Exposure of skin to ultraviolet radiation from sunlight presents both positive and negative health effects. On the positive side, UV exposure enables the synthesis of vitamin D3, which is essential for bone health [1] and potentially plays a role in inhibiting certain cancers. [2] [3] While vitamin D can also be obtained through dietary supplements, [4] UV exposure offers benefits such as enhanced subdermal nitric oxide production and improved endorphin levels, which are not achievable through supplementation alone. [5] [6] [7] [8] [9] Additionally, exposure to visible light supports melatonin synthesis, maintains circadian rhythms, and reduces the risk of seasonal affective disorder. [10]
However, UV radiation is also a mutagen and carcinogen for the skin, posing significant risks. [11] [12] Acute exposure can lead to painful sunburns and increase the likelihood of developing serious skin conditions later in life. [13] Prolonged exposure is associated with the development of skin cancers, photoaging or premature skin aging, immune suppression, and eye diseases like cataracts. [14] [15]
Given these dual effects, public health organizations emphasize the importance of striking a balance between the benefits and risks of UV exposure. They recommend avoiding sunburn at all costs and advocate for moderation in sun exposure to minimize the risks associated with UV radiation while still reaping its health benefits. [16]
UVB radiation with a wavelength of 290–315 nanometers penetrates uncovered skin and converts cutaneous 7-dehydrocholesterol to previtamin D3, which in turn becomes vitamin D3. [17] [18] [19] UVB radiation does not penetrate glass, so exposure to sunshine indoors through a window does not produce vitamin D. [20] Time of day, time of year, geographic latitude, ground altitude, cloud cover, smog, skin melanin content, and sunscreen are among the factors that greatly affect UV intensity and vitamin D synthesis, [19] making it difficult to provide general guidelines. It has been suggested by some researchers, for example, that adequate amounts of vitamin D can be produced with moderate sun exposure to the face, arms and legs, averaging 5–30 minutes twice per week without sunscreen. (The darker the complexion, or the weaker the sunlight, the more minutes of exposure are needed, approximating 25% of the time for minimal sunburn. Vitamin D overdose is impossible from UV exposure; the skin reaches an equilibrium where the vitamin degrades as fast as it is created.) [19] [21] [22] Individuals with limited sun exposure need to include good sources of vitamin D in their diet or take a supplement.
The only way to quantify adequate levels of vitamin D is with a serum 25(OH)D3 (calcifediol) test. [23] In the United States, serum 25(OH)D3 was below the recommended level for more than a third of white men in a 2005 study, with serum levels even lower in women and in most minorities. This indicates that vitamin D deficiency may be a common problem in the US. [24] Australia and New Zealand have had similar findings, which indicate insufficient protection against rickets for children and osteoporosis for adults. [25]
Over the past several years, levels of ultraviolet radiation have been tracked at over 30 sites across North America as part of the United States Department of Agriculture's UVB Monitoring and Research Program at Colorado State University. The first map at right shows levels of UVB radiation in June 2008, expressed in Vitamin D Equivalents. [26]
Using satellite data, measurements from the European Space Agency produce similar maps expressed in units of the widely followed UV Index, for locations around the world. [27] Effects of UV-radiation at high latitudes, where snow stays on the ground into early summer and the sun then remains at a low position even at its zenith, have been reviewed by Meyer-Rochow. [15]
Exposure to ultraviolet radiation from the sun is a source of vitamin D. One minimal erythemal dose of sunlight UV radiation provides the equivalent of about 20,000 IU of vitamin D2, taken as an oral supplement.[ citation needed ] If an adult's arms and legs are exposed to a half minimal erythemal UV radiation, it is the same as taking 3,000 IU of vitamin D3 through an oral supplement. This exposure of 10–15 minutes, on a frequency of two to three times per week, will cause the adult's skin to produce enough vitamin D. It is not necessary to expose the face to the UV, as facial skin provides little vitamin D3. Individuals whose metabolism makes taking oral vitamin D ineffective are able, through exposure to an ultraviolet lamp that emits UV-B radiation, to achieve a 25 (OH) D blood level. [28]
Three benefits of UV exposure are production of vitamin D, improvement in mood, and increased energy. [29]
UVB induces production of vitamin D in the skin at rates of up to 1,000 IUs per minute. This vitamin helps to regulate calcium metabolism (vital for the nervous system and bone health), immunity, cell proliferation, insulin secretion, and blood pressure. [30] In low and middle income countries, foods fortified with vitamin D are "practically nonexistent." Most people in the world depend on the sun to get vitamin D, [31] and elderly populations in low UVB countries experience higher rates of cancer. [32]
There are not many foods that naturally have vitamin D. [33] Examples are cod liver oil and oily fish. If people cannot get sunlight, then they will need 1,000 IU of vitamin D per day to stay healthy. [34] A person would have to eat oily fish three or four times per week in order to get enough vitamin D from that food source alone.
