Sunlight consists of a spectrum of several visible and invisible types of radiation with wavelengths ranging from 280 nm to 3000 nm. Radiation emitted by the sun is partly absorbed by the ozone layer, by clouds and by air pollutants.
The most important in terms of pathological damage to the skin are the invisible UVA and UVB rays (i), which stimulate the body's own photoprotective mechanisms in the different skin layers. According to leading photobiologists the shortwave UVC radiation, which has strong erythematogenic and carcinogenic effects on human skin, is completely absorbed in the stratosphere and atmosphere and never reaches the earth's surface.
Some types of radiation reach the earth directly and others indirectly after being scattered in the different layers of the earth's atmosphere. The amount of scattering depends on the wavelength: the shorter the wavelength, the greater the scattering. Only small doses of sunlight are needed to have positive effects on the human organism. The damage from UV radiation also decreases with less sun exposure.
UV rays and their effect on the skin
With increasing wavelengths both the percentage of penetrating radiation and the depth of penetration increase. At 300 nm, which is in the UVB region, 10 percent of the radiation still reaches the basal cell layer of the skin.
The highly erythematogenic UVB rays (i) are the main cause of DNA damage and sunburn (erythema solare), the most common acute light-induced damage. They are additionally responsible for epidermal changes accompanying chronic, light-induced damage.
The skin-burdening UVB portion of sunlight is influenced by geographical factors such as latitude and altitude (alpine, coastal regions, etc.), as well as the time of day and level of air pollution. Thinning of the ozone layer in particular has led to a rise in UVB radiation.
UVB radiation acts as a local immunosuppressant by damaging the Langerhans cells, which are responsible for antigen presentation in the epidermis. Langerhans cells respond to UV radiation by leaving the epidermis. Immunological studies on persons after prolonged exposure to UVB radiation reveal an additional, systemic immunosuppression. It is assumed that keratinocytes in the epidermis release immunosuppressive factors to the immune system.
UVA rays (i) penetrate as far as the connective tissue and cause changes in the dermis which can result in irreversible long turn damage, e.g. premature skin ageing (photoageing (i)). In addition, they are primarily responsible for the formation of cell-damaging free radicals (i).
Distribution of Langerhans cells (dark-coloured)
Other dermatological impacts of UVA radiation:
Most important trigger of sun allergy - polymorphous light eruptions (PLE)
PLE is the most common sun-induced skin disease. The formation of free radicals (i) induced by UV radiation is considered a causative factor in this disease which occurs mostly in younger women.
Photoallergic and phototoxic skin reactions
Photoallergic and phototoxic reactions can be triggered by chemical substances - including certain active ingredients in sunscreen and skincare products - under the influence of sunlight and/or by staying in the sun when taking certain medications.
Formation of free radicals (i) (oxidants)
UV radiation, particularly UVA, triggers skin damage through the formation of free radicals (i). Free radicals are chemical compounds with a free electron that are highly reactive. Free radicals damage the cells of the epidermis and dermis. The cumulative action of these processes over years gradually leads to the signs of chronic light-induced damage. They are also considered triggers polymorphous light eruptions (PLE).
Action of radical scavengers
A Free radicals
B Radical scavengers