colour blindness

colour blindness Some 8% of men exhibit a hereditary deficiency of colour perception, but so imprecise is our common coinage of words about colour that it was not until the eighteenth century that the existence of colour blindness was generally known — and only rather recently was it recognized that there are measurable differences in colour perception between people with ‘normal’ colour vision.

The novelist Fanny Burney, who became lady-in-waiting to Queen Charlotte, records in her journal an uncomfortable conversation with George III:
He still, however, kept me in talk, and still upon music. ‘To me,’ said he, ‘it appears quite as strange to meet with people who have no ear for music and cannot distinguish one air from another, as to meet with people who are dumb … There are people who have no eye for difference of colour. The Duke of Marlborough actually cannot tell scarlet from green!’ He then told me an anecdote of his mistaking one of those colours for another, which was very laughable, but I do not remember it clearly enough to write it. How unfortunate for true virtuosi that such an eye should possess objects worthy of the most discerning — the treasures of Blenheim! ‘I do not find, though,’ added His Majesty, ‘that this defect runs in his family, for lady Di Beauclerk draws very finely.’In fact, though His Majesty did not know it, most forms of colour blindness do run in families, but in an interesting way. The affected gene is typically on the X chromosome (of which normal females have two and males only one). A woman must carry similar defective genes on both her two X chromosomes if she is to be overtly colour blind; but a man will inescapably be colour blind if his single X chromosome bears the defect. So a woman may inherit an affected chromosome from one or other of her parents and transmit colour blindness to, on average, half her sons. She herself will pass the standard tests of colour vision, but such carriers may reveal themselves in the laboratory by, for example, their judgement of the relative brightness of different colours.

The genes that are affected are usually ones that encode and produce the light-sensitive pigments of the retina. Our daytime vision depends on three types of retinal cell, the ‘cones’, each type containing a different light-absorbing pigment. One of the pigments has its peak sensitivity in the violet part of the spectrum, a second peaks in the green, and the third peaks in the yellow– green. Our visual system is able to work out the colour by comparing the relative rates at which photons of light are absorbed in the different classes of cone in the area of retina exposed to the light.

In the type of colour blindness called dichromacy, one of the three pigments is missing. Typically the cone pigment that is lost is either the type that peaks in the green or the one that peaks in the yellow–green. About 2% of Caucasian men are dichromats of this kind. They are often well content with their residual colour vision, which depends on comparing the light absorbed in the two remaining cone types and allows them to distinguish ‘warm’ colours from ‘cold’. More common, affecting 6% of men, is the milder condition called anomalous trichromacy. In such cases, the absorption curve of one of the two pigments in the green–yellow range is shifted in its position in the spectrum so that it lies closer than usual to the other. Anomalous trichromats vary in their ability to discriminate colours: they may be almost as limited as dichromats, or they may be nearly as good as normals, but they always reveal themselves by making anomalous settings in a test called the Rayleigh match, where the subject is asked to find the proportion of red to green light in a mixture that will just match a spectral orange. In a lesser — but measurable — way, colour-normal people vary in their Rayleigh matches, and we now know that these differences in our subjective worlds are correlated with small variations in the DNA sequence of our X chromosomes.

In addition to these inherited forms of colour deficiency, there are also forms that arise from eye conditions, such as glaucoma, or systemic conditions, such as diabetes. In these cases, it is often the violet-sensitive cones (or the pathways that carry their signals) that are affected.

In Britain at the beginning of the twenty-first century, coloured lights are still used for signalling on the roads and the railways, and the particular red and green lights employed are easily confused by many colour blind individuals. It is reported that trains are daily driven through red lights and it is a matter of speculation whether any of these incidents arise because colour-deficient drivers slip through testing or monitoring procedures designed to exclude them from such employment. It is clearly critical to screen for colour blindness at entry to professions where coloured signals are used — aviation and navigation, as well as train driving. There are other, less obvious, occupations where colour deficiency is a disadvantage, such as dermatology and market gardening. On the whole, however, colour blindness is a minor handicap in the modern world. And some biologists believe that there must be some compensating advantage that maintains the high incidence of colour blindness in our population. Certainly, one can demonstrate some advantages in the laboratory. For instance, if a screen is filled with an array of small bars randomly coloured red or green, dichromats are more accurate than normals in quickly detecting in which quadrant of the screen there is variation in the size or the orientation of the bars. And so one possibility is that the colour blind person enjoys an advantage in detecting the texture of patterns in the natural world.

J. D. Mollon

Bibliography

Backhaus, W. G., Kliegl, R., and Werner, J. S. (ed.) (1998). Color vision. De Gruyter, Berlin.

See also blindness; eyes; vision.