Color blindness

"Colorblind" and "Colourblind" redirect here. For other uses, see Colorblind (disambiguation).

Color blindness or color deficiency
Classification and external resources
An 1895 illustration of normal vision and various kinds of color blindness
ICD-10	H53.5
ICD-9	368.5
DiseasesDB	2999
MeSH	D003117

Color blindness or color vision deficiency is the inability or decreased ability to see color, or perceive color differences, under lighting conditions when color vision is not normally impaired. "Color blind" is a term of art; there is no actual blindness but there is a fault in the development of either or both sets of retinal cones that perceive color in light and transmit that information to the optic nerve. The gene that causes color blindness is carried on the X chromosome, making the handicap more common among men (who have just one X chromosome) than among women (who have two, so must inherit the gene from both parents).

The symptoms of color blindness also can be produced by physical or chemical damage to the eye, optic nerve, or the brain generally. These are not true color blindness, however, but they represent conditions of limited actual blindness. Similarly, a person with achromatopsia, although unable to see colors, is not "color blind" per se but they suffer from a completely different disorder, of which an atypical color deficiency is only one manifestation.

The English chemist John Dalton published the first scientific paper on this subject in 1798, "Extraordinary facts relating to the vision of colours",^[1] after the realization of his own color blindness. Because of Dalton's work, the condition was often called daltonism, although this term is now used for a single type of color blindness, called deuteranopia.

Color blindness is usually classed as a mild disability but there are situations where color blind individuals can have an advantage over those with normal color vision. Some studies conclude that color blind individuals are better at penetrating certain color camouflages; this may be an evolutionary explanation for the surprisingly high frequency of congenital red–green color blindness.^[2]

This article is about color blindness in humans; for other species, see color vision.

Background

Main article: Trichromatic color vision

The typical human retina contains two kinds of light cells: the rod cells (active in low light) and the cone cells (active in normal daylight). Normally, there are three kinds of cones, each containing a different pigment, which are activated when the pigments absorb light. The spectral sensitivities of the cones differ; one is maximally sensitive to short wavelengths, one to medium wavelengths, and the third to long wavelengths, with their peak sensitivities in the blue, yellowish-green, and yellow regions of the spectrum, respectively. The absorption spectra of all three systems cover the visible spectrum. These receptors are often called S cones, M cones, and L cones, for short, medium, and long wavelength; but they are also often referred to as blue cones, green cones, and red cones, respectively.

Although these receptors are often referred to as "blue, green, and red" receptors, this terminology is not very accurate, especially as the "red" receptor actually has its peak sensitivity in the yellow region. The sensitivity of normal color vision actually depends on the overlap between the absorption spectra of the three systems: different colors are recognized when the different types of cone are stimulated to different degrees. Red light, for example, stimulates the long wavelength cones much more than either of the others, and reducing the wavelength causes the other two cone systems to be increasingly stimulated, causing a gradual change in hue.

Many of the genes involved in color vision are on the X chromosome, making color blindness more common in males than in females because males have only one X chromosome, while females have two. Because this is an X-linked trait about 1% of women have a 4th color cone and can be considered tetrachromats although it is not clear that this provides an advantage in color discrimination.

Classification

By cause

The colors of the rainbow as viewed by a person with no color vision deficiencies.

The colors of the rainbow as viewed by a person with protanopia.

The colors of the rainbow as viewed by a person with deuteranopia.

The colors of the rainbow as viewed by a person with tritanopia.

Color vision deficiencies can be classified as acquired or inherited.^[3][4]

• Acquired
• Inherited: There are three types of inherited or congenital color vision deficiencies: monochromacy, dichromacy, and anomalous trichromacy.^[3]

• Monochromacy, also known as "total color blindness,"^[5] is the lack of ability to distinguish colors; caused by cone defect or absence.^[6] Monochromacy occurs when two or all three of the cone pigments are missing and color and lightness vision is reduced to one dimension.^[5]

• Rod monochromacy (achromatopsia) is an exceedingly rare, nonprogressive inability to distinguish any colors as a result of absent or nonfunctioning retinal cones. It is associated with light sensitivity (photophobia), involuntary eye oscillations (nystagmus), and poor vision.^[6]
• Cone monochromacy is a rare total color blindness that is accompanied by relatively normal vision, electoretinogram, and electrooculogram.^[6]

• Dichromacy is a moderately severe color vision defect in which one of the three basic color mechanisms is absent or not functioning. It is hereditary and, in the case of Protanopia or Deuteranopia, sex-linked, affecting predominantly males.^[6] Dichromacy occurs when one of the cone pigments is missing and color is reduced to two dimensions.^[5]

