In the digital age, our day to day lives are increasingly surrounded by artificial light created by light filaments and digital devices. Natural sunlight cannot penetrate thick walls in large shopping centres, meaning commercial lighting fixtures are built as a replacement. Traditional use of pen and paper has declined with computer screens now in nearly every household, 762.15 per 1,000 people in the USA; combined with the new generation of tablet and smart phone devices. Increasing exposure to a certain type of light emitted from lighting and digital devices known as “blue light” has been documented on tabloids and many journal articles in the recent millennium. Short wavelength light such as UV light and blue light has a higher level of energy, less is required to cause severe damage to the retina and ocular structures. The recently introduced light-emitting diodes produce more blue light than previous forms of artificial lighting. With Age-related macular degeneration being the main cause of blindness in the western world and the number of patients likely to increase as the population’s age, blue light exposure has been highlighted as one of the risk factors. Furthermore, studies on the effects of blue light exposure on sleep and melatonin have also been in the limelight due to increasing numbers of people struggling with sleep, insomniacs. This literature review aims to scrutinise the integrity of existing literature allowing for a comprehensive understanding of the topic, as well as highlighting any areas that require further investigation.
Frequently used abbreviations
AMD/ARMD- Age-related macular degeneration
LED- light emitting diodes
ROS- Reactive oxygen species
RPE- Retinal pigment epithelium
NLRP3- Nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing protein 3 inflammasome
IOL- Intra ocular lens
SCN- Suprachiasmatic nuclei
IpRGC- Intrinsically photosensitive retinal ganglion cell
BB- Blue blocking glasses
CL- Clear lenses
ILC- Inappropriate line crossings
1. 1 Introduction to light and its characteristics
Light is a special form of electromagnetic energy explained Youssef et al. (2011). Light which interacts with the eye is known as optical radiation and includes multiple wavelengths, including ultraviolet light (100-400nm), visible light (400-760nm) and lastly infrared (760-10 000+). Industrial lighting is increasingly changing from high pressure sodium vapour lamps to new light emitting diodes (LEDS). LEDs work when voltage is applied to negatively charged semiconductors, this causes electrons to combine and generate a unit of light know as a photon. In layman terms, a LED is a chemical chip embedded in a plastic capsule (Pawson and Bader, 2014). By September 2016, incandescent lighting will no longer be available, making it important to know more about our next generation of lighting, light emitting diodes. Artificial white light is now being produced by LEDs in three ways and is depicted within the image below:
Figure 1: White light can be achieved with LEDs in three ways Lougheed (2014)
In the digital age, our eyes are increasingly being exposed to light from video display terminals manufactured with LEDs. Scientists and researchers are only now beginning to investigate long-term effects of harmful everyday light (Kitchel, 2000). One of the focuses of this literature review is among increasingly frequent household LED products that employ a chip emitting blue light; this is surrounded by a yellow phosphor coating. The phosphor-converted white LEDs consist of a blue colour emitting GaN chip over which phosphor is coated. Upon excitation, the GaN chip produces emissions of radiation which contains more than two or three colours. The resulting light will look white to the naked eye, although it can feature a spike in the short wavelength blue light end of the spectrum at wavelengths 460-500nm (Lougheed 2014).
Light has many roles in human processes; it is a potent stimulus for regulating circadian, hormonal and behavioural systems. These biological and behavioural effects of light are influenced by distinct photoreceptors in the eye; melanopsin-containing intrinsically photosensitive retinal ganglion cells (Lucas et al. 2014). The purpose of this literature review is to evaluate published research on the effects of blue light affecting ocular health and cardiac rhythms.
