Sunscreens: the ounce of prevention - includes patient information sheet

Author: J. Michael Wentzell
Date: April, 1996

Cutaneous exposure to sunlight decreases the body's immune response,[1,2] increases the risk of skin cancer, promotes photoaging,[3] exacerbates photosensitivity diseases[4] and interacts adversely with common drugs.[5] These adverse effects can be minimized by adequate photoprotection. However, a full understanding of sunscreen agents requires more than knowledge of the sun protection factor (SPF) or the spectrum of activity of a particular product.

The effects of exposure to sunlight are costly Products to combat the signs of photoaging account for much of the $14 billion a year cosmetic industry. Polymorphous light eruption, solar urticaria, actinic keratoses and a variety of prevalent diseases are directly attributable to sun exposure. Sunlight can aggravate diseases such as lupus erythematosus, porphyria, herpes simplex, rosacea, vitiligo and dermatomyositis.[4] Photoallergic and/or phototoxic reactions can be caused by over 100 commonly used drugs, including saccharin, oral contraceptives, nonsteroidal anti-inflammatory drugs (NSAIDs), tetracyclines, diuretics, diphenhydramine, sulfa, warfarin (Coumadin) and captopril (Capoten).[5]

By the year 2000, the lifetime incidence of melanoma in the United States will exceed one in 90. The annual incidence of basal cell and squamous cell carcinoma in the United States increased by 50 percent to 600,000 people from 1980 to 1990[6]; currently, as many as 900,000 people are estimated to be affected. Persons with fair skin are at highest risk for squamous cell carcinoma, and risk is proportional to chronic sun exposure and cumulative radiation. Basal cell carcinoma, although less clearly associated with chronic sun exposure, is also found most frequently on body surfaces that are frequently exposed to the sun. The risk of melanoma has also been linked to intermittent severe solar radiation exposure, especially in childhood. However, persons who work indoors are actually at greater risk for melanoma than those who work outdoors.[7]

Ultraviolet radiation (UVR) is responsible for most of the adverse effects of solar radiation. UVR wavelengths between 200 and 400 nm are divided into three bands: UVC (200 to 290 rim), UVB (290 to 320 run) and UVA (320 to 400 nm). UVC is stopped at the outer stratosphere. UVB is the most erythemogenic and melanogenic. It is particularly carcinogenic and is highly implicated in photoaging and most diseases exacerbated by exposure to sunlight. UVB is stopped by window glass and is effectively blocked by many sunscreens. For each 1 percent decrease in stratospheric ozone, there is a 2 percent increase in the amount of UVB that reaches the earth' surface. UVA tanning bulbs simultaneously emit up to 5 percent UVB, and as little as 1 percent UVB emission can increase the potential for skin cancer.[8]

Short wavelength UVA in the range of 320 to 340 nm is more damaging than long wavelength UVA. Although UVA is less carcinogenic than UVB on a dose-for-dose basis, 10 to 100 times as much UVA reaches the earth.[9] UVA is also clearly implicated in photoaging and tumor promotion.3,10 Together with UVB, UVA can be a significant factor in polymorphous light eruption, solar urticaria, actinic reticuloid, actinic keratosis and porphyria.[4] Much of UVA penetrates glass, penetrates well into the fat layer of the integument and is incompletely blocked by chemical sunscreens. UVA-induced tanning provides less protection against future sunburn than does tanning induced by UVB.

Environmental factors affect the degree of radiation exposure. For example, UVR increases by 4 percent for each 1,000 feet of elevation. In addition up to 80 percent of UVR can penetrate cloud cover. As much as 50 percent of UVR can penetrate to the skin of a summer covered by water Sand, snow and concrete reflect up to 85 percent of sunlight, and reflected UVR can even reach shaded areas. Seasonal variation accounts for New Orleans receiving 14 times as much UVR in winter as Philadelphia. Sixty percent of the day's UVR reaches earth during the midday hours. UVR is strongest between 10 a.m. and 3 p.m.[3,6,9]

Although the role of infrared radiation in skin damage is less clear, infrared radiation plays a role in accelerated aging of the skin seen in erythema abigne and in squamous cell carcinoma that arises from the scar tissue of a bum.

