SUNSCREENS
Skin Safety 101
More than 1 million people in the U.S. will be diagnosed with non-malignant skin cancer this year and another 60,000 will get malignant melanoma (NCI 2007). Many common sunscreens do little to protect users from the most harmful effects of sunlight caused by ultraviolet (UV) radiation. Approximately 5% of the solar light reaching the Earth is UV rays. The vast majority of this light is in the form of skin-penetrating UVA radiation. UVB, the fraction that causes sunburn, makes up just 4% of this UV light, while another variation, UVC, is filtered out by the atmosphere (Diffey 2002).
UV light can break the chemical bonds of skin cells — including DNA, enzymes, and proteins (Burren 1998; Kielbassa 1997; Kvam 1997; Wenczl 1998; Young 1998). This kills cells directly, causes cancerous cell growth, inhibits the body's anti-cancer defenses and does other damage to skin cells (Dalle Carbonare 1992; Herrling 2002; Scharffetter-Kochanek 1997; Vile 1995).
For years the sunscreen industry has focused primarily on UVB, the light that causes the most immediate skin damage, inflicting sunburn as well as increasing skin cancer risk. The SPF test is designed to measure the UVB protection of a sunscreen.
UVA, however, penetrates deeper into the skin than UVB, reaching the fragile subcutaneous tissue, and creates harmful free radicals when it interacts with certain chemicals in the skin. UVA-induced stress leads to immune suppression of skin (Bestak 1995; Damian 1997; Iwai 1999; Moyal 1997). Naturally occurring chemicals such as vitamin B2 (Marrot 2005) have been linked to tumor formation (Le Panse 2003; Bachelor 2004) after interacting with UVA. UVA also sensitizes skin for people taking antibiotics, hormonal contraceptives and other pharmaceuticals (Gould 1995; Ferguson 1995).
UVA damage occurs before any visible sunburn and is increasingly being recognized as the major contributor to UV-related skin damage and aging. This shift in our understanding of UV-related skin damage brings to light the pressing problem with many sunscreens: they effectively shield skin from UVB rays, but leave users vulnerable to UVA damage.
Basal-cell carcinoma is usually found in areas of the skin exposed to sunlight, and typically appears as a raised, hard, red or red-grey, pearly wound, often found on the forehead, eyelids, cheeks, nose, and lips. Squamous-cell carcinoma occurs most frequently on skin exposed to sunlight over long periods of time, and usually develops in areas where skin has been damaged by the sun — areas with blemishes or freckles. These blemishes develop into rough, scaly patches with small areas of open wound that do not heal. They eventually grow into larger wounds with crusts. BCC and SCC are localized and unlikely to spread. They are the most common forms of skin cancer.
Malignant melanoma is more rare and potentially deadly. It often shows itself as a mole or spot that begins to bleed, grow, or change its color, shape or texture. It usually spreads if not treated in the early stage. Malignant melanomas are responsible for 75% of skin cancer deaths and are the sixth most common cancer in American men and women (AAD 2007).
The most common places to develop skin cancer are those exposed to the most sun: the face, arms, neck, legs, and hands (NCI 2007, AFP 2007). Risk factors for skin cancer include sunburn or excessive sun damage, especially early in life. Review of nearly 30 studies indicates that just a few severe sunburns during childhood or adolescence can doubles the likelihood of developing malignant melanoma later in life (Oliveria 2006). Other risk factors include freckles, light skin color, eye color, or hair color, personal or family history of skin cancer, and the presence of certain types of moles.
The influence of UVA on skin cancer is still being studied. There is some evidence that UVA contributes to basal cell carcinoma (Agar 2004) and concerns that it may related to melanoma as well (Haywood 2003).
One study did find a reduced frequency of mutations in the p53 tumor suppressor gene among basal-cell carcinoma patients who regularly used sunscreen (Rosenstein 1999). Mutations in the p53 gene cause up to 80% of skin cancer cases (Nohynek citing Levine 1991); therefore this study suggests that sunscreen reduces sun-induced basal-cell carcinoma, while potentially leaving only individuals with genetic susceptibility to the disease's other pathways vulnerable (Rosenstein 1999).
