Madison Avenue has sold the idea to the American consumer that it is both healthy and fashionable to have a glowing suntan. However, "healthy" and "suntan" may be contradictory, as evidence is mounting that the sun can have not only short-term but also long-term deleterious effects. Public awareness of the hazards of long-term sun exposure were heightened when President Reagan developed a basal cell carcinoma on his nose. In spite of increased press coverage, a visit to the beach or local pool demonstrates that many people have not learned the lesson that the sun is not always their friend!
Solar energy consists of visible, infrared, and ultraviolet rays (Figure I). Visible rays have a minor effect on the skin, while infrared rays cause primarily a sensation of heat. Wavelengths which mainly affect the skin are in the ultraviolet range. Ultraviolet A (UVA) rays are those between 320 and 400 nanometers (nm), ultraviolet B (UVB) 290 and 320 nm, and ultraviolet C (UVC) between 200 and 290 nm. Longer wavelengths penetrate the skin further, so that UVA penetrates deeper into the dermis than UVB, and probably has more effect on the breakdown of collagen. UVB penetrates only as far as the epidermis and therefore a sunburn (which affects primarily the epidermis) is the major side effect of overexposure to UVB. Representing 0.2% of the sun's total energy, UVB is known as the "sunburn spectrum" of radiant energy.
UVA can cause inflammation and erythema of the skin but only at much higher doses than UVB. In the long run, UVA may be just as (if not more) damaging to cutaneous tissue as UVB, because UVA not only intensifies UVB erythema but also accelerates the aging process of skin and increases the risk of UVB carcinogenesis, In work done with hairless mice, those mice given UVA plus UVB as compared with those given either UVA or UVB alone had a greater number of skin cancers than controls. ' UVC is absorbed in the upper atmosphere so that it does not reach the earth. Experimentally produced UVC1 however, can cause erythema as well as carcinomas in mammalian skin.
In order for a photoreaction to occur, two events must take place. First, light must be absorbed by the molecules that undergo the reaction. Light that is transmitted through or reflected from the skin is not absorbed and will not evoke a chemical or biologic change. Secondly, the radiation must have sufficient energy to cause a reaction. The wavelengths of light (or energy) necessary to cause a reaction constitute the action spectrum. A photoreaction takes place when there is absorption of light by a molecule in a ground state with the resultant transfer of energy. Molecules that absorb ultraviolet light in the skin are mainly nucleic acids and proteins, and have specific absorption spectra which for the most part are in the UVC and UVB ranges. Photosensitizing chemicals which may also be in the skin or blood stream such as méthylène blue, 8-methoxypsoralen, or endogenous porphyrins can absorb radiant energy and cause photoreactions.
Figure 1. Energy spectrum of solar energy
When unprotected skin is exposed to sunlight, either a photoallergic or phototoxic reaction can occur. The most common adverse reaction to the sun is the phototoxic reaction, with sunburn as the classic example (Figure 2). Manifested clinically by erythema, pain, and edema, a sunburn usually begins several hours after exposure, reaches a peak at 14 to 20 hours, and lasts a total of 24 to 48 hours. If damage is severe, erythema may be followed by desquamation and/or hyperpigmentation (Figure 3).
Photoallergic reactions are uncommon, depend upon circulating antibodies, and occur either in the presence or absence of a photosensitizer. Clinically, one sees either an immediate urticarial wheal or a delayed eczematous eruption that can extend beyond the area of immediate exposure. Areas that have been previously involved may show reinvolvement if a distant site is challenged with UVL. In general, these reactions require less energy than do phototoxic reactions.
When sunburn takes place, three responses occur in the dermis: 1) vasodilatation, caused either by direct action of UV on the blood vessels or by chemical mediators; 2) increased vascular permeability with extravasation of fluid into tissues; and 3) leukocyte migration to the site of damage. Chemical mediators which have been implicated in these processes include histamine, serotonin, lysosomal hydrolytic enzymes, kinins, prostaglandins, leukotrienes, and vasoactive products from the activation of the complement cascade. Local prostaglandin formation is probably responsible for some of the clinical symptoms of sunburn.2
The tanning response actually occurs in two distinct phases, an immediate response and a delayed response. The first is caused by the photo-oxidation of melanin chromoproteins, which are already present in the melanocytes. Delayed tanning develops when there is an increase in the formation of melanosomes and increased transfer of melanosomes to the keratinocytes, notable at 2 days and reaching a peak at 19 days. Melanin protects the skin in two ways. It not only absorbs UVB but also serves as a "sponge" which mops up free radicals. This explains why fair skinned individuals with less melanin tend to have more actinic damage than darker skinned people who have more melanin.
Figure 2. Delayed erythema response to sunburn. The persistent redness (erythema) following UVL exposure is caused by the increased blood content in the superficial dermal blood vessels.
Figure 3. Acute sunburn reaction : Superficial desquamation several days after erythema.