1.2 The eyes natural protection against harmful light
The retina is part of the central nervous system, and is the only part that is exposed to light radiated between the wavelengths 400nm and 780nm (Osbourne et al. 2014). Due to the retinas specialised structure, the eye is at the most risk from damage from light in comparison to the skin for example (Glickman 2011). The eyes have multiple natural mechanisms which protect the retina from excessive exposure to light. Ocular geometry in the form of the eyelids, partly block light entering the eye through the pupil. A direct response to bright light, squinting of the eyes, further protects the retina from excessive exposure. Furthermore, through the papillary light, reflex light levels are adjusting meaning different levels of light reach the retina (Rozanowska 2015). Eyes have two important sources of natural tissue where electromagnetic radiation is absorbed. Firstly the cornea absorbs all of the ultraviolet radiation below 295 nm. Within this range, includes all the UVC light (100-280nm) and the majority UVB (280-315nm) and UVA light (315-400nm). Secondly, the crystalline lens absorbs a narrow range of UVB and all UVA light transmitted (Youseff (2011). Infrared wavelengths beyond 1,400 nm are heavily absorbed by water molecules and therefore do not penetrate the anterior structures (Glickman 2011). The macular pigment acts as an optical filter. In a young person’s eye, the ocular transmittance of blue light at 450nm is very high, reaching close to 90%. This is important as this could contribute to problems created by blue light exposure such as insomnia and age-related macular degeneration (ARMD). On the other hand, the transmittance of elderly lenses is much lower and has considerable inter-individual variation, but in general does not reach 75% until wavelengths of 540nm. In contrast to aphakic eyes, in which substantial high energy short wavelengths longer than 310nm including UVA and blue light will strike the retina (Algvere et al. 2006).
2.1 Blue light and the retina
The mammalian eye detects image generation, but is also capable of detecting changes in environmental light resulting in non-image forming responses (Arendt & Broadway 1986). Nevertheless, the bandwidth from 360 to 550nm penetrates through to the retina and contains photons which are increasingly energetic and can cause damage to the retina. There are three types of injury that can occur at the retina, photothermal, photomechanical and most relevant photochemical damage. Brief exposure to extremely bright lights can cause an immediate photothermal injury. Whereas, exposure to light for an extended time period may result in chemical changes to retinal cells which can result in retinal cell death. This is known as photochemical injury. Damage caused by blue light enhances oxygen presence and suggests that the basic mechanism of the photochemical injury is the photodynamic production of free radicals from the toxic combination of light and oxygen (Beatty et al. 2015).
A study conducted by Kuse et al. (2014) investigated cultured marine photoreceptor cells which were maintained with fetal bovine serum and a humidified atmosphere to replicate in vivo conditions. The methodology used in this study was one that is closest to actually seeing the effects of prolonged acute exposure to the eye. The 661 cells were seeded at a density of 3 × 103 cells per well into 96-well plates and incubated for 24 hours under a humidified atmosphere CO2 at 37° degrees. Following such, the cells were treated with N-acetylcystein (NAC) and incubated for 1 hour. Furthermore, the cells were exposed to 450 lux of blue LED light (464nm); 1,600 lux for white LED light (wavelength peak is at 456nm and 553nm) and 2,500 lux for green LED light 522nm. The 96 plates were then incubated for 12 hours alongside control cells obtained from the same stock and treated identically. This eliminated any pre-existing bias, which may have come from light or temperature. Kuse et al. (2014) evaluated the relationship between reactive oxygen species (ROS) generated through the exposure to the three coloured LED lights for 24 hours. The results found blue LED light induced a high ROS production in comparison to that of white LED light and green LED light. However, it would be unrealistic for a normal person to be exposed to 24 hours of light in our day to day lives. Therefore, the same experiment was done for 6 hours, which also induced ROS production. Specifically, blue LED light induced a 1.4 fold ROS increase and white LED light increased exposure induced 1.2 fold ROS increase. Important to note green LED light exposure had no affect and did not induce a ROS increase.
Observing the diagram above we can see blue LED light increased ROS production, changed the protein expression level and aggregated short-wavelength opsin, resulting in severe cell damage. Although the blue LED light damaged the primary retinal cells and was photoreceptor specific, a known antioxidant N-Acetylcysteine (NAC) protected against the harmful cellular damage induced by blue LED light. This may warrant research on how to increase NAC levels similar to carotenoids with supplements. White LED light (wavelength peak is at 456nm and 553nm) is what we typically experience being emitted from digital devices. From the research we can deduce that the blue light component of white light also causes ROS. This is more relevant to examples of artificial light sources used today where blue light is emitted, rather than exposure to an independent 450 lux blue light source.
