The blue light hazard is the experimental finding that blue light is highly toxic to the retina (photic retinopathy), in brief abnormally intense exposures, including sungazing or vitreoretinal endoillumination. This term has been misused commercially to suggest, falsely, that ambient environmental light exposure causes phototoxicity to the retina, leading to age-related macular degeneration (AMD). We analyze clinical, epidemiologic, and biophysical data regarding blue-filtering optical chromophores.
Analysis and integration of data regarding the blue light hazard and blue-blocking filters in ophthalmology and related disciplines.
Large epidemiologic studies show that blue-blocking intraocular lenses (IOLs) do not decrease AMD risk or progression. Blue-filtering lenses cannot reduce disability glare because image and glare illumination are decreased in the same proportion. Blue light essential for optimal rod and retinal ganglion photoreception is decreased by progressive age-related crystalline lens yellowing, pupillary miosis, and rod and retinal ganglion photoreceptor degeneration. Healthful daily environmental blue light exposure decreases in older adults, especially women. Blue light is important in dim environments where inadequate illumination increases risk of falls and associated morbidities.
The blue light hazard is misused as a marketing stratagem to alarm people into using spectacles and IOLs that restrict blue light. Blue light loss is permanent for pseudophakes with blue-blocking IOLs. Blue light hazard misrepresentation flourishes despite absence of proof that environmental light exposure or cataract surgery causes AMD or that IOL chromophores provide clinical protection. Blue-filtering chromophores suppress blue light critical for good mental and physical health and for optimal scotopic and mesopic vision.
Few patients or clinicians who hear about the blue light hazard know what the term means. Major health care organizations warn patients to “safeguard your eyes from harmful blue light.” Articles in professional magazines caution that the “sun is your worst enemy,” claiming that sunlight “is a risk factor for age-related macular degeneration” (AMD). Large manufacturers assert that their products provide “protection against harmful blue light,” , claiming that “a pedestrian can encounter toxic blue light levels on a sunny summer day.” Some fearful patients retreat to unhealthful indoor lifestyles with increased risk of insomnia, depression, and reduced longevity.
Manufacturers have devoted vast resources to creating a commercially expedient fear of blue light to market optical filters that reduce blue light transmission. These yellow-tinted blue-blocking (also known as “blue-filtering”) lenses decrease violet (400-440 nm) and blue (440-500 nm) wavelengths that are essential for dim environment vision, circadian photoreception, and good health. When blue-blocking chromophores are used in intraocular lenses (IOLs), light restriction is permanent. Manufacturers cannot produce conventional lenses that improve vision by amplifying light, so some choose to suppress useful light with colored chromophores, relying instead on marketing to convince people to pay more for “premium” products that provide less light for photoreception.
Decades of research have failed to provide conclusive evidence that environmental light exposure , or cataract surgery , increase the incidence or progression of AMD. There is strong and growing scientific evidence, however, that blue light is critical for dim environment vision and circadian photoreception, especially in aging eyes. Indeed, studies have shown that in comparison to yellow-tinted blue-blocking IOLs, colorless UV-blocking IOLs are associated with reduced depression and improved slow-wave sleep, cognition, and even longevity. Additionally, blue-blocking IOLs decrease dim-light photoreception, , and in some cases increase intraocular straylight, which is the cause of disability glare.
Large epidemiologic studies show that blue-filtering IOLs have no advantage over UV-blocking IOLs in reducing the incidence, progression, or severity of AMD, as predicted by earlier biophysical hazards analyses. , This perspective examines some of the myths and misperceptions used to promote blue light fright in consumers and clinical practice.
NORMAL ENVIRONMENTS DO NOT POSE A BLUE LIGHT HAZARD
The term blue light hazard describes an experimental finding that short-wavelength light is more phototoxic to the retina than longer wavelengths when delivered in brief, intense, exposures. , , The phenomenon could have been called the ultraviolet (UV) radiation hazard because UV radiation in aphakic eyes is potentially more phototoxic than violet light, which in turn is potentially more hazardous acutely than blue or longer wavelengths.
