Update on ultraviolet A and B radiation generated by the sun and artificial lamps and their effects on skin

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1 International Journal of Cosmetic Science, 2015, 37, doi: /ics Review Article Update on ultraviolet A and B radiation generated by the sun and artificial lamps and their effects on skin R. C. Romanhole*, J. A. Ataide*, P. Moriel*, and P. G. Mazzola*, *Department of Clinical Pathology, Faculty of Medical Sciences, University of Campinas (Unicamp), Campinas, Brazil and Faculty of Pharmaceutical Sciences, University of Campinas (Unicamp), Campinas, Brazil Received 6 October 2014, Accepted 19 February 2015 Keywords: effects of ultraviolet radiation on skin, photoageing, photodamage, ultraviolet light, visible light Synopsis Solar radiation, especially ultraviolet A (UVA) and ultraviolet B (UVB), can cause damage to the human body, and exposure to the radiation may vary according to the geographical location, time of year and other factors. The effects of UVA and UVB radiation on organisms range from erythema formation, through tanning and reduced synthesis of macromolecules such as collagen and elastin, to carcinogenic DNA mutations. Some studies suggest that, in addition to the radiation emitted by the sun, artificial sources of radiation, such as commercial lamps, can also generate small amounts of UVA and UVB radiation. Depending on the source intensity and on the distance from the source, this radiation can be harmful to photosensitive individuals. In healthy subjects, the evidence on the danger of this radiation is still far from conclusive. Resume Le rayonnement solaire, notamment ultraviolet A (UVA) et ultraviolets B (UVB), peut provoquer des dommages au corps humain, et l exposition au rayonnement peut varier en fonction de la localisation geographique, le temps de l annee et d autres facteurs. Les effets des UVA et UVB sur les organismes vont de la formation d erytheme, au bronzage et a la diminution de la synthese de macromolecules telles que le collagene et l elastine, jusqu a des mutations de l ADN cancerigenes. Certaines etudes indiquent que, en plus du rayonnement emis par le soleil, des sources artificielles de rayonnement, telles que les lampes commerciales, peuvent egalement produire de petites quantites de rayons UVA et UVB. En fonction de l intensite de la source et de la distance de la source, ce rayonnement peut ^etre nocif pour les personnes photosensibles. Chez les sujets sains, la preuve concernant le danger de ce rayonnement est encore loin d ^etre concluant. Radiation sources Correspondence: Priscila G. Mazzola, Faculty of Medical Sciences, University of Campinas (Unicamp) - Rua Tessalia Vieira de Camargo, 126, Cidade Universitaria Zeferino Vaz - Campinas - SP - CEP: Brazil. Tel.: ; fax: ; pmazzola@fcm.unicamp.br Solar radiation Earth is constantly irradiated by photons arriving from the sun [1]. Sunlight is not composed only of visible light, but contains a continuous spectrum of electromagnetic radiation, which is categorized into different spectral bands according to the ranges of wavelengths (k) [2]. The sunlight spectrum comprises a continuum of electromagnetic radiation with wavelengths ranging from 0.1 nm for gamma rays to nm (i.e. 20 km) for radio waves [3, 4]. The electromagnetic radiation comprises energy particles termed photons, the energy of which is inversely proportional to their wavelength. The frequency of the wave is proportional to the photon s energy. Because photons are emitted and absorbed by charged particles, they act as the carriers of energy. The energy of a photon is calculated using the Planck Einstein equation: [3]. E ¼ h f ð1þ In the above equation, E is the energy, h is the Planck s constant and f is the photon frequency. Thus, the lower the wavelength, the higher is the photon energy [3]. Infrared light photons comprise 56% of electromagnetic radiation energy reaching the Earth, 39% is attributed to the visible light ( nm) and 5% to the ultraviolet (UV) light ( nm) [1]. Ultraviolet radiation (UVR) is divided into three categories: ultraviolet A (UVA), ultraviolet B (UVB) and ultraviolet C (UVC). UVA