1.4 Clinical testing of animals exposed to blue light
The Ham and Ruffalo study in 1978 is a landmark trial into the pigmentary changes due to blue light. Despite this research dating back over 30 years it has been included within this review study because of the key arguments it poses. Here a histological analysis on 20 rhesus monkeys eyes with a 2500 W xenon lamp optical system with narrow bandpass (6 nm) filter at 441nm was carried out. The xenon lamp was a 1mm diameter retinal beam, centred on the fovea and covered most of the macula. These animals carried out daily visual acuity tests, both prior and after the exposure. Specimens examined after 1 hour exposure to the light found that the neural retina, retinal pigment epithelium (RPE) and choroid appeared unchanged except for a small number of rod nuclei with clumped chromatin and some dense cone cells. The same was true at 24 hours. Following 48 hours, a dramatic change was documented.
A, Response of RPE staining following prolonged exposure to blue light. Pigment epithelium just above Bruch’s membrane (BM) is damaged in more than 90% of image area. Arrowed areas are macrophages in sub retinal space, containing melanin and membrane debris. Photoreceptor outer segments (OS) appear to be undamaged.
B, Response of the RPE and choroid after blue light exposure. Evident extensive damage and disruption of the RPE, macrophages present in subretinal space engorged with melanin and membrane debris.
The RPE was disrupted, and accompanying choroidal damage was seen. The most evident feature of the lesion was a pigmentary change, whereby the RPE underwent hypopigmentation. The lesion was characterised by these pigmentary changes as first detected 48 hours after exposure through fundus examination. This initial lesion was localised largely in the RPE, causing widespread damage and some necrosis of cells.
1.5 The effects of blue light on Age-related macular degeneration
The fundamental study by Ham and Ruffalo opened more channels for development into research concerning blue light effects on a cellular level. Oxidative damage and endoplasmic reticulum stress from blue light is related to the pathogenesis of age-related macular degeneration (Zhao et al. 2014). Age-related macular degeneration, commonly called AMD or ARMD, is one of the leading causes of visual impairment in all industrialised countries, especially amongst individuals over the age of 65 (Biswas and Raman 2002). In ARMD, the retinal pigment epithelium (RPE) progressively becomes dysfunctional which then eventually degenerates, causing photoreceptor death and visual function loss. ARMD presents in two major forms, namely ‘wet’ or ‘dry’. The former is so-called because of the growth of new blood vessels, a process called angiogenesis, although less common than the dry (or non-neovascular) it is associated with more serious vision loss (Biswas and Raman 2002). The earliest clinical manifestations of ARMD are pigment changes and the presence of focal deposits of extracellular debris called Drusens (Abdelsalam et al. 1999). These deposits form between the RPE and the outer retina, specifically a many-layered membrane called the Bruch membrane. We have two major carotenoids characteristically yellow in colour, Zexanthin and its isomer Lutein. In the eye, these two carotenoids are found specifically in the human macula, specifically within the Henle fibre layer (O’Hare et al. 2015). The carotenoids have an absorbance spectrum peaking at 460nm; therefore acting as a natural filter for blue light and UV radiation (Krinsky et al. 2003).
A contributing factor to the pathogenesis of ARMD is excessive lysosomal accumulation of lipofucin in the RPE cells which impedes metabolic activity (Delori 1998). The innate immune signalling receptor involved in RPE cell pathology in AMD pathogenesis is nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome. Brandstetter et al. (2015) used a RPE cell culture model, where it was demonstrated that photo oxidative stress by irradiation with blue light activated the (NLRP3) infalmmasome. This activation mediates permeabilization of lysosomal membranes with subsequent cytosolic leakage of lysosomal enzymes. It is amplified further by the photosensitizer lipfuscin which accumulates in the RPE in vivo with age and has the highest concentration in the macula. NLRP3 inflammasome activation in the RPE has been reported in both atrophic and neovascualar ARMD. Therefore, this molecular mechanism of blue light induced inflammasome activation in the RPE links key pathogenic factors of ARMD. Due to the mentioned types of oxidative stress, macrophages are recruited and inflammatory cytokines are secreted in the macular area (Narimatsu et al. 2015).
