| Color blindness or color deficiency | |
|---|---|
| Classification and external resources | |
An 1895 illustration of normal vision and various kinds of color blindness |
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| 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 one or more sets of retinal cones that perceive color in light and transmit that information to the optic nerve. Color blindness is a sex-linked condition; the genes that produce photopigments are carried on the X chromosome; if some of these genes are missing or damaged, color blindness will be expressed in males with a higher probability than in females because males only have one X chromosome (in females, a good gene on only one of the two X chromosomes is enough to yield the needed photopigments).[1]
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",[2] 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.[3]
This article is about color blindness in humans; for other species, see color vision.
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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 an estimated 2-3% of women have a 4th color cone and can be considered tetrachromats[4] although it is not clear that this provides an advantage in color discrimination.
Color vision deficiencies can be classified as acquired or inherited.[5][6]
Based on clinical appearance, color blindness may be described as total or partial. Total color blindness is much less common than partial color blindness.[9] 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.[10][11]
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.[3][12] At one time the U.S. Army found that color blind people could spot "camouflage" colors that fooled those with normal color vision.[13][14] Humans have a higher percentage of color blindness than macaque monkeys according to recent research.[15]
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.[16]
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:
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.[17][18] 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 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. 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. Another factor that may affect color blindness includes a deficiency in Vitamin A (Beta-Carotene)[19]
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.
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 color vision deficiencies are subdivided based on the number of primary hues needed to match a given sample in the visible spectrum.
Monochromacy is the condition of possessing only a single channel for conveying information about color.[20] Monochromats possess a complete inability to distinguish any colors and perceive only variations in brightness.[20] It occurs in two primary forms:
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.
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.
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).[27]
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.[27]
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.
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.[28]
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.[29]
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.[30] 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. 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.[31]
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.[32]
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.[33] 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).[28] 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.
| Males | Females | Total | References | |
|---|---|---|---|---|
| Overall | — | — | — | |
| Overall (United States) | — | — | — | |
| Red–green (Overall) | 7 to 10% | — | — | [34][35] |
| Red–green (Caucasians) | 8% | — | — | [36] |
| Red–green (Asians) | 5% | — | — | [36] |
| Red–green (Africans) | 4% | — | — | [36] |
| Monochromacy | — | — | — | |
| Rod monochromacy (dysfunctional, abnormally shaped or no cones) | 0.00001% | 0.00001% | — | [37] |
| Dichromacy | 2.4% | 0.03% | 1.30% | [34][37] |
| Protanopia (red deficient: L cone absent) | 1% to 1.3% | 0.02% | — | [34][37] |
| Deuteranopia (green deficient: M cone absent) | 1% to 1.2% | 0.01% | — | [34][37] |
| Tritanopia (blue deficient: S cone absent) | 0.001% | 0.03% | — | [37] |
| Anomalous Trichromacy | 6.3% | 0.37% | — | [37] |
| Protanomaly (red deficient: L cone defect) | 1.3% | 0.02% | — | [37] |
| Deuteranomaly (green deficient: M cone defect) | 5.0% | 0.35% | — | [37] |
| Tritanomaly (blue deficient: S cone defect) | 0.01% | 0.01% | — | [37] |
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.
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. 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.[38]
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.[39] Electronic wiring, transformers, resistors, and capacitors are color-coded as well, using black, brown, red, orange, green, yellow, blue, violet, gray, white, silver, gold.[40]
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.[41]
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.
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.[42]
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.[43]
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.[44] 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.[45]
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.[3]
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 cannot 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 can 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.
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