Light microscopy reveals epidermal changes in sunburned skin within 24 hours of exposure. Dyskeratotic celts (damaged epidermal cells) in the Malpighian layer, known as "sunburn" cells, are seen first. By 48 hours there is damage throughout the epidermis, and by 72 hours regeneration begins to take place. The dyskeratotic cells then form a superficial desquamating layer. At 96 hours there is a great increase in the number of melanocytes which have arborized their dendrites, * beginning the tanning process.
SKIN TYPES AND RECOMMENDED SUNSCREEN PROTECTION FACTORS
Electron microscopic changes in the skin can be seen even earlier than light microscopy.4 Within 5 hours after exposure to UVB, the cytoplasm and keratinosomes of epidermal cells show cell injury.
Not only is there structural damage to epidermal cells, but functional damage occurs as well. Slowing of DNA, RNA, and protein synthesis and a depressed rate of mitosis is followed by a burst of activity probably related to the repair process. By 24 hours recovery takes place, and by 48 to 72 hours there is an acceleration of protein synthesis. With repeated UV exposure, accelerated cellular damage-repair cycles occur, thereby increasing the chance of errors in protein synthesis and with it the possibility of mutagenesis or carcinogenesis. 5
Whether or not a person develops a sunburn depends upon a number of factors: 1) the length of exposure; 2) the patient's skin type; 3) the direction of the sun's rays; 4) time of day during exposure; 5) geographical location; 6) altitude; and 7) age. Infants and young children are thought to be at risk because of the thinness of the outer epidermis. The body is better protected in older age groups when the skin becomes thicker and oilier.
Recognition of the basic differences in tanning and burning has led to the classification system (Table 1) that categorizes people according to clinical history.6 There are six basic types of skin (Figure 4).
Direct sun rays, high altitude, and tropical location are all factors which increase solar energy received by the skin. The time of day is important. For example, in Atlanta, Georgia on June 1, it takes approximately 46 minutes to turn average untanned skin red (the "minimal erythema dose") beginning at 10 AM, while it only takes 23 minutes to achieve the same effect at 12 noon.7 Dobes7 further points out that sun intensity is high from 10 AM until SPM, not 10 AM to 2 PM, which has been dogma in the past.
Repeated UV irradiation of caucasoid skin not only causes acute toxic reactions such as sunburn but also causes chronic changes, including wrinkling, hyperpigmentation, hypopigmentation, telangiectasias, atrophy, actinic kératoses, and nonmelanotic skin cancers3 (Figures 5 through 7). With increased exposure, leathery changes of the skin of the posterior neck, known as cutis rhomboidalis nuchae, are commonly seen (Figure 8).
An inverse relationship between solar elastosis and skin color exists, so that persons with skin types IV, V1 and VI will not have the same amount of acute and chronic sun damage as their fair skinned counterparts.
Histologically, the epidermis in chronic damage shows disorderly arrangement and thinning. The dermis demonstrates a loss of collagen and degeneration of elastic tissue, known as actinic elastosis, which can be seen as early as the first decade of life.8
Chronic sunlight exposure affects not only the epidermal cells and dermal nbroblasts but the systemic and epidermal immune systems as well. In mice, UVB radiation induces the generation of suppressor T lymphocytes, which suppress immune recognition of UV radiation induced skin tumors.9 In humans, an increase in circulating suppressor T cells and reduction in circulating helper T cells can be demonstrated.10 Commercial solarium irradiation (which has more UVA than sunlight) depletes immunocompetent Langerhans cells in man, with the resulting potential for skin cancer formation.11
Figure 4. Six basic skin types. A, Type I, bums easily, never tans. B, Type II, bums easily, tans minimally. C, Type III, bums moderately, tans gradually D, Type IV burns minimally tans well. E, Type V rarely burns, tans profusely. F, Type Vl, never bums, deeply pigmented.
ABNORMAL RESPONSES TO SUN
Other adverse reactions to the sun may be caused by the lack of melanin protection, or the presence of a photosensitizer in the skin. Diseases which cause disturbance in pigment formation and therefore a lack of protection include albinism, vitíligo, phenylketonuria, and Chediak-Higashi syndrome. Photosensitizers which may be either endogenous or exogenous can produce abnormal reactions when light energy is absorbed, causing either phototoxic or photoallergic reactions. The prototype of an endogenous photosensitivity is porphyria. Most types of porphyria cause photoreactions except acute intermittent porphyria and hereditary coproporphyria. The primary action spectrum for these diseases is 400 to 410 nm,12 the so-called Soret Band.
Systemically administered exogenous photosensitizers produce phototoxic reactions which clinically resemble an exaggerated sunburn. Such substances include psoralens, tetracycline, sulfonamides, and thiazide diuretics. Photosens i ti zers which can be applied topically include lime oil, oil of cedar, vanilla oils, oil of lavender, and sandalwood oil. Certain substances found in plants called furocoumarins may also cause photosensitive reactions which begin 24 hours after exposure. The severity of a photosensitive reaction can range from a mild erythema to severe blistering. Postinflammatory hyperpigmentation usually follows this type of photosensitive reaction.
Figure 5. Note the contrast between chronically exposed and unexposed skin.
Figure 6. Chronic actinic damage with actinic keratoses, atrophy, and purpura.