• Protanopia is a severe type of color vision deficiency caused by the complete absence of red retinal photoreceptors. It is a form of dichromatism in which red appears dark. It is hereditary, sex-linked, and present in 1% of males.^[6]
• Deuteranopia is a color vision deficiency in which the green retinal photoreceptors are absent, moderately affecting red–green hue discrimination. It is a form of dichromatism in which there are only two cone pigments present. It is likewise hereditary and sex-linked.
• Tritanopia is a very rare color vision disturbance in which there are only two cone pigments present and a total absence of blue retinal receptors.^[6]

• Anomalous trichromacy is a common type of inherited color vision deficiency, occurring when one of the three cone pigments is altered in its spectral sensitivity. This results in an impairment, rather than loss, of trichromacy (normal three-dimensional color vision).^[5]

• Protanomaly is a mild color vision defect in which an altered spectral sensitivity of red retinal receptors (closer to green receptor response) results in poor red–green hue discrimination. It is hereditary, sex-linked, and present in 1% of males.^[6]
• Deuteranomaly, caused by a similar shift in the green retinal receptors, is by far the most common type of color vision deficiency, mildly affecting red–green hue discrimination in 5% of males. It is hereditary and sex-linked.^[6]
• Tritanomaly is a rare, hereditary color vision deficiency affecting blue–yellow hue discrimination. Unlike most other forms, it is not sex-linked.^[6]

By clinical appearance

Based on clinical appearance, color blindness may be described as total or partial. Total color blindness is much less common than partial color blindness.^[7] There are two major types of color blindness: those who have difficulty distinguishing between red and green, and who have difficulty distinguishing between blue and yellow.^[8][9]

• Total color blindness
• Partial color blindness

• Red–green

• Dichromacy (protanopia and deuteranopia)
• Anomalous trichromacy (protanomaly and deuteranomaly)

• Blue–yellow

• Dichromacy (tritanopia)
• Anomalous trichromacy (tritanomaly)

Causes

Evolutionary arguments

Any recessive genetic characteristic that persists at a level as high as 5% is generally regarded as possibly having some advantage over the long term, such as better discrimination of color camouflaged objects especially in low-light conditions.^[2][10] At one time the U.S. Army found that color blind people could spot "camouflage" colors that fooled those with normal color vision.^{[11][not in citation given][12]} Humans have a higher percentage of color blindness than macaque monkeys according to recent research.^[13]

Another possible advantage might result from the presence of a tetrachromic female. Owing to X-chromosome inactivation, females who are heterozygous for anomalous trichromacy ought to have at least four types of cone in their retinae. It is possible that this affords them an extra dimension of color vision, by analogy to New World monkeys where heterozygous females gain trichromacy in a basically dichromatic species.^[14]

Genetics

Color blindness can be inherited. It is most commonly inherited from mutations on the X chromosome but the mapping of the human genome has shown there are many causative mutations – 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) database at Johns Hopkins University).

Some of the inherited diseases known to cause color blindness are:

• cone dystrophy
• cone-rod dystrophy
• achromatopsia (aka rod monochromatism, aka stationary cone dystrophy, aka cone dysfunction syndrome)
• blue cone monochromatism,
• Leber's congenital amaurosis.
• retinitis pigmentosa (initially affects rods but can later progress to cones and therefore color blindness)

Inherited color blindness can be congenital (from birth), or it can commence in childhood or adulthood. Depending on the mutation, it 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, certain forms of color blindness can progress to legal blindness, i.e., an acuity of 6/60 or worse, and often leave a person with complete blindness.

Color blindness always pertains to the cone photoreceptors in retinas, as the cones are capable of detecting the color frequencies of light.

About 8 percent of males, but only 0.5 percent of females, are color blind in some way or another, whether it is one color, a color combination, or another mutation.^[15][16] The reason males are at a greater risk of inheriting an X linked mutation is that males only have one X chromosome (XY, with the Y chromosome carrying altogether different genes than the X chromosome), and females have two (XX); if a woman inherits a normal X chromosome in addition to the one that carries the mutation, she will not display the mutation. Men do not have a second X chromosome to override the chromosome that carries the mutation. If 5% of variants of a given gene are defective, the probability of a single copy being defective is 5%, but the probability that two copies are both defective is 0.05 × 0.05 = 0.0025, or just 0.25%.

Other causes

Other causes of color blindness include brain or retinal damage caused by shaken baby syndrome, accidents and other trauma which produce swelling of the brain in the occipital lobe, and damage to the retina caused by exposure to ultraviolet light. Most ultraviolet light damage is caused during childhood and this form of retinal degeneration is the leading cause of blindness in the world.^{[citation needed]} Damage often presents itself later on in life.