and UVB rays comprise 5% of the total electromagnetic radiation energy that reaches the Earth. Below the wavelength of 200 nm are the X-rays with wavelengths that are sufficiently short to penetrate the human body [1, 2, 5]. The initial work on dividing the UV spectra into different bands can be attributed to W.W. Coblentz. His UVR classification, developed at the U.S. National Bureau of Standards during the 1930s, was soon adopted worldwide. Using different filters composed of barium, pyrex and flint, he categorized the UV light based on its capacity to be germicidal (UVC), erythemal (UVB) or black light producing (UVA) [6]. Ozone in the Earth s atmosphere absorbs 100% of UVC, approximately 90% of UVB and virtually no UVA. Therefore, depletion of the ozone layer, as a result of climatic changes, is likely to have a large impact on the amount of erythemogenic UVB reaching the Earth s surface, but very little effect on UVA. It is estimated that a 1% reduction in ozone concentration could increase the incidence of skin cancer two-fold, making it 4% [2]. Because of the atmospheric filtration, UVR reaching the Earth s surface is predominately UVB, with some UVA, with an approximate UVB UVA ratio of 20 : 1. Ultraviolet radiation can also interact with skin cells, causing extensive damage, thus becoming a health issue. UVA (wavelengths Society of Cosmetic Scientists and the Societe Francßaise de Cosmetologie

2 ranging from 320 to 360 nm) has relatively low energies, but is able to penetrate deep into the skin and interact with skin cells. Low doses of UVA can penetrate the dermis, stimulating the production of melanin, the pigment responsible for tanning and protecting the skin from further injury [2, 5, 7, 8]. UVB radiation (wavelengths ranging from 290 to 320 nm) causes the majority of skin lesions of immediate perception, such as redness, which is known as erythema or sunburn. This radiation can also penetrate the stratum corneum and the epidermis [2, 5, 7, 8]. UVC radiation (wavelengths ranging from 200 to 290 nm) has shorter wavelengths, and, consequently, carries the maximal energy, because energy and wavelength are inversely related. Nearly all light in this range is filtered by the atmosphere, although a small quantity is generated by arc lights and some sunbathing [2, 5, 7, 8]. The amount of solar UV radiation reaching the Earth s surface depends on the number of factors, such as the latitude, altitude, time of day and time of year. Many surfaces, including snow and sand, are UV-reflecting. Snow, for example, may reflect up to 85% of incident UV radiation; this explains why it is important for skiers to protect themselves using sunscreen. Sand has the reflection rate of 17%, and water has the reflection rate of 5%. Clouds and fog retain more long waves than short waves. Thus, infrared radiation (IR) is blocked effectively by clouds; however, a substantial amount of UV, particularly UVB, is transmitted through the clouds, which explains why an individual may suffer burns on a cloudy day [5, 9, 10]. Artificial sources of radiation: lamps Although the intensity of ultraviolet radiation is, in general, larger in the outdoor environment, the radiation penetrating through the windows and the radiation emitted by artificial lighting, generally available indoors, may potentially exert long-term effects [11]. The operation of a lamp is simple and basically amounts to releasing the energy by an atom in the form of photons. This process occurs when an electron receives energy, is excited, and shifts to a higher energy orbital. When this electron returns to its original orbital, energy is released in the form of photons, manifested as emission of light. The most commonly used artificial light sources in indoor and outdoor settings are incandescent and fluorescent bulbs [11]. Incandescent bulbs The basic structure of an incandescent lamp consists of two metal contacts on the base, connected to two rigid wires attached to a thin metal filament. This entire assembly is protected by a glass capsule filled with an inert gas [11]. Electrical current flowing from one contact to another excites the electrons of the tungsten