I. The properties and biological effects of light Sunlight is a continuous wave of electromagnetic radiation, a form of energy, with fluctuations (light waves) and particles (photons) two properties. Distinguished by wavelength from short to long, sunlight is mainly composed of cosmic rays, X-rays, ultraviolet, visible light, infrared, microwave and radio waves. The shorter the wavelength, the greater the energy. After the sunlight passes through the atmosphere, only 2/3 of the energy reaches the earth’s surface, including visible light, part of the infrared and ultraviolet, of which ultraviolet light accounts for about 5%. The wavelength range of ultraviolet light is 100 to 400 nm. usually divided into: short-wave ultraviolet (UVC), wavelength 100 to 290 nm; medium-wave ultraviolet (UVB), wavelength 290 to 320 nm; long-wave ultraviolet (UVA), wavelength 320 to 400 nm. in recent years, UVA has been divided into UVAI (340 to 400 nm) and UVAII (320 to 340 nm). 340nm). Visible light wavelengths are 400 to 760 nm. All of the UVC in the sun’s ultraviolet light is absorbed by the atmospheric ozone layer and cannot reach the earth’s surface. Artificial light source UV sterilization lamp wavelength is 254nm, can be absorbed by DNA, RNA, cell protein and stratum corneum, can kill living cells, and used for sterilization. UVB can not pass through the glass, because it is easy to cause acute or delayed erythema, so it is also called sunburn spectrum, can also cause pigmentation, photoaging and skin cancer. UVA can pass through glass and cannot be seen by the naked eye, but can cause fluorescence of certain substances. In the presence of certain photosensitive substances and light skin diseases produce skin reactions. Therefore, UVA and UVB are the main pathogenic spectra of light-based dermatoses. The process of biological reaction caused by light absorption by tissues is known as cutaneous photobiologic reaction (cutaneous photobiologic reaction). At room temperature, all molecules are in a low-energy state, i.e. the ground state. Special molecules or chromophores in the skin, such as nucleic acids, urocanic acid, aromatic amino acids (proteins), porphyrins and pigment precursors in the epidermis, absorb the energy of light (photons) and the molecules in the ground state are transformed into a high electronic state, usually called the excited electronic state. state). The excited state of a molecule is not stable and can undergo a chemical change in an instant (10-7 to 10-5s) to form a photo product, while transferring energy to other molecules in the vicinity, or returning to the ground state after releasing energy in the form of heat or fluorescence. This initiates complex biochemical processes such as enzyme repair, ion flow, induction of gene products and initiation of DNA replication. The accumulation of these biochemical reactions results in histological effects such as proliferation, mutation, loss of cell surface markers and intoxication. Eventually, photobiological effects can be observed, i.e., the ability to cause skin erythema, hyperplasia, and tumor induction, among others. There is some evidence that DNA damage and repair are associated with the release of cytokines and inflammatory mediators in the skin after UV exposure. These substances regulate the cellular activity of many cells, including keratin-forming cells, epidermal Langerhans cells (LCs), vascular endothelial cells, fibroblasts and lymphocytes, thus causing physiological and clinical changes. It is believed that 90% of the aging appearance of exposed skin is the result of sun-induced “photoaging”. A large number of epidemiological data show that the ultraviolet portion of sunlight, especially UVB and the occurrence of skin photoaging is closely related, but UVA, although less biologically active than UVB, UVA exists in large quantities in sunlight, especially in the summer daylight can be 1000 times UVB, and has a deep penetrating power, can have an impact on fibroblasts and connective tissue, while research shows that UVA has strengthen the role of UVB, so the role of UVA in the photochemical damage of the skin can not be ignored. The skin of photoaging is characterized by skin laxity, hypertrophy, and deep and coarse wrinkles, and diamond-shaped skin can be seen in the neck of long-term outdoor workers. Other manifestations include local hyperpigmentation and capillary dilation, presenting a “weathered” appearance, while various benign, pre-cancerous or malignant tumors can occur in the skin, such as heliokeratosis, squamous cell carcinoma, mesenchymal carcinoma and melanocytoma. Skin photoaging is different from natural aging. If reasonable photoprotection measures are taken, the effects of UVA and UVB on the skin can be blocked to prevent photochemical skin damage. Second, UV sources and exposure dose measurement 1, humans receive most of the UV from sunlight, other sources are artificial light sources, such as fluorescent lamps, incandescent lamps, xenon arc lamps, mercury arc lamps and medical phototherapy systems. The amount of individual exposure to UV dose is related to the surrounding UV intensity, clothing wear and whether to use sunscreens. 