Color blindness

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Color blindness
Other namesColor deficiency, impaired color vision [1]
Ishihara 9.svg
Specialty Ophthalmology
Symptoms Decreased ability to see colors [2]
DurationLong term [2]
Causes Genetic (inherited usually X-linked) [2]
Diagnostic method Ishihara color test [2]
TreatmentAdjustments to teaching methods, mobile apps [1] [2]
FrequencyRed–green: 8% males, 0.5% females (Northern European descent) [2]

Color blindness (color vision deficiency) is the decreased ability to see color or differences in color. [2] It can impair tasks such as selecting ripe fruit, choosing clothing, and reading traffic lights. [2] Color blindness may make some academic activities more difficult. [2] However, issues are generally minor, and the colorblind automatically develop adaptations and coping mechanisms. [2] People with total color blindness (achromatopsia) may also be uncomfortable in bright environments [2] and have decreased visual acuity.


The most common cause of color blindness is an inherited problem or variation in the functionality of one or more of the three classes of cone cells in the retina, which mediate color vision. [2] Males are more likely to be color blind than females, because the genes responsible for the most common forms of color blindness are on the X chromosome. [2] Non-color-blind females can carry genes for color blindness and pass them on to their children. [2] Color blindness can also result from physical or chemical damage to the eye, the optic nerve, or parts of the brain. [2] Screening for color blindness is typically done with the Ishihara color test. [2]

There is no cure for color blindness. [2] Diagnosis may allow an individual, or their parents/teachers to actively accommodate the condition. [1] Special lenses such as EnChroma glasses or X-chrom contact lenses may help people with red–green color blindness at some color tasks, [2] but they do not grant the wearer "normal color vision".[ citation needed ] Mobile apps can help people identify colors. [2]

Red–green color blindness is the most common form, followed by blue–yellow color blindness and total color blindness. [2] Red–green color blindness affects up to 1 in 12 males (8%) and 1 in 200 females (0.5%). [2] [3] The ability to see color also decreases in old age. [2] In certain countries, color blindness may make people ineligible for certain jobs, [1] such as those of aircraft pilots, train drivers, crane operators, and people in the armed forces. [1] [4] The effect of color blindness on artistic ability is controversial, [1] [5] but a number of famous artists are believed to have been color blind. [1] [6]

Signs and symptoms

Color blindness describes both a symptom of reduced color perception, as well as several conditions where colorblindness is the primary – or only – symptom. This section will focus only on color blindness as a symptom.

A colorblind subject will have decreased (or no) color discrimination along the red-green axis, blue-yellow axis, or both, though the vast majority of the colorblind are only affected on their red-green axis.

The first indication of colorblindness generally consists of a person using the wrong color for an object, such as when painting, or calling a color by the wrong name. The colors that are confused are very consistent among people with the same type of color blindness.

Confusion colors

Confusion colors are pairs or groups of colors that will often be mistaken by the colorblind. Confusion colors for red-green color blindness include:

Confusion colors for blue-yellow color blindness include:

Color tasks

Cole [7] describes four color tasks, all of which are impeded to some degree by color blindness:

Color blindness causes difficulty in all four kinds of color tasks. The following sections will describe specific color tasks that the colorblind typically have difficulty with.


Simulation of the normal (above) and dichromatic (below) perception of red and green apples Braeburn GrannySmith dichromat sim.jpg
Simulation of the normal (above) and dichromatic (below) perception of red and green apples

Colorblindness causes difficulty with the connotative color tasks associated with selecting or preparing food, for example:

Skin color

Changes in skin color due to bruising, sunburn, rashes or even blushing are easily missed by those with red-green colorblindness. These discolorations are often linked to the blood oxygen saturation, which affects skin reflectance.

Traffic lights

The colors of traffic lights can be difficult for the red-green colorblind. This includes distinguishing:

Signal lights

Navigation lights in marine and aviation settings employ red and green lights to signal the relative position of other ships or aircraft. Railway signal lights also rely heavily on red-green-yellow colors. In both cases, these color combinations can be difficult for the red-green colorblind. Lantern Tests are a common means of simulating these light sources to determine not necessarily whether someone is colorblind, but whether they can functionally distinguish these specific signal colors. Those who cannot pass this test are generally completely restricted from working on aircraft, ships or rail.


Aesthetic color tasks, such as matching clothes, can be particularly difficult. Most colorblind individuals will avoid brightly colored clothes to avoid making color clashing mistakes.


People with deuteranomaly may be better at distinguishing shades of khaki than people with normal vision and may be at an advantage when looking for predators, food, or camouflaged objects hidden among foliage. [8] [9] Dichromats tend to learn to use texture and shape clues and so may be able to penetrate camouflage that has been designed to deceive individuals with normal color vision. [10]


These color charts show how different colorblind people see compared to a person with normal color vision. Color blindness.svg
These color charts show how different colorblind people see compared to a person with normal color vision.

Much terminology has existed and does exist for the classification of color blindness, but the typical classification for color blindness follows the von Kries classifications, [11] which uses severity and affected cone for naming.

Based on severity

Based on clinical appearance, color blindness may be described as total or partial. Total color blindness (monochromacy) is much less common than partial color blindness. [12] Partial colorblindness includes dichromacy and anomalous trichromacy, but is often clinically defined as mild, moderate or strong.