filament, and energy in the form of photons is released when these excited electrons return to their lower energy levels [11]. Incandescent bulbs emit light in the ultraviolet range, but because their capsules (bulbs) are made of glass, much of the ultraviolet component is filtered and in principle there is no risk associated with these bulbs [11]. Even so, some data indicate the existence of 280 nm wavelength emission, and high emission levels in the UVA range were observed for intense illumination. Halogen lamps Halogen lamps are very similar to incandescent bulbs, but are more efficient than the latter [9]. Halogen lamps can generate UVA and UVB radiation, and if the quartz envelope is broken or damaged UVC radiation can be generated as well [9, 13]. Fluorescent lamps Low-energy light bulbs, also known as compact fluorescent lamps (CFLs), are set to replace the common incandescent lamps in an ongoing attempt to improve the lighting efficiency and reduce carbon dioxide emission [12]. A CFL works in the same manner as other fluorescent lamps. Electricity is supplied to the lamp, causing the mercury contained within it to generate UV radiation, especially at 254 nm (Fig. 2) [14]. The UV is absorbed by the phosphor-coated tubular walls and the specific composition of the phosphor implies that white visible light is emitted from a CFL. However, it is known that standard tubular fluorescent lamps produce mercury line emissions. In the UV range these lines occur at 254 nm, 313 nm and 365 nm and, potentially, replacing the incandescent lamps by CFLs could lead to increased levels of UV exposure, especially in reading lamps or in settings where close lighting is required [14]. Figures 1 and 2 illustrate the irradiance of an incandescent lamp and a CFL lamp. In both cases, small emissions, especially in the UVA range ( nm), are observed. In general, it can be noticed that the lamps commonly used in indoor environments, such as in offices and homes, can expose people to levels of UVB, UVA, visible and IR. Doses of exposure and its consequences depend on the source, the distance from the radiation source and the time of exposure. Individuals who are photosensitive to these light sources can be affected, and these patients should be advised that their health condition may be negatively affected by exposure to the radiation from incandescent, fluorescent and halogen lamps. Preventively, it can be suggested that using sunscreen products can help minimize the negative effects of these artificial light sources, and even lower the risks associated with exposure of normal people to these sources of artificial radiation [12]. Eadie and co-workers [12] found that CFLs emit UV radiation at wavelengths as low as 254 nm, and that a prolonged exposure of a normal individual s skin to this radiation produces erythema. Although unlikely to be a major problem for normal individuals, Irradiance (mw m 2 nm 1 ) Wavelength (nm) Figure 1 Spectral irradiance of incandescent lamp. Reprinted from A preliminary investigation into the effect of exposure of photosensitive individuals to light from compact fluorescent lamps by E. Eadie, J. Ferguson and H. Moseley, 2009, British Journal of Dermatology, 160, p Society of Cosmetic Scientists and the Societe Francßaise de Cosmetologie 367

3 Irradiance (mw m 2 nm 1 ) Wavelength (nm) Figure 2 Spectral irradiance of compact fluorescent lamp (CFL). Reprinted from A preliminary investigation into the effect of exposure of photosensitive individuals to light from compact fluorescent lamps by E. Eadie, J. Ferguson and H. Moseley, 2009, British Journal of Dermatology, 160, p the CFL can pose a serious risk to photosensitive individuals, particularly patients with chronic actinic dermatitis [15]. These authors also recommended that patients with photosensitivity issues should use only CFLs with protective envelopes [12]. Radiation and its interaction with skin The skin is the organ most exposed to the environment and sunshine, and in vitro as well as in vivo studies on skin cells have shown that UV rays can damage the skin molecules and structures [1, 2, 13]. Upon reaching bare skin, UV radiation triggers a