The Risk of Eye Damage from Bright and Blue Light Therapy

Retinal mitochondria damaged by blue light exposure a factor in AMD.

There is a growing understanding that chronic exposure of the eye to blue light causes mitochondrial dysfunction and the generation of ROS (Radical Oxygen Species) in the retina and contributes to the development of macular degeneration. Two recent papers discussing this are:

1) Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina. Aug 2019.

Distinct from other visible light components, blue light is characterized by short wavelength, high energy, and strong penetration that can reach the retina with relatively little loss in damage potential. Mitochondria are abundant in retinal tissues, giving them relatively high access to blue light, and chromophores, which are enriched in the retina, have many mitochondria able to absorb blue light and induce photochemical effects. Therefore, excessive exposure of the retina to blue light tends to cause ROS [Radical Oxygen Species] accumulation and oxidative stress, which affect the structure and function of the retinal mitochondria and trigger mitochondria-involved death signaling pathways.

In accordance with the vital importance of the RPE to the neural retina, especially the photoreceptor cells, mitochondrial dysfunction not only harms the RPE cells themselves but also affects adjacent photoreceptors. A similar mechanism is correlated with age-related macular degeneration (AMD).
Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina

and
2) Mitochondrial Dysfunction in the Aging Retina May, 2019.

Aging is a recognized factor associated with mitochondrial dysfunction in the outer retina. Other important risk factors for the development of AMD are genetics and environmental stressors, including exposure to blue light.
Mitochondrial Dysfunction in the Aging Retina

Since blue light damage to the retina is cumulative over a lifetime the repeated exposure to bright light or blue light therapy lamps causes increased levels of ROS and contributes to the age related mitochondrial dysfunction the causes the development of macular degeneration. The higher levels of blue light exposure from LEDs now widely used for indoor lighting further increases the risk of age related blindness for users of bright light therapy.

Newly discovered process show an additional pathway blue light attacks vision

An article in Safety and Health discusses a 2018 Nature Scientific Reports study about a newly discovered mechanism by which blue light damages cells in the human eye.

Exposure to blue light from the sun and electronic devices may destroy cells in the retina and accelerate the onset of blindness...Researchers discovered that emissions of blue light cause retinal molecules, which sense light and send signals to the brain, to produce toxic chemical molecules in photoreceptor cells that help the eye to see. The ensuing chemical reactions kill photoreceptors. The result is macular degeneration, an incurable eye disease that can trigger blindness, typically beginning in a person’s 50s or 60s.
“We are being exposed to blue light continuously, and the eye’s cornea and lens cannot block or reflect it,” Ajith Karunarathne, lead author ... “It’s no secret that blue light harms our vision by damaging the eye’s retina. Our experiments explain how this happens...."
Blue Light from Electronic Devices, Sun May Damage Vision

The study was also discussed in Science Alert in 2018.

“Excessive exposure to blue light isn't great for our eyes, contributing to a slow loss of vision over the course of a lifetime.” says chemist and senior researcher Ajith Karunarathne.”
“Age related macular degeneration involves the slow breakdown of cells that sit behind the light-sensitive tissue on the inside of the eyeball, preventing the transfer of nutrients and removal of waste. Little by little, the retina dies, leaving a growing blind spot that eventually robs an individual of their eyesight.”
See Blue Light Is Causing The Human Eye to Attack Itself

The Nature, Scientific Reports study can be accessed here.

AMD, blue light, macular pigment and diet.

Several studies discuss how macular pigment (MP) protects the eye by limiting the amount of blue light reaching the retina. A 2018 study in the journal Eye describes;

MP serves an ocular protective role through its ability to filter phototoxic blue light radiation... Epidemiological studies have supported this by showing that patients with lower concentrations of serum carotenoids and macular pigment optical density (MPOD) measurements are at a higher risk of developing AMD.