Color blindness may also present itself in the spectrum of degenerative diseases of the eye, such as age-related macular degeneration, and as part of the retinal damage caused by diabetes.

Types

There are many types of color blindness. The most common are red–green hereditary photoreceptor disorders, but it is also possible to acquire color blindness through damage to the retina, optic nerve, or higher brain areas. Higher brain areas implicated in color processing include the parvocellular pathway of the lateral geniculate nucleus of the thalamus, and visual area V4 of the visual cortex. Acquired color blindness is generally unlike the more typical genetic disorders. For example, it is possible to acquire color blindness only in a portion of the visual field but maintain normal color vision elsewhere. Some forms of acquired color blindness are reversible. Transient color blindness also occurs (very rarely) in the aura of some migraine sufferers.^{[citation needed]}

The different kinds of inherited color blindness result from partial or complete loss of function of one or more of the different cone systems. When one cone system is compromised, dichromacy results. The most frequent forms of human color blindness result from problems with either the middle or long wavelength sensitive cone systems, and involve difficulties in discriminating reds, yellows, and greens from one another. They are collectively referred to as "red–green color blindness", though the term is an over-simplification and is somewhat misleading. Other forms of color blindness are much more rare. They include problems in discriminating blues from yellows, and the rarest forms of all, complete color blindness or monochromacy, where one cannot distinguish any color from grey, as in a black-and-white movie or photograph.

Congenital

Congenital color vision deficiencies are subdivided based on the number of primary hues needed to match a given sample in the visible spectrum.

Monochromacy

Monochromacy is the condition of possessing only a single channel for conveying information about color.^[17] Monochromats possess a complete inability to distinguish any colors and perceive only variations in brightness.^[17] It occurs in two primary forms:

1. Rod monochromacy, frequently called 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. While normally rare, achromatopsia is very common on the island of Pingelap, a part of the Pohnpei state, Federated States of Micronesia, where it is called maskun: about 10% of the population there has it, and 30% are unaffected carriers. The island was devastated by a storm in the 18th century, and one of the few male survivors carried a gene for achromatopsia; the population is now several thousand.^[18]
2. Cone monochromacy is the condition of having both rods and cones, but only a single kind of cone. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues. Blue cone monochromacy (X chromosome) is caused by a complete absence of L and M cones (red and green). It is encoded at the same place 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).^[19] Visual acuity usually falls to the 20/50 to 20/400 range.

Dichromacy

Protanopes, deuteranopes, and tritanopes are dichromats; that is, they can match any color they see with some mixture of just two spectral lights (whereas normally humans are trichromats and require three lights). These individuals normally know they have a color vision problem and it can affect their lives on a daily basis. Protanopes and deuteranopes see no perceptible difference between red, orange, yellow, and green. All these colors, that seem so different to the normal viewer, appear to be the same color for this two percent of the population. The terms protanopia, deuteranopia, and tritanopia come from Greek, and literally mean "inability to see (anopia) with the first (prot-), second (deuter-), or third (trit-) [cone]", respectively.

Test for protanopia^{[Note 1]}
This image contains the number 37, but someone who is protanopic may not be able to see it.

• Protanopia (1% of males): Lacking the long-wavelength sensitive retinal cones, those with this condition are unable to distinguish between colors in the green–yellow–red section of the spectrum. They have a neutral point at a greenish wavelength around 492 nm – that is, they cannot discriminate light of this wavelength from white. For the protanope, the brightness of red, orange, and yellow are much reduced compared to normal. 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 and from greens 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 because their reddish components are so dimmed as to be invisible. for example, pink flowers, reflecting both red light and blue light, may appear just blue to the protanope. 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 below the neutral point as blue and those above it as yellow. This is a rare form of color blindness.

Test for deuteranopia^{[Note 1]}
This image shows a number 49, but someone who is deuteranopic may not be able to see it.

• Deuteranopia (1% of males): Lacking the medium-wavelength cones, those affected are again unable to distinguish between colors in the green–yellow–red section of the spectrum. Their neutral point is at a slightly longer wavelength, 498 nm. The deuteranope suffers the same hue discrimination problems as the protanope, but without the abnormal dimming. Similarly, violet, lavender, purple, and blue all seem much the same to a deuteranope. This form of colorblindness is also known as Daltonism after John Dalton. (Dalton's diagnosis was confirmed as deuteranopia in 1995, some 150 years after his death, by DNA analysis of his preserved eyeball.) Deuteranopic unilateral dichromats report that with only their deuteranopic eye open, they see wavelengths below the neutral point as blue and those above it as yellow.^[20]

Test for tritanopia^{[Note 1]}
This image shows the number 56, but someone who is tritanopic may not be able to see it.