Monochromacy is often called total color blindness since there is no ability to see color. Although the term may refer to acquired disorders such as cerebral achromatopsia, it typically refers to congenital color vision disorders, namely rod monochromacy and blue cone monochromacy). [13] [14]

In cerebral achromatopsia, a person cannot perceive colors even though the eyes are capable of distinguishing them. Some sources do not consider these to be true color blindness, because the failure is of perception, not of vision. They are forms of visual agnosia. [14]

Monochromacy is the condition of possessing only a single channel for conveying information about color. Monochromats are unable to distinguish any colors and perceive only variations in brightness. Congenital monochromacy occurs in two primary forms:

  1. Rod monochromacy, frequently called complete achromatopsia, where the retina contains no cone cells, so that in addition to the absence of color discrimination, vision in lights of normal intensity is difficult.
  2. Cone monochromacy is the condition of having only a single class of cone. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues. Cone monochromacy is divided into classes defined by the single remaining cone class. However, red and green cone monochromats have not been definitively described in the literature. Blue cone monochromacy is caused by lack of functionality of L (red) and M (green) cones, and is therefore mediated by the same genes as red–green color blindness (on the X chromosome). Peak spectral sensitivities are in the blue region of the visible spectrum (near 440 nm). People with this condition generally show nystagmus ("jiggling eyes"), photophobia (light sensitivity), reduced visual acuity, and myopia (nearsightedness). [15] Visual acuity usually falls to the 20/50 to 20/400 range.


Dichromats can match any color they see with some mixture of just two primary colors (in contrast to those with normal sight (trichromats) who can distinguish three primary colors). Dichromats usually know they have a color vision problem, and it can affect their daily lives. Dichromacy in humans includes protanopia, deuteranopia, and tritanopia. Out of the male population, 2% have severe difficulties distinguishing between red, orange, yellow, and green. (Orange and yellow are different combinations of red and green light.) Colors in this range, which appear very different to a normal viewer, appear to a dichromat to be the same or a similar color. The terms protanopia, deuteranopia, and tritanopia come from Greek, and respectively mean "inability to see (anopia) with the first (prot-), second (deuter-), or third (trit-) [cone]".

Anomalous trichromacy

Anomalous trichromacy is the least serious type of color deficiency [16] and includes protanomaly, deuteranomaly and tritanomaly. Anomalous trichromats exhibit trichromacy, but the color matches they make differ from normal trichromats. In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than a normal observer, and deuteranomalous observers need more green. The severity of anomalous trichromacy ranges from almost dichromacy (strong) to almost normal trichromacy (mild). In fact, many mild anomalous trichromats have very little difficulty carrying out tasks that require normal color vision and some may not even be aware that they have a color vision deficiency.

Based on affected cone

There are two major types of color blindness: difficulty distinguishing between red and green, and difficulty distinguishing between blue and yellow. [17] [18] [ dubious ] These definitions are based on the phenotype of the partial colorblindness. Clinically, it is more common to use a genotypical definition, which describes which cone/opsin is affected.

Red–green color blindness

Red-green color blindness includes protan and deutan CVD. Protan CVD is related to the L-cone and includes protanomaly (anomalous trichromacy) and protanopia (dichromacy). Deutan CVD is related to the M-cone and includes deuteranomaly (anomalous trichromacy) and deuteranopia (dichromacy). [19] [20] The phenotype (visual experience) of deutans and protans is quite similar. Common colors of confusion include red/brown/green/yellow as well as blue/purple. Both forms are almost always congenital (genetic) and sex-linked: affecting males much more often than females. [21] This form of colorblindness is sometimes referred to as daltonism after John Dalton, who had red-green dichromacy. In some languages, daltonism is still used to describe red-green color blindness.

Illustration of the distribution of cone cells in the fovea of an individual with normal color vision (left), and a color blind (protanopic) retina. The center of the fovea holds very few blue-sensitive cones. ConeMosaics.jpg
Illustration of the distribution of cone cells in the fovea of an individual with normal color vision (left), and a color blind (protanopic) retina. The center of the fovea holds very few blue-sensitive cones.

  • Protan (2% of males): Lacking, or possessing anomalous L-opsins for long-wavelength sensitive cone cells. Protans have a neutral point at a cyan-like wavelength around 492 nm (see spectral color for comparison)—that is, they cannot discriminate light of this wavelength from white. For a protanope, the brightness of red, is much reduced compared to normal. [22] This dimming can be so pronounced that reds may be confused with black or dark gray, and red traffic lights may appear to be extinguished. They may learn to distinguish reds from yellows primarily on the basis of their apparent brightness or lightness, not on any perceptible hue difference. Violet, lavender, and purple are indistinguishable from various shades of blue. A very few people have been found who have one normal eye and one protanopic eye. These unilateral dichromats report that with only their protanopic eye open, they see wavelengths shorter than neutral point as blue and those longer than it as yellow.

  • Deutan (6% of males): Lacking, or possessing anomalous M-opsins for medium-wavelength sensitive cone cells. Their neutral point is at a slightly longer wavelength, 498 nm, a more greenish hue of cyan. Deutans have the same hue discrimination problems as protans, but without the dimming of long wavelengths. Deuteranopic unilateral dichromats report that with only their deuteranopic eye open, they see wavelengths shorter than neutral point as blue and longer than it as yellow. [23]

Blue–yellow color blindness

Blue-yellow color blindness includes tritan CVD. Tritan CVD is related to the S-cone and includes tritanomaly (anomalous trichromacy) and tritanopia (dichromacy). Blue-yellow color blindness is much less common than red-green color blindness, and more often has acquired causes than genetic. Tritans have difficulty discerning between bluish and greenish hues. [24] Tritans have a neutral point at 571 nm (yellowish).[ citation needed ]

  • Tritan (<0.01% of individuals): Lacking, or possessing anomalous S-opsins or medium-wavelength sensitive cone cells. Tritans see short-wavelength colors (blue, indigo and spectral violet) as greenish and drastically dimmed, some of these colors even as black. Yellow and orange are indistinguishable from white and pink respectively, and purple colors are perceived as various shades of red. Unlike protans and deutans, the mutation for this color blindness is carried on chromosome 7. Therefore, it is not sex-linked (equally prevalent in both males and females). The OMIM gene code for this mutation is 304000 "Colorblindness, Partial Tritanomaly". [25]

  • Tetartan is the "fourth type" of colorblindness, and a type of blue-yellow color blindness. However, its existence is hypothetical and given the molecular basis of human color vision, it is unlikely this type could exist.[ citation needed ]

Summary of cone complements

The below table shows the cone complements for different types of human color vision, including those considered color blindness, normal color vision and 'superior' color vision. The cone complement contains the types of cones (or their opsins) expressed by an individual.