complex process associated with morphological and chemical reactions of cumulative action. The outcomes can include formation of reactive oxygen species, histochemical changes of varying severity, thickening of stratum spinosum and flattening of dermo-epidermal junction [1, 5, 16 18]. UV radiation is absorbed by various chromophores in the skin, such as melanin, DNA, RNA, proteins, aromatic amino acids (e.g. tyrosine and tryptophan) and urocanic acid, among others. The absorption of UV radiation by the chromophores triggers different photochemical reactions and secondary interactions, involving reactive oxygen species and results in harmful effects following excessive exposure [1]. DNA is the main target of UV radiation, and its pyrimidine bases are subject to different photochemical modifications forming cyclobutane dimers, hydration products, adducts and other photoproducts that can be repaired by specific enzymes. When the cell cannot repair the damage mutations occur that may be transmitted to the cell progeny after mitosis, especially regarding the changes in photoprotective mechanisms based on the inhibition of replication, apoptosis or cell death of mutation carriers [1, 19]. When UV radiation strikes the skin, some of it is reflected and some absorbed by the skin various layers. Wavelengths in the UVB range (~320 nm) are mainly absorbed by epidermal cell components (e.g. proteins or DNA). UVA radiation penetrates deeper into the skin compared with UVB, reaching the basal layer of the epidermis and even dermal fibroblasts [13, 19], and particularly affecting the connective tissue, producing reactive oxygen species (ROS) and stimulating the production of matrix metalloproteinase, besides being a potent immunosuppressant [2, 13, 19]. The damaging effects of sunlight on human skin cannot be attributed only to individual wavelengths. The interaction between different wavelength bands, such as visible light, UV radiation and infrared plays an important role in the development of these effects [20]. Infrared radiation (IR) can transmit energy as heat, raising the skin temperature. Human skin exposed directly to the IR can have its temperature raised to over 40 C owing to the conversion of IR into heat. Chronic exposure to heat can cause changes in human skin and diseases such as erythema ab igne, characterized by reticulate erythema, hyperpigmentation, fine scaling, epidermal atrophy and telangiectasias [20, 21]. Visible light and near infrared light can induce pigmentation. An in vivo study was conducted for determining colour changes that occur during irradiation. A polychromatic light source with wavelengths ranging from 390 to 1700 nm that simulated the solar spectrum was used, but without the UV radiation component. It was found that pigmentation occurred even without the presence of UV radiation. Other studies have shown that the exposure of normal skin to visible light can result in the induction of immediate pigmentation (immediate pigment darkening - IPD), immediate erythema and delayed tanning (DT) [22]. A recent study conducted by Chiarelli-Neto and co-workers [23] showed that visible light can damage melanocytes through melanin photosensitization and singlet oxygen ( 1 O 2 ) generation, thus decreasing cell viability, increasing membrane permeability and causing both DNA photooxidation and necro-apoptotic cell death. UVA (355 nm) and visible (532 nm) light photosensitize 1 O 2 with similar yields, and pheomelanin is more efficient than eumelanin at generating 1 O 2 and resisting photobleaching. Although melanin can protect against the cellular damage induced by UVB, exposure to visible light leads to pre-mutagenic DNA lesions, which may be mutagenic and may cause photoageing, as well as other health problems, such as skin cancer. UV radiation and cancer Skin cancer is a growing public health issue because the incidence of cutaneous malignant melanoma and non-melanoma skin cancer has increased by more than 600% worldwide since 1940s [24]. The Brazilian National Cancer Institute (NCI) registered about new cases of cancer in 2014, and the most frequent cancers in the Brazilian population this year would