|Other names||Color vision deficiency, impaired color vision |
|Example of an Ishihara color test plate. Viewers with normal color vision should clearly see the number "74".|
|Symptoms||Decreased ability to see colors |
|Duration||Long term |
|Causes||Genetic ( inherited usually X-linked) |
|Diagnostic method||Ishihara color test |
|Treatment||Adjustments to teaching methods, mobile apps  |
|Frequency||Red–green: 8% males, 0.5% females (Northern European descent) |
Color blindness or color vision deficiency (CVD) is the decreased ability to see color or differences in color.  It can impair tasks such as selecting ripe fruit, choosing clothing, and reading traffic lights.  Color blindness may make some academic activities more difficult.  However, issues are generally minor, and people with colorblindness automatically develop adaptations and coping mechanisms.  People with total color blindness (achromatopsia) may also be uncomfortable in bright environments  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.  The most common form is caused by a genetic disorder called congenital red–green color blindness. 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.  Females who are not color-blind can carry genes for color blindness and pass them on to their children.  Color blindness can also result from physical or chemical damage to the eye, the optic nerve, or parts of the brain.  Screening for color blindness is typically done with the Ishihara color test. 
There is no cure for color blindness.  Diagnosis may allow an individual, or their parents/teachers to actively accommodate the condition.  Special lenses such as EnChroma glasses or X-chrom contact lenses may help people with red–green color blindness at some color tasks,  but they do not grant the wearer "normal color vision".  Mobile apps can help people identify colors. 
Red–green color blindness is the most common form, followed by blue–yellow color blindness and total color blindness.  Red–green color blindness affects up to 1 in 12 males (8%) and 1 in 200 females (0.5%).   The ability to see color also decreases in old age.  In certain countries, color blindness may make people ineligible for certain jobs,  such as those of aircraft pilots, train drivers, crane operators, and people in the armed forces.   The effect of color blindness on artistic ability is controversial,   but a number of famous artists are believed to have been color blind.  
This article is about color blindness in humans, but other organisms also have color blindness. Many species have color vision that is different from human vision, with either a limited or extended range of visible colors as compared with humans.
A person who is colorblind will have decreased (or no) color discrimination along the red–green axis, blue–yellow axis, or both. However, the vast majority of people with colorblindness 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 are pairs or groups of colors that will often be mistaken by people with colorblindness. Confusion colors for red–green color blindness include:
Confusion colors for tritan include:
These colors of confusion are defined quantitatively by straight confusion lines plotted in CIEXYZ, usually plotted on the corresponding chromaticity diagram. The lines all intersect at a copunctal point, which varies with the type of color blindness.  Chromaticities along a confusion line will appear metameric to people with dichromacy of that type. People with trichromacy of that type will see the chromaticities as metameric if they are close enough, depending on the strength of their CVD. For two colors on a confusion line to be metameric, the chromaticities first have to be made isoluminant, meaning equal in lightness. Also, colors that may be isoluminant to the standard observer may not be isoluminant to a person with dichromacy.
Cole describes four color tasks, all of which are impeded to some degree by color blindness: 
The following sections describe specific color tasks with which people with colorblindness typically have difficulty.
Colorblindness causes difficulty with the connotative color tasks associated with selecting or preparing food. Selecting food for ripeness can be difficult. The green–yellow transition of bananas is particularly hard to identify. It can also be difficult to detect bruises, mold or rot on some foods, to determine when meat is done by color, to distinguish some varietals, such as a Braeburn vs. a Granny Smith apple, or to distinguish colors associated with artificial flavors (e.g. jelly beans, sports drinks).
Changes in skin color due to bruising, sunburn, rashes or even blushing are easily missed by people with red–green colorblindness.
The colors of traffic lights can be difficult for people with red–green colorblindness. This difficulty includes distinguishing red/amber lights from sodium street lamps, distinguishing green lights (closer to cyan) from normal white lights, and distinguishing red from amber lights, especially when there are no positional clues available (see image).
The main coping mechanism to overcome these challenges is to memorize the position of lights. The order of the common triplet traffic light is standardized as red–amber–green from top to bottom or left to right. Cases that deviate from this standard are rare. One such case is a traffic light in Tipperary Hill in Syracuse, New York, which is upside-down (green–amber–red top to bottom) due to the sentiments of its Irish American community.  However, the light has been criticized due to the potential hazard it poses for color-blind drivers. 
