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Comparative review of color blindness in different ethnic populations.

INTRODUCTION: The faculty by which one can distinguish between different colors and color tones as excited by light of different wavelengths is known as Color Sense. Sir John Dalton first gave a clear description of his own color blindness in 1794. His publication subsequently stimulated much research into the pathophysiology and genetics of the condition (1). In 1801-1802 Thomas Young postulated the existence of three 'Principal' colors (Red, Green and Violet), from which all colors and white light can be obtained (2). Von Helmholtz (1866) suggested that there are three types of cones, containing three photochemical substances corresponding to the three fundamental color sensations (3). Von Kries (1923) noted that anomalous Trichromats can see all the three colors, but the appreciation of one particular color is subnormal. He further described Protanomaly as sub-normal green vision and Tritanomaly as sub-normal blue vision. People who can see two colors but fail to see the third are designated as Dichromats. Dichromats lack red pigment gene and those lacking green pigment gene are known as Protanopes while those lacking blue green pigment are known as Tritanopes (4). In 1881, Lord Rayleigh introduced anomaloscope for scientific analysis of color defects (5).

Color blindness is a hereditary disorder of color vision, being transmitted by sex-linked recessives by two pairs of genes in the non-homologous part of the X chromosome. It is much more common in males than in females. Y-chromosome plays no role in the determination of color vision (6). The objective of the present article is to correlate the prevalence of colorblindness in various groups of ethnic populations. People with defective color vision are at a disadvantage especially for employment in defense services, technical fields like engineering, medical profession, textile industry, dyeing industry, pilots, drivers etc. This may influence their education and carrier choice.

MATERIAL AND METHODS: Seven studies were identified that examined the prevalence of color vision impairment. These studies are summarized in the table 1. Some of the percentages included in this table were calculated by the author of this report. The prevalence of color blindness was assessed in Tibetans, Turkish men, Jordanians, Singaporean children and Nepali school children & two other populations. Ishihara Pseudoisochromatic test plates were used for these populations while HRR (Hardy, Rand and Ritter) Pseudoisochromatic test plates were used in assessing male population of Lalima village, Terena, India. In addition, Pickford Nicolson anomaloscope was used in the Tibetan study used to distinguish the type and the extent of defect of color vision.

Ishihara plates consist of a series of cards in which a colored background is printed in spots of different sizes (7). A letter, figure or a number is printed against this background in spots of the same size. To a normal subject, the figure or letter at once becomes clear, but the color blind subject fails to distinguish it from the background. It is easy, quick to perform and type of color defect can be ascertained with a fair degree of accuracy. The detection of Tritan defect is not possible using this test. The Pickford Nicolson Anomaloscope is a simple colorimeter based on the use of integrating boxes which has color chance's optical glass filters. The wavelengths of the primary filters (red and green) used are 642nm and 555nm, to produce a yellow with a wavelength of 585nm. It is manually operated. It is the only instrument by means of which colour blindness can be correctly classified (8).

RESULTS AND DISCUSSION: The present article provides a met analysis of the prevalence of impaired color vision from 7 different studies in diverse populations.

The prevalence of color blindness in the Tibetan male population (n = 120) was 4.21%. No Tibetan female was found to be color blind (9). The prevalence of color blindness in the Tibetan males was lower than that reported in Turkish men (7.33%). (10) and Jordanian men 8.7% (11). On the other hand the prevalence of color blindness in the males in the Tibetan population was much higher than that reported in the Indian population of Lalima village, Terena 0% (12). Strikingly, the prevalence of color blindness in the Tibetan male population is in accord with those in Nepali school children 3.8% (15) (S.D. [+ or -] 0.4%) (13). The prevalence of color blindness in Singaporean children was assessed and found it to be 5.3% (SD+ 0.9%) (14) while found it to be 5.42% in Southern Calabria (variation [+ or -] 1.2%) (15). In the Muslim communities, consanguineous marriages are very common with more likelihood of transmission of hereditary disease. Consanguineous marriages also take place in Tibetan and Nepali communities but the frequency is quite low compared to Muslim community. This explains a lesser incidence of color blindness in the Tibetans and Nepalese compared with the Turkish and Jordanian groups.

None of the females was found to be color blind in the Tibetan, Turkish populations and Nepali school children (9, 10, 13) while the incidence in Jordanians was reported 0.33% (12) and 0.2% in Singaporean children (14).

