The human retina, under normal living conditions, undergoes irradiance of 10W cm, while direct observation of the sun increases that by 100,000 (Marshall).

A causal relation between certain types of retinal damage and sun watching has long been suspected. It has even been said that Galileo’s visual function suffered as a result of his frequent astronomic observations, since the entry pupil of the eye looking through a telescope is greater than with a bare eye (Silney and Wolbarsht). This damage had been initially assigned to thermal coagulation, but today we know that the increase in temperature faced by the retina is low, normally only reaching around 4_C if the pupil is normally restricted to not over 3mm in diameter (White and Coll). A pupil of 7 mm, as would occur during the observation of an eclipse, can make the temperature rise to more than 22_C; a temperature exceeding what occurs during a laser treatment. In which case, the thermal damage is denounced by the immediate whitening of the retina treated in small focuses. The rise in temperature grows if the exposure is prolonged, but not in a substantial way since the heat production is mitigated by choroidal circulation.

The possibility of UV being responsible for retinal lesions in the rear pole started growing after an observation made in 1902. In welders using an electric arc, a retinopathy, similar to that caused by an eclipse, was observed and often resulted in a macular hole (Naidoff and Sliney). While the rise in temperature may impact the whole eye globe, it bears little importance at the level of the retina. It is possible that the rise of temperature could favor the developing of the photochemical damage (White and Coll). If photochemical damage is produced mainly by short wavelength radiation, especially UV, we should assume that the retina would not suffer any damage from this process since it is situated behind the dioctric and the lens, both of which absorb UV. Additionally, the xantophill present in the plexiform internal and external layers supposedly protects the retina from radiation as it is not only capable of absorbing UV and short wavelength, high energy visible rays, but also offers protection from oxygen related damage (Kirshfeld).

This idea is incorrect. Even if only a small part of UV-A photons get to the retina, they can still start the damage process due to their high energy (Mellerio). This is particularly relevant for younger people whose lenses are more transmissive for this region of wavelengths There are two classes of photochemical damage to the retina; they are simply called type 1 and type 2. The damage of type 1 occurs after many hours of exposure (hours or even days) to non-elevated irradiances, and is usually viewable on vast areas of the retina at the photoreceptor’s level (Noell and coll.). Rats that have been exposed for a few hours a day to the light of a simple fluorescent lamp have suffered this kind of damage. After a single day of exposure to fluorescent lamps, the first elements of a photoreceptor to be attacked are the lamellas, located in the external segments of the cones, which are much more susceptible than the rods to this type of damage (Marshall, Mellerio, and Palmer). The characteristic aspect is that of the “wormed” nature of the phospholipidic membrane. Produced by the lipid peroxidation, it is likely made more sensitive by an endogenous retinal sensitizer--probably rhodopsin or visual pigment (van Norren and Schellekens). This kind of damage can result in color blindness (Howerth and Sperling). It is useful to remember that Arden and his colleagues have noted that ophthalmologists who spend a great deal of time working with argon lasers (green-blue) develop a change in color vision (tritanomalia). Type 2 Damage requires a shorter exposure time and a higher level of irradiance. The lesions are more localized (Ham and coll. Kremers van Norren) and the visual pigment is rapidly whitened and moved away from the photoreceptors towards the pigmented epithelium. Therefore, this kind of damage originates in the retinal-pigment epithelium and might be sensitized by some product associated with the whitening of the photoreceptors (Rapp and coll.). Ham and his colleague have measured the action spectrum of the damage, and have demonstrated that the shorter the wavelength of the light, the greater the sensitivity . As a consequence, Type 2 Damage is sometimes known as “Ham damage” or “blue light damage”. Melanin may be the initial sensitizer, but the action spectrum for blue light damage does not seem to correspond to the melanin absorption spectrum or the spectrum needed for the conversion of oxygen to superoxide in a melanin solution (Sarna and Sealy). In the case of blue light damage, Rapp and fellow colleagues suggested that the mitochondrial enzymes could behave as sensitizers. These organelless in fact are observed to swell significantly under blue light irradiation. Finally, one must remember that even an increase in the fraction of oxygen in air can accelerate the appearance and severity of the damage (Jaffe and coll).



Until recently, the damage caused by radiation to the retina , as compared to the damage to other ocular structures, has been mostly irreversible and untreatable. This retinal damage is most severe in the center of the retina at the macula. This behavior has been demonstrated both experimentally and clinically, but the reasons for it are not clear. In fact, the anatomic peculiarities of the retina in the macular region do not appear to be important, since the damage caused by light appears preferentially in this location even in animal species without an anatomically differentiated macula. The central area of the retina experiences a greater intensity of radiation for optical reasons.

The harmful effects of light associated with the prolonged use of ophthalmic diagnostic instruments or with the use of microscopes are now well known. Protective systems, which have been developed in the last few years, provide relief from these effects. However, it seems that the answer to the question of whether light produces long-term damage to the retina of human beings, still remains open. The epidemiological evidence suggests that it may not be so, while laboratory and other studies have raised doubts about the epidemiological conclusions and tend to support suspicions that long-term exposure to light may well be a causative factor.