People with higher levels of vitamin D tend to have lower rates of diabetes, heart disease, and stroke and tend to have lower blood pressure. However, it has been found that vitamin D supplementation does not improve cardiovascular health or metabolism, so the link with vitamin D must be in part indirect.[ citation needed ] People who get more sun are generally healthier, and also have higher vitamin D levels. It has been found that ultraviolet radiation (even UVA) produces nitric oxide (NO) in the skin, and nitric oxide can lower blood pressure. High blood pressure increases the risk of stroke and heart disease. Although long-term exposure to ultraviolet contributes to non-melanoma skin cancers that are rarely fatal, it has been found in a Danish study that those who get these cancers were less likely to die during the study, and were much less likely to have a heart attack, than those who did not have these cancers. [35]
People in certain situations, such as people with intellectual disabilities and neurodevelopmental disorders who stay inside most of the time have low vitamin D levels. Getting enough vitamin D can help stave off "autoimmune diseases, cardiovascular disease, many types of cancer, dementia, types 1 and 2 diabetes mellitus, and respiratory tract infections." [36]
Fetuses and children who do not get enough vitamin D can result in "growth retardation and skeletal deformities." [33]
Multiple sclerosis (MS) is least prevalent in the sunniest regions. [37] [38] [39] Exposure to the ultraviolet-B radiation of sunlight appears to be most important and this may operate via vitamin D synthesis. [40]
Ultraviolet (UV) irradiation present in sunlight is an environmental human carcinogen. The toxic effects of UV from natural sunlight and therapeutic artificial lamps are a major concern for human health. Skin surface lipids, including unsaturated lipids such as squalene, sebaleic acid, linoleic acid, and cholesterol can be a subject of oxidation by singlet oxygen and ozone as well as free radicals. Ultraviolet radiation activates lipoxygenase and cyclooxygenase, inducing specific enzymatic oxidation of lipids. Free radical mediated lipid peroxidation gives multiple oxidation products which may induce various skin diseases [41]
The major acute effects of UV irradiation on normal human skin comprise sunburn inflammation erythema, tanning, and local or systemic immunosuppression. [42] The most deadly form, malignant melanoma, is mostly caused by indirect DNA damage from UVA radiation.[ dubious – discuss ] This can be seen from the absence of a direct UV signature mutation in 92% of all melanoma. [43] [ failed verification ] UVC is the highest-energy, most-dangerous type of ultraviolet radiation, and causes adverse effects that can variously be mutagenic or carcinogenic. [44]
Despite the importance of the sun to vitamin D synthesis, it is prudent to limit the exposure of skin to UV radiation from sunlight [45] and from tanning beds. [46] According to the National Toxicology Program Report on Carcinogens from the US Department of Health and Human Services, broad-spectrum UV radiation is a carcinogen whose DNA damage is thought to contribute to most of the estimated 1.5 million skin cancers and the 8,000 deaths due to metastatic melanoma that occur annually in the United States. [45] [47] The use of sunbeds is reported by the World Health Organization to be responsible for over 450,000 cases of non-melanoma skin cancer and over 10,000 cases of melanoma every year in the U.S., Europe, as well as Australia. [48] Lifetime cumulative UV exposure to skin is also responsible for significant age-associated dryness, wrinkling, elastin and collagen damage, freckling, IGH, age spots and other cosmetic changes. The American Academy of Dermatology advises that photoprotective measures be taken, including the use of sunscreen, whenever one is exposed to the sun. [49] Short-term over-exposure causes the pain and itching of sunburn, which in extreme cases can produce more-severe effects like blistering.