Cone systemRedGreenBlueN=normal
1Normal visionTrichromacyNormal
2ProtanomalyAnomalous trichromacyPartial
4DeuteranomalyAnomalous trichromacy
6TritanomalyAnomalous trichromacyBlue–
8Blue Cone MonochromacyMonochromacyTotal color blindness
(carrier theory)


Color vision deficiencies can be classified as inherited or acquired.


Color blindness is typically an inherited genetic disorder. The most common forms of colorblindness are associated with the Photopsin genes, but the mapping of the human genome has shown there are many causative mutations that don't directly affect the opsins. Mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man [OMIM]).

Genetics of red-green color blindness

Punnett squares for each combination of parents' color vision status giving probabilities of their offsprings' status, each cell having 25% probability in theory Punnett square colour blindness.svg
Punnett squares for each combination of parents' color vision status giving probabilities of their offsprings' status, each cell having 25% probability in theory

By far the most common form of colorblindness is congenital red-green colorblindness (Daltonism), which includes protanopia/protanomaly and deuteranopia/deuteranomaly. These conditions are mediated by the OPN1LW and OPN1MW genes, respectively, both on the X chromosome. Protanopia and Deuteranopia (Dichromacy) could be caused by either a missing gene, or a mutation that renders the protein fully non-functional. Protanomaly and Deuteranomaly are caused by a mutation of the genes that causes the spectral sensitivity of the associated opsin proteins to shift towards the other. That is, either the spectral sensitivity of the L cone shifts towards the M cone (blue shift), or that of the M cone shifts towards the L cone (red shift). These are then called anomalous cones and denoted by an asterisk (L* or M*).

Since the mutated OPN1LW and OPN1MW genes are on the X chromosome, they are sex-linked, and therefore affected males and females disproportionately. Because the colorblind alleles are recessive, colorblindness follows X-linked recessive inheritance. Males have only one X chromosome (XY), and females have two (XX); Because the male only has one allele of each gene, if it is mutated, the male will be colorblind. Because a female has two alleles of each gene (one on each chromosome), if only one allele is mutated, the dominant normal alleles will "override" the mutated, recessive allele and the female will have normal color vision. However, if the female has two mutated alleles, she will still be colorblind. This is why there is a disproportionate prevalence of colorblindness, with ~8% of males exhibiting colorblindness and ~0.5% of females (0.08² = 0.0064 = 0.64%).

The following table shows the possible allele/chromosome combinations and how their interactions will manifest in an individual. The exact phenotype of some of the combinations depend on whether the mutation yields an anomalous or non-functioning opsin. Blue cone monochromacy also follows these inheritance patterns, since it essentially a superposition of protanopia and deuteranopia.

Ymale-only chromosome, no affect on colorblindness.
XX chromosome.
M(as subscript), normal M opsin.
L(as subscript), normal L opsin.
M*(as subscript), mutated M opsin.
L*(as subscript), mutated L opsin.
XML YUnaffected male
XM*L YDeutan male
XML* YProtan male
XM*L* YMale with possible blue cone monochromacy
XML XMLUnaffected female
Female Carrier (possible tetrachromat)
Female Carrier (possible pentachromat)
Protan/Deutan Female

The following table shows the pattern of inheritance for congenital red-green colorblindness (protan/deutan) given affected, unaffected or carrier parents. When daughter 1 and daughter 2 (or son 1 and son 2) differ, this indicates a 50% chance of each outcome. Some conclusions from the table include:

  • A male cannot inherit colorblindness from his father.
  • A colorblind female must have a colorblind father.
  • A female must inherit colorblindness alleles from both parents to be colorblind.
  • Colorblind females can only produce colorblind males.
  • Because carrier females often have a colorblind father, colorblind males often will have a colorblind maternal grandfather (or great grandfather). In this way, colorblindness is often said to 'skip a generation'.

Note: these conclusions do not apply to other forms of colorblindness (e.g. tritanopia).

MotherFatherDaughter 1Daughter 2Son 1Son 2
same color deficiency of mother
different color deficiency of mother
with 2 defective X
with 2 defective X
with 2 defective X
same color deficiency of mother
different color deficiency of mother
with 2 defective X

Genetics of blue-yellow color blindness

Blue-yellow color blindness is a rarer form of colorblindness including tritanopia/tritanomaly. These conditions are mediated by the OPN1SW gene on Chromosome 7.

Other genetic causes

Several inherited diseases are known to cause color blindness:

They can be congenital (from birth) or can commence in childhood or adulthood. They can be stationary, that is, remain the same throughout a person's lifetime, or progressive. As progressive phenotypes involve deterioration of the retina and other parts of the eye, many of the above forms of color blindness can progress to legal blindness, i.e. an acuity of 6/60 (20/200) or worse, and often leave a person with complete blindness.

Non-genetic causes

Physical trauma can cause color blindness, either neurologically – brain trauma which produces swelling of the brain in the occipital lobe – or retinally, either acute (e.g. from laser exposure) or chronic (e.g. from ultraviolet light exposure).

