Other causes of color blindness include brain or retinal damage caused by shaken baby syndrome, accidents and other trauma which produce swelling of the brain in the occipital lobe, and damage to the retina caused by exposure to ultraviolet light (10–300 nm). Damage often presents itself later on in life.

Color blindness may also present itself in the spectrum of degenerative diseases of the eye, such as age-related macular degeneration, and as part of the retinal damage caused by diabetes. Another factor that may affect color blindness includes a deficiency in Vitamin A.

Some subtle forms of colorblindness may be associated with chronic solvent-induced encephalopathy (CSE), caused by longtime exposure to solvent vapors.

Red–green color blindness can be caused by ethambutol, a drug used in the treatment of tuberculosis.

Protanopia, deuteranopia, protanomaly, and deuteranomaly are commonly inherited forms of red–green color blindness which affect a substantial portion of the human population. Those affected have difficulty with discriminating red and green hues due to the absence or mutation of the red or green retinal photoreceptors. It is sex-linked: genetic red–green color blindness affects males much more often than females, because the genes for the red and green color receptors are located on the X chromosome, of which males have only one and females have two. Females (46, XX) are red–green color blind only if "both" their X chromosomes are defective with a similar deficiency, whereas males (46, XY) are color blind if their single X chromosome is defective.

The gene for red–green color blindness is transmitted from a color blind male to all his daughters who are heterozygote carriers and are usually unaffected. In turn, a carrier woman has a fifty percent chance of passing on a mutated X chromosome region to each of her male offspring. The sons of an affected male will not inherit the trait from him, since they receive his Y chromosome and not his (defective) X chromosome. Should an affected male have children with a carrier or colorblind woman, their daughters may be colorblind by inheriting an affected X chromosome from each parent.

Because one X chromosome is inactivated at random in each cell during a woman's development, deuteranomalous heterozygotes (i.e. female carriers of deuteranomaly) are potentially tetrachromats, because they will have the normal long wave (red) receptors, the normal medium wave (green) receptors, the abnormal medium wave (deuteranomalous) receptors and the normal autosomal short wave (blue) receptors in their retinas. The same applies to the carriers of protanomaly (who have two types of short wave receptors, normal medium wave receptors, and normal autosomal short wave receptors in their retinas). If, by chance, a woman is heterozygous for "both" protanomaly and deuteranomaly she could be pentachromatic. This situation could arise if, for instance, she inherited the X chromosome with the abnormal long wave gene (but normal medium wave gene) from her mother who is a carrier of protanomaly, and her other X chromosome from a deuteranomalous father. Such a woman would have a normal and an abnormal long wave receptor, a normal and abnormal medium wave receptor, and a normal autosomal short wave receptor – 5 different types of color receptors in all. The degree to which women who are carriers of either protanomaly or deuteranomaly are demonstrably tetrachromatic and require a mixture of four spectral lights to match an arbitrary light is very variable. In many cases it is almost unnoticeable, but in a minority the tetrachromacy is very outspoken. However, Jameson "et al." have shown that with appropriate and sufficiently sensitive equipment all female carriers of red-green color blindness (i.e. heterozygous protanomaly, or heterozygous deuteranomaly) are tetrachromats to a greater or lesser extent.

Since deuteranamoly is by far the most common form of red-green blindness among men of northwestern European descent (with an incidence of 8%), then the carrier frequency (and of potential deuteranomalous tetrachromacy) among the females of that genetic stock is 14.7% (= [92% x 8%] x 2).

- Protanopia (1% of males): Lacking the red cones for long-wavelength sensitive retinal cones, those with this condition are unable to distinguish between colors in the green–yellow–red section of the spectrum. They have a neutral point at a cyan-like wavelength around 492 nm (see spectral color for comparison) – that is, they cannot discriminate light of this wavelength from white. For a protanope, the brightness of red, orange, and yellow are much reduced compared to normal. This dimming can be so pronounced that reds may be confused with black or dark gray, and red traffic lights may appear to be extinguished. They may learn to distinguish reds from yellows primarily on the basis of their apparent brightness or lightness, not on any perceptible hue difference. Violet, lavender, and purple are indistinguishable from various shades of blue because their reddish components are so dimmed as to be invisible. For example, pink flowers, reflecting both red light and blue light, may appear just blue to the protanope. A very few people have been found who have one normal eye and one protanopic eye. These "unilateral dichromats" report that with only their protanopic eye open, they see wavelengths shorter than neutral point as blue and those longer than it as yellow. This is a rare form of color blindness.

