Color blindness

This article is about color vision deficiencies. For the term describing activities undertaken and services provided without regard to the racial characteristics, see Race-blind.
Color blindness
Classifications and external resources
ICD-10 H53.5
ICD-9 368.5

Color blindness, or color vision deficiency, in humans is the inability to perceive differences between some or all colors that other people can distinguish. It is most often of genetic nature, but may also occur because of eye, nerve, or brain damage, or due to exposure to certain chemicals. The English chemist John Dalton in 1798 published the first scientific paper on the subject, "Extraordinary facts relating to the vision of colours",[1] after the realization of his own color blindness; because of Dalton's work, the condition is sometimes called Daltonism, although this term is now used for a type of color blindness called deuteranopia.

Color blindness is usually classed as a disability; however, in selected situations color blind people may have advantages over people with normal color vision.There is anecdotal evidence that color blind individuals are better at penetrating color camouflage and at least one scientific study confirms this under controlled conditions.[2] Monochromats may have a minor advantage in dark vision, but only in the first five minutes of dark adaptation.




The normal human retina contains two kinds of light sensitive 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. The cones are activated when the pigments absorb light. The absorption spectra of the pigments differ; one is maximally sensitive to short wavelengths, one to medium wavelengths, and the third to long wavelengths (their peak sensitivities are in the blue, yellowish-green, and yellow regions of the spectrum, respectively). The absorption spectra of all three systems cover much of the visible spectrum, so it is not entirely accurate to refer to them as "blue", "green" and "red" receptors, especially because the "red" receptor actually has its peak sensitivity in the yellow. 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 extents. For example, red light stimulates the long wavelength cones much more than either of the others, but the gradual change in hue seen, as wavelength reduces, is the result of the other two cone systems being increasingly stimulated as well.


Causes of color blindness

There are many types of color blindness. The most common are hereditary (genetic) 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 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.


Classification of color deficiencies


By etiology

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

  • 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 a 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 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 congential, sex-linked, and present in 1% of all males.[6]
  • Deuteranopia is a color vision deficiency, moderately affecting red-green hue discrimination in 1% of all males. It is hereditary and sex-linked form of dichromatism in which there are only two cone pigments present.[6]
  • Tritanopia is an exceedingly 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 congenital color vision deficiency caused by the reduced amount (not absence) of one of three cone photopigment types.[6] Anomalous trichromacy occurs when one of the three cone pigments is altered in its spectral sensitivity, but trichromacy or normal three-dimensional color vision is not fully impaired.[5]
  • Protanomaly is a mild color vision defect in which a deficiency of red retinal receptors results in poor red-green hue discrimination. It is congenital, sex-linked, and present in 1% of all males.[6]
  • Deuteranomaly is the most common type of color vision deficiency, mildly affecting red-green hue discrimination in 5% of all males. It is hereditary and sex-linked.[6]
  • Tritanomaly is a rare, hereditary color vision deficiency affecting blue-yellow hue discrimination.[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 those who have difficulty distinguishing between blue and yellow.[8][9]

  • Red-green
  • Dichromacy (protanopia and deuteranopia)
  • Anomalous trichromacy (protanomaly and deuteranomaly)
  • Blue-yellow
  • Dichromacy (tritanopia)
  • Anomalous trichromacy (tritanomaly)

Congenital color vision deficiencies

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.[10] Monochromats possess a complete inability to distinguish any colors and perceive only variations in brightness.[10] 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 1/12 of the population there has it. 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, of whom about 30% carry this gene.
  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. 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). They generally show nystagmus ("jiggling eyes"), photophobia (light sensitivity), reduced visual acuity, and myopia (nearsightedness).[11] Visual acuity usually falls to the 20/50 to 20/400 range


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.


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 stand point though, many protanomalous and deuteranomalous people breeze through life with very little difficulty doing tasks that require normal color vision. Some may not even be aware that their color perception is in any way different from normal. The only problem they have is passing that "Blank Blank" color vision test.

Protanomaly and deuteranomaly can be readily observed 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 men, as the proportion of red is increased from a low value, first a small proportion of people will declare a match, while most of the audience sees 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 everyone else is seeing the mixed light as definitely reddish.


Clinical forms of color blindness


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).

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.


Red-green color blindness

Those with protanopia, deuteranopia, protanomaly, and deuteranomaly have difficulty with discriminating red and green hues.

Genetic red-green color blindness affects men much more often than women, because the genes for the red and green color receptors are located on the X chromosome, of which men have only one and women have two. Such a trait is called sex-linked. Genetic females (46, XX) are red-green color blind only if both their X chromosomes are defective with a similar deficiency, whereas genetic males (46, XY) are color blind if their only 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 perceptually unaffected. In turn, a carrier woman passes on a mutated X chromosome region to only half her male offspring. The sons of an affected male will not inherit the trait, since they receive his Y chromosome and not his (defective) X chromosome.