Several countries (such as Australia) provide public forecasts of UV irradiation in the form of the UV Index. The index can be used as a guide to the public of dangers from over-exposure to sunlight, especially around noon, when direct sunlight is at its most intense.
Prolonged optical exposure to sunlight, especially intense ultraviolet light, may be linked to cortical cataracts, [50] [15] and high levels of visible light is maybe linked to macular degeneration.
However, significant daily exposure to bright light may be necessary for children to avoid myopia (nearsightedness). [51]
Short-term over-exposure can cause snow blindness, which is analogous to sunburn of the cornea, or can cause solar retinopathy, which is long-lasting retinal damage and vision impairment from sungazing. [52] [53]
Frequent exposure to the sun can cause yellow non-cancerous bumps on the middle part of the sclera of the eye, called pingueculae. It is most common in younger people, mainly those who spend a lot of their time outdoors and do not protect their eyes from UV rays. To decrease the risk of developing pingueculae, it may be wise to wear sunglasses when outdoors, even on overcast days. [54]
Light to the eyes, primarily blue-wavelength light, is important for the entrainment and maintenance of robust circadian rhythms. Exposure to sunlight in the morning is particularly effective; it leads to earlier melatonin onset in the evening and makes it easier to fall asleep. Bright morning light has been shown to be effective against insomnia, premenstrual syndrome and seasonal affective disorder (SAD). [10]
Blood levels of folate, a nutrient vital for fetal development, can be degraded by UV radiation, [55] raising concerns about sun exposure for pregnant women. [56] Lifespan and fertility can be adversely affected for individuals born during peaks of the 11-year solar cycle, possibly because of UV-related folate deficiency during gestation. [57]
A seasonal variation in blood pressure has been noted for decades. Research indicates that skin exposure to sunlight results in a modest reduction in systolic blood pressure. The effect is independent of vitamin D status, instead being mediated by nitric oxide release from skin upon exposure to UV light. The effect is greater in fair-skinned individuals. [58]
According to a 2007 study submitted by the University of Ottawa to the US Department of Health and Human Services, there is not enough information to determine a safe level of sun exposure that imposes minimal risk of skin cancer. [59] In addition, there is not yet conclusive evidence on which components of ultraviolet radiation (UVA, UVB, UVC) are actually carcinogenic. [12] UVC is almost completely absorbed by the atmosphere and does not reach the surface in any appreciable quantity. [60] As a result, only the broad-spectrum combination (UVA, UVB, UVC) known as "ultraviolet radiation" is listed as a carcinogen; the components are only "likely to become" known carcinogens. Solar radiation (sunlight) and sunlamps are listed as carcinogens because they contain ultraviolet radiation. [12]
There are currently no recommendations on a safe level of total lifetime sun exposure. [59] According to epidemiologist Robyn Lucas at Australian National University, analysis of lifespan versus disease shows that far more lives worldwide could be lost to diseases caused by lack of sunlight than to those caused by too much, [62] and it is inappropriate to recommend total avoidance of sunlight. [63]
Over thousands of years, in many climate zones, genetic selection has helped indigenous human populations adapt toward skin pigmentation levels that provide a healthy level of UV exposure. This largely explains the tendency toward darker-skinned populations in the sunniest tropical environments, and lighter skin tones in less-sunny regions and for those who most need vitamin D for rapid bone growth, specifically children and reproductive-age women. The map to the right illustrates the geographic distribution of skin color for native populations prior to 1940, based on von Luschan's chromatic scale. These long-term adaptations for optimal health can be confounded by patterns of food, clothing and shelter, especially at a time when large populations have migrated far from the climates for which their skin was genetically adapted. [64] [65]
Sunlight is a portion of the electromagnetic radiation given off by the Sun, in particular infrared, visible, and ultraviolet light. On Earth, sunlight is scattered and filtered through Earth's atmosphere as daylight when the Sun is above the horizon. When direct solar radiation is not blocked by clouds, it is experienced as sunshine, a combination of bright light and radiant heat (atmospheric). When blocked by clouds or reflected off other objects, sunlight is diffused. Sources estimate a global average of between 164 watts to 340 watts per square meter over a 24-hour day; this figure is estimated by NASA to be about a quarter of Earth's average total solar irradiance.