On the other hand, a study by Hirakawa et al. (2008) which evaluated sun light exposure and age related maculpouathy had inconclusive evidence. With sunlight, we are naturally exposed to moderate levels of blue light, hence an increased exposure would theoretically cause age related maculpouathy to increase. The collected data on this study did not firmly support any photochemical oxidated stress exacerbating ARMD due to sunlight. This may be due to the methodology Hirakawa et al. used in observing facial wrinkle length and area of hyper pigmentation, which are considered to be associated with exposure to sun.
1.5 Intra Ocular Lenses filtering blue light
Ham and Rufflow’s study in 1978 depicted the effects of blue light on mammals. As the population increases, the number of cataract surgeries will be on the rise, therefore cataract surgeons are increasingly interested in the colour of an intra-ocular lens (IOL) used in their operating theatre. One question that can be raised regarding visual function, ARMD and circadian rhythm is, whether there are any benefits using a blue light filtering lens (Ayaki et al. 2014). The natural ageing process of the crystalline lens, means it becomes cataractous and absorbs more shorter-wavelength light (Youseff 2011). This process happens through chromophore deposition which decreases transmission of blue light through the crystalline lens by 0.75% per year on average. When a cataract is removed, this protective filter is removed, therefore increasing the amount of short wavelength light reaching the retina (Lavric and Pompe 2014). In theory, a blue light filter should effectively reduce phototoxcity created by blue light (Herbst et al. 2012). Blue light XCC filters (SN60AT lens which has an IMPRUV filter) are yellow tinted in appearance (yellow complementing the colour blue); this filters light up to approx 400nm. Orange lens filters(PCC40Y) are also manufactured, which are shown to filter more blue light but removes part of the visible light spectrum filtering up to 550nm (Díez-Ajenjo et al. 2014).
A clinical trial by Kara-Junior et al. was conducted in 2011; the possible side effects and potential protection 5 years after an IOL was implanted were studied. Two IOL’s were used, one which filtered UV and blue light (SN60AT) VS a UV light filter (SA60AT) only. The study used 30 patients of which 60 eyes in turn tested. Random allocation of either IOL was implanted into either eye. The cohort study found no significant clinical or optical coherence tomography findings in terms of ARMD and protection of tinted IOL to the macular remains unclear. The SN60AT lens used in the study filtered up to 400nm of short wavelength light. We know that blue light is emitted after 400nm in the spectrum of light and peaks between 450-500nm, therefore the SN60AT lens is not cutting out blue light and is a flaw of the product. This could have compromised the study, but no clinical findings even with light above 400nm transmitted through the lens were found.
3.1 The involvement of blue light on circadian rhythms
Insomnia has been associated with irregularities in the timing of circadian rhythms. These difficulties are often chronic rather than acute and are accompanied by a total amount of decreased sleep, impaired daytime functioning and agitated moods and anxiety. There are two types of insomnia symptoms, sleep-onset and early morning-awakening insomnia; these may be referred to as an abnormal circadian rhythm. Sleep and wake cycles across a 24 hour period are regulated by a sophisticated interaction between two biologic mechanisms: the homeostatic and circadian processes. The homeostatic process is one that refers to the increase in pressure for sleep with continued wakefulness, similar to an increase in hunger as one goes without food. Once asleep, the fix for sleep decreases rapidly in the initial stages before declining at a slower rate through the remaining sleep period. The second process explored further in this literature review is involved in the regulation of sleep via the circadian process which is largely independent of the prior wake time and is therefore distinct from the homeostatic process. Sleep propensity is regulated by this circadian process through self sustaining cycles of physiological activity, known as circadian rhythms. These rhythms are originated and regulated by the body clock located in the suprachiasmatic nuclei (SCN) (Edinger 2013).
