Glare Terminology

The human visual system is sensitive to a trillionfold range of luminances but it responds effectively at a particular moment only to a thousandfold range of luminances in nighttime environments and a hundredfold range in bright daylight. Visual adaption adjusts the range of simultaneous visual sensitivity to the prevailing environmental luminance, also termed the adaptation luminance. Luminances substantially lower or higher than adaptation luminance appear dark or brilliant, respectively. Adaptation occurs in seconds for increases in environmental illumination (light adaptation) but can take minutes for luminance decreases (dark adaption). Transient perceptual difficulties occur when the visual system adjusts to sudden changes in adaptation luminance, as, for example, when driving into or out of a tunnel on a bright day.

Glare means different things in different professions. Automotive and road lighting designers use it to describe adverse headlight or streetlight exposures. Architects use it to characterize unfavorable lighting that causes fatigue, errors, and accidents in working environments. Patients use it inconsistently and unpredictably for numerous phakic and pseudophakic phenomena of photic and nonphotic origin. The current plethora of conflicting terminology and quantifying metrics in diverse disciplines is a barrier to understanding glare a century after Sir Herbert’s address, confirming W. S. Stiles’ pessimistic, prescient 1929 caveat that “Any attempt to frame a precise definition of glare … is foredoomed to failure on account of the very varied character of the glare phenomena.” The Table provides a summary of contemporary glare nomenclature and mechanisms.

Glare is caused by “light entering the eye that does not aid vision,” typically environmental luminance that is too intense or variable across the visual field. W. S. Stiles first differentiated discomfort from disability glare in 1929, based partly on earlier work by Luckiesh and Holladay. Disability glare , which is also known as physiological glare, is glare that impairs vision. Discomfort glare , which is also known as psychological glare, is glare that causes annoyance. Disability and discomfort glare can range from insignificant to incapacitating. They are usually concurrent but can occur independently. For example, brilliant street lighting can produce discomfort without disability glare, whereas poor street lighting can cause disability without discomfort glare.

Two other well-recognized forms of glare are dazzling and scotomatic glare. Dazzling glare (dazzle) is glare that produces squinting, annoyance, aversion, and visual disability when bright environments spread high illuminance across large retinal areas. Momentary dazzle is sometimes called adaptation glare. Prolonged dazzle has been termed saturation or blinding glare. Scotomatic glare (also termed photostress or flashblindness ) is glare that causes afterimages and visual disability when a brilliant but localized light exposure excessively bleaches macular photopigment (“puts a retinal area temporarily out of business by exhaustion of its active material” ). Aging and ocular or systemic disease can increase susceptibility to and recovery time from scotomatic and disability glare.

Disability Glare

Disability glare is caused by intraocular light scattering ( straylight ) that reduces the contrast of retinal images by spreading a veiling luminance across them. Contrast is decreased by a factor equal to background luminance divided by the sum of veiling and background luminances. Contrast loss is more significant in dim than bright environments because rod photoreceptors need larger contrast differences for target detection than cones (roughly 20% vs 1%, respectively).

Disability glare is determined by straylight, which is an optical phenomenon not dependent on neurophysiology. Veiling luminance from straylight depends on (1) the illuminances that glare sources produce at the observer’s eye and the angular distance between those sources and the observer’s visual axis (as described by the Holladay-Stiles equation), and (2) the observer’s age and pigmentation. These effects are embodied in the international-consensus general disability glare equation of the International Commission on Illumination (Commission Internationale de l’Éclairage or CIE).

Entopic straylight arises from light scattering by particles or inhomogeneities in ocular media or intraocular lenses (IOLs). When these defects are smaller than, roughly the same size as, or larger than the wavelength of visible light (0.4–0.7 μm), they produce Rayleigh-type , Rayleigh-Gans-type , or Mie-type light scattering , respectively. Rayleigh-type light scattering is largely nondirectional. It is proportional to λ ⁻⁴ , where λ is the wavelength of the scattered light, so small particle light scattering efficiency increases with decreasing wavelength. The daytime sky is blue because Rayleigh-type scattering by atmospheric oxygen and nitrogen molecules scatters shorter-wavelength (bluer) solar photons more effectively than longer-wavelength (redder) ones. Conversely, Mie-type large particle scattering is wavelength independent but it preferentially forward-scatters light. The color of light from streetlamps at night does not change when scattered by a fog’s large water droplets, but shadows are dense (sharply bordered) because light is preferentially forward-scattered.