- Deuteranopia (1% of males): Lacking the green cones for medium-wavelength cones, those affected are again unable to distinguish between colors in the green–yellow–red section of the spectrum. Their neutral point is at a slightly longer wavelength, 498 nm, a more greenish hue of cyan. A deuteranope suffers the same hue discrimination problems as protanopes, but without the abnormal dimming. Purple colors are not perceived as something opposite to spectral colors; all these appear similarly. This form of colorblindness is also known as "Daltonism" after John Dalton (his diagnosis was confirmed as deuteranopia in 1995, some 150 years after his death, by DNA analysis of his preserved eyeball). Equivalent forms for daltonism in Romanic languages such as "daltonismo" (Spanish, Portuguese and Italian), "daltonisme" (French), "daltonism" (Romanian) are still used to describe color blindess in a broad sense or deuteranopia in a more restricted sense. Deuteranopic unilateral dichromats report that with only their deuteranopic eye open, they see wavelengths shorter than neutral point as blue and longer than it as yellow.

- Protanomaly (1% of males, 0.01% of females): Having a mutated form of the long-wavelength (red) pigment, whose peak sensitivity is at a shorter wavelength than in the normal retina, protanomalous individuals are less sensitive to red light than normal. This means that they are less able to discriminate colors, and they do not see mixed lights as having the same colors as normal observers. They also suffer from a darkening of the red end of the spectrum. This causes reds to reduce in intensity to the point where they can be mistaken for black. Protanomaly is a fairly rare form of color blindness, making up about 1% of the male population. Both protanomaly and deuteranomaly are carried on the X chromosome.

- Deuteranomaly (most common—6% of males, 0.4% of females): These individuals have a mutated form of the medium-wavelength (green) pigment. The medium-wavelength pigment is shifted towards the red end of the spectrum resulting in a reduction in sensitivity to the green area of the spectrum. Unlike protanomaly the intensity of colors is unchanged. The deuteranomalous person is considered "green weak". For example, in the evening, dark green cars appear to be black to Deuteranomalous people. Similar to the protanomates, deuteranomates are poor at discriminating small differences in hues in the red, orange, yellow, green region of the spectrum. They make errors in the naming of hues in this region because the hues appear somewhat shifted towards green. One very important difference between deuteranomalous individuals and protanomalous individuals is deuteranomalous individuals do "not" have the loss of "brightness" problem.

Dichromacy ("di" meaning "two" and "chroma" meaning "color") is the state of having two types of functioning color receptors, called cone cells, in the eyes. Organisms with dichromacy are called dichromats. Dichromats can match any color they see with a mixture of no more than two pure spectral lights. By comparison, trichromats require three pure spectral lights to match all colors that they can perceive, and tetrachromats require four.

Dichromacy in humans is a color vision defect in which one of the three basic color mechanisms is absent or not functioning. It is hereditary and sex-linked, predominantly affecting males. Dichromacy occurs when one of the cone pigments is missing and color is reduced to two dimensions.

There are various kinds of color blindness:

- Protanopia is a severe form of red-green color blindness, in which there is impairment in perception of very long wavelengths, such as reds. To these individuals, reds are perceived as beige or grey and greens tend to look beige or grey like reds. It is also the most common type of dichromacy today. This problem occurs because patients do not have the red cone cells in the retina. Protanomaly is a less severe version.

- Deuteranopia consists of an impairment in perceiving medium wavelengths, such as greens. Deuteranomaly is a less severe form of deuteranopia. Those with deuteranomaly cannot see reds and greens like those without this condition; however, they can still distinguish them in most cases. It is very similar to protanopia. In this form, patients do not have green cone cells in the retina, which makes it hard to see the green color.

- A rarer form of color blindness is tritanopia, where there exists an inability to perceive short wavelengths, such as blues. Sufferers have trouble distinguishing between yellow and blue. They tend to confuse greens and blues, and yellow can appear pink. This is the rarest of all dichromacy, and occurs in around 1 in 100,000 people. Patients do not have the blue cone cells in the retina.