J. F. Nash and Paul R. Tanner
P&G Beauty, Sharon Woods Technical Center, Cincinnati, Ohio, U. S.A.
There is consensus among the scientific and medical communities that exposure to sunlight is a major factor in the etiology of the progressive unwanted changes in the appearance of skin, i. e., photoaging, and in the risk of skin cancers (1-3). The evidence supportive of this view comes from epidemiology, clinical studies, and experimental studies in humans, laboratory animals, and in vitro systems. It is well established that acute exposure of unprotected skin to ultraviolet (UV) radiation in sunlight produces numerous physiological effects beyond the most obvious which is sunburn (4). Such insults or damage following repeated, lifetime exposure to solar UV lead to skin cancers (5-8), and as presented in Table 1, a myriad of degenerative events responsible for the visible signs of skin aging (10,11). Recent years have seen a very rapid increase in knowledge concerning the etiology and prevention of solar damage (12-14). Since exposure to UV radiation in sunlight is associated with deleterious dermatological events, it is logical that reducing solar UV exposure will diminish such damage to the skin.
Arguably, the complete avoidance of solar UV is neither achievable nor entirely healthy. For example, it is known that exposure to sunlight has health benefits including production of vitamin D (15). As such, moderation seems prudent when considering the balance between the established damage and benefits of solar exposure. To this end, a “safe sun” strategy has been developed and promoted by healthcare professionals worldwide (16-18). An important part of this “safe sun” strategy is the use of sunscreens.
Once the energy from UV is absorbed in the skin, it may produce new chemical entities, e. g., 60,40-DNA photoproducts, free radicals, etc., or dissipate the excess energy as heat or phosphorescence. This absorption and subsequent conversion of energy contribute to the processes involved in the etiology of skin cancer and photoaging. Preventing solar UV from interacting with skin chromophores is the primary function of sunscreens. To this end, sunscreen products are quite simple; they absorb/reflect/scatter UV radiation from sunlight before this energy can be absorbed by chromophores residing in the skin. As it turns out, sunscreen products are technically complex. Moreover, such products must be applied to be effective, and as with any other preventative measure, compliance is the key to achieving health benefits.
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Table 1 Features of Chronological (Intrinsic) and Photo-Induced Skin Aging
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Fine wrinkles |
Increase variability in epidermal thickness |
Varying degrees of thickness |
Epidermal acanthosis |
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Skin laxity |
Decrease in epidermal filaggrin |
Coarse wrinkles |
Thickened stratum corneum |
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Dry skin |
Reduction in the number |
Marked dryness |
Marked cellular |
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of melanocytes |
and scaliness |
dysplasia |
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Even skin tone |
Reduction in number |
Uneven pigmenta- |
Variability in size and |
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of Langerhans cells |
tion and lenti – gines |
shape of keratinocytes |
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Impaired wound |
Decrease in dermal |
Benign, premalig- |
Pronounced flattening |
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healing |
thickness Increase in cross-linkage and disorganization of collagen fibers Decrease in number of eccrine, apocrine, and sebaceous glands Flattened dermoepidermal junction |
nant, and malignant skin lesions |
of epidermal-dermal junction Reduction in number of Langerhans cells Solar elastosis resulting from hyperplasia of abnormal elastic tissue Blood vessels dilated and on the face called telangiectasias |
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Sebaceous gland hyperplasia and pore size |
Source: Modified from Ref. 9.