They say that the fashion for tanning was instilled in the Parisians by the legendary Coco Chanel, when she returned from a Mediterranean cruise, struck the pale Parisian beauties with a bronze tan. Soon, capricious fashion made a turn of 180 °, and the ladies who had not previously left the house without wide-brimmed hats, long gloves and veils, went to the beaches, where they first timidly, and then boldly bared their bodies, substituting them for the hot rays of the sun.
According to another theory, the fashion for sunburn appeared when pale skin became associated with heavy work in closed premises of factories and plants, and sunburn became the privilege of those who could afford to spend a lot of time outdoors, resting and playing sports. Be that as it may, in almost all European countries and in America, a tan turned into a symbol of health and an active lifestyle, and so many people, especially at a young age, were lying under the scorching sunbeams to burns and dizziness, trying to get it.
In America, the generation that became so actively friends with the sun was a generation of people born during the postwar boom in the 1940s and 1950s or by the baby boomers. Years went by, and the doctors began to notice that the aging of the skin of the baby boomers has its own peculiarities - sharp wrinkles, irregularity, tuberosity of the skin, pigment spots, the presence of the areas of densified skin and the branches of dilated vessels on the cheeks. Such changes are found only in areas subjected to increased solar irradiation, while in places usually protected from the sun (for example, in the lower abdomen on the inner thighs, etc.), the skin tends to look much better. It took careful research before the doctors came to a unanimous conclusion - not age, but solar radiation is responsible for the appearance of these signs. As it turned out, UV radiation, although it does not have such destructive effects as ionizing radiation, nevertheless has enough energy to cause damage to DNA and other skin molecules.
Now, the following signs of sun damage to the skin, or photo-staining:
- wrinkles appearing in the areas of collagen damage;
- uneven skin, occurring in areas of accumulation of atypical elastin (soyaellic elastosis);
- dry skin;
- expansion of surface vessels (telangiectasia);
- pigment spots (solar lentigo);
- actinic, or sunny, keratosis (patches of reddish condensed, flaky skin).
Most often photoaging is observed in light-skinned people aged after 50 years as in people with a swarthy skin it appears less often. The concept of photoaging has revolutionized cosmetology. Before that, scientists believed that neither aging can be prevented nor the aged skin rejuvenated and that all attempts to create a means that smooth wrinkles or restore the radiance of youth are doomed to failure in advance. It turned out that the skin, damaged by the sun, keeps a reserve of vitality that can be awakened. Now a number of tools and methods have been developed that can partially eliminate the signs of photoaging. Although they are all advertised as a means of "wrinkles" or "from aging", one must understand that in this case it is not a question of true rejuvenation, but of "treating" (more accurately - restoring) the skin damaged by the sun.
To date, extensive information has been accumulated about the negative effect of ultraviolet action on the skin. The ultraviolet spectrum is represented by three groups of rays.
- Ultraviolet rays C (UVC, short UV, far UV) - rays with the shortest wavelength (100-280 nm). They have the most damaging effect on the human body. However, their influence is minimal, since they are adsorbed by the ozone layer and practically do not reach the earth's surface
- Ultraviolet rays B (UVB, mid UV) are rays with an average wavelength range (280-320 nm). They damage the skin as much as possible, but their effect is significantly weakened by cloudiness, and penetration is delayed by clothing and ordinary window panes. Adsorption and dispersion of UVB in the atmosphere is observed when the sun is low near the horizon (early morning and late evening), at high latitudes, and also in winter.
The smallest absorption and dispersion of these rays is observed on a half day, at low latitudes and in summer.
- Ultraviolet rays A (UVA, long UV, near UV, black light) - rays with the largest wavelengths (320-400 nm) The damaging effect of UVA is 1000 times weaker than UVB. However, they reach the surface of the earth much better, and their penetration does not depend on the time of day, latitude and season. It is known that these rays are not retained by the ozone layer, the clothes are not tinted through the clouds. That is why many modern buildings use tinted glass, which is not only a certain architecture and aesthetic solution, but also a protection against UVA.
The source of ultraviolet radiation is not only the sun, but also the solarium lamps. It is believed that a small fraction of the ultraviolet can produce gas-discharge lamps. With regard to fluorescent lamps andhalogen lamps, television screens and computer screens, they are not sources of ultraviolet radiation. It is important to remember that white sand, snow, water reflect up to 85% of solar radiation. Therefore, staying on the beach or in the mountains, a person receives almost twice as much energy due to reflection and scattering of rays.
Ultraviolet rays A and B differ in the depth of penetration into the skin - it is directly proportional to the wavelength. It is known that 90% of UVB is blocked by the stratum corneum, while UVA is able to penetrate deeper layers of the epidermis and more than 50% of them can enter the papillary and reticular layers of the dermis. For this reason, when the rays B are exposed, the epidermis changes, and when the rays A are affected, the structural changes in the basic substance of the dermis, its fibrous structures, microcirculatory bed and cell elements.