Entopic scattering in older and lightly pigmented eyes is quite different from atmospheric scattering. It is not heavily wavelength dependent because predominantly short-wavelength light scattered by the cornea and crystalline lens is balanced by primarily long-wavelength light scattering in the iris, retina, choroid, and sclera. Straylight increases with aging, due partly to large-particle light scattering by multilamellar bodies roughly 1–4 μm in diameter in senescent crystalline lenses. Scattering abnormalities have diameters of approximately 200 μm in asteroid hyalosis and 5 to 20 μm in “glistenings” (water-filled vacuoles) that occur in some acrylic IOL materials. These defects all cause Mie-type light scattering in which light entering the eye is preferentially forward-scattered toward the retina.

The point spread function (PSF) describes how light energy from a point stimulus is imaged on the retina. It embodies information on both ocular aberrations and intraocular light scattering. Straylight accounts for light energy spread beyond 1 degree from the center of the PSF. Optical aberrations determine the central 0.1 degree of the PSF. Aberrations and neural processing affect visual acuity and contrast sensitivity, so changes in these psychophysical measures may not be well correlated with straylight and thus disability glare measurements.

Disability Glare

Disability glare is caused by intraocular light scattering ( straylight ) that reduces the contrast of retinal images by spreading a veiling luminance across them. Contrast is decreased by a factor equal to background luminance divided by the sum of veiling and background luminances. Contrast loss is more significant in dim than bright environments because rod photoreceptors need larger contrast differences for target detection than cones (roughly 20% vs 1%, respectively).

Disability glare is determined by straylight, which is an optical phenomenon not dependent on neurophysiology. Veiling luminance from straylight depends on (1) the illuminances that glare sources produce at the observer’s eye and the angular distance between those sources and the observer’s visual axis (as described by the Holladay-Stiles equation), and (2) the observer’s age and pigmentation. These effects are embodied in the international-consensus general disability glare equation of the International Commission on Illumination (Commission Internationale de l’Éclairage or CIE).

Entopic straylight arises from light scattering by particles or inhomogeneities in ocular media or intraocular lenses (IOLs). When these defects are smaller than, roughly the same size as, or larger than the wavelength of visible light (0.4–0.7 μm), they produce Rayleigh-type , Rayleigh-Gans-type , or Mie-type light scattering , respectively. Rayleigh-type light scattering is largely nondirectional. It is proportional to λ ⁻⁴ , where λ is the wavelength of the scattered light, so small particle light scattering efficiency increases with decreasing wavelength. The daytime sky is blue because Rayleigh-type scattering by atmospheric oxygen and nitrogen molecules scatters shorter-wavelength (bluer) solar photons more effectively than longer-wavelength (redder) ones. Conversely, Mie-type large particle scattering is wavelength independent but it preferentially forward-scatters light. The color of light from streetlamps at night does not change when scattered by a fog’s large water droplets, but shadows are dense (sharply bordered) because light is preferentially forward-scattered.

Entopic scattering in older and lightly pigmented eyes is quite different from atmospheric scattering. It is not heavily wavelength dependent because predominantly short-wavelength light scattered by the cornea and crystalline lens is balanced by primarily long-wavelength light scattering in the iris, retina, choroid, and sclera. Straylight increases with aging, due partly to large-particle light scattering by multilamellar bodies roughly 1–4 μm in diameter in senescent crystalline lenses. Scattering abnormalities have diameters of approximately 200 μm in asteroid hyalosis and 5 to 20 μm in “glistenings” (water-filled vacuoles) that occur in some acrylic IOL materials. These defects all cause Mie-type light scattering in which light entering the eye is preferentially forward-scattered toward the retina.