MP has its peak absorption at 460 nm (Fig. 3) where it can absorb 40–90 % of incident high-energy, short-wavelength [blue] visible light depending on its concentration [7]. A primary function of MP is the reduction of blue-light scattering in the central retina, and the deep yellow color and anatomical location of MP are thought to be ideal to protect the foveal region from photo-oxidative damage.
MP... must be obtained by dietary ingestion. Several studies have shown that increased dietary consumption of lutein and zeaxanthin results in a lower incidence of AMD. What Do We Know About the Macular Pigment in AMD: the Past, the Present, and the Future. Eye 32:992–1004 (2018)

Blue light is a much greater hazard than UV for AMD.

A paper in the Journal of Ophthalmology, explained:

"In adults, the lens absorbs UV-B and all the UV-A (295-400 nm); therefore only visible light (>400 nm) reaches the retina".
"short-wavelength blue visible light damages the retinas of those over 50 years of age through a photooxidation reaction with an accumulated chromophore, lipofuscin. Lipofuscin...is mainly derived from the chemically modified residues of incompletely digested photoreceptor outer segments. Photoreceptor cells (rods and cones) shed their outer segments (disc shedding) daily to be finally phagocytosed (digested) by RPE cells." ... "In response to [Upon the absorption of] short blue visible light, lipofuscin efficiently produces singlet oxygen and lipid peroxy radicals; there is also some production of superoxide and hydroxyl radicals...leading to damage to RPE cells.
Because the rods and cones survival is dependent on healthy RPE, these primary vision cells will eventually die, resulting in a loss of (central) vision (macular degeneration) and other retinopathies"
"Ocular exposure to sunlight, UV, and short blue light-emitting lamps directed at the human eye can lead to the induction of cataracts and retinal degeneration. This process is particularly hazardous after the age of 40 because there is a decrease in naturally protective antioxidant systems and an increase in UV and visible light-absorbing endogenous phototoxic chromophores that efficiently produce singlet oxygen and other reactive oxygen species."
The Photobiology of Lutein and Zeaxanthin in the Eye. J Ophthalmology

Studies continue to find that increased exposure to sunlight over a lifetime increases the likelihood of developing AMD. Since only the visible light wavelengths from sunlight reach the retina, hese studies support the premise that cumulative exposure to visible blue light wavelengths contributes to the development of AMD.

PURPOSE: To evaluate effects of current and past sunlight exposure and iris color on early and late age-related macular degeneration (AMD)
CONCLUSION: Sunlight exposure during working life is an important risk factor for AMD, ... Therefore, preventive measures, for example, wearing sunglasses to minimize sunlight exposure, should start early to prevent development of AMD later in life.
History of Sunlight Exposure is a Risk Factor for Age-Related Macular Degeneration

While many studies are concerned with the long term effects of repetitious blue light exposure, others also discuss the contribution of blue light wavelengths to retinal damage from acute exposure to high intensity light.

“Light causes damage to the retina (phototoxicity) and decreases photoreceptor responses to light. The most harmful component of visible light is the blue wavelength (400–500 nm)”
Removal of the Blue Component of Light Significantly Decreases Retinal Damage after High Intensity Exposure. PLOS (the Public Library of Science) March 15, 2018.

However, it is the harmful effects of repeated exposure of the eye to blue light that appears to pose the most significant risk to vision. The paper Effects of Blue Light on the Circadian System and Eye Physiology. discusses the role of blue light in the development of blindness from AMD.

"Experimental evidence indicates that wavelengths in the blue part of the spectrum (400-490 nm) can induce damage in the retina, and although the initial damage following exposure to blue light may be confined to the RPE, a damaged RPE eventually leads to photoreceptor death. ...some studies have reported that sub-threshold exposure to blue light can also induce damage in photoreceptors. In addition, several authors have proposed that the amount of blue light received during an individual's entire lifespan can be an important factor in the development of age-related macular degeneration (AMD)."

The paper concludes:

"Because light has a cumulative effect and many different characteristics (e.g., wavelength, intensity, duration of the exposure, time of day), it is important to consider the spectral output of the light source to minimize the danger that may be associated with blue light exposure....Although we are convinced that exposure to blue light from LEDs in the range 470-480 nm for a short to medium period (days to a few weeks) should not significantly increase the risk of development of ocular pathologies, this conclusion cannot be generalized to a long-term exposure (months to years)."