The mechanisms of action of ultraviolet rays on the skin and their consequences have been thoroughly studied. It is known that UVC have a pronounced mutagenic effect. UVB causes sunburn, in part, sun tan. The main negative consequence of UVB is the proven carcinogenesis, which is induced due to cell mutations. Ultraviolet rays A cause pigmentation of the skin, i.e. Sun tan. These rays are the least erythemogenic, which is why this spectrum of ultraviolet radiation is represented in the lamps of solariums. UVA, as well as UVB, cause carcinogenesis, while the potentiating effect of rays A on rays B is known. Some researchers believe that rays A play a greater role in the development of melanoma than rays B. In this connection, it is necessary to emphasize the importance of using sunscreens means from the action of rays A and B simultaneously.
The combined effects of ultraviolet rays on the skin include a number of morphological changes. So, influence on the proliferation and differentiation of keratinocytes, fibroblasts, melanocytes (stimulation of alteration of cellular elements, violation of DNA repair) is known. It is proved that the combined effects of rays A and B lead to a number of serious violations of local immunological surveillance. In particular, the development of a number of immunosuppressive cytokines in the skin (for example, IL-10), a decrease in the number of killer lymphocytes involved in the elimination of tumor cells, the appearance of CD8 lymphocytes stimulating apoptosis of Langerhans cells, induction in the epidermis of trans-cisomerization of urocanic acid (endogenous component, to which the immunosuppressive effect is attributed). In addition, UVA are the main cause of the development of photosensitivity. Most dermatoses associated with increased congenital or acquired sensitivity to ultraviolet light, arise or exacerbated by the action of the longwave spectrum. Such dermatoses include photoallergic reactions, porphyria, solar urticaria, lupus erythematosus, pigmentary xeroderma and other diseases.
It should be especially emphasized that ultraviolet rays A are associated with the growth of the skin aging - photo-aging. It is characterized by certain morphological manifestations, different from biological aging. Under the influence of UVA in the epidermis there is an uneven thickening of the stratum corneum and the epidermis itself as a whole due to uneven acceleration of basal keratinocyte proliferation and disruption of keratinization processes. Dysplasia of keratinocytes develops. In the dermis, chronic inflammation is formed, fibrous structures are destroyed, especially elastic fibers (homogenization, thickening, twisting and fragmentation of elastic fibers, reduction in their diameter and quantity - "solar elastosis"), serious changes in small-caliber vessels occur. The latter subsequently leads to the restructuring of the microcirculatory bed and the formation of telangiectasias
It is known that prolonged exposure to UVA, for example excessive use of tanning salons, causes structural changes in the skin, similar to prolonged exposure to the sun. It is appropriate to emphasize the importance of dosed use of tanning beds.
Isolate acute and chronic ultraviolet effect, causing various clinical manifestations.
Clinical signs of acute ultraviolet exposure include sunburn and skin pigmentation. Sunburn is a simple dermatitis and is manifested by erythema and edema (1 st degree) or erythema and the formation of blisters (2nd degree). The third degree burn is extremely rare, mainly in infants, and is accompanied by heat shock. It is believed that the occurrence of sunburn of the 1st degree is possible if a person within 24 hours received 4 minimal erythematous doses, and 2 nd degree - 8. Pigmentation, or sun tanning, is instantaneous and delayed. Instantaneous darkening of the skin occurs a few minutes after insolation and is associated with the photoxidation of the already synthesized melanin and its rapid redistribution into dendrites of melanocytes and, subsequently, into the epidermal cells. Delayed pigmentation occurs after 48-72 hours and is associated with active melanin synthesis in melanosomes, an increase in the number of melanocytes and activation of synthetic processes in previously inactive melanocytes. These changes are a reflection of the protective properties of the skin in response to ultraviolet radiation. Delayed pigmentation can also be explained by the formation of secondary post-inflammatory pigmentation as a result of simple dermatitis or a burn.
Clinical signs of chronic exposure to ultraviolet radiation are as follows: vascular changes, pigmentation disorders, new skin formation, changes in turgor, elasticity, skin pattern. Vascular changes as a result of chronic UV exposure are presented by persistent diffuse erythema, the formation of telangiectasias, and ecchymoses in areas most prone to irradiation (face, hands, parietal and occipital areas, posterior surface of the neck, etc.). Disturbances of pigmentation are manifested in the form of freckles, sun lentigo, dyschromia, chronic drop-shaped idiopathic hypomelanosis and poikiloderma. This complex of clinical manifestations, along with the signs of photoaging, was named in the English-language literature "sun-damaged skin" ("sun-damaged skin"). Excessive UFD is most often associated with the development of skin tumors such as actinic keratosis, basioma, squamous cell carcinoma, melanoma.
Changes in turgor, elasticity and skin pattern are the basis for photoaging. Clinically photoaging is manifested by dry skin, its coarse, accentuated skin pattern, decreased turgor and elasticity of the skin. The consequence of these changes are shallow superficial and deep wrinkles. In addition, during photoaging, a yellowish skin tone, dyschromia, lentigo, telangiectasias, seborrheic keratoses, comedo senilis are noted. It is noteworthy that the complex of changes in the skin associated with the chronic exposure of UFOs is well described in dermatology as early as the beginning of the last century (for example, "skin of seamen", "peas skin", "rhomboid neck atrophy", Favre-Racouchot disease, etc.) .
When assessing the nature of age-related skin changes, it is important to take into account the type of aging. Morphological and clinical signs of photoaging have their own characteristic picture, which differs from that in other types of aging.
, , , , , , ,