Colour Blindness

Statistics

  • The most common forms of colour blindness are inherited and are associated with the inability to discriminate red and green wavelengths (a.k.a. red-green colour blindness). They arise from alterations in the genes located on the X-chromosome, which encode the middle-wave (green) and long-wave (red) sensitive photopigment molecules
  • Because these defects are inherited as recessive traits, the incidences are much higher in UK males (c. 8.0%), who possess a single X-chromosome, than in females (c. 0.5%), who possess two
  • Incidences of red-green colour deficiencies vary between human populations of different racial origin. The highest rates are found in Europeans and the Brahmins of India (c. 8% of males) and Asians (c. 4%); the lowest in Africans (c. 2.5%) and the aborigines in Australia (c. 2%), Brazil, North America (c. 2.0%) and the South Pacific Islands (c. 1.0%)
  • (Source: Opsin genes, cone photopigments, color vision, and color blindness in Color Vision: from Genes to Perception, Cambridge University Press, New York, 1999)


What is it?

Colour blindness is the reduced ability to distinguish between certain colours or wavelengths of light. To see colours properly, light detecting photoreceptor cells, called cones, are needed in the retina of the eye. Three different types exist, each containing a different photopigment: the short-wave (S, sometimes called 'blue'), middle-wave (M, sometimes called 'green')- and long-wave (L, sometimes called 'red') sensitive cones. These have distinct, spectral sensitivities, which define the probability curve of photon capture as a function of wavelength. The absorbance spectra of the S-, M- and L-cone photopigments overlap considerably, but have their wavelengths of maximum absorbance in different parts of the visible spectrum. If one or more of these types of cells is faulty then colour blindness results.

Colour blindness is normally diagnosed through clinical testing and a number of tests have been devised. The most common test is the use of special test plates called "pseudo-isochromatic" plates or colour confusion plates. The plates are made up of a series of spots of varying hues and lightnesses so that a central number or letter stands out from the background. Those with defective vision are unable to distinguish these figures or will see a different figure due to the different appreciation of the hues. By changing the figure and background colours, the basic types of defective colour vision can be identified. Other more specific tests, such as the anomaloscope, can pinpoint the more subtle defects in colour vision and provide a more accurate classification.

There is no cure for colour blindness, however there are techniques that can be used to help discriminate between colours, for example: hand held filters, tinted spectacles and monocular contact lenses. However, such devices must be used with caution. For instance, wearing a coloured filter over one eye reduces luminance, and can actually diminish colour discrimination and visual acuity, induce visual distortions, alter stereopsis and impair depth perception. And, indeed, a review of research on whether tinted lenses or filters improve visual performance in low vision concluded they actually worsen colour vision. It should be emphasised that improving test scores on specialized colour vision tests is not the same thing as curing colour blindness.


Types

Phenotypically, there are 3 main types of inherited colour blindness, resulting from alterations in the cone photopigments: (i) anomalous trichromacy (when one of the three cone pigments is altered in its spectral sensitivity, but trichromacy or normal three-dimensional colour vision is not fully impaired); (ii) dichromacy (when one of the cone pigments is missing and colour is reduced to two dimensions); or (iii) monochromacy (when two or all three of the cone pigments are missing and colour and lightness vision is reduced to one dimension).

The most common, hereditary colour blindnesses are known as red-green colour vision deficiencies, they are associated with disturbances in either the L-cone photopigment (protan defects, with protanomaly being the alteration form and protanopia being the loss form) or M-cone photopigment (deutan defects, with deuteranomaly being the alteration form and deuteranopia being the loss form). Generally, the loss forms are more severe than the alteration forms, with some people not able to tell green and red apart and others able to make some discriminations.

Tritan defects affect the S-cones. They are often referred to as yellow-blue disorders, but the term blue-green disorder is more accurate because they affect the ability to discriminate colours in the short- and middle-wave regions of the spectrum. Tritan defects arise from alterations in the gene encoding the S-cone photopigment and are autosomal dominant (linked to chromosome 7) in nature. Incidences are equivalent in males and females. In the UK, the frequency of inherited tritan defects has been estimated as being as low as 1:13,000 to 1:65,000. Tritanopia is the loss form of tritan defects. Like many autosomal dominant disorders, it is complicated by frequent incomplete manifestation. Tritanomaly, the alteration form, has never been satisfactorily documented.