References:
AAD (American Academy of Dermatology). 2007 New Formulations Improve Sunscreen Effectiveness. Available at: http://www.aad.org/aad/Newsroom/New+Formulations+Improve+Sunscreen+Effective ness.htm. Accessed 31 May, 2007.
ACS (American Cancer Society, Inc.) 2006. Surveillance Research. Cancer Facts & Figures.
AFP (American Family Physicians). 2007 Saving your skin from sun damage. Available at: http://www.aafp.org/afp/20060901/815ph.html. Accessed 31 May, 2007.
Agar N, Halliday G, Barnetson R, Ananthaswamy H, Wheeler M, Jones A. 2004. The basal layer in human squamous tumors harbors more UVA than UVB fingerprint mutations: a role for UVA in human skin carcinogenesis. Proceedings of the National Academy of Sciences of the USA 101(14):4954-9.
Armeni T, et al. 2004. Lack of in Vitro Protection by a Common Sunscreen Ingredient on UVA-Induced Cytotoxicity in Keratinocytes. Toxicology 203: 165-78.
Bachelor MA, et al. 2004 UVA-mediated activation of signaling pathways involved in skin tumor promotion and progression. Semin.Cancer Biol. 14 131-38.
Baron E, et al. 2003. High Ultraviolet a Protection Affords Greater Immune Protection Confirming That Ultraviolet a Contributes to Photoimmunosuppression in Humans. J Invest Dermatol 121(4): 869-75.
Bestak R, Barnetson RSC, Nearn MR, Halliday GM. 1995. Sunscreen Protection of Contact Hypersensitivity Responses from Chronic Solar-Simulated Ultraviolet-Irradiation Correlates with the Absorption-Spectrum of the Sunscreen. Journal of Investigative Dermatology 105(3): 345-51.
Burren R, Scaletta C, Frenk E, Panizzon R, Applegate L. 1998. Sunlight and Carcinogenesis: Expression of P53 Pyramidine Dimers in Human Skin Following Va I, Ii and Solar Stimulating Radiations. Int J Cancer 76: 201-06.
Chapman, M. 2002. Sunscreens: the importance of UVA protection. Medscape Today. Available at: http://www.medscape.com/viewarticle/431185. Accessed 31 May, 2007.
Dalle Carbonare M, et al. 1992. Skin Photosensitizing Agents and the Role of Reactive Oxygen Species in Photoaging. Journal of Photochemistry and Photobiology B 14: 105-24.
Damian D, et al. 1997. Broad-Spectrum Sunscreens Provide Greater Protection against UV-Radiation-Induced Suppression of Contact Hypersensitivity to a Recall Antigen in Humans. J Invest Dermatol 109: 146-51.
Diffey. 2002. What Is Light? Photodermatol Photoimmunol Photomed 18: 68-74.
Ferguson J 1995 Fluoroquinolone photosensitization: a review of clinical and laboratory studies Photochem. Photobiol. 62: 954-58.
Fourtanier A, Bernerd F, Bouillon C, Marrot L, Moyal D, Seite S. 2006. Protection of skin biological targets by different types of sunscreens. Photoderm. Photoimmunol. Photomed. 22: 22-32.
Fuchs J. 1998. Potentials and Limitations on the Natural Antioxidants Rrr-Alpha-Tocopherol, L-Ascorbic Acid and Beta-Carotene in Cutaneous Photoprotection. Free Radical Biology and Medicine 25: 848-73.
Gould JN, et al. 1995 Cutaneous photosensitivity diseases induced by exogenous agents J. Am. Acad. Dermatol. 33: 551-73.
Green et al. 1999 Daily sunscreen application and betacarotene supplementation in prevention of basal-cell and squamous-cell carcinomas of the skin: a randomised controlled trial Lancet 354(9180): 723-9.