be skin (about cases) [25]. Skin cancer is universally distributed and is often present in three main forms: melanoma, basal cell carcinoma and squamous cell carcinoma (or epidermoid). The basal and squamous cell carcinomas are also known as non-melanoma skin cancer and are the more common type of skin cancer and the most common cancer in light-skinned people. Excessive sun exposure is the main risk factor for the development of melanoma skin cancer and non-melanoma. The squamous cell carcinoma occurs almost exclusively in areas continuously exposed to the solar radiation, whereas the basal cell carcinoma can occur in areas of the body intermittently exposed to the solar radiation. For melanoma, the presence of numerous skin nevi increases the risk [25]. Unlike non-melanoma skin cancers that can usually be cured, melanoma skin cancers are more likely to spread to nearby tissues and other body parts, thereby making the mortality rate higher than in non-melanoma cancers [26]. Risk factors for melanoma and non-melanoma cancers include the exposure to UV radiation and sensitivity of a person s skin to UV radiation [27] Society of Cosmetic Scientists and the Societe Francßaise de Cosmetologie

4 The risk of melanoma is related to UV exposure through several factors, such as the timing of exposure, the age at exposure, the behavioural components, the modulating effects of host susceptibility factors on exposure and the biological mechanisms of melanoma induction. However, in contemporary environmental health regime, two basic issues complicate establishing solar UV exposure as a melanoma risk factor. First, measurements of solar exposure are neither well codified nor precise; second, exposure effects are highly modified by host factors and behaviours [28]. The role of UVA in tumour induction was ignored for decades, and the contribution from UVB has always been acknowledged. However, several studies have now gathered evidence on the involvement of UVA in tumour development and immunosuppressant action [13]. The carcinogenic effect of UVA radiation is smaller, but no less important than that of UVB radiation, and both are considered as risk factors for melanoma. Similar to UVB, the UVA radiation can act directly on the DNA structure, but most of its activity is indirect, where the UVA reacts with molecular oxygen to form ROS, which can interact with the DNA, leading to changes in its structure [13, 19]. UVB radiation can cause DNA damage directly, by inducing the formation of dimers of DNA bases, or indirectly, via free radicals. In both cases, this damage can lead to mutations, which can be detected and corrected by defence systems. When these lesions are irreparable, cell death (apoptosis) is triggered, which is a form of systemic defence for preventing the affected cells from multiplying. Thus, the potential risk of developing a malignant tumour appears when a mutation occurs, and the mechanisms of protection and cellular repair are ineffective [19]. UVA irradiances are not significantly affected by ozone levels, whereas UVB irradiances with wavelengths below 320 nm are reduced by ozone absorption, aerosols and clouds and are also affected by ground albedo, altitude and Rayleigh scattering in the atmosphere. Consequently, the thinning of the atmospheric ozone layer has led to elevated levels of UVB on the Earth s surface, resulting in an increase in health risks due to DNA damage in living organisms [29]. Melanoma incidence is also related to age, gender, race, geography and intervention efforts. All age groups are affected by melanoma with an average age of onset being 55, but the younger age group (15 30 years) and the older age group (60+) are more sensitive to increasing UV radiation [30]. Studies have shown that UV overexposure in childhood is a major risk factor for future melanoma development [31 34], suggesting that the damaging effect of ultraviolet radiation on the skin cumulates over the years. Sunburn in childhood leads to premature ageing and may be responsible for the onset of skin cancer in adulthood. Thus, children should be targeted early on to protect skin from the sun on the daily basis during