2, the measurement of exposure dose: the unit of energy of light is joule (J), the biological dose unit is J/m2, the biological effect caused by light exposure is generally expressed in terms of the minimum erythema dose (minimal erythema dose, MED). MED is just perceptible erythema after 24 hours of UV exposure (just perceptible erythema, JPE). erythema (JPE) or the minimum dose required for a clearly defined erythema after 24 hours. Recent studies have shown that the MED dose is judged by JPE, and the error is much smaller. Third, the role of UV on normal skin and the defense function of the skin 1, the acute effect of UV radiation can cause a series of changes in the skin, mainly including erythema (sunburn inflammation), pigmentation (tanning), local (skin) and systemic immunosuppression, thickening of the stratum corneum, epidermis, dermis, and vitamin D photosynthesis. The most significant of these are the production of erythema and hyperpigmentation. (1) UV skin erythema and tanning: rapid appearance of transient skin erythema within 1 second or a few seconds after UV exposure, i.e. rapid erythema (common in animals and humans with type I and II skin); or the appearance of brownish gray pigment (easily seen in darker skin tones), called rapid pigment darkening (immidiate pigment darkening, IPD). This is followed by delayed erythema, which peaks at 6 to 24 hours depending on the dose and lasts for one or several days; the erythema fades to produce delayed pigmentation (tanning), i.e., new melanin formation, which occurs clinically 72 hours after exposure. UVB and short-wavelength UVA can directly damage the DNA of skin keratin-forming cells, resulting in the synthesis and release of many inflammatory mediators and cytokines, among which the pharmacological mediators that produce erythema are arachidonic acid products (eicosanoids), histamine, bradykinin, prostaglandins, cytokines and other chemokines. cytokines and other chemokines, which together regulate the expression of adhesion molecules in vascular endothelial cells and keratin-forming cells, thus causing the aggregation and activation of monocytes and neutrophils in the skin, resulting in erythema due to vasodilation and inflammation. Biphasic hyperpigmentation after UV exposure is a protective response of the skin. The changes leading to IPD are due to oxidation of melanin and redistribution of melanosomes in melanocytes from the perinuclear to the peripheral dendrites. The function of IPD is not well understood and may have a specific role in preventing damage to the basal cell nuclei; delayed tanning is due to increased melanin synthesis and accelerated transport to keratin-forming cells as a result of increased activity and number of epidermal melanocytes after UV exposure The result of this is the increase in melanin synthesis and its transport to keratin-forming cells. However, the erythema effect decreases rapidly with increasing wavelength, and UVA with energy equivalent to 1000 times that of UVB can produce the same erythema effect, so usually the erythema effect of skin is mainly due to UVB. Erythema still plays an important role, the role of UVA in the strongest sunlight accounts for about 15%, and when the sun position is low, UVB in the atmospheric attenuation, then the role of UVA increased, causing skin tanning effect spectrum similar to the erythema effect spectrum, but UVB irradiation skin pigmentation increase in 72 hours can be seen, and usually quickly fade; UVA irradiation tanning time occurs earlier, the duration is long, and thus the effect is stronger. UVA irradiation has a much earlier onset and longer duration, and thus has a stronger effect. Individual differences affecting the erythema and tanning response of human skin are largely genetically determined and the mechanism is not yet clear. Recent studies have suggested a possible association with melanocyte stimulating hormone (MSH) receptor polymorphisms. Other influencing factors are the pigmentation of the irradiated skin, thickness, antioxidant status of the skin, humidity, age and anatomical location. According to the degree of acute skin reaction to sunlight, human skin is classified into sun-reactive skin types I to VI (see table). Chinese people have the most type IV (81.1%), followed by type V (13.3%) and type III (5.6%). Type III was predominant among Americans (63, 0%), followed by Type II (21, 0%), and Type II and III were also predominant among the British. The typing of sun-reactive skin type typing sun spot reaction tanning reaction skin color sensitivity I very