3.2 Photoreceptors and circadian rhythm
A paper by Woodland Hasting and Beatric M. Sweeney tested the ability of multiple wavelengths of light, to shift the circadian rhythm in a marine dinoflagellate Gonyaulax in 1958. Nobody in their millennium thought it had any relevance to humans, whose circadian rhythms were then widely believed to be relative to light intensities. The Woodland Hasting and Beatric M. Sweeney research was an overlooked landmark in blue light research only being recognised recently in the past two decades changing the uninterested opinions. Light resets the human circadian rhythm, but the same blue light that has the strongest impact on dinoflagellates has the equivalent power to reset our sleep wake cycles. Although most visible wavelengths can rest the cycle, the blue short wavelength light does the job most convincingly. In 1998, a major discovery of melanopsin retinal ganglion cells led to finding a new type of photoreceptor in the eye. “These biological and behavioural effects of light are influenced by a distinct photoreceptor in the eye, melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs), in addition to conventional rods and cones” (Lucas et al. 2014, p. 1). These cells provide signals to the brains master clock (SCN) which provides entertainment to the light-dark cycles (Holzman 2010). Melanopsin is structurally and evolutionary more closely related to the opsins of invertebrate rhabadomeric photoreceptors than ciliary photoreceptors we vertebrates use (Borges et al. 2012).
Fig 4.0 (A) Relevant retinal circuitry in humans (B) Photoreceptive mechanisms from retinal irradiance input (Lucas et al. 2014)
Shown in schematic Fig 4.0 (A), all retinal photoreceptor classes are upstream to response of light for circadian, neuroendocrine and neurobehavioral response to light. Responses which are non image-forming originate in the retina and are attributed to a specific class of retinal ganglion cell (ipRGC). Direct photosensitivity from ipRGCs expresses melanopsin, which allows them to respond to light even if isolated from the retina. On site they are connected to the outer retinal rods and cones via conventional retinal circuitry. Shown in the schematic are major connections with on cone bipolar cells (on CBC) which connect them to cones and via amacrine cells (All) and rod bipolar cells (RBC), rod photoreceptors. Due to this network of connections, the firing pattern of ipRGCs can be influences by both intrinsic malanopsin photoreception and extrinsic signals which originate in rods and each of the spectrally distinct cone types (shown in red, green and blue). Fig 4.0 (B) shows a number of photoreceptive mechanisms, “(R for rod opsin; MC for M cone opsin: LC for L cone Opsin; SC for S cone opsin and M for melanopsin)” (Lucas et al. 2014, p 3), each responsible for absorbing light in accordance to its own spectral sensitivity profile, generating a distinct measure of luminance. Retinal rewiring combines the five inputs and within the ipRGC itself produce an integrated signal that is delivered to non-image-forming centres in the brain (Lucas et al. 2014).
Provencio et al. (2000) stated that the discovery of melanopsin is the most sensitive at the wavelengths ranging from 420 to 480nm (blue light). Holzman (2010) later narrowed this down further, across 10 published studies including humans, rodents and monkeys. Holzman found that the peak sensitivity appeared to span 459-485nm. A study by Lockley et al. (2003) studied 16 healthy subjects. Briefly, the subjects were studied for nine consecutive days in an environment free of time cues and then circadian phases were assessed by monitoring the melatonin secretory profile during two constant routine methods, before and after exposure to monochromatic light. Subjects were randomised in a clinical trial for exposure to either 460nm or 555nm monochromatic light (+/- 10 nm half-peak bandwidth of equal photon density). Irradiances were then measured with an IL1400 radiometer and SEL-033/F/W detector. Monochromatic light exposure caused a delay of melatonin production in all subjects. Exposure to 6.5 hours of 460nm monochromatic light caused a significantly greater phase delay than exposure to longer wavelength monochromatic light at 555nm. The results demonstrated that the strength of light in phase shifting circadian rhythms in humans is wavelength dependent and that the human circadian pacemaker is more sensitive to short (460nm) wavelength light in comparison to (555nm) longer wavelength visible light.