Haywood R, Wardman P, Sanders R, Linge C. 2003. Sunscreens inadequately protect against ultraviolet-A-induced free radicals in skin: implications for skin aging and melanoma? Journal of Investigative Dermatology 121(4):862-8.
Herrling T, et al. 2002. Electron Spin Resonance Detection of UVA-Induced Free Radicals. Skin Pharmacology and Applied Skin Physiology 15: 381-83.
Hidaka H, et al. 2006 DNA Damage Photoinduced by Cosmetic Pigments and Sunscreen Agents under Solar Exposure and Artifical UV Illumination. J Oleo Sci 55(5): 249-61.
Iwai I, et al. 1999. UVA-Induced Immune Suppression through an Oxidative Pathway. J Invest Dermatol 112: 19-24.
Kielbassa C, et al. 1997. Wavelength Dependence of Oxidative DNA Damage Induced by Uv and Visible Light. Carcinogenesis 18: 811-16.
Kvam E. 1997. Induction of Oxidative DNA Base Damage in Human Skin Cells by UV and near Visible Radiation. Carcinogenesis 18: 2379-84.
Le Panse R, 2003 P38 mitogen-activated protein kinase activation by ultraviolet A radiation in human dermal fibroblasts Photochem Photobiol 78: 168-74.
Levine AJ,et al. 1991 Click here to read The p53 tumour suppressor gene. Nature. 1991 Jun 6;351(6326):453-6.
Marrott L, et al. 2005 Importance of UVA photoprotection as shown by genotoxic related endpoints: DNA damage and p53 status. Mutation Research. 571: 175-84.
Moyal D, et al. 1997. Immunosuppression Induced by Chronic Solar-Simulated Irradiation in Humans and Its Prevention by Sunscreens. Eur J Dermatol 7: 223-5.
NCI. 2007. National Cancer Institute: General Information about Skin Cancer. Available: www.cancer.gov/cancertopics/pdq/treatment/skin/melanoma [accessed May 31, 2007.
NCI. 2007. National Cancer Institute: Cancer Topics: What you need to know about melanoma. http://wwwcancergov/cancertopics/wyntk/melanoma.
Nohnyek, GJ 2001 Benefit and risk of ultraviolet filters Oliveria SA, Saraiya M, Geller AC, Heneghan MK, Jorgensen C. 2006. Sun exposure and risk of melanoma. Archives of disease in childhood 91(2): 131-138.
Rosenstein B, et al. 1999 Mutations in basal cell carcinomas arising in routine users of sunscreens Photochem. Photobiol. 70: 798-806.
Scharffetter-Kochanek K, et al. 1997. UV-Induced Reactive Oxygen Species in Photocarcinogenesis and Photoaging. Biol Chem 378: 1247-57.
Schindo Y, et al. 1994. Enzymatic and Non-Enzymatic Antioxidants in Epidermis and Dermis of Human Skin. J Invest Dermatol 102: 122-24.
Selgrade M, et al. 2001. Dose-Response for UV-Induced Immune Suppression in People of Color: Differences Based on Erythemal Reactivity Rather Than Skin Pigmentation. Photochem Photobiol 74: 88-95.
Van der Pols 2006 Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer Epidem. Biomark. Prev. 15(12): 2546-8.
Vile GF, et al. 1995. UVA Radiation-Induced Oxidative Damage to Lipids and Proteins in Vitro and in Hman Skin Fibroblasts Is Dependent on Iron and Singlet Oxygen. Free Radical Biology and Medicine 18: 721-30.
Wenczl E, et al. 1998. (Pheo)Melanin Photosensitizes UVA-Induced DNA Damage in Cultured Human Melanocytes. J Invest Dermatol 111: 678-82.
Young A, et al. 1998. Human Melanocytes and Keratinocytes Exposed to UVB or UVA in Vivo Show Comparable Levels of Thymine Dimers. J Invest Dermatol 111: 936-40.
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