The concern these authors express relates to blue light wavelengths from indirect ambient lighting emitted by LEDs providing white light. The authors explain

"The white-light LED (i.e., the most common type of LED) is essentially a bichromatic source that couples the emission from a blue LED (peak of emission around 450-470 nm with a full width at half max of 30-40 nm) with a yellow phosphor ...that appears white to the eye when viewed directly. ...
white-light LEDs degrade over time ..[with]..increasing blue emission from the device with time."
See Effects of Blue Light on the Circadian System and Eye Physiology

In 2018 Healthy but Smart reviewed the evidence regarding eye damage from personal electronic devices and ambient lighting. Do Blue Light Blocking Glasses Do Anything? A Review of The Research

In May 2019, a 400 page report from ANSES, the French Agency for Food, Environmental and Occupational Health & Safety updated their 2010 expertise on the health effects of LEDs in light of the new scientific knowledge. According to English language press reports,

New scientific evidence confirms the "phototoxic effects" of short-term exposures to high-intensity blue light, as well as an increased risk of age-related macular degeneration after chronic exposure to lower-intensity sources." "even chronic exposure 'can accelerate the aging of retinal tissue, contributing to a decline in visual acuity and certain degenerative diseases such as age-related macular degeneration', the agency concluded CTV - French authorities warn of health dangers from LED lighting. CNN on ANSES report

The ANSES Report can be seen here

With respect to ambient lighting, the paper Light in Man's Environment in the journal EYE stated:

"Many studies have demonstrated the spectral dependence of eye health, with the retinal hazard zone associated with wavelengths in the blue, peaking at 441 nm - many of today's low-energy sources peak in this region. Given the increased longevity and artificial light sources emitting at biologically unfriendly wavelengths, attention has to be directed towards light in man's environment as a risk factor in age-related ocular diseases."
Light in Man's Environment

The risk to vision from blue light wavelengths has also been addressed in several studies examining the benefit of blue blocking artificial lenses implanted due to cataracts. The research was reviewed in the journal Eye.

"With the arrival of blue-filtering intraocular lenses (BFIOLs) in 1990's, a further debate was ignited as to their safety and potential disadvantages. ... The potential disadvantages raised in the literature over the last 25 years since their introduction, regarding compromise of visual function and disruption of the circadian system, have been largely dispelled. The clear benefits of protecting the retina from short-wavelength light make [blue-filtering intraocular lenses] BFIOLs a sensible choice"
Ultraviolet or Blue-Filtering Intraocular Lenses: What is the Evidence?

The amount of blue light entering the eye from a personal electronic device or ambient lighting is a tiny fraction of the light emitted by a therapy lamp used to influence mood or regulate circadian rhythms. The direct exposure to high intensity light provided by white or blue light therapy lamps presents a significantly greater hazard to the eye than exposure to personal electronic devices.

The eye has several built in robust systems that protect the retina from blue light damage. While many of these systems become less effective with age, they may still be capable of preventing permanent damage from the very low levels of blue light that enter the eye from personal devices or indirect lighting, or they may limit the amount retinal damage to a point where the advance in onset of AMD could be in the order of days or weeks. This would not be meaningful as a measurable advance in onset of AMD would be expressed in years.

Harvard University Finds Humans are Most Responsive to GreenLIGHT Therapy, not Blue Light.

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In 2022 a group of light therapy researchers in the Sleep Medicine Department at Harvard university (plus G.C. Brainard), published a paper in PNAS (Proceedings of the National Academy of Sciences) on the effects of several different wavelengths in the visible light spectrum on human circadian physiology, which indicated that the light wavelengths provided by Sunnex Biotechnologies Lo-LIGHT lamps, i.e. those in the 500 - 510 nm portion of the visible green light spectrum, are the most effective light wavelengths for light therapy.