outdoor activities and not only during holidays [13, 19]. Chang and collaborators found strong positive associations between skin cancer and past UV exposure or cumulative UV exposure over 3 or 4 years. These researchers used an ecological approach for incorporating more accurate UVB incidence measures across the continental U.S. population [26]. Unfortunately, no data on UV incidence exist for Brazilian population. Benefits from UV radiation It is known that UV radiation has beneficial health effects. It stimulates the production of vitamin D3 (cholecalciferol), which is involved in bone metabolism and immune system functioning. It is also used to treat skin diseases such as psoriasis and vitiligo. Regular exposure to UV radiation characterizes phototherapy, which can be used in combination with drugs that increase sensitivity to radiation, improving the symptoms of certain skin diseases [1, 5, 16 18]. The benefits of vitamin D for skeletal health have been well established and described in literature. Optimization of bone mass from infancy until adolescence forms the foundation for primary prevention of osteoporosis. The name vitamin D is a misnomer as it is not a vitamin but a fat-soluble steroid hormone, which can be procured through dietary sources, vitamin supplements and from sunlight exposure. Cutaneous formation of vitamin D after sunlight exposure is the most recognized source of this vitamin, thus labelling it as the sunshine vitamin. The action spectrum of cutaneous vitamin D synthesis is in the UVB portion of sunlight, specifically, at a wavelength of nm. With additional exposure to UVB, pre-vitamin D3 can also be non-enzymatically converted into inactive products, lumisterol and tachysterol. Photoconversion of previtamin D3 into inactive products regulates production of vitamin D3 for preventing vitamin D intoxication with prolonged sun exposure [35].There is also evidence of the relationship between sun exposure, increased production of hormones and improved disposition and mood. Prolonged deprivation of sunlight, such as in countries of the far north during winter, can lead to seasonal order disorders [2, 5]. Conclusion Every day the sun generates different types of radiation that can reach the Earth s surface, and the intensity of this radiation varies with latitude, altitude and the Earth s surface. The effects of the radiation reaching the Earth s surface, mainly UVA and UVB, on organisms and structures, especially on human skin, are clear and well documented. Effects such as sunburn, premature ageing and cancer are well distributed throughout the population, which requires using sunscreen products. It is known that even when indoors, small amounts of UVA and UVB rays can penetrate glass, and commercial lamps, such as Tungsten and Fluorescent lamps, can also emit small amounts of UVA and UVB radiation at certain wavelengths. This radiation may cause rash and other types of blemish on the skin, suggesting that sunscreen should be used indoors as well. References 1. Gonzalez, S., Fernandez-Lorente, M. and Calzada, Y. The latest on skin photoprotection. Clin. Dermatol. 26, (2008). 2. Balogh, T.S., Velasco, M.V., Pedriali, C.A., Kaneko, T.M. and Baby, A.R. Ultraviolet radiation protection: Current available resources in photoprotection. An. Bras. Dermatol. 86, (2011). 3. Csele, M. (ed.) Fundamentals of Light and Lasers, p. 26. John Wiley & Sons, Inc., Hoboken, New Jersey (2004). 4. Khan, A. Device physics: a bug-beating diode. Nature 441, 299 (2006). 5. Palm, M.D. and O 0 Donoghue, M.N. Update on photoprotection. Dermatol. Ther. 20, (2007) Society of Cosmetic Scientists and the Societe Francßaise de Cosmetologie 369