Macular degeneration is among those diseases in which a certain level of light exposure is assumed. This disease deteriorates sight by attacking the macular retina, the focal point of visual acuteness. As a result, a blind area obscures the fixation point. The loss in sight occurs because the visual cells, both cones, and rods degenerate and die in the macular area of the retina. Similar to cataracts, macular degeneration is the final result of a deteriorative process that occurs over a time span of decades. Therefore, the probability of its occurrence increases with age. People older than 75, have a 30% probability of suffering visual deterioration due to this disease (Young). About 46-50% of older patients have become blind as a result of age related macular degeneration (Gibson and Coll). Nothing can be done for patients affected with this disease since the central scotomal damage is permanent.

Deterioration occurs in the centrally located external layers of the retina, the layer of the pigmented epithelial cells, and in adjacent cones and rods. Starting from youth, incompletely assembled, residual molecules called lipofuscins start to accumulate in the pigmented epithelial cells. Lipofuscin comes from the substrates of cells, which have been so badly damaged that they have become inassimilable Over time, these sacs of denaturated molecules start to release abnormal secretions from their basal surface, which fill the cells. These abnormal products produce a mechanical distortion in the cell and, interfere with the exchange of fluids and metabolites between the retina and choroids and reduce cellular adhesion. Within a few years, the visual function starts to be affected; sight is lost when the cells of photoreceptors die. This death is a secondary effect resulting from the destruction of pigmented epithelial cells, which the photoreceptors depend upon. Also, blood vessels that invade the increased, abnormal cellular deposits can have destructive consequences.

The same factors which are involved in the deterioration of the lens namely , heat, oxygen, and solar light, also lead to the deterioration of the retina. In the case of the retina ,however, it is the high-energy visible radiation( HEV) part of the solar spectrum rather than the ultraviolet part that is responsible for solar generated damage. It is not that UV photons are not potentially dangerous to the retina , indeed they are the most dangerous; however, they are strongly absorbed before reaching the retina. UV photons are progressively absorbed by the cornea and the lens and do not normally reach the retina. Although, if the lens is removed, as in a cataract operation, and a UV blocking IOL is not substituted, UV radiation can reach the retina and be even more harmful than the HEV radiation (Cech. and Coll., Stamler and Coll., Werner and Coll). It is important to mention that this maculopathy, which could also be called experimental, has a spontaneous tendency to recover within a few months after the onset (Lindquist and coll.).

Higher energy photons, which penetrate and reach the retina, are perceived as violet. As the energy level decreases, violet changes to blue. It is this blue-violet component of solar light that is harmful to the retina; the rest of the visible solar spectrum is less harmful. Experimental studies have provided clues to why the retina may be so susceptible to damage from HEV radiation. It seems related to the following factors: a high concentration of oxygen, the presence of thick layers of lipids , which are sensitive to oxidation, and to the presence of pigmented molecules that serve to absorb photons. Additionally, it is well known that molecular destruction is more likely to start at the energy of blue photons since it is at this level of photon energy for which electron excitation becomes possible.

People with a lot of pigmentation have a lower risk of macular degeneration, which seems logical since melanin absorbs radiation efficiently and releases this energy in the form of heat which is less damaging .

People with cataracts have a lower risk of experiencing macular degeneration as their lenses absorb and dissipate even more of the incident blue/green photons. Studies involving people exposed to strong sunlight for extended periods of time , as were prisoners of war in South-east Asia (Young) and fishermen (Taylor and coll.), confirm that the risk for age related macular degeneration increases in proportion to the duration of their exposure. Even if it seems clear that light is not a causal factor (though it does enhance age related macular degeneration), it is not clear if this disease should be considered as Type 1 damage, because of the decades duration of exposure required, or Type 2, because of the greater danger caused by UV radiation (Mellerio).

The fact that an abundance of melanin present in ocular tissues decreases the probability of suffering from age related macular degeneration is indirect proof of a correlation between exposure to radiation and retinal damage.

In 1985, Weitter and his colleagues conducted a study on 650 subjects affected by senile macular degeneration. The results showed that 76% of the affected subjects had lighter colored irises, and 57% had fair hair. These statistics, when compared to a control group, underline a significant correlation between the prevalence of macular degeneration and color of the iris.

Epidemiological studies have showed that age related macular degeneration is more prevalent in white people than it is in black people. As it has been stated before, radiation absorbed by the lens plays a role in determining the possibility of age-related cataract. Nevertheless, it is surprising how this situation turns out to be protective for the retina. There are documented studies that reveal that in the presence of opacity of the lens, and in particular opacity of the nucleus, the incidence of age related macular degeneration is markedly lower. In a study by Gjessing of Norway in 1953, on a population of 8,694 people of 55 years of age, or 17,314 eyes, the frequency of macular alteration was strikingly lower among subjects who had lenses with impaired clarity .

From the data presented in Fig.11 we can draw an interesting conclusion: radiation absorbed by the lens contributes to the development of age related cataracts, yet these opacities, by increasing the capacity of the lens to filter short wavelength radiation, is an added factor for the protection for the retina. It is interesting that the transmission spectrum of the aged lens is very similar to that of melanin.