Role of Sunscreens

Sunscreens reduce the incidence of actinic keratoses, which are precursors to squamous cell carcinoma and are markers for patients who are at risk for basal cell carcinoma and melanoma.[11] Sunscreens reduce the incidence of UVR-induced tumors in laboratory animals.[12] Sunscreens also protect against UVR-induced damage to Langerhans cells,[13] and they decrease the incidence of sunburn cells,[13,14] which are markers of DNA damage. It has been estimated that adequate use of sunscreens before 18 years of age could reduce the lifetime risk of nonmelanoma skin cancer by 78 percent.[15]

UVB protection and sunscreen potency is measured in terms of sun protection factor (SPF). SPF describes the minimum dose of radiation required to produce erythema (MED) in sun-protected skin compared with the MED of unprotected skin. A sunscreen product with an SPF of 15 confers 15 times more protection against UVB than using no sunscreen at all. Although most sunburns are primarily due to UVB exposure, about 15 to 20 percent of sunburn erythema is due to UVA exposure.[16] Various proposals to standardize terminology for UVA protection have been set forth. Among these is the phototoxic protection factor (PPF), which measures the vulnerability of skin that has been pretreated with photosensitizing psoralen to UVA-induced erythema. A monograph by the U.S. Food and Drug Administration (FDA) regarding UVA protection ratings is currently being finalized.

Proper clothing is the most effective sunscreen. However, wet clothing or clothing made from loosely woven fabrics can transmit up to 30 percent of the sun's UVR. A typical dry, white T-shirt provides an SPF between 5 and 9. Wet fabrics and fabrics with light weight, color and weave increase transmission of UVR. A ball cap shields little more than the upper central forehead. Effective UVR-shielding clothing includes tightly woven fabrics, long sleeves and pants, and broad-brimmed hats with adequate neck and ear protection. Proper clothing can provide an SPF of up to 60 for UVB and protects over the entire UVR spectrum.[3,17]

Commercial sunscreen lotions generally fall into two broad categories: physical sunscreens that scatter or reflect UVR and chemical sunscreens that absorb UVR. Physical sunscreens generally have a broader spectrum of coverage than chemical sunscreens and protect throughout the UVB/UVA/visible range. Physical sunscreens are useful for persons who require very broad-spectrum protection and for those who are sensitive to chemical sunscreens. Many people who are not actually allergic to chemical sunscreens still find that many chemical sunscreens irritate their skin.

PHYSICAL SUNSCREENS

Physical sunscreens include zinc oxide, titanium dioxide, magnesium silicate, talc, ferric chloride, kaolin and red veterinary petrolatum. Compared with chemical sunscreens that absorb UVR, the effectiveness of physical sunscreens is less dependent on application technique. Some products tend to melt with heat and can discolor clothing and/or can promote miliaria and folliculitis.[18,19] Because of the need for broader spectrum sunscreens with limited allergenic potential, more cosmetically acceptable physical sunscreens are becoming available (Neutrogena Chemical-Free Sunblocker, Ti Screen Natural, Sundown Sport Sunblock, Clinique Special Defense Sunblock).

CHEMICAL SUNSCREENS

The first chemical sunscreen was a salicylate introduced in the 1920s. Chemical sunscreens that absorb UVR have the cosmetic advantage of being invisible after skin application. They are available in creams, lotions, gels, wax sticks and sprays. The delivery medium is largely a matter of personal preference. People with dry skin generally prefer sunscreens with an emollient base (PreSun 46, 29, 25, Vaseline Intensive Care 30, 15, Coppertone Moisturizing Sunblock 30, 25). Some children prefer sprays (PreSun Spray Mist). Ranchers, farmers and construction workers often dislike the use of creams and lotions because airborne dust sticks to the oily film left on their skin. In these persons, compliance often improves with use of sunscreen gels that dry on the skin (PreSun Active, Shade Gel, Bullfrog, Hawaiian Tropic).

Chemical sunscreens are also available in "waterproof" or "very water-resistant" formulations (80-minute submersion resistance) and "water-resistant" formulations (40-minute submersion resistance). Most of these products are available as lotions or creams, but some water-resistant gel formulations are also available.