The reason for the wide variation of frequency in the two sexes can be explained on the basis of heredity of color vision defects. Red and green defects in color vision are transmitted as sex-linked recessive by two pairs of genes in the non-homologous part of the X-chromosome, each of which might mutate into one of the 3 different alleles. The incidence of color blindness in females is much less compared with males because a female must carry a pair of homologous abnormal genes which however is rare. This explains very low frequency of color blindness in females (6). As color blindness is a congenital defect, its incidence does not have any relation with age.

The Tibetan study (9) showed 14 (n = 14) cases simple Deuteranomaly, 8 Extreme Deuteranomaly followed by 9 cases of Protanopia, 9 Deuteranopia, 7 Protanomaly, 3 Extreme Protanomaly and 1 case of Tritanopia. The Jordanians (Al Aqtum and Al Qawasmeh (2001) had 8 cases of Deuteranomaly, 4 Deuteranopia, 4 Protanomalia and 3 cases of Protanopia and 4 of deuteranopia. Strikingly in these 2 studies Deuteranomaly is the predominant finding followed by Deuteranopia. [Table 2]. However, the study in Nepali school children showed the maximum number of cases of Deuteranopia (n = 9), followed by Deuteranomaly 6, Protanomaly 3 (13). Among the anomalous trichomats the frequency of Deuternanomaly is more than that of protanomaly. This could be explained by genetic factors (16). Males with normal color vision always have one red pigment gene. However the number of green pigment genes differs among those individuals and ranges between 1 and 3. Most people have 2 green pigment genes. Larger number of genes for the green pigment explains the higher frequency of Deuteranomaly as compared with protanomaly (17).

SUMMARY AND CONCLUSION: The percentage distributions of color blindness in our studies were found different in different

Ethnic populations: highest in Jordanian men [8.7%] followed by Turkish men [7.33%]. Since Color blindness is genetically transmitted, its distribution varies from race to race and is different in the different geographical regions of the world inhabited by people of different ethnicity.

The prevalence of Deuteranomaly was highest among different male ethnic populations and that of Tritanopia was the lowest. Although several therapies have been proposed [eg. Electrical eye stimulation, Iodine injections, Large doses of vitamins], there are no treatments or surgical procedures to improve the quality of an individual's chromatic vision. The natural history of color vision impairment cannot be altered, the importance of identifying individuals with color vision defects is to ensure that adequate provision and advice is given.

It may be concluded that the major benefit of color vision screening is to ensure adequate carrier advice. It would also be interesting to genetically examine the various populations and verify the genes that code for photo pigments.


(1.) Dalton J: Edin J Sci., 9; 97: 1798. Quoted from Duke Elder. Physiology of the Eye and Vision. System of Ophthalmology 1968; 4: 667.

(2.) Young T: Theory of colour vision. Phil Trans 1801; 91: 23-A, A course of lecturers on natural Physiology and the mechanical Arts London 18-07. Quoted by Duke Elder. The physiology of eye and vision 1968; iv: 643.

(3.) Helmholtz V: Ann Phys (LPZ) 1852; 87: 45. Quoted from Duke Elder. Physiology of the Elder. Physiology of the Eye and Vision. System of Ophthalmology 1968; 4: 620.

(4.) Kries V: Psychol Physiol Sinnes 1896; 9: 81. Quoted from Duke Elder. Physiology of the Eye and Vision. System of Ophthalmology 1968; 4: 545.

(5.) Rayleigh Lord: Nature (London) 1881; 25, 64. Quoted by Duke-Elder. The Physiology of Eye and Vision 1968; IV: 636.

(6.) Dalton J: Inheritance of protanopic and deuteranopic defects. Mem Manchester Lit and Phil Soc 1798; 5(1): quoted by Duke-Elder. Physiology of the Eye and Vision. System of Ophthalmology 1968; 4: 650.

(7.) Ishihara S: Test for colour--blindness, 15th complete edition with 38 plates KancharsSuppan. Co. Ltd., London. H. K. Leivis and Co., Ltd. Made in Japan, 1960.

(8.) Pickford RW and LakowskiR: Anomaloscope Brit J Physiol Optics 1961; 17: 131.