Blue light hazard data originated from experiments on anesthetized rhesus monkeys using a 2500-watt xenon lamp and retinal exposures ranging from 1 to 1000 seconds in duration. It has nothing to do with ordinary indoor or ambient outdoor lighting, which produce retinal irradiances that are a million times lower in magnitude. , , , The blue light hazard refers only to exposures from brilliant light sources that can cause acute chorioretinal injuries such as solar, welder’s, and operating microscope maculopathies. , , Misrepresentation of this term recently prompted the International Commission on Illumination to issue a position statement emphasizing that the term blue light hazard should be used only for conditions involving staring at brilliant light sources such as the sun or welding arcs.
THE CENTURY-OLD PHOTOTOXICITY-AMD HYPOTHESIS IS UNPROVEN
Some manufacturers use the unproven phototoxicity-AMD hypothesis to justify blue-blocking chromophores. This hypothesis was proposed in 1975 based on histopathologic similarities between acute solar retinopathy and AMD. It conjectures that hypothetical cumulative retinal damage from repetitive acute environmental retinal phototoxicity (also known as photic retinopathy) may increase the risk of AMD. A similar conjecture was proposed in 1920 based on cataract-AMD incidence correlations that were later proven erroneous.
The phototoxicity-AMD hypothesis was first applied to IOLs in 1978. It was shown that IOLs in use then transmitted visually-unnecessary and potentially harmful UV radiation that could be blocked fully with IOL chromophores. UV-absorbing IOL chromophores were incorporated into IOLs shortly thereafter but their protective value remains unproven. Indeed, some IOLs marketed as “premium” because of their accommodative properties did not incorporate UV-absorbing chromophores for many years.
The potential role of cumulative environmental light exposure in the pathogenesis of AMD remains unproven despite decades of intensive investigation. Most major epidemiologic studies found no association between light exposure and AMD. , A recent meta-analysis of 14 previous studies involving >40,000 people also found no association between AMD risk and sunlight exposure. The Centers for Medicare & Medicaid Services concluded that the “relationship between blue light and macular degeneration is speculative and not proven by available evidence.” , Fourteen years later, the International Commission on Illumination published the same conclusion.
RPE CELL CULTURES ARE NOT VALID MODELS OF CLINICAL AMD
Retinal phototoxicity experiments involving RPE cell cultures are used to suggest that blue-blocking IOL and spectacle chromophores can decrease AMD. Retinal phototoxicity is a useful technique for studying perturbations of retinal pigment epithelium (RPE) physiology if the cells exhibit characteristic properties of confluence, polarity, and barrier function. It requires high retinal irradiances that overwhelm RPE monolayer repair mechanisms acutely, especially when cells have been incubated with a photosensitizer. Some investigators have used a blue-blocking filter to reduce experimental blue light irradiance in phototoxicity experiments, predicably decreasing cell culture damage. , , The experiments are then said to support the “efficacy” or “protection” of blue-blocking IOLs. ,
An important development in the last 15 years is improved understanding of how AMD does proceed, using data from human eye pathology, genetics, gene expression profiling, clinical imaging and epidemiology, among other approaches. , Additionally, there are well-supported biologically defensible actions for patients to slow AMD progression including smoking cessation and dietary modification. Knowledge gaps remain but studies collectively implicate pathways of complement, lipid transfer, and extracellular matrix remodeling that reflect the biology of cone- and rod-specific support systems and sequelae of inflammation, in a vasculogenic disease not dependent on retinal phototoxicity. , , The A2E bisretinoid compound used as a photosensitizer in many in vitro light damage studies has been repeatedly shown to be lower in human macula than in the periphery, raising questions about its role in macular disease.
RPE cell culture experiments have been described in recent manufacturer-supported studies as an “in vitro model of AMD.” Conversely, more than a decade of anti–vascular endothelial growth factor therapy monitored by optical coherence tomography has demonstrated that AMD pathophysiology is multilayer and only partly represented by a single cell layer, even an important one such as the RPE. , Additionally, lifelong aging cannot be simulated by acute injury. , , Acute phototoxicity can damage the macula but cannot simulate a lifetime of normal environmental light exposure just as scalding water can scar skin but cannot simulate a lifetime of normal bathing. Intense blue light is harmful to nonphysiologic RPE cell cultures but ordinary environmental light exposure has not been proven to be harmful to normal human retinas.