Ultraviolet (UV) light is electromagnetic radiation of wavelengths of 10–400 nanometers, shorter than that of visible light, but longer than X-rays. UV radiation is present in sunlight, and constitutes about 10% of the total electromagnetic radiation output from the Sun. It is also produced by electric arcs, Cherenkov radiation, and specialized lights, such as mercury-vapor lamps, tanning lamps, and black lights.
Electromagnetic radiation can be classified into two types: ionizing radiation and non-ionizing radiation, based on the capability of a single photon with more than 10 eV energy to ionize atoms or break chemical bonds. Extreme ultraviolet and higher frequencies, such as X-rays or gamma rays are ionizing, and these pose their own special hazards: see radiation poisoning. The field strength of electromagnetic radiation is measured in volts per meter (V/m).
7-Dehydrocholesterol (7-DHC) is a zoosterol that functions in the serum as a cholesterol precursor, and is photochemically converted to vitamin D3 in the skin, therefore functioning as provitamin-D3. The presence of this compound in human skin enables humans to manufacture vitamin D3 (cholecalciferol). Upon exposure to ultraviolet UV-B rays in the sun light, 7-DHC is converted into vitamin D3 via previtamin D3 as an intermediate isomer. It is also found in the milk of several mammalian species. Lanolin, a waxy substance that is naturally secreted by wool-bearing mammals, contains 7-DHC which is converted into vitamin D by sunlight and then ingested during grooming as a nutrient. In insects 7-dehydrocholesterol is a precursor for the hormone ecdysone, required for reaching adulthood. 7-DHC was discovered by Nobel-laureate organic chemist Adolf Windaus.
Skin cancers are cancers that arise from the skin. They are due to the development of abnormal cells that have the ability to invade or spread to other parts of the body. Skin cancer is the most commonly diagnosed form of cancer in humans. There are three main types of skin cancers: basal-cell skin cancer (BCC), squamous-cell skin cancer (SCC) and melanoma. The first two, along with a number of less common skin cancers, are known as nonmelanoma skin cancer (NMSC). Basal-cell cancer grows slowly and can damage the tissue around it but is unlikely to spread to distant areas or result in death. It often appears as a painless raised area of skin that may be shiny with small blood vessels running over it or may present as a raised area with an ulcer. Squamous-cell skin cancer is more likely to spread. It usually presents as a hard lump with a scaly top but may also form an ulcer. Melanomas are the most aggressive. Signs include a mole that has changed in size, shape, color, has irregular edges, has more than one color, is itchy or bleeds.
Sunscreen, also known as sunblock, sun lotion or sun cream, is a photoprotective topical product for the skin that helps protect against sunburn and prevent skin cancer. Sunscreens come as lotions, sprays, gels, foams, sticks, powders and other topical products. Sunscreens are common supplements to clothing, particularly sunglasses, sunhats and special sun protective clothing, and other forms of photoprotection.
Cholecalciferol, also known as vitamin D3 or colecalciferol, is a type of vitamin D that is produced by the skin when exposed to UVB light; it is found in certain foods and can be taken as a dietary supplement.
Sun tanning or tanning is the process whereby skin color is darkened or tanned. It is most often a result of exposure to ultraviolet (UV) radiation from sunlight or from artificial sources, such as a tanning lamp found in indoor tanning beds. People who deliberately tan their skin by exposure to the sun engage in a passive recreational activity of sun bathing. Some people use chemical products that can produce a tanning effect without exposure to ultraviolet radiation, known as sunless tanning.
Indoor tanning involves using a device that emits ultraviolet radiation to produce a cosmetic tan. Typically found in tanning salons, gyms, spas, hotels, and sporting facilities, and less often in private residences, the most common device is a horizontal tanning bed, also known as a sunbed or solarium. Vertical devices are known as tanning booths or stand-up sunbeds.