• Tritanopia (less than 1% of males and females): Lacking the short-wavelength cones, those affected are unable to distinguish colors along the blue–yellow dimension. This form of color blindness is not sex-linked.

Anomalous trichromacy

Those with protanomaly, deuteranomaly, or tritanomaly are trichromats, but the color matches they make differ from the normal. They are called anomalous 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. From a practical standpoint though, many protanomalous and deuteranomalous people have very little difficulty carrying out tasks that require normal color vision. Some may not even be aware that their color perception is in any way different from normal.

Protanomaly and deuteranomaly can be diagnosed using an instrument called an anomaloscope, which mixes spectral red and green lights in variable proportions, for comparison with a fixed spectral yellow. If this is done in front of a large audience of males, as the proportion of red is increased from a low value, first a small proportion of the audience will declare a match, while most will see the mixed light as greenish; these are the deuteranomalous observers. Next, as more red is added the majority will say that a match has been achieved. Finally, as yet more red is added, the remaining, protanomalous, observers will declare a match at a point where normal observers will see the mixed light as definitely reddish.

• Protanomaly (1% of males, 0.01% of females):^[21] Having a mutated form of the long-wavelength (red) pigment, whose peak sensitivity is at a shorter wavelength than in the normal retina, protanomalous individuals are less sensitive to red light than normal. This means that they are less able to discriminate colors, and they do not see mixed lights as having the same colors as normal observers. They also suffer from a darkening of the red end of the spectrum. This causes reds to reduce in intensity to the point where they can be mistaken for black. Protanomaly is a fairly rare form of color blindness, making up about 1% of the male population. Both protanomaly and deuteranomaly are carried on the X chromosome.
• Deuteranomaly (most common — 6% of males, 0.4% of females):^[21] These individuals have a mutated form of the medium-wavelength (green) pigment. The medium-wavelength pigment is shifted towards the red end of the spectrum resulting in a reduction in sensitivity to the green area of the spectrum. Unlike protanomaly the intensity of colors is unchanged. This is the most common form of color blindness, making up about 6% of the male population. The deuteranomalous person is considered "green weak". For example, in the evening, dark green cars appear to be black to Deuteranomalous people. Similar to the protanomates, deuteranomates are poor at discriminating small differences in hues in the red, orange, yellow, green region of the spectrum. They make errors in the naming of hues in this region because the hues appear somewhat shifted towards red. One very important difference between deuteranomalous individuals and protanomalous individuals is deuteranomalous individuals do not have the loss of "brightness" problem.
• Tritanomaly (equally rare for males and females [0.01% for both]):^[21] Having a mutated form of the short-wavelength (blue) pigment. The short-wavelength pigment is shifted towards the green area of the spectrum. This is the rarest form of anomalous trichromacy color blindness. Unlike the other anomalous trichromacy color deficiencies, the mutation for this color blindness is carried on chromosome 7.^[22] Therefore it is equally prevalent in both male & female populations. The OMIM gene code for this mutation is 304000 "Colorblindness, Partial Tritanomaly".^[23]

Total color blindness

Achromatopsia is strictly defined as the inability to see color. Although the term may refer to acquired disorders such as color agnosia and cerebral achromatopsia, it typically refers to congenital color vision disorders (i.e. more frequently rod monochromacy and less frequently cone monochromacy).^[24]

In color agnosia and 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.^[24]

Red–green color blindness

X-linked recessive inheritance

Those with protanopia, deuteranopia, protanomaly, and deuteranomaly have difficulty with discriminating red and green hues. It is sex-linked: genetic red–green color blindness affects males much more often than females, because the genes for the red and green color receptors are located on the X chromosome, of which males have only one and females have two. Females (46, XX) are red–green color blind only if both their X chromosomes are defective with a similar deficiency, whereas males (46, XY) are color blind if their single X chromosome is defective.

The gene for red–green color blindness is transmitted from a color blind male to all his daughters who are heterozygote carriers and are usually unaffected. In turn, a carrier woman has a fifty percent chance of passing on a mutated X chromosome region to each of her male offspring. The sons of an affected male will not inherit the trait from him, since they receive his Y chromosome and not his (defective) X chromosome. Should an affected male have children with a carrier or colorblind woman, their daughters may be colorblind by inheriting an affected X chromosome from each parent.