(9.) Kaur N and Kumar A: Study of colour blindness in Tibetan migrant population. Delhi J Opthalmol 2009; Vol.21 (3):45-47.

(10.) Citirik M, Acaroglu G, Batman C et al: Congenital color blindness in young Turkish men. Ophthalmic Epidemiology 2005 Apr; Vol. 12(2): 133-7.

(11.) Al-Aqtum MT and Al-Qawasmeh MH: Prevalence of colour--blindness in young Jordanians. Ophthalmologica 2001; 215(1): 39-42.

(12.) Piccinin MR, Cunha JF, de Almeida HP et al: Low prevalence of dyschromatopsia using the fourth edition of HRR (Hardy, Rand & Rittler) pseudoisochromatic plate test among the Indian Population of Lalima village, Terena. Arq Bras ophthalmol 2007; 70(2): 259-69.

(13.) Niroula DR and Saha CG: The Incidence of colour blindness among some school children of Pokhara, Western Nepal. Nepal Med Coll J 2010 Mar; 12(1): 48-50.

(14.) Chia A, Gazzard G, Tong L et al: Red-green colour blindness in Singaporean children. Clinical & Experimental Ophthalmology 2008, July: 36{5}: 464-7, Experiment Ophthalmology 2008 July; 36(5): 464-7.

(15.) Tagarelli A, Piro A and Tagarelli G et al: Colour blindness in Calabria (Southern Italy): A North-South decreasing trend. Am J. Human Biol 2000; 12(1): 17-24.

(16.) Ganong WF: Vision. Ganong's Review of Medical Physiology. 2003; 21:168.

(17.) Wald G: Defective colour vision and its inheritance in Symposium on mechanism of colour vision. Proc Nat Acad S USA 55(6): 1347-63. Bio Abstract 1967; 48:11.


[1.] Navjot Kaur

[2.] Kawalpreet Singh


[1.] Assistant Professor, Department of Physiology, Dr. H.S. Judge Institute of Dental Sciences, P.U, Chandigarh.

[2.] Consulting Anaesthetist, Columbia Asia Hospital, Patiala.


Dr. Navjot Kaur, Dept. of Physiology, Dr. Harvansh Singh Judge Institute of Dental Sciences, Sector 25, Punjab University, Chandigarh.

Date of Submission: 07/08/2013.

Date of Peer Review: 08/08/2013.

Date of Acceptance: 03/09/2013.

Date of Publishing: 05/09/2013
Table 1: Summary of studies examining the
prevalence of colour blindness

Reference                    Colour vision test      Sample size

(Navjot et al 2009)            Ishihara charts        n = 2010
                              Pickford Nicolson     Males = 1210
                                Anomaloscope        Females = 800

(Citirik et al, 2005)          Ishihara charts       Males= 941
Turkish men                                          Females = 0

(Chia et al.., 2008)           Ishihara charts        n = 1249
Singaporean Children

Al-Aqtum and                   Ishihara charts        n = 1418
(Al-Qawasmeh 2001)                                   Males = 218
Jordanians                                         Females = 1200

(Niroula and Saha 2010)        Ishihara charts         n = 964
Nepali School Children                               Males = 474
                                                    Females = 490

(Tagarelli et al.., 2000)      Ishihara charts       n = 13,072
Italian population                                     (Males)

(Piccinin et al.., 2010)            HRR-               n = 226
Indian population            Pseudoisochromatic         Males
                                 plate test

Reference                              Results

(Navjot et al 2009)                 Males = 4.21%
                                     Females = 0%

(Citirik et al, 2005)        Males = 7.33 [+ or -] 0.98%
Turkish men                          Females = 0%

(Chia et al.., 2008)                 Males = 5.3%
Singaporean Children                Females = 0.2%

Al-Aqtum and                         Males = 8.7%
(Al-Qawasmeh 2001)                 Females = 0.33%

(Niroula and Saha 2010)              Males = 3.8%
Nepali School Children               Females = 0%

(Tagarelli et al.., 2000)             n = 5.42%
Italian population

(Piccinin et al.., 2010)               n = 0%
Indian population
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Author:Kaur, Navjot; Singh, Kawalpreet
Publication:Journal of Evolution of Medical and Dental Sciences
Article Type:Report
Geographic Code:9INDI
Date:Sep 9, 2013
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