5 6. Matts, P.J. Solar ultraviolet radiation: definitions and terminology. Dermatol. Clin. 24, 1 8 (2006). 7. Schueller, R. and Romanowki, P. Introducß~ao aos produtos fotoprotetores. Cosmet. Toilet. 12, (2000). 8. Forestier, S. Rationale for sunscreen development. J. Am. Acad. Dermatol. 58, S133 S138 (2008). 9. Godar, D.E. UV doses worldwide. Photochem. Photobiol. 81, (2005). 10. Grant, R.H. and Heisler, G.M. Effect of cloud cover on UVB exposure under tree canopies: will climate change affect UVB exposure? Photochem. Photobiol. 82, (2006). 11. Pupo, M. (ed.) Tratado de fotoprotecß~ao. S~ao Paulo, 83 92, (2012). 12. Eadie, E., Ferguson, J. and Moseley, H. A preliminary investigation into the effect of exposure of photosensitive individuals to light from compact fluorescent lamps. Br. J. Dermatol. 160, (2009). 13. Marrot, L. and Meunier, J.R. Skin DNA photodamage and its biological consequences. J. Am. Acad. Dermatol. 58, S139 S148 (2008). 14. Moseley, H. Medical Physics Handbooks 18: Non-Ionising Radiation. Adam Hilger, Bristol (1988). 15. Dawe, R.S., Crombie, I.K. and Ferguson, J. The natural history of chronic actinic dermatitis. Arch. Dermatol. 136, (2000). 16. Sgarbi, F.C., Carmo, E.D. and Rosa, L.E.B. Radiacß~ao ultravioleta e carcinog^enese. Rev. Cienc. Med. 16, (2007). 17. Wilkinson, J.B. and Moore, R.J. Cosmetologia de Harry, pp Dıaz de Santos, Madrid (1990). 18. Pathak, M.A. Photoprotection against harmful effects of solar UVB and UVA radiation: an update. In: Sunscreens: Development, Evaluation and Regulatory Aspects (Lowe, N.J., Shaath, N.A. and Pathak, M.A., eds.), pp Marcel Dekker, New York (1997). 19. Gallagher, R.P. and Lee, T.K. Adverse effects of ultraviolet radiation: a brief review. Prog. Biophys. Mol. Biol. 92, (2006). 20. Cho, S., Shin, M.H., Kim, Y.K., Seo, J.E., Lee, Y.M., Park, C.H. and Chung, J.H. Effects of infrared radiation and heat on human skin aging in vivo. J. Investig. Dermatol. Symp. Proc. 14, (2009). 21. Weber, M.B., Ponzio, H.A., Costa, F.B. and Camini, L. Eritema ab igne: relato de um caso. An. Bras. Dermatol. 80, (2005). 22. Mahmoud, B.H., Hexsel, C.L., Hamzavi, I.H. and Lim, H.W. Effects of visible light on skin. Photochem. Photobiol. 84, (2008). 23. Chiarelli-Neto, O., Ferreira, A.S., Martins, W.K. et al. Melanin photosensitization and the effect of visible light on epithelial cells. PLoS ONE 9, e (2014). 24. Osterlind, A., Hjalgrim, H., Kulinsky, B. and Frentz, G. Skin-cancer as a cause of death in Denmark. Br. J. Dermatol. 125, (1991). 25. Estimativa Incid^encia de C^ancer no Brasil. Rio de Janeiro: Instituto Nacional de C^ancer Jose de Alencar Goes da Silva, (2014). 26. Chang, N.B., Feng, R., Gao, Z. and Gao, W. Skin cancer incidence is highly associated with ultraviolet-b radiation history. Int. J. Hyg. Environ. Health 213, (2010). 27. NCI. Study of Individuals and Families at High Risk for Melanoma (2009). 28. Hatfield, L.A., Hoffbeck, R.W., Alexander, B.H. and Carlin, B.P. Spatiotemporal and spatial threshold models for relating UV exposures and skin cancer in the central United States. Comput. Stat. Data Anal. 53, (2009). 29. Leaf, A. Loss of stratospheric ozone and health effects of increased ultraviolet radiation. In: Critical condition: Human Health and Environment (Chivian, E.M.M., Hu, H. and Haines, A., eds.), pp The MIT Press, Cambridge, MA (1993). 30. Jensen, E.H., Kim, A., Margolin, A., Sondak, V.K. Melanoma and other skin cancers. In: Cancer Management: A Multidisciplinary Approach CMP Medica LLC. (2007). 31. Weinstock, M.A., Colditz, G.A., Willett, W.C. et al. Nonfamilial cutaneous melanoma incidence in women associated with sun exposure before 20 years of age. Pediatrics 84, (1989). 32. Autier, P. and Dore, J.F. Influence of sun exposures during childhood and during adulthood on melanoma risk. EPIMEL and EORTC Melanoma Cooperative Group. European Organisation for Research and Treatment of Cancer. Int. J. Cancer 77, (1998). 33. Naldi, L., Imberti, G.L., Parazzini, F. et al. Pigmentary traits, modalities of sun reaction, history of sunburns, and melanocytic nevi as risk factors for cutaneous malignant melanoma in the Italian population: results of a collaborative case control study. Cancer 88, (2000). 34. Whiteman, D.C., Whiteman, C.A. and Green, A.C. Childhood sun exposure as a risk factor for melanoma: a systematic review of epidemiologic studies. Cancer Causes Control 12, (2001). 35. Kannan, S. and Lim, H.W. Photoprotection and vitamin D: a review. Photodermatol. Photoimmunol. Photomed. 30, (2013). doi: /phpp Society of Cosmetic Scientists and the Societe Francßaise de Cosmetologie

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