The ultraviolet index, or UV index, is an international standard measurement of the strength of the sunburn-producing ultraviolet (UV) radiation at a particular place and time. It is primarily used in daily and hourly forecasts aimed at the general public. The UV index is designed as an open-ended linear scale, directly proportional to the intensity of UV radiation, and adjusting for wavelength based on what causes human skin to sunburn. The purpose of the UV index is to help people effectively protect themselves from UV radiation, which has health benefits in moderation but in excess causes sunburn, skin aging, DNA damage, skin cancer, immunosuppression, and eye damage, such as cataracts.
UV-induced apoptosis UV-induced apoptosis is an adequate (physiological) reaction of a cell damaged by UV radiation (UVR) in a sufficiently large (lethal) dose and it prevents the disordered destruction of UV damaged cells by help necrosis. Cell elimination by apoptosis occurs when UV-induced cell damage which cannot be repaired by the intracellular repair system exceeds at it certain limit. Through apoptosis, the cells are self-disassembled into compartments with their subsequent utilization. The first time sign of the beginning of the apoptosis system is working in a UV damaged cell is the activation of restriction enzymes, which divide cell DNA into fragments convenient for utilization. But too large a dose of UVR can lead to breakdown (inactivation) of the energy-dependent mechanism of apoptosis. In this case, cell destruction occurs randomly, not orderly, and during a significantly longer time interval. UV-irradiated cells do not change their appearance for a long time [1, 6], as a result of which the researchers may make the erroneous conclusion that “revealed an unexpected response to a dose at which a higher dose of UV increased the viability of keratinocytes” [2]. The fact that UV-induced apoptosis at high doses of UVR begins to be replaced by necrosis was established in 2000 [3]. For keratinocytes, the proportion of cells that have elimination by help apoptosis, with an increase in UVR dose can reach to achieve 45%, but with a further increase in the dose of UVR, destruction of damaged cells by help necrosis and the part of cells that eliminated by apoptosis begins to decrease [4, 11]. In the dose range of UVR from “lethal” to “super-lethal”, “pro-inflammatory” apoptosis can be manifested, which was experimentally discovered in 2003 [5]. This may be the result of partial damage to the apoptosis mechanism by UV radiation [1]. If at moderate doses “pure” apoptosis does not cause an inflammatory reaction, then at sufficiently large doses, an inflammatory reaction arises due to pro-inflammatory apoptosis, which leads to the appearance of “fast” erythema for UV irradiated skin keratinocytes. Kinetic of “fast” erythema is much faster by the time of development of UV erythema caused by necrosis of UV damaged keratinocytes [6]. The most erythemogenic is UVB the spectral range of UVR, since radiation in this range is less absorbed by the outer layers of the skin, which allows UVB radiation, in contrast to UVC, to reach more deep layers skin and act on keratinocytes of the deep-lying basal layer of the epidermis of the skin. The ability to induce apoptosis for UVB and UVC radiation is due to the fact that the DNA of the nucleus [7] and / or mitochondria [8] of the cell absorbs UVR well in the UVC and UVB spectral range. Keratinocytes of the skin are in a state of programmed apoptosis, during which the keratinocytes of the basal layer are removed from it and during the transition through all layers of the epidermis within 28 days turn into flakes of the outer stratum corneum, which are subsequently desquamated. It is clear that the keratinocyte response to UV exposure will depend on what phase of programmed apoptosis the keratinocyte experienced UV exposure, and this is the main reason for the difference of the UV effect for UVC and UVB on the skin. There are also differences in the initiation of mitochondrial (internal) and caspase-dependent (external) apoptosis for the UVC and UVB spectral ranges [9]. Sunburn cells (SBS) are the keratinocytes in the process of UV-induced apoptosis. The appearance of SBC may be not associated with an inflammatory reaction, but the role of UV-induced apoptosis of skin keratinocytes in the development of UV erythema of the skin has been established, which allowed the development of a patent-protected METHOD FOR QUANTITATIVE ASSESSMENT OF APOPTOSIS SYSTEM [10], in which “the brightest lamp of skin display "(photoerythema) is used to diagnose the state of the body systems involved in the elimination of UV-induced damage. Such systems include the immune system, the intracellular repair system, the microcirculation system and not only.
