Colour vision defects can be tested by recording discriminated patterns or numbers on the Ishihara colour vision plates, and sometimes further diagnosis occurs in specially equipped colour vision clinics. Defective colour vision is not ‘colour blindness and is common and inherited.
1 in 12 men (8 per cent)
1 in 200 women (0.5%)
Present at birth and remains unchanged.
There is no treatment, but different techniques to allow the colour to be inferred by brightness are being researched and developed. Sometimes tints can be used to select more specific wavelengths but will not cure colour vision defects. Typically greens, yellows, oranges and reds can be confused. It causes colour matching problems, colour naming problems and the inability to perceive the brightness of colours.Retinal cone photoreceptors, either contain red, green and blue responsive photopigments. These human eye cone cells can hundreds of shades, and millions of colours. Some rare individuals have a genetic mutation granting them an extra, fourth cone cell. Colour confusion line can be plotted on the CIE

The CIE 1931 RGB colour space and CIE 1931 XYZ color space were created by the International Commission on Illumination (CIE))

What causes colour vision defects?
Accidents and trauma to the retina or brain can cause defects, and acquired colour defects can be crucial in pathology diagnosis.
Nutritional causes such as deficiency of vitamin A and degenerative diseases of the eye – macular degeneration, glaucoma, diabetes and cataracts can all bear on the quality of colour vision.
Inherited colour blindness is the most common cause of loss or partial loss of the different cone systems within the eye due to missing or damaged genes.
Further tests are required to assess this provided by an optometrist, sometimes in specially equipped colour vision clinics featuring such equipment such as the Nagel anomaloscope, D15 test where hue samples are recorded and referenced in a juxtaposed fashion to a reference and the Farnsworth lantern.
The Ishihara test doesn’t measure the extent of the defect.
Further tests are required to assess this.
Follow up can be provided by an optometrist or ophthalmologist.
The rod cells are active in low light, and the cone cells (active in average daylight). A normal eye has three kinds of colour receptors.
For red, green and blue light, Responses are relayed to the brain.
Here they are mixed to perceive many thousands of colours.
Defects occur by:
One receptor is missing.
One receptor is abnormal.
Two or even three receptors are missing is a rarer and a more severe problem.
Colour vision and your job
Everyday problem examples of coping with a colour vision defect:
Recognising the colour of traffic lights.
Seeing coloured flowers on trees.
Judging ripeness of fruit.
Knowing when meat is cooked.
Job requirements where colour vision could be an issue
e.g. Airline pilot
Air traffic controller
Train and tram driver
Policeman
Fireman
Careers in the defence forces
Seafarer
What is the most common colour vision defect?
Red-green colour blindness is the most common type of colour defect because the genes that lead to red-green colour blindness are on the X chromosome, with males having just one X chromosome, whilst females have two.
Blue colour blindness is far less common, being present in just 5% of all colour blindness sufferers. The genes affected are equal in both sexes.