beauty

Sunlight: Effects of light on the skin

UV sunlight

The solar spectrum is formed by electromagnetic energy, with a wavelength ranging from 200 to 1800 nanometers (nm).

The shortest wavelengths, which reach the earth, are ultraviolet (UV) radiations, which are divided into UVC (200-290 nm), UVA (320-400 nm) and UVB (290-320 nm); in particular:

  • UV-C (100-280 nm): they have very high energy but are filtered by atmospheric ozone and do not reach the earth's surface
  • UV-A (320-400 nm): these are the least energetic rays (the energy is inversely proportional to the wavelength), but they manage to penetrate to the dermis where they can damage collagen and elastin. UV-A radiations promote the maturation process of melanin already present in melanosomes transferred to keratinocytes: these radiations are therefore responsible for the immediate pigmentation of the skin, which appears already during exposure to the sun and regresses within 2-3 hours ("Meyrowsky phenomenon")
  • UV-B (280-320 nm): they induce the most common biological reactions due to sun exposure, they are erythematogens and they are the real responsible for a long-lasting tan, because they stimulate melanogenesis, which continues even after exposure.

Numerous variables influence the quality of irradiation: season, altitude, latitude, time of day and also humidity and atmospheric pollution. With regard to altitude, its increase of 1000 m determines an increase of 15-20% of UVB rays, while UVA rays do not undergo modification. The reflection of UV radiation takes place from the sky, clouds, soil and this phenomenon is particularly evident if you are in the presence of snow (with fresh snow 80% of the light is reflected, with old snow 50 %), dry sand (24%), water (9%) (3V Cosmetic division technical report No 3 Edition 1/1).

Until a few years ago, the focus was mainly on UVB, as responsible for the immediate and visible effects of solar radiation on the skin. Today, instead, there is the awareness that UVAs, being more penetrating, are more correlated to the formation of skin tumors, to photoaging, to photoimmunosuppression and to phototoxicity and photoallergy phenomena.

Effects of sunlight on the skin

The radiations that reach the skin are partly reflected by the stratum corneum and partly absorbed and transmitted to the structures of the epidermis and dermis.

Their ability to penetrate the epidermis and their effects depend on the wavelength: the larger this is, the lower the frequency, therefore the greater the penetration; consequently the UVA, shorter wavelength rays, have greater penetration capacity and can cause greater damage over time; UVB are instead the rays mainly responsible for immediate damage, such as skin rash or burns.

When the skin is irradiated, some biological responses are activated:

  • the stratum corneum begins to thicken (hyperkeratosis) following an increased mitosis of the basal cells of the epidermis, in order to protect the skin from UV radiation;
  • b-carotene, an antioxidant molecule that acts as a singlet oxygen silencer and as a membrane stabilizer, starts to accumulate;
  • there is secretion, with eccrine sweat, urocanic diacid, a molecule deriving from the deammination of histidine, capable of absorbing UVA rays;
  • the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH) are activated, as scavengers of reactive oxygen forms;
  • DNA repair and replication mechanisms are activated;
  • the main mechanism of UV self-protection is activated: pigmentation . First an immediate and transient pigmentation induced by UVA rays and Visible light is produced, which starts after a few minutes from the first exposure and lasts 24-36 hours. This first tan is due to the photo-oxidation of the melanin already present in the melanocytes, but the resulting color is ephemeral and has no protective function. Two days after the first exposure, time required for melanocytes to produce melanin, delayed pigmentation begins in response to UVA and UVB rays (P. Kullavanijaya, HWLim "Photoprotection" J Am Acad Dermatol 2005; 52: 937-58);
  • the production of vitamin D in the layer of spiny cells (anti-rachitic action) is induced by UVB rays.

In addition to the anti-rachitic action attributable to ultraviolet rays, the sun has further beneficial effects, such as a disinfectant action at the level of the skin and an anti-inflammatory action against atopic dermatitis and psoriasis.

However, when the exposure is excessive, the physiological responses are insufficient and the sun's rays can cause harmful effects such as:

  • acute erythema due to vasodilation of the papillary dermis microcirculation and to the production of inflammatory substances by keratinocytes.
  • The hyperkeratosis which, on the one hand is a physiological response of the organism, on the other hand can reach pathological levels if it affects not only the stratum corneum, but the epidermis in its entirety and the superficial dermis. The hyperkeratosis typically develops in the areas more exposed to ultraviolet rays. Very often it is associated with other signs of photodamage and skin aging, such as actinic elastosis, deep wrinkles or solar freckles.
  • Actinic photoaging (photoaging) or solar elastosis: this is an alteration with an exclusive hypertrophic character of photoexposed skin, with aspects of proliferative disorder that can sometimes give rise to neoplasia.

The most significant histopathological features are found at the level of the dermis, where UVA rays can penetrate; the dermis takes on a yellowish color, is strongly thickened, with similar-reparative areas and makes the skin inelastic and lacking in tone. On a histological level, there are a number of changes in both the constituents of the extracellular matrix and the dermis cells. The collagen is degraded, the fibrillar proteins suffer a serious depletion, the elastic fibers become abnormal, tortuous and there is an imbalance of their components; fibroblasts increase in number. Histiocytes and mast cells are also more numerous and the latter release mediators that favor fibroblast proliferation and leukocyte chemotaxis. Melanocytes are irregularly dispersed along the basement membrane and Langerhans cells are significantly reduced. The blood vessels are tortuous and dilated. All this imbalance could be due both to the production of reactive oxygen species (ROS) induced by UVA, and to damage to the DNA level caused by UVB. As a consequence there is generally a defective structural organization and an irregular dermo-epidermal junction for the development of papillae and crests of irregular shape and size. In particular, UVB rays cause direct damage to the DNA of keratinocytes, with the formation of thymine dimers that bring cells to programmed death; moreover they are more responsible, compared to UVA, for the onset of skin neoplasms other than melanoma (basal-cell and spino-cell carcinomas).

More recently, the harmful effects of UVA rays associated with the formation of oxidative species, which cause immunosuppression, oxidative DNA damage, induction of specific mutations in oncogenes, have also been identified: these phenomena are attributed a direct role in the pathogenesis of melanoma mainly associated to sporadic exposure to the sun in the first years of life (S.Lautenschlager, HCWulf, MRPittelkow "Photoprotection" Lancet 2007; 370: 528-37).

It emerges that the skin damages caused by UV rays are caused both by UVB and UVA and this is why it is agreed that complete protection is essential, shielding both UVB rays, which are responsible for direct damage to the skin, and UVA, preventing indirect damage to the epidermis and dermis in the long term.