Pyrimidine dimers represent molecular lesions originating from thymine or cytosine bases within DNA, resulting from photochemical reactions. These lesions, commonly linked to direct DNA damage, are induced by ultraviolet light (UV), particularly UVC, result in the formation of covalent bonds between adjacent nitrogenous bases along the nucleotide chain near their carbon–carbon double bonds, the photo-coupled dimers are fluorescent. Such dimerization, which can also occur in double-stranded RNA (dsRNA) involving uracil or cytosine, leads to the creation of cyclobutane pyrimidine dimers (CPDs) and 6–4 photoproducts. These pre-mutagenic lesions modify the DNA helix structure, resulting in abnormal non-canonical base pairing and, consequently, adjacent thymines or cytosines in DNA will form a cyclobutane ring when joined together and cause a distortion in the DNA. This distortion prevents DNA replication and transcription mechanisms beyond the dimerization site.
Light skin is a human skin color that has a low level of eumelanin pigmentation as an adaptation to environments of low UV radiation. Due to migrations of people in recent centuries, light-skinned populations today are found all over the world. Light skin is most commonly found amongst the native populations of Europe, East Asia, West Asia, Central Asia, Siberia, and North Africa as measured through skin reflectance. People with light skin pigmentation are often referred to as "white" although these usages can be ambiguous in some countries where they are used to refer specifically to certain ethnic groups or populations.
UV-B lamps are lamps that emit a spectrum of ultraviolet light with wavelengths ranging from 290–320 nanometers. This spectrum is also commonly called the biological spectrum due to the human body's sensitivity to light of such a wavelength. UV-B light does not tan the skin very much, compared to the UV-A lamps that are used in tanning beds.
Sunburn is a form of radiation burn that affects living tissue, such as skin, that results from an overexposure to ultraviolet (UV) radiation, usually from the Sun. Common symptoms in humans and other animals include red or reddish skin that is hot to the touch or painful, general fatigue, and mild dizziness. Other symptoms include blistering, peeling skin, swelling, itching, and nausea. Excessive UV radiation is the leading cause of (primarily) non-malignant skin tumors, which in extreme cases can be life-threatening. Sunburn is an inflammatory response in the tissue triggered by direct DNA damage by UV radiation. When the cells' DNA is overly damaged by UV radiation, type I cell-death is triggered and the tissue is replaced.
Vitamin D deficiency or hypovitaminosis D is a vitamin D level that is below normal. It most commonly occurs in people when they have inadequate exposure to sunlight, particularly sunlight with adequate ultraviolet B rays (UVB). Vitamin D deficiency can also be caused by inadequate nutritional intake of vitamin D; disorders that limit vitamin D absorption; and disorders that impair the conversion of vitamin D to active metabolites, including certain liver, kidney, and hereditary disorders. Deficiency impairs bone mineralization, leading to bone-softening diseases, such as rickets in children. It can also worsen osteomalacia and osteoporosis in adults, increasing the risk of bone fractures. Muscle weakness is also a common symptom of vitamin D deficiency, further increasing the risk of fall and bone fractures in adults. Vitamin D deficiency is associated with the development of schizophrenia.
Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, along with numerous other biological functions. In humans, the most significant compounds within this group are vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol).
Animal-type melanoma is a rare subtype of melanoma that is characterized by heavily pigmented dermal epithelioid and spindled melanocytes. Animal-type melanoma is also known to be called equine-type melanoma, pigment synthesizing melanoma, and pigmented epithelioid melanocytoma (PEM). While melanoma is known as the most aggressive skin cancer, the mortality for PEM is lower than in other melanoma types. Animal-type melanoma earned its name due to the resemblance of melanocytic tumors in grey horses.
Dark skin is a type of human skin color that is rich in melanin pigments. People with dark skin are often referred to as black people, although this usage can be ambiguous in some countries where it is also used to specifically refer to different ethnic groups or populations.
Vitamin D deficiency has become a worldwide health epidemic with clinical rates on the rise. In the years of 2011–12, it was estimated that around 4 million adults were considered deficient in Vitamin D throughout Australia. The Australian Bureau of Statistics (ABS) found 23%, or one in four Australian adults suffer from some form of Vitamin D deficiency. Outlined throughout the article are the causes of increase through subgroups populations, influencing factors and strategies in place to control deficiency rates throughout Australia.