Following on from this study, a number of researchers including Lockley et al. did a similar project with Gooley et al. (2010) which followed similar methodology to their previous reviewed paper. This time using a sample of 66 health subjects who again did a 9 day inpatient study. Results confirmed what previously was found, showing 460nm blue light suppressed melatonin following 6.5 hours exposure. While already established that the studies demonstrated the peak sensitivity of the circadian pacemaker to light is the blue-shift relative to the three-cone visual photopic system, it is by the fourth quarter of the 6.5 hours light exposure, a difference in log relative sensitivity at these white and blue light wavelengths was consistent with a melanopsin only response. Based on the studies of short-wavelength shift in spectral sensitivity, Gooley et al. (2010) hypothesised that cone receptors provide for temporary suppression of the circadian rhythm, whereas melanopsin signals light information continuously across long-duration exposure to light. This is consistent with the interpretation of a blind individual with no detectable rod or cone functionality. Tests showed constant levels of melatonin suppression across a 6.5-hours exposure to 460nm light; whereas 555nm light did not suppress melatonin at all.
3.3 Reducing blue light exposure
A quantitative study performed recently by Van der Lely et al. (2015) involved studying thirteen healthy male high-school students between the ages of 15 and 17. The study lasted 16 days and was organized in two study parts with a balanced crossover design which was separated by an intervening period of 1 week to 5 weeks. The study comprised a 15.5-hour stay in the laboratory and a further preceding ambulatory week. The participants maintained their usual sleep-wake cycles and were not permitted to go out in the evenings or nap during the 3 days before the in-laboratory element. Caffeinated drinks were also restricted and alcohol consumption was limited to three glasses per week. The ambulatory part compromised of participants wearing orange-tinted blue blocking (BB) glasses or glasses of equal design with clear lenses (CL) as a control; these had to be worn from 18:00 hours until sleep onset. At the end of each ambulatory week, the in-laboratory testing took place where participants reported for chronobiology. Participants entered the laboratory 5.5 hours before their scheduled sleep time.
Figure 6.0 Melatonin profiles of 13 male participants. Astrix(*) indicates noticeable difference between BB and CL (Van der Lely et al. 2015)
As show from the above graph, an increase in salivary melatonin signifies reduction in melatonin suppression. The graph represents the data from the study and showed BB glasses can decrease specifically LED screen induced melatonin suppression and allow users to regulate sleep and attention levels in the late evening hours far better. Foster and Roenneberg, (2008) recognised the circadian clock of adolescents has a markedly later circadian phase compared with older adults. Eveningness can be associated with the lack of morning light exposure and evening exposure to artificial created light sources (Figueiro and Rea, 2010). Blue-enriched light exposure in the evening hours being the most problematic, further phase delay in sleep timing and reduction in sleep duration is the price that may be paid (Van der Lely et al. 2015). Although the results show good indications of melatonin suppression, sample size was restricted to 13 males; lack of statistical power lowers the creditability of the results and indicates further research is needed.
3.4 Necessity of blue light and other uses
It is important to add, blue light in itself is very good for us and exposure to blue light (preferably outdoors) is crucial in maintaining our circadian rhythms. A study composed on the delayed sleep phase, which is common in the Antarctic winter due to a lack of natural sunlight was undertaken highlighting why blue light is important. In these conditions, optimizing the artificial light conditions becomes desirable. This study evaluated sleep when using 17 000 k blue enriched lamps compared with standard 5000 k white maps for personal and communal lighting to make up for no natural sunlight. 15 subjects in total including 10 males and 5 females took part. Over a six month period, light exposure alternated between a 5 week period of standard white light and blue-enriched lamps. A 3 week control was put into place before and after extra light. Subjects sleep and light exposure was assessed by actigraphy and sleep diaries. Results here showed that with blue-enriched light the onset of sleep was earlier by 19 minutes and sleep latency (ability to fall from full wakefulness to sleep) tended to be shorter by 4 min. The research undertaken added to the artificial polar light research, concluding that artificial blue-enriched white light during daytime is capable of replicating the sun and correcting circadian phase delay and sleep loss during polar winter that would have otherwise occurred less effectively under a standard daytime white light (Mottram et al. 2010).
