Color blindness, a color vision deficiency, is the inability to perceive differences between some of the colors that others 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", 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 disability; however, in selected situations color blind people have an advantage over people with normal color vision. There are some studies which conclude that color blind individuals are better at penetrating certain camouflages. Monochromats may have a minor advantage in dark vision, but only in the first five and a half minutes of dark adaptation.
The normal 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. The cones are activated when the pigments absorb light. The absorption spectra of the cones 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. Red light, for example, stimulates the long wavelength cones much more than either of the others, and reducing 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.
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. In World War II it was discovered that analysis of color aerial photos yielded more information if at least one team member was color blind. Significantly, humans are the only trichromatic primates with such a high percentage of color blindness. As the color blind test example (next to analysis) demonstrates, color blind people see different patterns. WWII teams that analyzed aerial photographs were looking for unusual patterns, so a color blind person could prove useful. From an evolutionary perspective a hunting group will be more effective if it includes a color blind hunter (one in twenty) who can spot prey that others cannot.
Another possible advantage might result from the presence of a tetrachromic female. Owing to X-chromosome inactivation, women 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.
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 our retina as the cones are capable of detecting the color frequencies of light we perceive.
About 5—8 percent of males, but less than 1 percent of females, are color blind in some way or another, whether it be one color, a color combination, or another mutation. The reason males are at a greater risk of inheriting an X linked mutation is because males only have one X chromosome (XY, with the Y chromosome being significantly shorter than the X chromosome), and females have two (XX); if the women inherit a normal X chromosome in addition to the one which carries the mutation, they will not display the mutation, while men have no 'spare' normal chromosome to override the chromosome which 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%.
Shaken Baby Syndrome (this can cause damage to the retina and brain damage and therefore cause color blindness); Accidents and other trauma to the retina and brain; UV damage (not wearing appropriate protection). Most UV damage is caused during childhood and this form of retinal degeneration is the leading cause of blindness in the world. Damage often presents later in life.
There are many types of color blindness. The most common are red-green 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 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.
Color vision deficiencies can be classified as acquired or inherited.
Based on clinical appearance, color blindness may be described as total or partial. Total color blindness is much less common than partial color blindness. 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.
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. Monochromats possess a complete inability to distinguish any colors and perceive only variations in brightness. 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.
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 a 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.
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.
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. 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 women are tetrachromats, since they require a mixture of four spectral lights to match an arbitrary light.
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 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 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. 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 (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.
|Overall (United States)||—||—||1.30%|
|Red-green (Overall)||7 to 10%||—||—|
|Rod monochromacy (no cones)||0.00001%||0.00001%||—|
|Protanopia (L-cone absent)||1% to 1.3%||0.02%||—|
|Deuteranopia (M-cone absent)||1% to 1.2%||0.01%||—|
|Tritanopia (S-cone absent)||0.001%||0.03%||—|
|Protanomaly (L-cone defect)||1.3%||0.02%||—|
|Deuteranomaly (M-cone defect)||5.0%||0.35%||—|
|Tritanomaly (S-cone defect)||0.01%||0.01%||—|
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 (for example) to collect thorough datasets, identify copunctal points, and measure just noticeable differences.
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. Optometrists can supply a singular red-tint contact lens to wear in the dominant eye. This may enable the wearer to pass color blindness tests for certain occupations. The effect of wearing such a device is akin to wearing red/blue 3D glasses and can take some getting used to as certain wavelengths can "jump" out and be overly represented. Additionally, computer software has been developed to assist those with visual color difficulties.
The Gnome Desktop 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 the colors. The software enables, for instance, a color blind person to see the numbers in the ishihara test.
The National Eye Institute is doing research into treating/curing color blindness, and it is now required to donate 5% of its resources to this cause under instruction of the National Institutes of Health.
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. For an example of a map that could present a significant problem to a color blind reader, see this graphic from a recent New York Times article. The typical red-green color blind reader will find the green sections of the map nearly indistinguishable from the orange, rendering the graphic unreadable.
Designers, should 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. Thirdly, 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.
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 inability to recognize colors such as red and green, some countries (e.g., Singapore prior to the 1990s or Romania even to the present day) have refused to grant individuals with color blindness driving licenses. In Romania there is an undergoing effort to remove the legal restrictions that prohibit its colorblind citizens from getting drivers' licenses.
Color blindness is not the swapping of colors in the observer's eyes. Grass is never red, and 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 may find it difficult to distinguish a Braeburn from a Granny Smith and in some cases, the red and yellow of a traffic light without other clues (e.g., shape or location). This is demonstrated in this simulation of the two types of apple as viewed by a trichromat or by a dichromat.
Anomalous Trichromats are often able to readily spot camouflage clothing, netting, and paint that has been designed for individuals with color-normal vision. They tend to learn to see texture and shape. This lets them see through some camouflage patterns.
Traffic light colors are confusing to some dichromats: there is insufficient apparent difference between the red and amber and sodium street lamps and the green can be confused with a grubby white lamp. This is a risk factor on a high-speed undulating road where angular cues can't be used. British Rail color lamp signals use more easily identifiable colors: the red is really blood red, the amber is quite yellow and the green is a bluish color.
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.
It should also be noted that even though some people are unable to see some or maybe even any of the numbers in (e.g. red-green) color blindness tests, they might still be able to tell the difference between the colors in their everyday lives.
Firefox add on for colorblind people https://addons.mozilla.org/en-US/firefox/addon/5001
Na(+)-Ca(2+)-K(+) currents measured in insect cells transfected with the retinal cone or rod Na(+)-Ca(2+)-K(+) exchanger cDNA
Oct 01, 2000; ABSTRACT The recently cloned retinal cone Na+-Ca2+-K+ exchanger (NCKX) was expressed in cultured insect cells, and whole-cell...