye diseases in humans. There are only data on the effects of visible blue light irradiation on rat and monkey retinas. Based on the available evidence, the Association of Optometrists (AOP) concludes that there is insufficient evidence to support the claim that exposure to visible blue light from digital devices leads to eye pathologies and damage to eye health [22]. However, blue light is not all harmful. It can be essentially divided into two ranges: blue-violet light (380–455 nm) and turquoise light (455–495 nm), and these can affect the ocular tissues quite differently [23]. Turquoise light is essential for synchronizing our biological rhythms (the circadian cycle). It helps to maintain and regulate memory, cognition, mood and hormonal balance [24]. It urges a scientific commitment to develop solutions to the potential risk of blue light exposure and it is necessary to know which wavelengths help guide technological decisions and research.

Retinal damage, changes in the lens and cornea, dry-eye syndrome, digital eye fatigue, aging, sleep disorders and circadian rhythm are the most investigated topics. The present review has blue light as its central object. Recent concerns about this radiation impact on visual health and environment due to increased exposure to artificial sources of blue light (mainly from digital devices) are also relevant.

Animal models have shown that phototoxicity results in human degenerative pathologies, such as age-related macular degeneration (AMD). A recent model of blue LED-induced phototoxicity in rats was developed, causing damage to the outer layers of the retina [26]. Progressive reduction in retinal thickness was noted in these in vivo studies. The photoreceptor layer was the most affected, and in electroretinogram evaluation, a transient reduction in the amplitude of waves a and b was observed [27]. The progressive reduction in the cones and the involvement of retinal pigment epithelium cells around the injury perfectly circumscribes the damage to the outer layer of the retina [28].

Many models of phototoxicity use white light due to its similarity to sunlight when studying the effect of blue light on the retina and retinal pigment epithelium (RPE) [27,29,30,31,32]. Knowing that lipofuscin accumulation intensifies aging in RPE, the relationship between phototoxicity and AMD supports the hypothesis of the potential risk of retinal phototoxicity in the elderly [33,34]. However, six of the eight most significant epidemiological studies found no correlation between AMD and light exposure over the users’ lifetime [35,36,37,38,39,40,41,42]. Figure 2 shows the blue light intensities’ radiance used in each referenced laboratory research study [43,44,45,46]. Only studies that used comparable units were included. Values represent the intensity used in each research study, which one can compare with the intensities produced by personal digital devices, such as those that can be found in the study by Gringas et al. (iPhone 5s, Kindle Paperwhite and iPad Air) [47]. Naturally, due to the fast evolution of these devices, future tests will always require updates on their emission spectra and intensity. Furthermore, the values can be useful for further studies about damage induced by blue light, and they are easily measured. Blue light irradiance (W/cm²) can be compared with peak spectral radiance (nm) or the ability of each source to stimulate different photopigments of the retina of a human eye, i.e., the capacity of each source to stimulate different photopigments to the S, M and L cones, rods and intrinsically photosensitive retinal ganglion cells [47]. No such comparison was found in the literature search considered in this article.

Compared to natural outdoor light, artificial light is often lower and has a different spectral distribution than sunlight. Outdoor light illuminance can reach values of up to 130,000 lux, depending on location, climate and elevation. Countries located on the equator receive a daily average of 7.7 kW/m² of solar radiation between September and December [48]. In the CIE 62471 risk classification, irradiance is an important radiometric parameter to assess the level of harmful radiation produced by a light source [49]. CIE photobiological safety data, which compare the effective irradiance values of some common office light sources used for general lighting (LED, incandescent and halogen lamps) and digital devices (laptop and smartphone), indicate that the blue-light-effective radiance of general lighting was at least 20 times that of LED (cold-white, LW W5AP) and, in the case of the two electronic devices, 200,000 times less [49].

