Prevalence of colour blindness in young Bangladeshis

Humans are distinguishable from non-primates by their trichromatic vision. In
human, different combinations of the primary colors (red, green and blue) produce unique color sensation(1). Three spectrally-distinct types of cone photoreceptors in the retina are responsible for the discrimination of colors. They are known as short, medium and long wavelength sensitive cones which can sense light, at around 420, 530 and 560 nm, respectively. The location of red/green pigment genes are on the long arm of X chromosome (Xq 28) while blue pigment gene resides on the chromosome 7 of the human genome(2). Color blindness or color vision deficiencies (CVD), sometimes, occurs due to different forms of mutation, for instance, missense mutation in hybrid long/medium (L/M) cone opsin genes known as OPN1LW and OPNL1MW which are arranged in a
head-to-tail tandem array on the X chromosome(2,3). Although, CVD is a hereditary trait but it is also reported that some acquired properties such as damage to eyes, nerves, brain; metabolic disorder like diabetes, sickle cell anemia; drugs (e.g., plaquenil, digoxin, ethambutols, chloroquineetc); and some other chemicals may cause color blindness(4). Color blind people may suffer from partial (-anomaly) or complete (-anopia) inability to sense any of the primary colors. Red-green colorblindness is the most prevalent form of CVD which can be broadly categorized into protan (red) and deutan (green) according to the abnormality of sensing red and green color, respectively(2). Absence or anomaly in L-cone function is known as protan defects whereas deutan defects is characterized by disruption of M-cone function. Individuals with complete absence of photopigment of the green or red cone suffer from deuteranopia or protanopia.