Color blindness may also present itself as a symptom of degenerative diseases of the eye, such as cataract and age-related macular degeneration, and as part of the retinal damage caused by diabetes. Vitamin A deficiency may also cause color blindness. [27]

Color blindness may be a side effect of prescription drug use. For example, red–green color blindness can be caused by ethambutol, a drug used in the treatment of tuberculosis. [28] Blue-yellow color blindness can be caused by sildenafil, an active component of Viagra. [29] Hydroxychloroquine can also lead to hydroxychloroquine retinopathy, which includes various color defects. [30] Exposure to chemicals such as styrene [31] or organic solvents [32] [33] can also lead to color vision defects.


Color blindness is any deviation of color vision from normal trichromatic color vision (often as defined by the standard observer) that produces a reduced gamut. Mechanisms for color blindness are related to the functionality of cone cells, and often to the expression of photopsins, the photopigments that 'catch' photons and thereby convert light into chemical signals.

When an individual does not satisfy the requirements for trichromatic vision, they will express dichromacy or monochromacy and be colorblind. The main requirement for trichromacy is three cone cell classes that are each sensitive to different wavelengths of light and therefore have different spectral sensitivities. Dichromats only express two cone classes and cone monochromats express one. For each cone missing, one of the opponent channels (red-green and blue-yellow) that are responsible for color discrimination are disabled. This is the mechanism for protanopia, deuteranopia, blue cone monochromacy and tritanopia.

Even when there is trichromatic color vision and all three opponent channels are active, the size of an individual's color gamut is determined by the dynamic range of the opponent channels, which can be affected by several factors. One of these factors is the peak wavelengths of the spectral sensitivities of the three cones, namely the spectral distance between two cones contributing to an opponent channel. When this distance is smaller, the dynamic range is smaller and the color gamut is smaller, leading to a color vision deficiency. This is the mechanism for congenital protanomaly and deuteranomaly, though not of tritanomaly.

The opponent channels can also be affected by the prevalence of certain cones in the retinal mosaic. The cones are not equally prevalent and not evenly distributed in the retina. When the number of one of these cone types is significantly reduced, this can also lead to or contribute to a color vision deficiency. This is one of the causes of tritanomaly.

Simple colored filters can also create mild color vision deficiencies. John Dalton's original hypothesis for his deuteranopia was actually that the vitreous humor of his eye was discolored:

I was led to conjecture that one of the humours of my eye must be a transparent, but coloured, medium, so constituted as to absorb red and green rays principally... I suppose it must be the vitreous humor.

John Dalton, Extraordinary facts relating to the vision of colours: with observations (1798)

An autopsy of his eye after his death in 1844 showed this to be definitively untrue, [34] though other filters are possible. Actual physiological examples usually affect the blue-yellow opponent channel and are named Cyanopsia and Xanthopsia, and are most typically an affect of yellowing or removal of the lens.

Tetrachromacy in carriers of CVD

Females that are heterozygous for anomalous trichromacy (i.e. carriers) may be tetrachromats. These females have two alleles for either the OPN1MW or OPN1LW gene, and therefore express both the normal and anomalous opsins. Because one X chromosome is inactivated at random in each photoreceptor cell during a female's development, those normal and anomalous opsins will be segregated into their own cone cells, and because these cells have different spectral sensitivity, they can functionally operate as different opsins. This theoretical female would therefore have cones with peak sensitivities at 420nm (S cone), 530nm (M cone), 560nm (L cone) and the fourth (anomalous) cone between 530nm and 560nm (either M* or L* cone). [35] [36] [37]

If a female is heterozygous for both protanomaly and deuteranomaly, she could be pentachromatic. The degree to which women who are carriers of either protanomaly or deuteranomaly are demonstrably tetrachromatic and require a mixture of four spectral lights to match an arbitrary light is very variable. Jameson et al. [38] have shown that with appropriate and sufficiently sensitive equipment it can be demonstrated that any female carrier of red–green color blindness (i.e. heterozygous protanomaly, or heterozygous deuteranomaly) is a tetrachromat to a greater or lesser extent.

Since the incidence of anomalous trichromacy in males is ~6%, which should equal the incidence of anomalous M opsin or L opsin alleles, it follows that the prevalence of unaffected female carriers of colorblindness (and therefore of potential tetrachromats) is 11.3% (i.e. 94% × 6% × 2), based on the Hardy–Weinberg principle. [21] One such woman has been widely reported to be a true or functional tetrachromat, as she can discriminate colors most other people can't. [36] [37]


An Ishihara test image as seen by subjects with normal color vision and by those with a variety of color deficiencies Ishihara compare 1.jpg
An Ishihara test image as seen by subjects with normal color vision and by those with a variety of color deficiencies

There are several color perception tests, or color vision standards that are capable of diagnosing or screening for color blindness. The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to detect red–green color deficiencies and most often recognized by the public. [1] However, this can be attributed more to its ease of application, and less to do with its precision. In fact, there are several types of common color perception tests. Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect precise datasets, identify copunctal points, and measure just noticeable differences. [39]

Pseudoisochromatic plates

A pseudoisochromatic plate (from Greek pseudo, meaning "false", iso, meaning "same" and chromo, meaning "color") is the type of test exemplified by the Ishihara test, where a figure (usually one or more numerals) is embedded in the plate as a number of spots surrounded by spots of a slightly different color. The figure can be seen with normal color vision, but not with a particular color defect. The figure and background colors must be carefully chosen to appear isochromatic to a color deficient individual, but not an individual with normal color vision.