easy to occur (heavy) does not occur (-) white very sensitive II very easy to occur (moderate) rarely occurs (very light) white very sensitive III sometimes occurs (light) sometimes occurs (light brown) white more sensitive IV less often occurs (very light) often occurs (brown) light brown light sensitive V rarely occurs (±) very easy to occur ( Dark brown) brown less sensitive VI does not occur (-) black black not sensitive (2) Hyperplasia of the skin after UV exposure: The increase in the erythema threshold of the skin after UV exposure is not only due to tanning, but also as a result of hyperplasia of the dermis, epidermis and stratum corneum. Sunlight-induced hyperplasia occurs 24 to 48 hours after acute UV irradiation and is mainly associated with increased mitosis of epidermal and dermal cells (dermis is weaker), but also with increased DNA, RNA and protein synthesis. The mechanism is not well understood, but several UVB-induced inflammatory mediators, especially TGFα and ornithine dehydrogenase, can be induced to produce the same keratin-forming cell proliferation. A single UVB irradiation can cause an increase in epidermal thickness and the proliferation returns to normal after about 6 weeks, whereas a single UVA irradiation does not cause an increase in epidermal thickness, and multiple repeated irradiations may cause an increase in epidermal thickness, but it is weaker than UVB. UVB-induced hyperplasia is also a protective response of the skin to UVB, which is especially important for those with white complexion and vitiligo. (3) Photosynthesis of vitamin D in the skin after UVB exposure: UVB exposure promotes vitamin D3 synthesis through photochemistry, which is the only positive beneficial effect of UVB on the skin. This process starts with the absorption of 7-dehydrocholesterol in the epidermis at a wavelength of <320nm, which is converted into vitamin D3 precursors, and then the heat-absorbing isomerization of vitamin D3 precursors to form vitamin D3. 2. Chronic effects Long-term exposure to large amounts of sunlight (mainly UV) can cause chronic changes in the skin, mainly photoaging and skin cancer. Photoaging is a skin change caused by prolonged and severe exposure to sunlight, with the typical clinical manifestations being skin hypertrophy and wrinkling, yellow nodules and dilated capillaries. Photoaging may be related to UV-induced epidermal and dermal hyperplasia. UV-induced skin cancers are mainly solar keratosis, basal cell epithelioma, squamous cell carcinoma and malignant melanoma. UV carcinogenesis may be related to the damage to DNA molecules, the body's ability to repair DNA damage and the immunosuppressive effect of UV light, which reduces the body's immune surveillance role. Some diseases are sensitive to UVA and even visible light, including ordinary fluorescent lamps, and need absolute light avoidance. As far as possible to find out photosensitizers, in daily life and work environment to avoid re-exposure, exposure or take. 2, sunscreening agent (sunscreening) use requires high photoprotection index (SPF), stable and long-lasting effect, non-toxic and non-alterative and easy to use. Commonly used: (1), chemical shading agents can absorb UVB and / or UVA, such as p-aminobenzoic acid (PABA), PABA ester and its derivatives, phenol derivatives, cinnamic acid, salicylic acid and tannic acid compounds. (2), physical shading agents can reflect or scatter the entire UV band and visible light, such as titanium dioxide, zinc oxide, kaolin, etc., which can be appropriately added to iron oxide red and iron oxide brown and other pigments to make patients happy to use. The effect of the mixture of several shading agents is often better, such as PABA, dimethyloctyl and benzophenone, dihydroxyacetone and naphthoquinone, etc., the shading range is improved and has a better anti-wash effect. Shading agents should be applied evenly to the exposed skin 10-15 minutes before going out; for people with whiter skin prone to sunburn, high-efficiency shading agents with SPF>15 should be used, while people with darker skin pigmentation should apply medium-effect shading agents (SPF=6-8). 3, medication Vitamin B, especially nicotinamide (NAA) orally has the effect of reducing skin photosensitivity; antimalarial chloroquine and hydroxychloroquine in small intermittent doses are often effective for certain polymorphic heliotrope and porphyria; antihistamines are still needed during the attack, and sometimes corticosteroids or immunosuppressants such as azathioprine are needed to control severe cases. Beta carotene, which absorbs 360-600 nm spectrum, is effective for certain porphyrias and polymorphic heliotropic rashes. 4, other such as PUVA therapy, cyclosporine oral, etc., have been reported to be effective for certain polymorphic heliotropic rash, persistent photoreactivity and photochemical reticulocytosis, etc.