YELLOW CHROMOPHORES CANNOT DECREASE DISABILITY GLARE
Clinical disability glare occurs when intraocular light scattering (straylight) reduces the contrast of retinal images by spreading a veiling luminance across them. Disability glare is determined by straylight, an optical phenomenon that does not depend on neurophysiology and is embodied in the International Commission on Illumination’s consensus disability glare equation. In common real-world situations, retinal targets are illuminated by light sources (eg, the sun) with a spectrum similar to the glare source (eg, the sun). Blue-blocking filters decrease image and glare illumination in exactly the same proportion so they cannot affect retinal image contrast or reduce disability glare. A recent study found that blue-blocking IOLs increase straylight, the cause of disability glare, an effect probably caused by glistenings rather than light filtering.
Discomfort glare occurs when natural or artificial illumination is too bright or variable for a person’s light adaptation state. It is manifested by squinting, light aversion, blinking, tearing, and related responses. Discomfort glare is a normal reaction to abnormal illumination, whereas photophobia is an abnormal response to normal illumination that can be aggravated by excessive illumination. Sunglasses are useful for reducing discomfort glare but blue-blocking IOLs are not effective substitutes for sunglasses.
Psychophysical tests can be biased to show that blue-blocking filters decrease artificial glare by using laboratory glare sources that are bluer than target illumination. , In one manufacturer-supported study, the spectrum of the blue-weighted glare source was labeled falsely as the redder target illumination spectrum, , and contrast testing was performed on a violet-blue background. The Centers for Medicare & Medicaid Services twice concluded that product-biased experiments fail to demonstrate that blue-filtering IOLs produce “clinically meaningful, improved outcomes” in “driving safety under glare conditions.” A recent independent scientific study documented that blue-blocking spectacles do not improve pedestrian detection or reduce headlight glare in nighttime driving situations.
BLUE LIGHT IS IMPORTANT FOR ROD PHOTORECEPTION
Colorless UV-blocking and yellow-tinted blue-blocking IOLs are seldom implanted in contralateral eyes because blue-filtering chromophores can produce a noticeable yellowish cast even in photopic viewing situations. This imbalance occurs because yellow IOL chromophores block 67% to 83% of violet and 27% to 40% of pseudophakic blue light, depending on their dioptric power. , In bright conditions, more retinal illuminance is available than needed for cone photoreceptors, so blue-blocking filters do not affect performance adversely on standard photopic tests such as visual acuity, contrast sensitivity, or color vision. Some tests have shown, however, that colorless UV-blocking IOLs provide photopic luminance contrast and color discrimination superior to yellow-tinted blue-filtering IOLs. , For example, pseudophakic differentiation of navy from black clothing is significantly better with colorless lenses.
Violet and blue light provide 45% of aphakic rod-mediated scotopic sensitivity but only 7% of photopic sensitivity. Rod-mediated vision including scotopic and mesopic sensitivity declines with aging because of crystalline lens yellowing, progressive pupillary miosis, selective loss of macular rods before cones, and slowed rod-mediated dark adaptation due to impairment of retinoid recycling. Cataract surgery increases blue light available for rod photoreception, regardless of IOL spectral transmittance. In dim environments when retinal illuminance is marginal, however, older pseudophakes benefit from having as much blue light reception as possible. , Yellow IOL chromophores decrease available blue light, permanently. , , ,
Mesopic vision is decreased in patients with yellow-tinted blue-blocking compared to colorless UV-blocking IOLs, , supporting prior biophysical analyses showing that blue-blocking IOLs reduce rod-mediated vision. , , Blue-blocking IOLs also decrease scotopic vision at violet and blue wavelengths. Reduced rod-mediated dim-environment vision is correlated with an increased risk of falling and its resultant serious morbidities as well as with nighttime driving problems.
BLUE LIGHT IS CRITICAL FOR RETINAL GANGLION PHOTORECEPTION
Blue light-sensitive retinal ganglion photoreceptors profoundly influence mental and physical health. , , , Only approximately 1% of retinal ganglion cells are photoreceptive and express the blue light–sensitive photopigment melanopsin. Their primary function is to monitor environmental light levels and send this information to the suprachiasmatic nuclei to synchronize the human body’s circadian clock. , , , They require high retinal illuminances well above typical indoor illumination levels. The maximal sensitivity for human retinal ganglion photoreceptors is 460 nm, , , in the middle of the blue part of the spectrum.