Pseudoisochromatic Plates are used as screening tools because they are cheap, fast and simple, but they do not provide precise diagnosis of CVD, and are often followed with another test if a user fails the Ishihara test.[ citation needed ]

The basic Ishihara test may not be useful in diagnosing young, preliterate children, who can't read the numerals, but larger editions contain plates that showcase a simple path to be traced with a finger, rather than numerals.[ citation needed ]

One of the most common alternative color vision tests based on pseudoisochromatic plates is the HRR color test (developed by Hardy, Rand, and Rittler), which solves many of the criticisms of the Ishihara test. For example, it detects blue-yellow color blindness, is less susceptible to memorization and uses shapes, so it is accessible to the illiterate and young children. [40]


Instead of the Ishihara test, the US Navy and US Army also allow testing with the a lantern, such as the Farnsworth Lantern Test. Lanterns project small colored lights to a subject, who is required to identify the color of the lights. The colors are those of typical signal lights, i.e. red, green and yellow, which also happen to be colors of confusion of red-green CVD. Lanterns do not diagnose colorblind, but they are occupational screening tests to ensure an applicant has sufficient color discrimination to be able to perform a job. This test allows 30% of color deficient individuals, generally with mild CVD, to pass. [41]

Arrangement tests

An Farnsworth D-15 test Huetestfmd15-2.jpg
An Farnsworth D-15 test

Arrangement tests can be used as screening or diagnostic tools. The Farnsworth–Munsell 100 hue test is sensitive enough that it not only can detect color blindness, but also evaluate the color vision of color normals, ranking them as low, average or superior.[ citation needed ] The Farnsworth D-15 is simpler and is used for screening for CVD. In either case, the subject is asked to arrange a set of colored caps or chips to form a gradual transition of color between two anchor caps. [42]


An instrument called an anomaloscope can also be used for diagnosis. These instruments are very expensive and require expertise to administer, so are generally only used in academic settings. However, they are very precise, being able to diagnose the type and severity of color blindness with high confidence. An anomaloscope designed to detect red-green colorblindnesses is based on the Rayleigh Equation, which compares a mixture of red and green light in variable proportions to a fixed spectral yellow of variable luminosity. The subject must change the two variables until the colors appear to match. The values of the variables at match (and the deviation from the variables of a color normal subject) are used to diagnose the type and severity of colorblindness. For example, deutans will put too much green in the mixture and protans will put too much red in the mixture.

Genetic testing

Most tests evaluate the phenotype of the subject, i.e. the functionality of their color vision, but the genotype can also be directly evaluated. This is especially useful for progressive forms that do not have a strongly deviant phenotype at a young age. However, it can also be used to sequence the L and M opsins on the X Chromosome. The most common anomalous alleles of these two genes are known and have even been related to exact spectral sensitivityies and peak wavelengths. A subject's anomalous alleles can therefore be classified through genetic testing. [43]


There is no cure for color deficiencies. The American Optometric Association reports that a contact lens on one eye can increase the ability to differentiate between colors, though nothing can cause a person to actually perceive the deficient color. [44]


There are several kinds of lenses that an individual can wear that can increase their accuracy in some color related tasks. However, none of these will "fix" color blindness or grant the wearer normal color vision. There are three kinds of lenses:


Many mobile and computer applications have been developed to aid color blind individuals in completing color tasks:


Rates of color blindness[ clarification needed ][ citation needed ]
Protanopia (red deficient: L cone absent)1.3%0.02%
Deuteranopia (green deficient: M cone absent)1.2%0.01%
Tritanopia (blue deficient: S cone absent)0.001%0.03%
Anomalous trichromacy6.3%0.37%
Protanomaly (red deficient: L cone defect)1.3%0.02%
Deuteranomaly (green deficient: M cone defect)5.0%0.35%
Tritanomaly (blue deficient: S cone defect)0.0001%0.0001%

Color blindness affects a large number of individuals, with protans and deutans being the most common types. [19] In individuals with Northern European ancestry, as many as 8 percent of men and 0.4 percent of women experience congenital color deficiency. [51] Interestingly, even Dalton's very first paper already arrived upon this 8% number: [52] is remarkable that, out of 25 pupils I once had, to whom I explained this subject, 2 were found to agree with me...

John Dalton, Extraordinary facts relating to the vision of colours: with observations (1798)

However, despite his accuracy, the number varies among groups. Isolated communities with a restricted gene pool sometimes produce high proportions of color blindness, including the less usual types. Examples include rural Finland, Hungary, and some of the Scottish islands.[ citation needed ] In the United States, about 7 percent of the male population—or about 10.5 million men—and 0.4 percent of the female population either cannot distinguish red from green, or see red and green differently from how others do (Howard Hughes Medical Institute, 2006[ clarification needed ]). More than 95 percent of all variations in human color vision involve the red and green receptors in male eyes. It is very rare for males or females to be "blind" to the blue end of the spectrum. [53]

Prevalence of red–green color blindness among males [54]
Arabs (Druzes)33710.0
Aboriginal Australians 4,4551.9
Belgians 9,5407.4
Bosnians 4,8366.2
Britons 16,1806.6
Chinese 1,1646.9
DR Congolese 9291.7
Dutch 3,1688.0
Fijians 6080.8
French 1,2438.6
Germans 7,8617.7
Hutu 1,0002.9
Indians (Andhra Pradesh)2927.5
Inuit 2972.5
Iranians 16,1806.6
Japanese 259,0004.0
Mexicans 5712.3
Navajo 5712.3
Norwegians 9,0479.0
Russians 1,3439.2
Scots 4637.8
Swiss 2,0008.0
Tibetans 2415.0
Tswana 4072.0
Tutsi 1,0002.5
Serbs 4,7507.4


An 1895 illustration of normal vision and various kinds of color blindness. It is not accurate
, but shows the views on this subject at the time. US Flag color blind.png
An 1895 illustration of normal vision and various kinds of color blindness. It is not accurate , but shows the views on this subject at the time.