Because one X chromosome is inactivated at random in each cell during a woman's development, it is possible for her to have four different cone types, as when a carrier of protanomaly has a child with a deuteranomalic man. Denoting the normal vision alleles by P and D and the anomalous by p and d, the carrier is PD pD and the man is Pd. The daughter is either PD Pd or pD Pd. Suppose she is pD Pd. Each cell in her body expresses either her mother's chromosome pD or her father's Pd. Thus her red–green sensing will involve both the normal and the anomalous pigments for both colors. Such females are tetrachromats, since they require a mixture of four spectral lights to match an arbitrary light.

Blue–yellow color blindness

Those with tritanopia and tritanomaly have difficulty discriminating blueish versus yellowish hues.

Color blindness involving the inactivation of the short-wavelength sensitive cone system (whose absorption spectrum peaks in the bluish-violet) is called tritanopia or, loosely, blue–yellow color blindness. The tritanopes neutral point occurs near a yellowish 570 nm; green is perceived at shorter wavelengths and red at longer wavelengths. Mutation of the short-wavelength sensitive cones is called tritanomaly. Tritanopia is equally distributed among males and females. Jeremy H. Nathans (with the Howard Hughes Medical Institute) proved that the gene coding for the blue receptor lies on chromosome 7, which is shared equally by males and females. Therefore it is not sex-linked. This gene does not have any neighbor whose DNA sequence is similar. Blue color blindness is caused by a simple mutation in this gene.^[25]

Diagnosis

Example of an Ishihara color test plate.^{[Note 1]} The numeral "74" should be clearly visible to viewers with normal color vision. Viewers with dichromacy or anomalous trichromacy may read it as "21", and viewers with achromatopsia may not see numbers.

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

The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to diagnose red–green color deficiencies. A figure (usually one or more Arabic digits) is embedded in the picture as a number of spots in a slightly different color, and can be seen with normal color vision, but not with a particular color defect. The full set of tests has a variety of figure/background color combinations, and enable diagnosis of which particular visual defect is present. The anomaloscope, described above, is also used in diagnosing anomalous trichromacy.

Because the Ishihara color test contains only numerals, it may not be useful in diagnosing young children, who have not yet learned to use numerals. In the interest of identifying these problems early on in life, alternative color vision tests were developed using only symbols (square, circle, car).

Besides the Ishihara color test, the US Navy and US Army also allow testing with the Farnsworth Lantern Test. This test allows 30% of color deficient individuals, whose deficiency is not too severe, to pass.

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 thorough datasets, identify copunctal points, and measure just noticeable differences.^[26]

Management

There is generally no treatment to cure color deficiencies. However, certain types of tinted filters and contact lenses may help an individual to better distinguish different colors. Optometrists can supply a singular red-tint contact lens to wear on the non-dominant eye.^[27] This may enable the wearer to pass some color blindness tests, but they have little practical use. The effect of wearing such a device is akin to wearing red/blue 3D glasses and can take some time getting used to as certain wavelengths can "jump" out and be overly represented.^{[citation needed]} Additionally, computer software and cybernetic devices have been developed to assist those with visual color difficulties such as an eyeborg, a "cybernetic eye" that allows individuals with color blindness to hear sounds representing colors.^[28]

The GNOME desktop environment provides colorblind accessibility using the gnome-mag and the libcolorblind software. Using a gnome applet, the user may switch a color filter on and off choosing from a set of possible color transformations that will displace the colors in order to disambiguate them. The software enables, for instance, a color blind person to see the numbers in the Ishihara test.

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.^[29]

Epidemiology

Color blindness affects a significant number of people, although exact proportions vary among groups. In Australia, for example, it occurs in about 8 percent of males and only about 0.4 percent of females.^[30] 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. 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).^[25] It has been found that 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.

Prevalence of color blindness

	Males	Females	Total	References
Overall	—	—	—
Overall (United States)	—	—	—
Red–green (Overall)	7 to 10%	—	—	[31][32]
Red–green (Caucasians)	8%	—	—	[33]
Red–green (Asians)	5%	—	—	[33]
Red–green (Africans)	4%	—	—	[33]
Monochromacy	—	—	—
Rod monochromacy (dysfunctional, abnormally shaped or no cones)	0.00001%	0.00001%	—	[34]
Dichromacy	2.4%	0.03%	1.30%	[31][34]
Protanopia (red deficient: L cone absent)	1% to 1.3%	0.02%	—	[31][34]
Deuteranopia (green deficient: M cone absent)	1% to 1.2%	0.01%	—	[31][34]
Tritanopia (blue deficient: S cone absent)	0.001%	0.03%	—	[34]
Anomalous Trichromacy	6.3%	0.37%	—	[34]
Protanomaly (red deficient: L cone defect)	1.3%	0.02%	—	[34]
Deuteranomaly (green deficient: M cone defect)	5.0%	0.35%	—	[34]
Tritanomaly (blue deficient: S cone defect)	0.01%	0.01%	—	[34]

Society and culture

Design implications of color blindness

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

Good graphic design avoids using color coding or using color contrasts alone to express information; this not only helps color blind people, but also aids understanding by normally sighted people.