Bright, well-timed blue light exposure is needed for effective suprachiasmatic nuclei circadian control and optimal neurobiologic health. Insufficient exposure dampens hormonal and physiological signaling, reducing physical and psychological health and contributing to sleep problems, depression, and the risk of all-cause mortality. , , Daily bright light exposure declines markedly in elderly adults, with women averaging half that of men. Institutionalized Alzheimer patients may receive fewer than 10 minutes of daily light exceeding 1000 lux. Morbidity from environmental light deficiency is reversable, with effective environmental light exposure shown to be beneficial for insomnia, depression, cognition, and degenerative disorders including Alzheimer disease. , Light exposures from artificial devices such as computer monitors and cell phones can disrupt circadian rhythms but there is no evidence they can cause retinal damage or AMD. ,
Retinal ganglion photoreceptor function is diminished by progressive age-related ocular changes, including crystalline lens yellowing, pupillary miosis, and retinal ganglion cell degeneration. Cataract surgery cannot reverse age-related pupillary miosis or retinal ganglion cell loss but it can compensate for crystalline lens yellowing and increase blue light transmission to optimize the function of the remaining retinal ganglion and rod photoreceptors. Retinal ganglion degeneration is accelerated in neurodegenerative disorders including Parkinson and Alzheimer diseases, glaucoma, and diabetic retinopathy, which all potentially benefit from the additional blue light available after cataract surgery.
It is difficult to perform studies that directly compare the circadian effects of colorless UV-blocking vs yellow-tinted blue-blocking IOLs because numerous factors must be controlled, including individual daily outdoor light exposure and sleep habits. Nonetheless, most circadian-related studies show either (1) no advantage for yellow-tinted blue-blocking IOLs , or (2) advantages for colorless UV-blocking IOLs vs yellow-tinted blue-blocking ones in functions including cognitive performance, sleep, , , and depression. Additionally, a 15-year-long cohort study showed that colorless UV-blocking IOLs in comparison to yellow-tinted blue-filtering ones were associated with a significantly reduced risk of all-cause mortality.
Photic retinopathy from intense light is sometimes referred to as a blue light hazard because shorter, bluer wavelengths are more acutely phototoxic, experimentally, than longer ones. , Ordinary ambient environmental light exposure does not cause this injury. The hazard has been used as a marketing ploy to alarm consumers and clinicians into using lenses that restrict blue light. People are encouraged to pay more for less light, motivated by misleading advertisements and the affirmations of professional “thought-leaders” that blue-filtering may protect them from AMD. , This blue light marketing stratagem persists despite (1) the absence of scientific proof that sunlight or cataract surgery causes AMD , or that blue-filtering IOLs reduce the risk of AMD, , (2) accumulating evidence that blue light is essential for good mental and physical health , , as well as for optimal scotopic and mesopic vision, , , , and (3) scientific evidence that AMD pathophysiology involves major biological processes in the photoreceptor support system and does not require light damage as an explanation. , ,
Pseudophakes with colorless IOLs are free to choose any outdoor sunglass filter they wish and still have optimal mesopic, scotopic, and circadian photoreception. Pseudophakes lose this freedom of photoreception when manufacturers incorporate ever-present blue-blocking filters into their IOLs. Blue-filtering IOL pseudophakes usually achieve improved photopic vision after cataract surgery. Most are unaware that blue light valuable for their declining populations of rod and retinal ganglion photoreceptors has been restricted, permanently.
Funding/Support: Martin A. Mainster is a consultant for Ocular Instruments, Inc. Oliver Findl is a scientific advisor to Alcon, Carl Zeiss Meditec, Croma, Johnson & Johnson, and Merck. Christine A. Curcio receives research support from Genentech/Hoffman LaRoche and Regeneron and is a stockholder in MacRegen Inc. Fundamental research in autofluorescence imaging was supported by NIH grants R01EY06019 and R01EY027948 (to C.A.C.). The other authors declare no conflicts of interest. Financial Disclosures: The sponsor had no role in the design or conduct of the research. All authors attest that they meet the current ICMJE criteria for authorship.
Acknowledgments: We thank many authors for contributions that we could not cite due to journal policy for Perspective publications. We direct readers to prior comprehensive reviews by authors M.A.M. and P.L.T.