During the XVII and XVIII century, several philosophers hypothesized that not all individuals perceived colors in the same way. For example, French philosopher Nicolas Malebranche wrote in 1674 that:

there is no reason to suppose a perfect resemblance in the disposition of the Optic Nerve in all Men, since there is an infinite variety in every thing in Nature, and chiefly in those that are Material, 'tis therefore very probable that all Men see not the same Colours in the same Objects. [55]

More than a hundred years later, in 1792, Scottish philosopher Dugald Stewart suggested that individuals could perceive colors differently: [56]

In the power of conceiving colors, too, there are striking differences among individuals: and, indeed, I am inclined to suspect, that, in the greater number of instances, the supposed defects of sight in this respect ought to be ascribed rather to a defect in the power of conception. [57]

The phenomenon only came to be scientifically studied in 1794, when English chemist John Dalton gave the first account of colour blindness in a paper to the Manchester Literary and Philosophical Society, which was published in 1798 as Extraordinary Facts relating to the Vision of Colours: With Observations. [58] [52] Genetic analysis of Dalton's preserved eyeball confirmed him as having deuteranopia in 1995, some 150 years after his death. [59]

Influenced by Dalton, German writer J. W. von Goethe studied color vision abnormalities in 1798 by asking two young subjects to match pairs of colors. [60]

Society and culture

Design implications

Testing the colors of a web chart, (center), to ensure that no information is lost to the various forms of color blindness. Safe Chart Colors-F99-FEC-ADD.jpg
Testing the colors of a web chart, (center), to ensure that no information is lost to the various forms of color blindness.

Color codes present particular problems for those with color deficiencies as they are often difficult or impossible for them to perceive. [61]

Good graphic design avoids using color coding or using color contrasts alone to express information; [62] this not only helps color blind people, but also aids understanding by normally sighted people by providing them with multiple reinforcing cues. [63] [ citation needed ]

Designers need to take into account that color-blindness is highly sensitive to differences in material. For example, a red–green colorblind person who is incapable of distinguishing colors on a map printed on paper may have no such difficulty when viewing the map on a computer screen or television. In addition, some color blind people find it easier to distinguish problem colors on artificial materials, such as plastic or in acrylic paints, than on natural materials, such as paper or wood. Third, for some color blind people, color can only be distinguished if there is a sufficient "mass" of color: thin lines might appear black, while a thicker line of the same color can be perceived as having color.[ citation needed ]

Designers should also note that red–blue and yellow–blue color combinations are generally safe. So instead of the ever-popular "red means bad and green means good" system, using these combinations can lead to a much higher ability to use color coding effectively. This will still cause problems for those with monochromatic color blindness, but it is still something worth considering.[ citation needed ]

When the need to process visual information as rapidly as possible arises, for example in an emergency situation, the visual system may operate only in shades of gray, with the extra information load in adding color being dropped. [64] This is an important possibility to consider when designing, for example, emergency brake handles or emergency phones.


Color blindness may make it difficult or impossible for a person to engage in certain occupations. Persons with color blindness may be legally or practically barred from occupations in which color perception is an essential part of the job (e.g., mixing paint colors), or in which color perception is important for safety (e.g., operating vehicles in response to color-coded signals). This occupational safety principle originates from the Lagerlunda train crash of 1875 in Sweden. Following the crash, Professor Alarik Frithiof Holmgren, a physiologist, investigated and concluded that the color blindness of the engineer (who had died) had caused the crash. Professor Holmgren then created the first test using different-colored skeins to exclude people from jobs in the transportation industry on the basis of color blindness. [65] However, there is a claim that there is no firm evidence that color deficiency did cause the collision, or that it might have not been the sole cause. [66]

Color vision is important for occupations using telephone or computer networking cabling, as the individual wires inside the cables are color-coded using green, orange, brown, blue and white colors. [67] Electronic wiring, transformers, resistors, and capacitors are color-coded as well, using black, brown, red, orange, yellow, green, blue, violet, gray, white, silver, gold. [68]


Red-green colorblindness can make it difficult to drive, primarily due to the inability to differentiate red-amber-green traffic lights. Protans are further disadvantaged due to the darkened perception of reds, which can make it more difficult to quickly recognize brake lights. [69] In response, some countries have refused to grant driver's licenses to individuals with color blindness:

Horizontal traffic light in Halifax, Nova Scotia, Canada Colourblind traffic signal.JPG
Horizontal traffic light in Halifax, Nova Scotia, Canada

There are several features available that help the colorblind compensate for their color vision deficiency:

Piloting aircraft

Although many aspects of aviation depend on color coding, only a few of them are critical enough to be interfered with by some milder types of color blindness. Some examples include color-gun signaling of aircraft that have lost radio communication, color-coded glide-path indications on runways, and the like. Some jurisdictions restrict the issuance of pilot credentials to persons with color blindness for this reason. Restrictions may be partial, allowing color-blind persons to obtain certification but with restrictions, or total, in which case color-blind persons are not permitted to obtain piloting credentials at all. [76]