There are other several features of traffic lights available that help accommodate people with colorblindness. British Rail signals use more easily identifiable colors: The red is blood red, the amber is yellow and the green is a bluish color.[ citation needed] Most British road traffic lights are mounted vertically on a black rectangle with a white border (forming a "sighting board"), so that drivers can more easily look for the position of the light. In the eastern provinces of Canada, traffic lights are sometimes differentiated by shape in addition to color: square for red, diamond for yellow, and circle for green (see image).
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 people with red–green colorblindness. 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.
Color analysis is the analysis of color in its use in fashion, to determine personal color combinations that are most aesthetically pleasing.[ citation needed] Colors to combine can include clothing, accessories, makeup, hair color, skin color, eye color, etc. Color analysis involves many aesthetic and comparative color task that can be difficult for people with color blindness.
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 person with protanopy.  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.  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. 
People with deuteranomaly are better at distinguishing shades of khaki,  which may be advantageous when looking for predators, food, or camouflaged objects hidden among foliage.  People with dichromacy 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.  
Some tentative evidence finds that people with color blindness are better at penetrating certain color camouflages. Such findings may give an evolutionary reason for the high rate of red–green color blindness.  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.  In World War II, color blind observers were used to penetrate camouflage. 
In the presence of chromatic noise, people with colorblindness are more capable of seeing a luminous signal, as long as the chromatic noise appears metameric to them.  This is the effect behind most "reverse" Pseudoisochromatic plates (e.g. "hidden digit" Ishihara plates) that are discernible to people with colorblindness but unreadable to people with typical color perception.[ citation needed]
Color codes are useful tools for designers to convey information. The interpretation of this information requires users to perform a variety of Color Tasks, usually comparative but also sometimes connotative or denotative. However, these tasks are often problematic for people with colorblindness when design of the color code has not followed best practices for accessibility.  For example, one of the most ubiquitous connotative color codes is the "red means bad and green means good" or similar systems, based on the classic signal light colors. However, this color coding will almost always be undifferentiable to people with either deutan or protan CVD, and therefore should be avoided or supplemented with a parallel connotative system ( symbols, smileys, etc.).
Good practices to ensure design is accessible to people with colorblindness include:
A common task for designers is to select a subset of colors (qualitative colormap) that are as mutually differentiable as possible ( salient). For example, player pieces in a board game should be as different as possible.
Classic advice suggests using Brewer palettes, but several of these are not actually accessible to people with colorblindness.
Unfortunately, the colors with the greatest contrast to the red–green colorblind tend to be colors of confusion to the blue–yellow colorblind, and vice versa. However, since red–green is much more prevalent than blue–yellow CVD, design should[ according to whom?] generally prioritize those users (people with deutan CVD then protan CVD).
A common task for data visualization is to represent a color scale, or sequential colormap, often in the form of a heat map or choropleth. Several scales are designed with special consideration for people with colorblindness and are widespread in academia, including Cividis,  Viridis  and Parula. These comprise a light-to-dark scale superimposed on a yellow-to-blue scale, making them monotonic and perceptually uniform to all forms of 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,  which uses severity and affected cone for naming.
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.  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).  
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. 
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:
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 is the mildest type of color deficiency, but the severity 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. The types of anomalous trichromacy include protanomaly, deuteranomaly and tritanomaly. It is approximately three times more common than dichromacy.  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. This difference can be measured by an instrument called an Anomaloscope, where red and green lights are mixed by a subject to match a yellow light. 
There are two major types of color blindness: difficulty distinguishing between red and green, and difficulty distinguishing between blue and yellow.  [ 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 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).   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 symptomatic of congenital red–green color blindness, so affects males disproportionately more than females.  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.
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.  Tritans have a neutral point at 571 nm (yellowish).[ citation needed]
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.
|8||Blue Cone Monochromacy||Monochromacy||Total color blindness|
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.
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]).
By far the most common form of colorblindness is congenital red–green color blindness (Daltonism), which includes protanopia/protanomaly and deuteranopia/deuteranomaly. These conditions are mediated by the OPN1LW and OPN1MW genes, respectively, both on the X chromosome. An 'affected' gene is either missing (as in Protanopia and Deuteranopia - Dichromacy) or is a chimeric gene (as in Protanomaly and Deuteranomaly).
Since the OPN1LW and OPN1MW genes are on the X chromosome, they are sex-linked, and therefore affect males and females disproportionately. Because the colorblind 'affected' alleles are recessive, color blindness specifically follows X-linked recessive inheritance. Males have only one X chromosome (XY), and females have two (XX); Because the male only has one of each gene, if it is affected, the male will be colorblind. Because a female has two alleles of each gene (one on each chromosome), if only one gene is affected, the dominant normal alleles will "override" the affected, 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.