"Examination of the fitted half-maximum value of each irradiance response curve shows that 507 nm light is more effective than 480 nm light at suppressing melatonin and resetting circadian phase"
Lockley et al., Short-Wavelength sensitivity for the Direct Effects of Light on Alertness, Vigilance, and the Waking Electroencephalogram in Humans

It appears that this 2022 PNAS paper was a response to a 2006 Sleep editorial that was critical of a study by the Harvard Sleep Medicine led group which was published in the same issue of Sleep. as the editorial. The 2006 SLEEP paper had been considered particularly significant in the study of human chronobiology because it appeared to establish the importance of blue light wavelengths for light therapy, by indicating that human physiology is most sensitive to exposure to blue light wavelengths; a misunderstanding that persists until today among several circadian researchers as well as the public.
This misunderstanding was promoted by several of the authors of the 2006 Sleep paper. For example in 2008 Lockley made a presentation to the Aerospace Medical Association (AsMA) where he stated:

"A wavelength-dependent shift in the sensitivity of the dose-response curves showed that 460 nm light was at least twice as effective as 555 nm light for circadian phase resetting and melatonin suppression (range, ~1.0-3.0 x 1013 photons/cm2/s). The short wavelength-sensitivity of human circadian responses to light is consistent with a role for the blue light-sensitive photopigment melanopsin in circadian phototransduction. These findings have important implications for light therapy-based treatments for sleep and circadian rhythm disorders associated with shiftwork, insomnia, and jet-lag."
AsMA presentation- Lockley et al

While the 2006 Harvard study only compared 460 nm blue light with 555 nm yellow-green light, the 2022 PNAS paper examined the effects of several wavelengths across the visible light spectrum, which addressed one of the criticisms in the editorial. Another reason the PNAS paper appears to be a response to the 2006 Sleep editorial is because the study described in the 2022 PNAS paper was conducted prior to 2010, even though it was not published until 2022.

"We constructed radiance-response curves and action spectra for melatonin suppression and circadian resetting responses in participants exposed to 6.5-h monochromatic 420, 460, 480, 507, 555, or 620 nm light exposures initiated near the onset of nocturnal melatonin secretion."
"Healthy research subjects (n =122), ages 18 to 30 y were enrolled in a 9-d inpatient study at the Intensive Physiologic Monitoring Unit (IPM) in the Enter for Clinical Investigation (CCI) at Brigham and Women’s Hospital (BWH; Boston, MA) between 2000 and 2009."
PNAS study, 2022

Although the editorial by S.S. Campbell in the February 2006 issue of Sleep addressed several comments and conclusions of the Lockley et al. paper from that issue, the Lockley paper has led to a major misunderstanding regarding spectral sensitivity of light therapy, and circadian regulation of humans with light in chronobiology that is now common. Specifically the editorial raised the following points;

Based on these findings, and on the tenor and focus of the authors’ discussion, it would be easy to come away from this paper with the distinct impression that light-induced improvements in alertness and performance are mediated almost exclusively by wavelengths in the 460nm range. This conclusion would be inaccurate, on several counts. First, despite the authors’ repeated use of the term, it appears that neither performance nor alertness were actually “improved” by exposure to either light source. Rather, the typical circadian dip in those measures appears to have been attenuated more so by exposure to 460nm than by exposure to 555nm. Yet, comparisons to other wavelengths, combinations thereof, a broad-spectrum, 460nm “knockout” light source, or some other appropriate control were not made. As such, the only conclusion that can be drawn from this study is that we are more sensitive to monochromatic blue light than we are to monochromatic yellow light. Moreover, because the study did not include a control condition, and because the authors did not analyze each condition relative to a circadian phase-equivalent baseline, it is impossible to assess the degree to which alertness and performance were actually affected by exposure to either wavelength."
"Another methodological problem involves the fact that timing of light exposure was scheduled to occur during an interval that can also result in significant circadian phase delays (6.5 hours, ending 15 minutes prior to the presumed nadir of body temperature). It is impossible, therefore, to effectively differentiate between possible circadian effects on alertness and performance and those attributed by the authors solely to acute activating effects. This confound is particularly problematic when trying to interpret the finding that subjective sleepiness remained relatively low for up to an hour after exposure to the short-wavelength light was terminated. While the authors conclude that this likely reflects a carry-over effect of the direct activating effects of light, the alternative interpretation that it was the result of a differential phase delay induced by exposure to 460nm cannot be ruled out."
Short-Wavelength Sensitivity for Activating Effects of Light: An Ascent to the Arcane?