In the United States, the Federal Aviation Administration requires that pilots be tested for normal color vision as part of their medical clearance in order to obtain the required medical certificate, a prerequisite to obtaining a pilot's certification. If testing reveals color blindness, the applicant may be issued a license with restrictions, such as no night flying and no flying by color signals—such a restriction effectively prevents a pilot from holding certain flying occupations, such as that of an airline pilot, although commercial pilot certification is still possible, and there are a few flying occupations that do not require night flight and thus are still available to those with restrictions due to color blindness (e.g., agricultural aviation). The government allows several types of tests, including medical standard tests (e.g., the Ishihara, Dvorine, and others) and specialized tests oriented specifically to the needs of aviation. If an applicant fails the standard tests, they will receive a restriction on their medical certificate that states: "Not valid for night flying or by color signal control". They may apply to the FAA to take a specialized test, administered by the FAA. Typically, this test is the "color vision light gun test". For this test an FAA inspector will meet the pilot at an airport with an operating control tower. The color signal light gun will be shone at the pilot from the tower, and they must identify the color. If they pass they may be issued a waiver, which states that the color vision test is no longer required during medical examinations. They will then receive a new medical certificate with the restriction removed. This was once a Statement of Demonstrated Ability (SODA), but the SODA was dropped, and converted to a simple waiver (letter) early in the 2000s. [77]

Research published in 2009 carried out by the City University of London's Applied Vision Research Centre, sponsored by the UK's Civil Aviation Authority and the U.S. Federal Aviation Administration, has established a more accurate assessment of color deficiencies in pilot applicants' red/green and yellow–blue color range which could lead to a 35% reduction in the number of prospective pilots who fail to meet the minimum medical threshold. [78]


Inability to distinguish color does not necessarily preclude the ability to become a celebrated artist. The 20th century expressionist painter Clifton Pugh, three-time winner of Australia's Archibald Prize, on biographical, gene inheritance and other grounds has been identified as a protanope. [79] 19th century French artist Charles Méryon became successful by concentrating on etching rather than painting after he was diagnosed as having a red–green deficiency. [80] Jin Kim's red–green color blindness did not stop him from becoming first an animator and later a character designer with Walt Disney Animation Studios. [81]

Rights of the color blind


A Brazilian court ruled that people with color blindness are protected by the Inter-American Convention on the Elimination of All Forms of Discrimination against Person with Disabilities. [82] [83] [84]

At trial, it was decided that the carriers of color blindness have a right of access to wider knowledge, or the full enjoyment of their human condition.[ citation needed ]

United States

In the United States, under federal anti-discrimination laws such as the Americans with Disabilities Act, color vision deficiencies have not been found to constitute a disability that triggers protection from workplace discrimination. [85]

A famous traffic light on Tipperary Hill in Syracuse, New York, is upside-down due to the sentiments of its Irish American community, [86] but has been criticized due to the potential hazard it poses for color-blind persons. [87]


Some tentative evidence finds that color blind people are better at penetrating certain color camouflages. Such findings may give an evolutionary reason for the high rate of red–green color blindness. [10] There is also a study suggesting that people with some types of color blindness can distinguish colors that people with normal color vision are not able to distinguish. [88] In World War II, color blind observers were used to penetrate camouflage. [89]

In September 2009, the journal Nature reported that researchers at the University of Washington and University of Florida were able to give trichromatic vision to squirrel monkeys, which normally have only dichromatic vision, using gene therapy. [90]

In 2003, a cybernetic device called eyeborg was developed to allow the wearer to hear sounds representing different colors. [91] Achromatopsic artist Neil Harbisson was the first to use such a device in early 2004; the eyeborg allowed him to start painting in color by memorizing the sound corresponding to each color. In 2012, at a TED Conference, Harbisson explained how he could now perceive colors outside the ability of human vision. [92]

See also

Related Research Articles

Color Characteristic of visual perception

Color or colour is the visual perceptual property deriving from the spectrum of light interacting with the photoreceptor cells of the eyes. Color categories and physical specifications of color are associated with objects or materials based on their physical properties such as light absorption, reflection, or emission spectra. By defining a color space, colors can be identified numerically by their coordinates.

Color vision Ability to perceive differences in light frequency

Color vision, a feature of visual perception, is an ability to perceive differences between light composed of different wavelengths independently of light intensity. Color perception is a part of the larger visual system and is mediated by a complex process between neurons that begins with differential stimulation of different types of photoreceptors by light entering the eye. Those photoreceptors then emit outputs that are propagated through many layers of neurons and then ultimately to the brain. Color vision is found in many animals and is mediated by similar underlying mechanisms with common types of biological molecules and a complex history of evolution in different animal taxa. In primates, color vision may have evolved under selective pressure for a variety of visual tasks including the foraging for nutritious young leaves, ripe fruit, and flowers, as well as detecting predator camouflage and emotional states in other primates.

Tetrachromacy Type of color vision with four types of cone cells

Tetrachromacy is the condition of possessing four independent channels for conveying color information, or possessing four types of cone cell in the eye. Organisms with tetrachromacy are called tetrachromats.

Trichromacy Possessing of three independent channels for conveying color information

Trichromacy or trichromatism is the possessing of three independent channels for conveying color information, derived from the three different types of cone cells in the eye. Organisms with trichromacy are called trichromats.

Pentachromacy describes the capability and capacity for capturing, transmitting, processing, and perceiving five independent channels of color information through the primary visual system. Organisms with pentachromacy are termed pentachromats. For these organisms, it would take at least five differing ranges of wavelengths along the electromagnetic spectrum to reproduce their full visual spectrum. In comparison, a combination of red, green, and blue wavelengths of light are all that is necessary to simulate most of the common human trichromat visual spectrum.

In visual physiology, adaptation is the ability of the retina of the eye to adjust to various levels of light. Natural night vision, or scotopic vision, is the ability to see under low-light conditions. In humans, rod cells are exclusively responsible for night vision as cone cells are only able to function at higher illumination levels. Night vision is of lower quality than day vision because it is limited in resolution and colors cannot be discerned; only shades of gray are seen. In order for humans to transition from day to night vision they must undergo a dark adaptation period of up to two hours in which each eye adjusts from a high to a low luminescence "setting", increasing sensitivity hugely, by many orders of magnitude. This adaptation period is different between rod and cone cells and results from the regeneration of photopigments to increase retinal sensitivity. Light adaptation, in contrast, works very quickly, within seconds.