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 consider that no one is simply red-blue, green-blue, yellow-blue, or yellow-red colorblind. using these color combinations, instead of the ever popular red means bad and green means good system, 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.

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.^{[citation needed]} This is an important possibility to consider when designing, for example, emergency brake handles or emergency phones.

Occupations

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.^[35]

Driving motor vehicles

Some countries (for example, Romania) have refused to grant individuals with color blindness driving licenses. In Romania, there is an ongoing campaign to remove the legal restrictions that prohibit colorblind citizens from getting drivers' licenses.^[36]

The usual justification for such restrictions is that drivers of motor vehicles must be able to recognize color-coded signals, such as traffic lights or warning lights.

Piloting aircraft

While 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 who suffer from 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.

In the United States, the Federal Aviation Administration requires that pilots be tested for normal color vision as part of the medical certification that is prerequisite to obtaining a pilot's license. 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 working for an airline. 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, he or she will receive a restriction on their medical certificate that states- "Not valid for night flying or by color signal control." He/she 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, and the color signal light gun will be shone at the pilot from the tower, and he or she must identify the color. If he passes, he may be issued a waiver, which states that the color vision test is no longer required during medical examinations. He 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.^[37]

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 US 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.^[38]

Art

Inability to distinguish color does not necessarily preclude the ability to become a celebrated artist. The 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.^[39] 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.^[40]

Problems and compensations

Simulation of the normal (above) and dichromatic (below) perception of red and green apples.

Horizontal traffic light in Halifax, NS Canada

Color blindness very rarely means complete monochromatism. In almost all cases, color blind people retain blue–yellow discrimination, and most color-blind individuals are anomalous trichromats rather than complete dichromats. In practice this means that they often retain a limited discrimination along the red–green axis of color space, although their ability to separate colors in this dimension is severely reduced.

Dichromats often confuse red and green items. For example, they may find it difficult to distinguish a Braeburn apple from a Granny Smith and in some cases, the red and green of a traffic light without other clues (for example, shape or location). The vision of dichromats may also be compared to images produced by a color printer that has run out of the ink in one of its three color cartridges (for protanopes and deuteranopes, the magenta cartridge, and for tritanopes, the yellow cartridge). Dichromats tend to learn to use texture and shape clues and so are often able to penetrate camouflage that has been designed to deceive individuals with color-normal vision.^[2]

Traffic light colors are confusing to some dichromats as there is insufficient apparent difference between the red/amber traffic lights, and that of sodium street lamps; also the green can be confused with a grubby white lamp. This is a risk factor on high-speed undulating roads where angular cues can't be used. British Rail color lamp signals use more easily identifiable colors: the red is blood red, the amber is yellow and the green is a bluish color. Most British road traffic lights are mounted vertically on a black rectangle with a white border (forming a "sighting board") and so dichromats simply look for the position of the light within the rectangle — top, middle or bottom. In the Eastern provinces of Canada horizontally-mounted traffic lights are generally differentiated by shape to facilitate identification for those with color blindness.

See also

• Articles with images not understandable by color blind users
• Cerebral achromatopsia
• Ishihara color test
• Motion blindness
• Tetrachromacy

Notes

1. ^ ^{a b c d} Because of variations in computer displays, these illustrations may not be accurately rendered.