In 2024, Dr. C.A. Czeisler, the head of Harvard's Department of Sleep Medicine, a leading authority on light therapy research, along with several longtime researchers of light therapy at Harvard, published an acknowledgenent in the journal Sleep Health that the initial 90 minutes of light exposure, the human physiological response to light, as measured by either melatonin suppression or by its capacity to shift circadian rhythms, is not in the blue region of the visible light spectrum, as is widely presented in the light therapy literature, but is in the green portion of the spectrum, in the region of the spectrum emitted by Lo-LIGHT lamps. i.e. 500-510 nm.

"given the effectiveness of monochromatic blue-green light (507 nm) at both suppressing melatonin secretion and delay resetting circadian phase and our earlier finding that dim monochromatic 555 nm green light may be more effective than dim blue light at inducing circadian phase resetting, these findings with green-enriched polychromatic light challenge the oversimplification that blue light is always more effective than green light in inducing circadian resetting responses in humans."
"for subjects whose eyes are not dilated, and who have not been restricted to very dim light exposure for about a day prior to the therapy, and who use light therapy for less than 90 minutes per session.]
"In the GREEN light conditions (GG and GS) the ambient room light was generated by ceiling-mounted green, fluorescent lamps (melDER 2.07) (Sunnex Biotechnologies, Winnipeg, MB Canada)"
Harvard's NASA study with Lo-LIGHT lamp

A paper published by the Harvard (plus Brainard) group in 2010 in Science Translational Medicine indicated that prior to 2010 the authors were well aware that for the first 90 minutes of exposure, blue light wavelengths are not paricularly effective for light therapy. Since light therapy sessions usually last less than 60 minutes, often closer to 30 minutes, blue light does not contribute to the effectiveness of light therapy. Though this 2010 study only examined the blue wavelengths near 460 nm and the yellow/green wavelengths near 550 and was published much earlier than the 2022 PNAS paper that examined the relative response to a range of light wavelengths referred to above, the study described in the 2022 paper was conducted prior to the publication of the 2010 Sleep study and had by many of the same authors as the 2010 study.
The earlier paper by Harvard University's Department determined that increasing the level of blue light wavelengths does not improve the effectiveness of a light therapy lamp to influence human physiological functioning. See Link Experts in the spectral sensitivity of human circadian physiology have recommended that all light therapy devices screen out potentially hazardous blue light wavelengths, and that light therapy devices emitting blue wavelengths of light should not be used. As one expert in light therapy stated,

"It should be noted that broad-spectrum white light, traditionally used for bright light therapy, also contains blue light of potential concern particularly for very high intensity, long-duration exposure. Clearly, the safety of bright light therapy for people needs investigating. In the meantime it would be suggested that light in the 500 to 530 nm wavelength range (blue-green) should still be effective while avoiding the putative blue hazard". REF

Although some earlier studies indicated that blue light would be highly effective for light therapy, it has now been determined that hazardous blue light wavelengths do not contribute to the effectiveness of light therapy. Studies have shown that monochromatic blue (479 nm) light is no more effective for light therapy than regular fluorescent white (polychromatic) light. see REF These studies were unable to demonstrate any benefit or increase in efficiency from increasing the proportion of blue light wavelengths, i.e. visible light wavelengths shorter than 480 nm, from a light therapy lamp. It has been known for many years that the inclusion of blue light is not necessary for effective light therapy.

Several studies using Lo-LIGHT lamps have been published in highly rated journals by leading authorities in light therapy. These studies demonstrate the effectiveness of low intensity GreenLIGHT technology in regulating human circadian rhythms and treating mood disorders. One shows that Lo-LIGHT lamps are least as effective at inducing physiological responses than a blue-enhanced (465 nm) light therapy device that emits 10 times as much light. Lo-LIGHT lamps emit no blue light and cannot damage the eye. see REF.