Dichromacy is the state of having two types of functioning photoreceptors, called cone cells, in the eyes. Organisms with dichromacy are called dichromats. Dichromats can match any color they see with a mixture of no more than two pure spectral lights. By comparison, trichromats need three pure spectral lights to represent their visible gamut, and tetrachromats need four.

Monochromacy Type of color vision

Monochromacy is the ability of organisms or machines to perceive only light intensity, without respect to spectral composition (color). Organisms with monochromacy are called monochromats.

Opponent process Theory regarding color vision in humans

The opponent process is a color theory that states that the human visual system interprets information about color by processing signals from cone cells and rod cells in an antagonistic manner. There is some overlap in the wavelengths of light to which the three types of cones respond, so it is more efficient for the visual system to record differences between the responses of cones, rather than each type of cone's individual response. The opponent color theory suggests that there are three opponent channels the cone photoreceptors are linked together to form three opposing color pairs: red versus green, blue versus yellow, and black versus white. It was first proposed in 1892 by the German physiologist Ewald Hering.

A color model is an abstract mathematical model describing the way colors can be represented as tuples of numbers, typically as three or four values or color components. When this model is associated with a precise description of how the components are to be interpreted, taking account of visual perception, the resulting set of colors is called "color space."

OPN1MW Protein-coding gene in the species Homo sapiens

Green-sensitive opsin is a protein that in humans is encoded by the OPN1MW gene. OPN1MW2 is a similar opsin.

OPN1LW Protein-coding gene in the species Homo sapiens

OPN1LW is a gene on the X chromosome that encodes for long wave sensitive (LWS) opsin, or red cone photopigment. It is responsible for perception of visible light in the yellow-green range on the visible spectrum. The gene contains 6 exons with variability that induces shifts in the spectral range. OPN1LW is subject to homologous recombination with OPN1MW, as the two have very similar sequences. These recombinations can lead to various vision problems, such as red-green colourblindness and blue monochromacy. The protein encoded is a G-protein coupled receptor with embedded 11-cis-retinal, whose light excitation causes a cis-trans conformational change that begins the process of chemical signalling to the brain.

Evolution of color vision in primates Loss and regain of colour vision during the evolution of primates

The evolution of color vision in primates is highly unusual compared to most eutherian mammals. A remote vertebrate ancestor of primates possessed tetrachromacy, but nocturnal, warm-blooded, mammalian ancestors lost two of four cones in the retina at the time of dinosaurs. Most teleost fish, reptiles and birds are therefore tetrachromatic while most mammals are strictly dichromats, the exceptions being some primates and marsupials, who are trichromats, and many marine mammals, who are monochromats.

The Farnsworth Lantern Test, or FALANT, is a test of color vision originally developed specifically to screen sailors for tasks requiring color vision, such as identifying signal lights at night. It screens for red-green deficiencies, but not the much rarer blue color deficiency.

Impossible color Color that cannot be perceived under ordinary viewing conditions

Impossible colors are colors that do not appear in ordinary visual functioning. Different color theories suggest different hypothetical colors that humans are incapable of seeing for one reason or another, and fictional colors are routinely created in popular culture. While some such colors have no basis in reality, phenomena such as cone cell fatigue enable colors to be perceived in certain circumstances that would not be otherwise.

Gene therapy for color blindness is an experimental gene therapy aiming to convert congenitally colorblind individuals to trichromats by introducing a photopigment gene that they lack. Though partial color blindness is considered only a mild disability, it is a condition that affects many people, particularly males. Complete color blindness, or achromatopsia, is very rare but more severe. While never demonstrated in humans, animal studies have shown that it is possible to confer color vision by injecting a gene of the missing photopigment using gene therapy. As of 2018 there is no medical entity offering this treatment, and no clinical trials available for volunteers.

The evolution of human colour vision in Homo sapiens produced a trichromatic view of the world in comparison to a majority of other mammals that only have a dichromatic view. Early human ancestors are believed to have viewed the world using UV vision as far back as 90 million years ago. It is thought that the shift to trichromatic vision capabilities and the ability to see blue light have evolved as an adaptive trait over time.

Blue cone monochromacy (BCM) is an inherited eye disease that causes severely impaired color discrimination, low vision, nystagmus and photophobia due to the absence of functionality of red (L) and green (M) cone photoreceptor cells in the retina. This form of retinal disorder is a recessive X-linked disease and manifests its symptoms in early infancy.

Colour anomaly, sometimes referred to as partial colour blindness, is an inherited condition in which people have full trichromatic colour vision, but do not make the same colour matches as the majority of the human population. It is much more common than dichromacy or other forms of colour blindness, affecting about 6% of human males in Northern European populations. Two forms are common, known as protanomaly and deuteranomaly. In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than the majority of observers, and deuteranomalous observers need more green. Tritanomaly, affecting mixtures involving blue, is much less common. Colour anomalies can be measured by an instrument called an anomaloscope, in which coloured lights are mixed in a controlled way; typical demonstration anomaloscopes are set up for measuring the red/green anomalies, but with appropriate choices of colours to mix, tritanomaly can also be measured.

EnChroma Eyeglasses designed to help color-blind people

EnChroma lenses are glasses which are designed to alleviate symptoms of red–green color blindness. Studies have shown that while the lenses alter the perception of already perceived colors, they do not restore normal color vision. Initial claims in excess of this by the manufacturer have been criticised and characterized as marketing hype. Recent research has shown the lenses have a positive impact on those with red-green color blindness.


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