The point spread function (PSF) describes how light energy from a point stimulus is imaged on the retina. It embodies information on both ocular aberrations and intraocular light scattering. Straylight accounts for light energy spread beyond 1 degree from the center of the PSF. Optical aberrations determine the central 0.1 degree of the PSF. Aberrations and neural processing affect visual acuity and contrast sensitivity, so changes in these psychophysical measures may not be well correlated with straylight and thus disability glare measurements.

Discomfort Glare and Photophobia

Discomfort glare is caused by illumination that is too intense or variable for a particular person, place, and time. It is a normal response to abnormal illumination, whereas photophobia is an abnormal response to normal illumination exaggerated by abnormal light exposure. Discomfort glare threshold ( photosensitivity ) varies considerably between individuals. Discomfort can be manifested as annoyance, squinting, distraction, blinking, tearing, and light aversion. Photophobia may additionally include blepharospasm and/or cortical pain. Discomfort glare is commonplace. Photophobia is uncommon, potentially excruciatingly uncomfortable, and associated with anterior segment inflammation or trauma, optic neuropathy, migraine, trigeminal neuralgia, mental illness, and numerous other ocular or nonocular disorders.

Discomfort glare depends on an individual’s adaptation luminance and the characteristics of surrounding natural and artificial light sources (luminaires). It is intensified by increasing the number, luminance (or luminous exposure), and angular subtense of light sources and by decreasing the adaptation luminance or the angular separation between glare sources and the visual axis. Discomfort glare and photophobia are summed binocularly and diminished in people with normal binocular vision by shutting 1 eye. Discomfort glare varies little with age, unlike disability and scotomatic glare.

Discomfort glare is often quantified using subjective scales such as the De Boer index, which ranges from 9 (unnoticeable) to 1 (unbearable). Empirical equations based on human factors studies can be used to predict discomfort glare. These methodologies provide reasonable estimates of a group’s average discomfort but are poor predictors of individual discomfort, which is highly variable. Different algorithms are used in North America and Europe to estimate discomfort from automobile headlights, roadway illumination, sports facility lighting, and natural or artificial office illumination. Inconsistencies persist because the origins of discomfort glare remain poorly understood despite over 50 years of interdisciplinary research. Additionally, discomfort glare issues often have a low priority in comparison to disability glare considerations in illumination engineering.

Light source spectrum also affects visual discomfort. Results vary greatly with experimental methodology, but recent data show that sensitivity spectra for discomfort glare peak between 510 and 550 nm (green) for light exposures within 5 degrees of the visual axis. In general, the relative contributions of rod, cone, and retinal ganglion photoreceptors to visual discomfort probably vary considerably for different people and glare situations.

Visual and nonvisual photoreception both contribute to discomfort glare and photophobia. Retinal ganglion photoreceptors send information primarily to nonvisual brain centers, but they also transmit environmental irradiance data to the lateral geniculate nuclei, helping set adaptation luminance involved in discomfort glare. Nonvisual retinal ganglion photoreception accounts for photophobia in the visually blind, probably also contributing to it in sighted people. Pupillary hippus is not an important factor in discomfort glare.

The thalamus is involved in visual discomfort, photophobia, and dazzle. Retinal ganglion and possibly rod and cone photoreceptors modulate thalamic nuclei that are involved in a trigeminovascular pathway extending from dural vessels through the trigeminal ganglion to the thalamus. These thalamic nuclei have projections to the somatosensory and visual cortices, probably contributing to light’s exacerbation of migraine pain and migraineurs’ enhanced photosensitivity during headaches. Between headaches, migraineurs have reduced discomfort glare thresholds. Thalamic damage itself can increase dazzle photosensitivity.

For people with normal bilateral vision, shutting 1 eye decreases binocularly summed retinal illuminance, thereby reducing discomfort glare, photophobia, and dazzle. Conversely, if someone with normal binocular vision views a scene with a neutral-density filter over 1 eye, shutting that eye increases image brightness even though total retinal illuminance has decreased (this phenomenon is known as Fechner’s paradox). Thus, discomfort glare does not depend on brightness, emphasizing important differences between brightness perception and the luminance of light sources.