The risk of damage to the retina from blue light is increased in people who smoke, people with pre-existing retinal damage and people who use photosensitizing medications or supplements. The eye is more susceptible to damage from bright light after extended periods of darkness, like in in the morning after awakening. Older people are at greater risk because the defense mechanisms that protect the retina from oxidative damage progressively deteriorate after age 40. For a more complete, annotated discussion of bright / blue light therapy and vision loss, please see Risk factors of bright and blue therapy

Assessing the risk to vision from blue light for an individual is not simple. In addition to the amount of blue light entering the eye, individual risk depends on genetics, age, personal habits such as smoking and diet, and the use of photosensitizing medications. see REF

Specialists in macular degeneration research often recommend sunglasses that block blue visible light be used by people of all ages to limit the amount of blue light reaching the retina over a lifetime.

The pathogenesis of Age-Related Macular Degeneration (AMD) involves chronic elevated levels of oxidative stress, chronic inflammation, and the accumulation of oxidative debris in the outer retina. The outer retina includes the photoreceptor cells, an adjacent monolayer of retinal pigment epithelium (RPE) cells, and Bruch's membrane - a complex that acts as a retinal-blood barrier through which the nutrients and oxygen needed to sustain photoreceptor cells and RPE cells must pass. AMD occurs within a small area of the retina called the macula and is associated with malfunctioning of RPE cells adjacent to the macula and with the accumulation of oxidative debris within these cells (lipofuscin). When RPE cells, which are responsible for providing oxygen and nutrients to the photoreceptor cells as well as for removing the metabolic waste and oxidative debris generated from photoreceptor cells, are not functioning properly, adjacent photoreceptor cells cannot function or survive.

Blue light wavelengths penetrating to the outer retinal region is absorbed by elements within RPE cells that induce the formation of radical oxygen species (ROS) and can result in oxidative stress. Oxidative stress occurs within a cell when the level of radical oxygen species (ROS) exceeds the capacity of the protective anti-oxidative mechanisms within the cell to negate the harmful effects of ROS, and an inflammatory response is induced. Chronic, low-grade inflammation of RPE cells has been directly linked to the development of AMD.

Malfunctioning mitochondria, the power plant organelles within the cell, generate high levels of ROS. Blue light absorption by RPE mitochondria can cause their malfunctioning, as can retinal stress within the RPE cell. Lipofuscin accumulates in RPE cells over a lifetime and generates radical oxygen species when it absorbs blue visible light. Damage resulting from blue light absorption by the DNA of RPE cells can also cause them to malfunction, though it is generally accepted that damage to mitochondrial DNA induced by blue light absorption and the resulting ROS generation by these damaged organelles is a more significant contributor to heightened oxidative stress levels within RPE cells.

Retinal melanin is one of the protective elements regarding blue light damage within the outer retina. However, absorption of blue light by retinal melanin causes its degradation, and retinal melanin is not regenerated. The reduction in levels of functional retinal melanin by blue light absorption over a lifetime attenuates the capacity of this protective mechanism from blue light exposure.

Within the macular region of the retina is, the fovea, the retinal structure primarily responsible for vison. Light entering the eye is focused towards the macula, so this is the retinal region where the highest level of oxidative damage takes place. Damage to this region of the retina also has the greatest effect on vision. When RPE cells malfunction, an accumulation of oxidative debris on the basal side of the RPE occurs, where this material can become cross-linked to the Bruch's membrane complex, and form drusen. The formation of drusen is considered to be the initiation of the process of AMD. Much of the indigestible material generated from oxidative damage to lipids and lipoproteins within photoreceptors and adjacent RPE cells that accumulates within RPE cells generates ROS upon exposure to blue light wavelengths.

An accumulation of material between the RPE cells, which nourish and remove waste materials from photoreceptor cells, and the Bruch's membrane complex limits the access of RPE cells to the blood supply for absorbing nutrients and disposing of metabolic waste. Impairment of all of these processes are associated with the slow deterioration of vision called "dry macular degeneration".

The generation of the large amounts of radical oxygen species and the resulting oxidative stress can induce damage to the Bruch's membrane complex separating the retina from the blood supply, and promote its permeation by small weak capillaries. When these small capillaries invade the macular region of the retina they are susceptible to leakage. This leakage into the retinal space results in a rapid deterioration of vision that is known as the "wet" form of macular degeneration.