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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.
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. 
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.  Blue–yellow color blindness can be caused by sildenafil, an active component of Viagra.  Hydroxychloroquine can also lead to hydroxychloroquine retinopathy, which includes various color defects.  Exposure to chemicals such as styrene  or organic solvents   can also lead to color vision defects.
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,  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 effect of yellowing or removal of the lens.
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.
The main method for diagnosing a color vision deficiency is in testing the color vision directly. The Ishihara color test is the test most often used to detect red–green deficiencies and most often recognized by the public.  Some tests are clinical in nature, designed to be fast, simple, and effective at identifying broad categories of color blindness. Others focus on precision and are generally available only in academic settings. 
While genetic testing cannot directly evaluate a subject's color vision ( phenotype), most congenital color vision deficiencies are well-correlated with genotype. Therefore, the genotype can be directly evaluated and used to predict the phenotype. This is especially useful for progressive forms that do not have a strongly color deficient phenotype at a young age. However, it can also be used to sequence the L- and M-Opsins on the X-Chromosome, since the most common alleles of these two genes are known and have even been related to exact spectral sensitivities and peak wavelengths. A subject's color vision can therefore be classified through genetic testing,  but this is just a prediction of the phenotype, since color vision can be affected by countless non-genetic factors such as your cone mosaic.
Despite much recent improvement in gene therapy for color blindness, there is currently no FDA approved treatment for any form of CVD, and otherwise no cure for CVD currently exists. Management of the condition by using lenses to alleviate symptoms or smartphone apps to aid with daily tasks is possible.
There are three kinds of lenses that an individual can wear that can increase their accuracy in some color related tasks (although none of these will "fix" color blindness or grant the wearer normal color vision):
Many mobile and computer applications have been developed to aid color blind individuals in completing color tasks:
In 2003, a cybernetic device called eyeborg was developed to allow the wearer to hear sounds representing different colors.  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. 
Color blindness affects a large number of individuals, with protans and deutans being the most common types.  In individuals with Northern European ancestry, as many as 8 percent of men and 0.4 percent of women experience congenital color deficiency.  Interestingly, even Dalton's very first paper already arrived upon this 8% number: 
...it 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)
During the 17th and 18th century, several philosophers hypothesized that not all individuals perceived colors in the same way: 
...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.
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.
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.   Genetic analysis of Dalton's preserved eyeball confirmed him as having deuteranopia in 1995, some 150 years after his death. 
In 1875, the Lagerlunda train crash in Sweden brought color blindness to the forefront. 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 for color vision using multicolored skeins of wool to detect color blindness and thereby exclude the colorblind from jobs in the transportation industry requiring color vision to interpret safety signals.  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. 
In 1920, Frederick William Edridge-Green devised an alternative theory of color vision and color blindness based on Newton's classification of 7 fundamental colors ( ROYGBIV). Edridge-Green classified color vision based on how many distinct colors a subject could see in the spectrum. Normal subjects were termed hexachromic as they could not discern Indigo. Subjects with superior color vision, who could discern indigo, where heptachromic. The colorblind were therefore dichromic (equivalent to dichromacy) or tri-, tetra- or pentachromic (anomalous trichromacy).  
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.
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.    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]
Color blindness may make it difficult or impossible for a person to engage in certain activities. 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 aftermath of the 1875 Lagerlunda train crash, which Alarik Frithiof Holmgren blamed on the color blindness of the engineer and created the first occupational screening test ( Holmgren's wool test) against the colorblind. 
...I consider that to [Holmgren] above all others do we owe the present and future control of color-blindness on land and sea, by which life and property are safer, and the risks of travelling less.— Benjamin Joy Jeffries, Color-blindness: Its Danger & Its Detection (1879)
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.  Electronic wiring, transformers, resistors, and capacitors are color-coded as well, using black, brown, red, orange, yellow, green, blue, violet, gray, white, silver, gold. 
Participation, officiating and viewing sporting events can be impacted by color blindness. Professional football players Thomas Delaney and Fabio Carvalho have discussed the difficulties when colour clashes occur, and research undertaken by FIFA has shown that enjoyment and player progression can be hampered by issues distinguishing the difference between the pitch and training objects or field markings. 
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.  In response, some countries have refused to grant driver's licenses to individuals with color blindness:
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. 
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. 
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. 
Description, user reviews, drug side effects, interactions–prescribing information
Description, user reviews, drug side effects, interactions–prescribing information