 |
Get exposed at your own risk
|
|
|
|
|
If the immediate perception of sun exposure results in a feeling of warmth and well-being, solar rays are responsible for chemical reactions in the skin with often harmful biological effects. The two layers concerned by solar rays are the epidermis and the dermis - 15 % of UVB rays reach the basal layer of the epidermis and more than 20 % of UVA rays penetrate as far as deep in the dermis.
|
|
|
|
After being exposed to the sun, skin pigmentation occurs in two stages:
Immediate skin coloration develops within minutes of being exposed to the sun. This initial tan, which disappears after a few hours, is due to oxidation, by the UVA rays, of the melanin pigments already in the skin.
True suntan only appears after 48 hours, resulting from the synthesis of melanin, a defensive and protective reaction against solar rays. Melanin filters the UVB rays by absorbing them.
(Left) No irradiation. (Right) Active melanin synthesis after irradiation UV.
Eumelanin
in black skin absorbs 90 % of UVB rays, and therefore offers higher protection than the pheomelanin found in very fair skins. The synthesis of these two types of pigment is determined genetically and enables an individual's phototype
to be defined.
Human phototypes
|
| Phototype |
Hair |
Skin colour |
Freckles |
Sun burn |
Tanning |
| 0 |
White |
Albino |
0 |
Constantly |
0 |
| I |
Red |
Milky |
Many |
Constantly |
0 |
| II |
Blonde |
Light |
Yes |
Constantly |
Very light |
| III |
Blonde: Auburn |
Light to dark |
Few |
Frequently |
Light to medium |
| IV |
Brown |
Dark |
0 |
Rare |
Dark |
| V |
Brown |
Brown |
0 |
Very rare |
Very dark |
| VI |
Black |
Black |
0 |
Absent |
Black |
In the hours following excessive exposure to the sun's rays, the skin becomes red, swollen and painful, with genuine burns appearing in extreme cases. Sunburn is essentially produced by UVBs. Initially, cells release molecules, which dilate the blood vessels and begin the inflammation process responsible for the redness and pain. After 24 hours, tissue lesions appear in the epidermis leading to the formation of distinctive "sunburn cells". These keratinocytes, which have entered into a process of apoptosis
(cellular suicide) are eliminated more rapidly than by normal desquamation as the skin peels.
|
|
|
|
Other effects are unvisible and delayed in time. They can be positive as the vitamin D synthesis. But most are harmfull, as the reduced immune defences, the carcinogenic effect, and the cutaneous photo-ageing.
|
|
|
|
Although UV rays are largely harmful to cells, they do have some beneficial effects on the organism. One of these is the synthesis of vitamin D in the epidermis. Short periods of sun exposure - and UVB rays - during summer, is enough to build the body's annual reserves of vitamin D, well-known for the its contribution in preventing rickets. However, some deficiencies are observedeither among people with black skins, or living in regions with little direct sunlight or who constantly remain in the shade. For people with black skins, the melanin absorbs 90 % of the UVBs, not enough rays are able to penetrate the epidermis and trigger the process of synthesising this vitamin. The necessary Vitamin D must therefore be supplied by the diet.
|
|
Zoom
|
|
Fewer atrophied Langerhans cells after irradiation.
|
|
|
Genomic modifications caused by UV rays contribute to the development of malignant cells, which are difficult to eliminate since the sun reduces the level of immune surveillance in the skin. UVA and UVB rays are responsible for reducing numbers of Langerhans cells and altering their morphology. These cells are the skin's guardians, responsible for identifying foreign bodies. In the longer term therefore, lower levels of immunological surveillance have a harmful effect since pre-cancerous cells can no longer be eliminated.
|
|
|
|
Ultraviolet rays can trigger off the formation of free oxygen radicals in the cellular cytoplasm. These radicals are powerful oxidants, attacking various components of the cell including lipids, proteins and DNA. The main targets are the lipids, essential components of the cell's internal and external membranes. Once oxidized, these cellular membranes stiffen and are no longer capable of adapting to changes in their environment.
The DNA, containing the record of the cell's genetic heritage, is also targeted by free radicals which bring about lesions in the genetic material. These lesions are normally eliminated by the cell's own repair machinery, but if they are overwhelmed by excessively long or excessively frequent exposure, they lose their efficacy. The lesions will then become mutations, leading to imperfect transmission of genetic codes and thereby create irreversible disturbances in the cell's activities.
When exposure to the sun is intense and frequent, the cell's repair mechanisms are no longer able to eliminate the lesions and DNA mutations become apparent. Affected cells can then multiply uncontrollably and become cancerous.
The UVA and UVB rays reach the keratinocytes in the basal layer, those which divide and differentiate to finally form the upper layer of the epidermis. If the process of cellular division is affected, skin cancer may develop. The keratinocytes are thereby responsible for the most common cancers, although melanocytes can also degenerate into melanoma, which is rarer but more dangerous.
Three types of skin cancer have been identified - basocellular cancers, spinocellular cancers affecting the keratinocytes and malignant melanoma, cancers of the melanocytes.
The occurrence of melanoma varies according to phototype, the risk of developing such a cancer being higher among fair-skinned people with blond or red hair who are more prone to sunburn. But it can also occur among people who have frequently suffered sunburn before the age of 15. The melanocytes have the particular characteristic of only dividing once every five years and are not fully mature before the age of puberty. They are therefore particularly sensitive to any excessive sun exposure during childhood, which is why sunburn can be particularly dangerous for children.
|
|
Zoom
|
|
Collagen and elastin fibre aggregates after UVA irradiation
|
|
Deep wrinkles characteristic of solar elastosis.
|
|
|
UV and especially UVA rays bring about a premature ageing of the skin, known as cutaneous photoageing. The harms caused to the skin resulting from this sun-induced ageing are different from and added to those of natural ageing. They involve changes in the skin clinically characterised by wrinkles, roughness, a lack of elasticity, depigmentation or hyperpigmentation marks and a variety of benign or malignant tumours. Although exposure to the sun enables the quality of the horny layer to be improved, this is only a short-term benefit. Over time, the rate of thickening diminishes, and ultimately the sun brings about epidermal atrophy. On the surface, the process of keratinocyte maturation is disturbed and corneocyte desquamation is delayed. Furthermore, disorganisation of melanocytes can result in the creation of pigmented marks.
In the event of repeated exposure to the sun and UVA rays, fibroblasts number diminishes. These cells become atrophied, gradually losing their capacity to produce collagen while at the same time their ability to digest it increases. The elastin fibres synthesised by the fibroblasts are also modified - produced in large quantities, they are unable to become attached to the collagen and gather in clusters. These form small white lumps which can be seen beneath the surface of the skin surrounded by the network of blood vessels which also become visible, giving the skin a reddened aspect punctuated by white spots. The skin, which has now lost its elasticity, slackens and deep folds appear in the flesh. These are the symptoms of solar elastosis, which can take months or even years to appear.
|
|
|
|
|