Although congenital tritan defects are rare, the most frequently acquired colour vision defects, whether due to ageing or to choroidal, pigment epithelial, retinal or neural disorders are the acquired blue-yellow defects. These are similar, but not identical to tritan defects. Unlike tritan defects, which are assumed to be stationary, acquired defects are usually progressive and have other related signs, such as associated visual acuity deficits.

Total colour blindness or monochromacy occurs when a person has only a single functioning cone class (blue or S-cone monochromacy, green or M-cone monochromacy or red or L-cone monochromacy) or has no functioning cones (complete achromatopsia or rod monochromacy). These forms of colour blindness are extremely rare.

Fruit stall
 
A fruit stall as seen by colour normal (A), protanopic - a form of red-green blindness (B), deuteranopic - another form of red-green blindness (C) and tritanopic - a form of
blue-green blindness (D) shoppers.
     
A. Colour Normal   C. Deuteranopic
Picture showing a fruit stall as seen by colour normal shoppers.   Picture showing a fruit stall as seen by green blind shoppers.
     
B. Protanopic   D. Tritanopic
Picture showing a fruit stall as seen by red blind shoppers.   Picture showing a fruit stall as seen by blue blind shoppers.


Causes

Red-green colour blindness is hereditary and is passed via the X chromosome. Women, who have two X chromosomes, are usually not colour blind. But about 15% of them are carriers (i.e., they inherit an X-chromosome carrying an abnormal photopigment gene array from one parent) and may share in part in the colour blindness that they pass on to their sons, owing to a process of dosage compensation known as X-chromosome inactivation of lyonization. As carriers, they have a 50% chance of having a colour blind son, and a 50% chance of having a daughter who is a carrier too.

If a girl inherits one of the affected X chromosomes from her mother (who must be a carrier), and an affected X chromosome from her father (who must therefore be colour blind), she will also be colour blind. However, this set of circumstances is rare.

The less common forms of colour blindness arise from other factors, including cortical trauma, cerebral infarction, disorders of the ocular media of the eye, fundus detachment, progressive cone dystrophies, macular degenerations, vascular and hematological diseases, glaucoma, optic nerve disorders, diabetes, multiple sclerosis, and toxic agents (e.g., lead, tobacco, alcohol) that affect the retina or the optic tracts.


Further information

  • BBCi Health
  • Colour Blind Resource Centre
  • Colour vision
  • Ishihara test for colour blindness
  • NHS Direct Online
  • Safe colours
  • Variantor - An experience-based tool to aid colour universal design
  • Vischeck - Online colour vision model that allows simulation of how the world looks to people with various sorts of colour deficiency
  • Eperjesi F, Fowler C W and Evans B J W. Do tinted lenses or filters improve visual performance in low vision? A review of the literature, Ophthal. Physiol. Opt. 22, 68 - 77, 2002
  • McIntyre D. Colour Blindness - Causes and Effects. Dalton Publishing, ISBN 0954188608, 2002
  • Rigden C. 'The Eye of the Beholder' - Designing for Colour-Blind Users. British Telecommunications Engineering, Vol 17, January 1999
  • Sharpe L T and Jägle H. Ergonomic Consequences of Dichromacy; I Used To Be Color Blind. Color Research and Application, 269-272, 2001
  • Sharpe L T, Stockman A, Jägle H and Nathans J. Opsin genes, cone photopigments, color vision, and color blindness. Chapter 1 in Gegenfurtner K R and Sharpe L T (editors). Color Vision: From Genes to Perception, pp. 1-51. Cambridge University Press, Cambridge, 1999


Acknowledgements:
This section has been developed with the help of Prof Lindsay Sharpe, Professor of Vision Science, University of Newcastle.

Last updated: 20.11.2009   © Copyright reserved    Website design: Digital Accessibility Team