A more recent study by Taillard et al. (2012) involved using blue light as an in-car countermeasure to prevent sleep-related accidents. The study evaluated whether continuous exposure to monochromatic blue light, improved night-time driving performance. The study was a gold standard, consisting of randomised, double blind, placebo-controlled and cross-over study with 48 healthy male participants (aged 20-50 years) who drove 250 miles on the motorway after dusk. The participants randomly received either continuous blue light exposure via GOlite, (Philips 468nm) placed on the dashboard during driving or 2*200mg of caffeine or a placebo of caffeine before and during a break. Treatments were separated by a minimum of 1 week. The quality of driving criteria was the number of inappropriate line crossings (ILC). This measure was chosen due to epidemiologic findings showing 65% of sleep-related accidents occur after an ILC. ILC was identified by a Conteinental Automotive video system, which measured and logged the lateral position of the car. Both counter measures improved driving performance, with coffee being the best. The numbers of ILC’s were higher with the placebo than with coffee (26.42 vs 12.51) and continuous blue light exposure (26.42 vs 14.58). It is paramount to note that coffee being a central nervous stimulant and orally ingested, held very close figures with blue light exposure which is non oral. From the study, drivers can use blue light for increasing alertness while driving, although 17% of the drivers in this study experienced eye-related discomfort and visual problems.
Following this literature review we can conclude that, as the use of LED based digital devices and lighting increases, general health and well being is at risk from blue light exposure. Ham and Rufflo (1978) identitified RPE changes due to prolonged blue light exposure; this was the foundation for the conclusive evidence that followed. Artificial suns in the form of LED screens in to our homes is one of the factors causing sleep deprivation in this modern age especially to young adolescents as seen from the extensive research into this area already available. Although we know blue light is emitted from these devices, there is no such research into the amount of blue light emitted from popular devices used today. Furthermore, as the brightness on screens/lighting is adjustable, common sense tells us the blue light transmittance varies from device to device. Algvere et al. (2006) explained that in the young eye, ocular transmittance of blue light is very high reaching close to 90% due to incomplete development of the ocular pigment. Our concrete understanding of melanopsin-containing intrinsically photosensitive retinal ganglion cells means the sleep phase delay that can be experienced due to peak spectral sensitivity in the short-wavelength range (460–480 nm blue-light) can be validated. This is further verified by the various clinical studies on circadian rhythm changes due to blue light and how circadian rhythm can be controlled in Antarctica to allow melatonin production.
Yellowing of the crystalline lens serves as an intra-ocular blue light filter restricting circadian rhythm delays. Therefore, when lenses are removed due to cataract and clear lenses are implanted, we know it proves to be a problem for the patient and sleep synchronisation is affected, hence having an IOL which serves a purpose even though no current macular degeneration was found in Kara-Junior et al. (2011) cohort study. Yellow IOL’s filtering blue light needs further investigation to clarify findings in accordance with ARMD prevention. This is because; current clinical as well as epidemiological studies have not provided sufficient proof of blue-light filtering intra ocular lenses protection against the onset of ARMD. With regards to blue light and ARMD, because of the numerous factors involved in ARMD, clinical trials with a large number of patients and a cohort study which considers these other risk factors should be taken. Risk factors such as smoking and patients antioxidants levels may allow us to quantify the effects of blue light on this ocular disease. Beatty et al. (2015) more recent study highlighted the damage caused by blue light enhancing photodynamic product of free radicals from the basic mechanism of photochemical injury. We know an increase in ROS is detrimental for ocular cells and in turn ocular health.
Products on the market such as BB glasses and more recently lens coatings to cut blue light transmittance through spectacle lenses enhances the conclusion reached, that short wavelength blue light is harmful. Ocular health and sleep directly affected as a result. Therefore it is important for all eye care professionals to grasp the key points of blue light and its potential dangers.
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