References

1. ^ Dalton J (1798). "Extraordinary facts relating to the vision of colours: with observations". Memoirs of the Literary and Philosophical Society of Manchester 5: 28–45. 
2. ^ ^{a b c} Morgan MJ, Adam A, Mollon JD (June 1992). "Dichromats detect colour-camouflaged objects that are not detected by trichromats". Proc. Biol. Sci. 248 (1323): 291–5. doi:10.1098/rspb.1992.0074. PMID 1354367. http://rspb.royalsocietypublishing.org/cgi/pmidlookup?view=long&pmid=1354367. 
3. ^ ^{a b} "Color Blindness." University of Illinois Eye Center, Department of Ophthalmology and Visual Sciences. Retrieved September 29, 2006.
4. ^ Kokotailo R, Kline D. "Congenital Colour Vision Deficiencies." University of Calgary, Department of Psychology, Vision & Aging Lab. Retrieved September 29, 2006.
5. ^ ^{a b c d} "Guidelines: Color Blindness." Tiresias.org. Retrieved April 2, 2011.
6. ^ ^{a b c d e f g h i} Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainsville, Florida: Triad Publishing Company, 1990.
7. ^ Spring, Kenneth R.; Matthew J. Parry-Hill; Thomas J. Fellers; Michael W. Davidson. "Human Vision and Color Perception". Florida State University. http://micro.magnet.fsu.edu/primer/lightandcolor/humanvisionhome.html. Retrieved 2007-04-05. 
8. ^ Paul S. Hoffman. "Accommodating Color Blindness" (PDF). http://www.digitalspaceart.com/articles/ColorBlindness.pdf. Retrieved 2009-07-01. 
9. ^ Neitz, Maureen E., PhD. "Severity of Colorblindness Varies". Medical College of Wisconsin. http://healthlink.mcw.edu/article/999211295.html. Retrieved 2007-04-05. 
10. ^ Saito, Atsuko; Akichika Mikami, Takayuki Hosokawa, Toshikazu Hasegawa (2006-02). "Advantage of Dichromats Over Trichromats in Discrimination of Color-Camouflaged Stimuli in Humans^1,2". Perceptual and Motor Skills 102 (1): 3–12. doi:10.2466/pms.102.1.3-12. ISSN 0031-5125. http://www.amsciepub.com/doi/abs/10.2466/pms.102.1.3-12. Retrieved 2011-06-25. 
11. ^ Waggoner, Terrace L.. "About Color Blindness (Color Vision Deficiency) :Clinical information about color blindness". Colors for the Color Blind. http://www.toledo-bend.com/colorblind/aboutcb.asp. Retrieved 2009-10-29. 
12. ^ REIT, SEYMOUR. (1979). MASQUERADE: THE AMAZING CAMOUFLAGE DECEPTIONS OF WORLD WAR 2. 
13. ^ Onishi A, Koike S, Ida M, et al. (November 1999). "Dichromatism in macaque monkeys". Nature 402 (6758): 139–40. doi:10.1038/45963. PMID 10647004. 
14. ^ Jordan G, Mollon JD (July 1993). "A study of women heterozygous for colour deficiencies". Vision Res. 33 (11): 1495–508. doi:10.1016/0042-6989(93)90143-K. PMID 8351822. http://linkinghub.elsevier.com/retrieve/pii/0042-6989(93)90143-K. 
    Jameson KA, Highnote SM, Wasserman LM (June 2001). "Richer color experience in observers with multiple photopigment opsin genes". Psychon Bull Rev 8 (2): 244–61. doi:10.3758/BF03196159. PMID 11495112. http://pbr.psychonomic-journals.org/cgi/pmidlookup?view=long&pmid=11495112. 
15. ^ Sharpe, LT; Stockman A, Jägle H, Nathans J (1999). "Opsin genes, cone photopigments, color vision and color blindness". In Gegenfurtner KR, Sharpe LT. Color Vision: From Genes to Perception. Cambridge University Press. ISBN 9780521004398. http://books.google.com/?id=4zQMQLLVkFYC. 
16. ^ colblindor.com
17. ^ ^{a b} Byrne A, Hilbert D. "A Glossary of Color Science." Originally published in Readings on Color, Volume 2: The Science of Color. (MIT Press, 1997). Retrieved November 7, 2006.
18. ^ [1]^{[dead link]}
19. ^ Weiss AH, Biersdorf WR (1989). "Blue cone monochromatism". J Pediatr Ophthalmol Strabismus 26 (5): 218–23. PMID 2795409. 
20. ^ David L. MacAdam (ed.) and Deane B. Judd (1979). Contributions to color science. NBS. p. 584. http://books.google.com/books?id=jgz_iI8NAzYC&pg=PA584. 
21. ^ ^{a b c} Kalloniatis, Michael and Luu, Charles. "Psychophysics of Vision: The Perception of Color". http://webvision.med.utah.edu/KallColor.html#deficiencies. Retrieved 2007-04-02. 
22. ^ Montgomery, Ted M., O.D.. "The Macula". http://www.tedmontgomery.com/the_eye/macula.html#X-chrome. Retrieved 2007-04-02. 