Damage induced by digital devices can be of a photothermal nature, which results from the increase in temperature induced by light in the retina, or of a photochemical nature induced by ambient light [50,51,52]. Photochemical damage to the retina is produced at wavelengths in the visible blue light range [53]. Many new devices have a greater intensity of light in blue wavelengths than conventional light sources [33,46]. Exposure to blue light from some of these light sources, more specifically from light-emitting diodes (LEDs), can damage the retina and produce other potentially harmful physiological changes [33,45,49,54,55,56,57]. Thus, the aim of this review is to explore the state of the art on whether exposure to blue light emitted by computers, tablets and smartphones can, when used frequently and for prolonged periods, can be harmful to the retina.

The lens is composed of structural proteins, enzymes and metabolites that absorb the most energetic visible light. These substances produce yellow pigments that gradually cause the crystalline lens to opacify and turn yellow. This radiation absorption by the lens blocks and protects the retina from potential damage from blue light exposure [37]. Some studies have shown that blue light can induce the production of reactive oxygen species (ROS) in the mitochondria of lens epithelial cells, which can anticipate cataract occurrence [13,15].

The lens blocks most UV radiation between 300 nm and 420 nm and light transmission decreases with aging, with medical–surgical intervention being the only effective solution to treat cataracts, which is one of the main causes of blindness in the world [14,58,59,60]. In around 1980, specialists realized that the intraocular lens (IOL) could not only provide major optical power (in diopters), but it could also filter short light waves, reducing the risks of retinal damage. Consequently, most IOLs used in cataract surgery have incorporated UV-blocking filters since 1986 [61]. Blue light loss is permanent for pseudophakes with blue-blocking IOLs, and despite the lack of evidence, blue light hazard is often discussed [62].

The hypothesis of phototoxicity by exposure to light has increased concern and interest in blocking, in addition to ultraviolet radiation, part of visible light, by causing or accelerating age-related macular degeneration (AMD) [63,64,65,66,67,68,69,70,71,72].

Carotenoids found in the lens, such as lutein and zeaxanthin, are effective in absorbing blue light due to their antioxidant characteristics [73]. In the oxidative stress of the lens, antioxidants provide greater protection [74].

Some articles have shown that after exposure to blue radiation, the survival rate of corneal epithelial cells decreases [75]. The oxidative increase in corneal epithelial cells triggers inflammation and causes oxidative damage and, consequently, cell apoptosis and formation of xerophthalmia [11].

The cornea, aqueous humor and vitreous are the ocular refractive media, permeable to wavelengths between 300 nm and 400 nm. UVA radiation causes damage to the basal layer of keratinocytes, which is responsible for the occurrence of most skin tumors. Sunburn, photokeratitis, cataracts and retinal damage are common consequences of UV-B exposure rays (290 nm to 320 nm) [76]. Digital device users with digital eye strain (DES) experience symptoms such as eye irritation, burning, tiredness and redness, dryness, blurred vision and double vision. During digital devices’ prolonged use, a significant proportion of users (40–60%) experience visual or ocular symptoms. Most blue-light-blocking lenses used to reduce DES symptoms have not shown to be effective in reducing visual symptomatology, such as reading a task on a computer for 30 min [77].

Other studies have investigated the relationship between the use of digital monitors and changes in the ocular surface. Tear film break-up time (BUT), tear film volume (tear film meniscus and Schirmer’s test) and the lipid layer of the tear film state were quantified. Cardona et al. verified several changes in the tear film. Twenty-five healthy young adults were exposed to 20 min of video games. The lacrimal meniscus decreased, the time and area of tear rupture increased, and the interference patterns of the lipid layer were also altered after the game [78]. Another article studied changes in tear film over an 8-h workday in computer users [79]. The results did not demonstrate significant changes in Schirmer’s test, but BUT (tear break-up time test) decreased after screen exposure [80]. Reading on a computer, the conjunctival surface presents greater hyperemia compared to reading on a smartphone. When using a smartphone, a smaller extent of the exposed ocular surface was identified, due to convergence, in comparison with a computer [81,82]. Most results suggest that there is a relationship between deterioration in tear film quality and the use of digital devices.