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 women 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 with discriminating blue and yellow 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 at 570 nm; where 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 men and women. 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 (2006, Howard Hughes Medical Institute).



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.[12] 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 21 million men - and 0.4 percent of the female population either cannot distinguish red from green, or see red and green differently (Howard Hughes Medical Institute, 2006). 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
Men Women Total References
Overall - - -
Overall (United States) - - 1.30% [1]
Red-green (Overall) 7 to 10% - - [2][3]
Red-green (Caucasians) 8% - - [4]
Red-green (Asians) 5% - - [5]
Red-green (Africans) 4% - - [6]
Monochromacy - - -
Rod monochromacy (no cones) 0.00001% 0.00001% - [7]
Dichromacy 2.4% 0.03% - [8]
Protanopia (L-cone absent) 1% to 1.3% 0.02% - [9][10]
Deuteranopia (M-cone absent) 1% to 1.2% 0.01% - [11][12]
Tritanopia (S-cone absent) 0.001% 0.03% - [13]
Anomalous Trichromacy 6.3% 0.37% - [14]
Protanomaly (L-cone defect) 1.3% 0.02% - [15]
Deuteranomaly (M-cone defect) 5.0% 0.35% - [16]
Tritanomaly (S-cone defect) 0.0001% 0.0001% - [17]


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.

However, the Ishihara color test is criticized for containing only numerals and thus not being useful for young children, who have not yet learned to use numerals. It is often stated that it is important to identify these problems as soon as possible and explain them to the children to prevent possible problems and psychological traumas. For this reason, alternative color vision tests were developed using only symbols (square, circle, car).

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 ([18], for example) to collect thorough datasets, identify copunctal points, and measure just noticeable differences.


Treatment and management

There is generally no treatment to cure color deficiencies, however, certain types of tinted filters and contact lenses may help an individual to distinguish different colors better. Additionally, software has been developed to assist those with visual color difficulties.


Design implications of color blindness

Color codes present particular problems for color blind people as they are often difficult or impossible for color blind people to understand.

Good graphic design avoids using color coding or color contrasts alone to express information, as this not only helps color blind people, but also aids understanding by normally sighted people. The use of Cascading Style Sheets on the world wide web allows pages to be given an alternative color scheme for color-blind readers. This color scheme generator helps a graphic designer see color schemes as seen by eight types of color blindness. When the need to process visual information as rapidly as possible arises, for example in a train or aircraft crash, the visual system may operate only in shades of grey, 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.

Due to this inablity to recognise colours such as red and green, some countries like Singapore for example have refused to grant individuals with colour blindness Driving licences. They are also not allowed to enroll for some technical courses at tertary instutons due to their conditions.


Misconceptions and compensations

Color blindness is not the swapping of colors in the observer's eyes. Grass is never red, stop signs are never green. The color impaired do not learn to call red "green" and vice versa. However, dichromats often confuse red and green items. For example, they find it difficult to distinguish a Granny Smith from a Braeburn or the red and green of a traffic light without other clues (for example, shape or location). This is demonstrated nicely in this simulation of the two types of apple as viewed by a trichromat or by a dichromat.


Color blindness almost never 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.



  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. Morgan MJ, Adam A, Mollon JD. "Dichromats detect colour-camouflaged objects that are not detected by trichromats." Proc Biol Sci. 1992 Jun 22;248(1323):291-5. PMID 1354367.
  3. 3.0 3.1 "Color Blindness." University of Illinois Eye Center, Department of Ophthalmology and Visual Sciences. Accessed September 29, 2006.
  4. Kokotailo R, Kline D. "Congenital Colour Vision Deficiencies." University of Calgary, Department of Psychology, Vision & Aging Lab. Accessed September 29, 2006.
  5. 5.0 5.1 5.2 5.3 "Guidelines: Color Blindness." Accessed September 29, 2006.
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainsville, Florida: Triad Publishing Company, 1990.
  10. 10.0 10.1 Byrne A, Hilbert D. "A Glossary of Color Science." Readings on Color, Volume 2: The Science of Color. (MIT Press, 1997). Accessed November 7, 2006.
  11. *Weiss AH, et al 1989. "Blue cone monochromatism" J Pediatr Ophthalmol Strabismus. 1989; 11: 315-7

External links

Color vision [Edit]
Color vision | Color blindness
Monochromat | Dichromat | Trichromat | Tetrachromat | Pentachromat

Retrieved from "http://localhost../../../art/a/h/m.html"

This text comes from Wikipedia the free encyclopedia. Permission is granted to copy, distribute and/or modify this document under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation; with no Invariant Sections, no Front-Cover Texts, and no Back-Cover Texts. For a complete list of contributors for a given article, visit the corresponding entry on the English Wikipedia and click on "History" . For more details about the license of an image, visit the corresponding entry on the English Wikipedia and click on the picture.