23. ^ "Disease-causing Mutations and protein structure". UCL Biochemistry BSM Group. http://www.biochem.ucl.ac.uk/bsm/humgen/chr__034.html#304000. Retrieved 2007-04-02. 
24. ^ ^{a b} Jan Dirk Blom (2009). A Dictionary of Hallucinations. Springer. p. 4. ISBN 9781441912220. http://books.google.com/books?id=KJtQptBcZloC&pg=PA4. 
25. ^ ^{a b} "Seeing, Hearing and Smelling the World, a Report for the Howard Hughes Medical Institute". Howard Hughes Medical Institute. http://www.hhmi.org/senses/b130.html. Retrieved 2010-02-18. 
26. ^ Toufeeq A (October 2004). "Specifying colours for colour vision testing using computer graphics". Eye (Lond) 18 (10): 1001–5. doi:10.1038/sj.eye.6701378. PMID 15192692. 
27. ^ Zeltzer,, Harry I. (March 1991). "Patent application for contact lens for correction of color blindness". freepatentsonline.com. FreePatentsOnline.com. http://www.freepatentsonline.com/4998817.html. Retrieved 2009-10-28. 
28. ^ Anon (19 January 2005). "Seeing things in a different light". BBC Devon features. BBC. http://www.bbc.co.uk/devon/news_features/2005/eyeborg.shtml. Retrieved 2009-10-30. 
29. ^ Dolgin E (2009-09-16). "Colour blindness corrected by gene therapy". Nature News. doi:10.1038/news.2009.921. http://www.nature.com/news/2009/090916/full/news.2009.921.html. 
30. ^ "Colour blindness". Better Health Channel. http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Colour_blindness. Retrieved 2007-04-02. 
31. ^ ^{a b c d} "Prevalence and Incidence of Color blindness". WrongDiagnosis.com. 2008-06-22. http://www.wrongdiagnosis.com/c/color_blindness/prevalence.htm. Retrieved 2008-07-10. 
32. ^ "Color Blindness: More Prevalent Among Males". Hhmi.org. http://www.hhmi.org/senses/b130.html. Retrieved 2009-04-16. 
33. ^ ^{a b c} Masataka Okabe, Kei Ito (2008-02-15). "Colorblind Barrier Free". J*Fly. http://jfly.iam.u-tokyo.ac.jp/color/. Retrieved 2008-07-10. 
34. ^ ^{a b c d e f g h i} Archive.org
35. ^ Vingrys AJ, Cole BL (1986). "Origins of colour vision standards within the transport industry". Ophthalmic Physiol Opt 6 (4): 369–75. doi:10.1111/j.1475-1313.1986.tb01155.x. PMID 3306566. 
36. ^ "Petition to European Union on Colorblind’s condition in Romania". http://discromat.wordpress.com/2007/08/15/time-out/. Retrieved 2007-08-21. 
37. ^ "Aerospace Medical Dispositions — Color vision". http://www.faa.gov/about/office_org/headquarters_offices/avs/offices/aam/ame/guide/app_process/exam_tech/item52/amd/. Retrieved 2009-04-11. 
38. ^ Warburton, Simon (29 May 2009). "Colour-blindness research could clear more pilots to fly: UK CAA". Air transport. Reed Business Information. http://www.flightglobal.com/articles/2009/05/29/327137/colour-blindness-research-could-clear-more-pilots-to-fly-uk.html. Retrieved 29 October 2009. 
39. ^ Cole BL, Harris RW (September 2009). "Colour blindness does not preclude fame as an artist: celebrated Australian artist Clifton Pugh was a protanope". Clin Exp Optom 92 (5): 421–8. doi:10.1111/j.1444-0938.2009.00384.x. PMID 19515095. 
40. ^ Anon. "Charles Meryon". Art Encyclopedia. The Concise Grove Dictionary of Art.. Oxford University Press. http://www.answers.com/topic/charles-m-ryon. Retrieved 7 January 2010. 

Bibliography

• Kaiser, Peter K.; Boynton, R.M. (1996). Human Color Vision (2nd ed.). Washington, DC: Optical Society of America. ISBN 1-55752-461-0. 
• McIntyre, Donald (2002). Colour Blindness: Causes and Effects. UK: Dalton Publishing. ISBN 0-9541886-0-8. 
• Shevell, Steven K. (2003). The Science of Color (2nd ed.). Oxford, UK: Optical Society of America. p. 350. ISBN 0-444-512-519. 
• Smal, James; Hilbert, D.S. (1997). Readings on Color, Volume 2: The Science of Color (2nd ed.). Cambridge, Massachusetts: MIT Press. ISBN 0-262-52231-4. 
• Wyszecki, Günther; Stiles, W.S. (2000). Color Science: Concepts and Methods, Quantitative Data and Formulae (2nd ed.). Wiley-Interscience. ISBN 0-471-39918-3. 

External links

• Color blindness at the Open Directory Project
• Watch the short documentary No Such Thing As Color