Anomalous colour vision is usually a genetically determined normal state, predominantly in men since it is carried in the X chromosome
More than 95% of people exhibit nearly the same responses when matching and identifying colours in objective tests, so there seems to be a normal colour vision that most of us share. The remainder, however, cannot make certain distinctions that the majority can, and are usually called colour blind, a misleading term coined by Dr G. Wilson of Edinburgh in 1855 to replace the even less satisfactory daltonism, from the famous possessor, John Dalton the chemist, who first recognized it. Dr Wilson was the first to study colour blindness extensively and apply it to practice, in which he was aided by James Clerk Maxwell, who was also interested in the subject. When I write colour blind in what follows, I mean simply anomalous colour vision, which perhaps could better be abbreviated ACV, but this is not customary. There are no people who can make more delicate colour distinctions than the majority, so anomalous colour vision is always a decrease in fineness of colour perception. However, it may also give increased acuteness of vision in low light. The types of colour blindness are not distinct, and occur in different degrees, but there is sufficient disparity to make classification useful. Colour-blindness is not a lesion, just a difference.
Men are more than ten times more likely to be colour blind than women. This, besides being unfair, shows that the commonest varieties of colour blindness are congenital, due to genetic differences in the sex-determining Y chromosome (where some genes are not duplicated), and that colour blindness is a recessive characteristic, like haemophilia. Men exhibit colour blindness when they receive one anomalous gene, while women must receive two, and are asymptomatic carriers when they have only one anomalous gene. None of the offspring of a women without anomalous genes and a colour-blind man will be colour-blind, but the daughters will all be carriers. The genetic source of colour blindness makes its incidence different in different genetic groups. Fiji islanders and Navajo indians have very little colour blindness, but among Norwegians, Poles and Czechs over 10% of the men are colour blind. Genes control protein synthesis, so congenital colour blindness is largely the result of errors in producing the colour-sensitive protein absorbers in the cone cells of the retina. The third colour-sensitive visual protein appears to be a recent evolutionary development; two do for most creatures. Colour blindness can also be the result of disease or poisoning, where it has no genetic basis, or due to other faults than those of the visual proteins.
Monochromatism or achromatopia, in which distinctions of hue cannot be made, is very rare (2 to 3 in 100,000 males and females). In the typical variety, the rod system of receptors is absent or nonfunctional. In the atypical, the difference is in the visual perception system of nerves and brain. In dichromatism, colour matches can be made using only two basic stimuli, instead of the three normally required. The colours perceived are said to be blue and yellow, as if there were no distinction between red and green. In protanopia, the red limit is shifted up to about 680 nm, and the peak sensitivity occurs at 540 nm. In deuteranopia, the blue limit is affected, and the peak sensitivity occurs at 560 nm. (In normal colour vision it is at 555 nm.) Each of these two anomalies is found in about 1% of males. In the very rare (1 in 1 million males) tritanopia, red-green distinctions can be made, but blue-yellow discrimination is affected. The three classes would seem to be due to severe deficiencies or abnormalities in one of the three colour-sensitive retinal proteins, but it is not clear that simple deficiencies are a complete explanation. Protanopia and deuteranopia are the principal forms of severe color blindness.
Anomalous trichromatism is the most common form of colour blindness, in which colour distinctions are merely less accurately or easily made than in normal colour vision, and three stimuli are still usually necessary to produce a match. The varieties of this condition are called protanomaly, deuteranomaly and tritanomaly, and seem to be simply less-serious versions of the corresponding dichromatic types. Again, protoanomaly and deuteranomaly are the most prevalent, and the severity ranges continuously from that of dichromatism down to normal perception.
Acquired colour blindness can be the result of disease, such as multiple sclerosis, optic neuritis, anaemia, lukaemia, vitamin B1 deficiency, or the result of poisioning by carbon disulphide, lead, sulfanilamide, iodoform, thallium, tobacco and alcohol. These causes attack the conducting paths of the optical system, and can be temporary or permanent. They can progress as far as monochromatism if the poisoning or disease continues. If the rod-cone mechanism is damaged, acquired tritanopia may occur, in which there is a reduced discrimination between blue and yellow. This may be stable and localized in small regions of the retina. A dose of half a gram to a gram of sodium santoninate produces temporary violet-blindness (accompanied by nausea and visual hallucinations). A violet haze is seen over the visual field.
Most kinds of anomalous colour vision can be quickly diagnosed without elaborate colour-matching apparatus by dichotomous tests designed principally to screen for red-green color blindness. A good example is the Ishihara colour plate book, one of many pseudoisochromatic (PIC) tests. These plates use patterns of discs of random size coloured so that a number can easily be seen if the observer can make the colour distinction involved. If an incorrect distinction is made, a different number, or no number at all, may be perceived. In the use of any published test plates, there is always the danger that the subject may have learned to identify the plates by some other characteristic in an attempt to conceal colour blindness. Other tests are wool-sorting (e.g., the Holmgren Wool Test), widely used before the PIC tests were developed in 1878 by Stilling, the New London Navy Lantern Test, specially adapted to signal lights, and many others. When screening, there should always be some other, improvised test for severe deuteranopia with, say coloured yarns, papers or posters that cannot have been studied in advance like publshed tests, as well as pointing out the dangers and traps of trying to conceal colour blindness when it has an effect on public safety. The Ishihara test, and others, are also qualitatively diagnostic to a various degrees, and can identify the more common types of anomalous colour vision that may be presented. More precise quantitative diagnosis requires equipment like the Nagel anomaloscope, developed in the 1890's, which mixes red and green lights to make a match with yellows. Reliable screening and testing is a subject requiring considerable expertise, and is not as easy as it might appear.
People with anomalous colour vision learn to use other clues in distinguishing colours where they carry an important message, as in traffic lights or railway signals. Position and brightness are two generally useful clues, as well as the slight differences that may be perceived even with severe anomalous trichromatism. It must be remembered that anomalous colour perception is not a yes-no question, but a continuum. It is unfortunate that colour is used where its recognition is essential to safety, and not simply as an aid to distinguishing objects, as nature intended.
The perception of colour is not entirely that exhibited under standard laboratory conditions, as in the assessment of anomalous colour vision, but in nature is influenced by illumination, contrast, fatigue and other factors. A coloured board can appear achromatic on a bright sunny day when the sun is behind it, but the colour is evident on a dull, cloudy day. A green light shining through fog and mist may appear yellow. Edwin Land found that mixtures of red and white light could give the sensation of green in certain cases. In any case, it must be remembered that colour is a property of perception, not of an object, and exists only subjectively. It can be made apparently objective only because 95% of us make the same behavioural responses to it.
G. Wilson, Proc. Edinb. Soc. III, 226-227 (1854), Monthly J. Med. Sci., Nov. 1853 to Dec. 1854, Edinb. Jour. (2) IV, 322-327, Researches on Colour Blindness (Edinburgh, 1855).
J. Dalton, Mem. Lit. & Phil. Soc. Manch. V, Edin. J. of Science IX, 97.
A. Seebeck, Pogg. Ann. XLII, 177-233 (1837). "Über den bei manchen Personen vorkommenden Mangel an Farbensinn"
J. Tyndall, Phil. Mag. (4) XI, 329-333(1856).
J. C. Maxwell, Edinb. Trans. XXI, 275-297 (1855).
See Helmholtz, Phys. Optik (English translation, Dover 1962), v. II, pp. 146-154.
Composed by J. B. Calvert
Created 29 March 2000
Last revised 29 March 2000