[1.] Gilchrest BA, Soter NA, Stoff JS, Mihm MC Jr. The human sunburn reaction: histologic and biochemical studies. J Am Acad Dermatol 1981;5:411-22. [2.] Krutmann J, Elmets CA. Recent studies on mechanisms in photoimmunology. Photochem Photobiol 1988:48:787-98. [3.] Taylor CR, Stern RS, Leyden JJ, Gilchrest BA. Photoaging/photodamage and photoprotection. J Am Acad Dermatol 1990;9?:1-15. [4.] Willis I. Photosensitivity and phototherapy. In: Moschella SL, Hurley HJ, eds. Dermatology. 2d ed. Philadelphia: Saunders, 1985:389-415. [5.] Gould JW, Mercurio MG, Elmets CA. Cutaneous photosensitivity disease induced by exogenous agents. J Am Acad Dermatol 1995;33:551-73. [6.] Sunlight, ultraviolet radiation and the skin. Natl Inst Health Consens Dev Conf Consens Statement 1989;7(8):I-10. [7.] FDA proposes to establish conditions under which OTC sunscreen drug products are GRAS. Federal Regist 1993;58(90):28194-302. [8.] Koh HK, Lew RA. Sunscreens and melanoma: implications for prevention [Editorial]. J Natl Cancer Inst 1994;86:78-9. [9.] Hebert AA. Photoprotection in children. Adv Dermatol 1983;8:309-24. [10.] Matsui MS, DeLeo VA. Longwave ultraviolet radiation and promotion of skin cancer. Cancer Cells 1991;3:8-12. [11.] Naylor MF, Boyd A, Smith DW, Cameron GS, Hubbard D, Neldner KH. High sun protection factor sunscreens in the supression of actinic neoplasia. Arch Dermatol 1995;131:170-5. [12.] Kligman LH, Akin FJ, Kligman AM. Sunscreens prevent ultraviolet photocarcinogenesis. J Am Acad Dermatol 1980;3:30-5. [13.] Elmets CA, Vargas A, Oresajo C. Photoprotective effects of sunscreens in cosmetics on sunburn and Langerhans cell photodamage. Photodermatol Photoimmunol Photomed 1992,9:113-20. [14.] Kaidbey KH. Photoprotective potential of the new superpotent sunscreens. J Am Acad Dermatol 1990;22:449-52. [15.] Stem RS, Weinstein MC, Baker SG. Risk reduction for nomnelanoma skin cancer with childhood sunscreen use. Arch Dermatol 1986;122:537-45. [16.] Diffey BL. Human exposure to ultraviolet radiation. Semin Dermatol 1990;9:2-10. [17.] Menter JM, Hollins TD, Sayre RM, Etemadi AA, Willis I, Hughes SN. Protection against UV photocarcinogenesis by fabric materials. J Am Acad Dermatol 1994;31(5 Pt 1):711-6. [18.] Fisher AA. Sunscreen dermatitis: part IV - the salicylates, the anthranilates, and physical agents. Cutis 1992;50:397-8. [19.] Dromgoole SH, Maibach HI. Sunscreening agent intolerance: contact and photocontact sensitization and contact urticaria. J Am Acad Dermatol 1990; (6 Pt 1):1068-78. [20.] Agin P. Photoaging/photodamage and photoprotection [Letter]. J Am Acad Dermatol 1991;24(2 Pt 1):315-7. [21.] Shade UVAGuard - a second broad-spectrum sunscreen. Med Lett Drugs Ther 1993;35(898):53-4. [22.] O'Donoghue MN. Sunscreen: one weapon against melanoma. Dermatol Clin 1991,9:789-93. [23.] Rhodes LE, O'Farrell S, Jackson MJ, Friedmann PS. Dietary fish-oil supplementation in humans reduces UVB-erythemal sensitivity but increases epidermal lipid peroxidation. J Invest Dermatol 1994;103:151-4. [24.] Marks R, Foley PA, Jolley D, Knight KR, Harrison J, Thompson SC. The effect of regular sunscreen use on vitamin D levels in an Australian population. Results of a randomized controlled source. Arch Dermatol 1995;131:415-21. [25.] Wolf P, Donawho CK, Kripke ML. Effect of sunscreens on UV radiation-induced enhancement of melanoma growth in mice. J Natl Cancer Inst 1994;86:99-105. [26.] Klein-Szanto AJ, Silvers WK, Mintz B. Ultraviolet radiation-induced malignant skin melanoma in melanoma-susceptible transgenic mice. Cancer Res 1994;54:4569-72. [27.] Gilchrest BA. Sunscreens--a public health opportunity [Editorial]. N Engl J Med 1993;329:1193-4. [28.] Drug facts and comparisons. St. Louis: Facts and Comparisons, 1994:562a-k. [29.] Stenberg C, Larko O. Sunscreen application and its importance for the sun protection factor. Arch Dermatol 1985;121:1400-2. [30.] Loesch H, Kaplan DL. Pitfalls in sunscreen application [Letter]. Arch Dermatol 1994;130:665-6. [31.] Mommaas AM, van Praag MC, Bouwes Bavinck JN, Out-Luiting C, Vermeer BJ, Claas FH. Analysis of the protective effect of topical sunscreens on the UVB-radiation-induced suppression of the mixed-lymphocyte reaction. J Invest Dermatol 1990; 95:313-6.

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