Figure 7. Telangiectasias over the cheek of a man who had many basal cell carcinomas.
Figure 8. Cutis rhomboidalis nuchae. Thickened, lichenified. leathery skin of the neck.
Polymorphic light eruption (PMLE) is an uncommon eczematous dermatitis which involves sunexposed sites and may spill over on to uninvolved skin. Several hours or days after exposure the dermatitis appears. It can begin at any age from childhood to old age and has no sex predilection. Although PMLE may be chronic and tends to flare every spring, it often paradoxically becomes better with repeated sun exposure throughout the summer (called "hardening").
Other diseases which may be exacerbated by sunlight include herpes simplex and systemic lupus erythematosus, as well as rare conditions such as pellegra (niacin deficiency), Hartnup disease, Rothmund-Thomson syndrome, Bloom's syndrome, Cockayne's syndrome, and xeroderma pigmentosa. Xeroderma pigmentosa is a genetic disorder characterized by impaired DNA repair after UVL exposure and cutaneous malignancies that develop at a very early age. Psoriasis, which under most circumstances is helped by sunlight exposure, may be exacerbated if a sunburn occurs (Figure 9). Therefore, it is important to caution psoriatic patients not to burn their skin while sunbathing or undergoing light therapy.
Because sunlight may exacerbate certain skin problems and cause both acute and chronic changes, fair skinned individuals should be protected as much as possible (Figure 10). Skin cancer increases with increased sun exposure. Although skin cancers occur more commonly in whites than in blacks, no person is immune. The overall annual incidence of malignant melanoma in the United States among Caucasians is 4-5/100,000 per year, while Blacks have an incidence of 0.6/100,000 per year.13 Nonmelanotic tumors are associated with the total amount of accumulated sun exposure, whereas melanomas have been associated with short, intense sun exposure.14 In other words, severe sunburns during childhood may predispose a susceptible person to develop melanoma in later life.
Some of the risk factors for the development of nonmelanotic skin cancers are: 1) fair skin (types I and II); 2) residence in the southern United States; 3) positive family history of skin cancer; and 4) outdoor lifestyle. A study of professional women golfers demonstrated that they developed basal cell carcinomas more frequently and at a younger age than their amateur counterparts.15
Sun damage is cumulative. Therefore, it makes sense to avoid any extended exposure. Ideally, this would be accomplished by staying out of the sun entirely, but this is neither practical nor desirable. The next best advice is to avoid the strongest radiant energy and to use sunscreens liberally.
Topical sunscreens are divided into three major types: those which form a physical barrier, those which absorb UVB, and those which block UVA (Table 2). Zinc oxide and titanium dioxide form physical barriers which reflect and scatter UVB. Absorbers of UVB include para-aminobenzoic acid (PABA) and its derivatives. An example of a UVA-absorbing chemical is benzophenone. The effectiveness of an absorbing sunscreen is rated by its "sun protection factor" (SPF) (Table 3), which is the ratio of the time it takes to develop erythema (redness) with the sunscreen applied compared to the time it takes to develop erythema without the sunscreen. li> With an SPF of 10, for example, a person may spend 10 times longer in the sun without getting a sunburn.
EXAMPLES OF COMMON SUNSCREENS
In general, those people with skin which bums easily and tans poorly should use the most protection, such as SPF 15-23. In addition to a chemical sunscreen, children should wear protective clothing that covers as much skin as possible, for example, a light long sleeve shirt and broad brimmed hat. Some methods of "protection," however, are not as effective as commonly thought. Thin, wet clothing may actually be transparent to UV light. Beach umbrellas and other shade devices may reduce sun exposure only by 50%.
UVB unfortunately does not generate a perception of warmth unless the skin is already burned. Consequently, a person does not realize the damage until it is too late. On cloudy and overcast days, visible light and infrared rays, both of which cause a sensation of warmth, are filtered out. However, as much as 80% of the UVB radiation can get through. Therefore, a person can easily get burned on a cloudy day.
Sunscreens, in order to be effective, must be used! And in order to be used they should be cosmetically acceptable, reasonably priced, retained on the skin through swimming and sweating, and not allergenic or irritating (Table 4). PABA has been widely accepted for these reasons. However, some patients may become allergic to PABA or to related chemicals such as sulfonamides and benzocaine.17 PABA may stain clothing and have a tingling sensation when applied. Despite these objections, PABA is the most effective and the most used UVB blocker on the market. Benzophenones partially block UVA1 and should be used primarily to protect patients with porphyria or polymorphous light eruption where UVA is part of the action spectra.
Children are more likely to use the lotion or gel forms of sunscreens rather than the alcohol forms because the alcoholic solutions of PABA tend to bum and sting when applied. Children definitely should use the water-resistant and sweat-resistant forms (see Table 3). Most sunscreens will cause ocular irritation, so patients should be warned against rubbing their eyes.
It has been estimated that with the regular use of an SPF 15 sunscreen during the first 18 years of life, the lifetime incidence of nonmelanoma skin cancers would be reduced by 78%. 18
TOPICAL SUNSCREENS ARE EVALUATED BY SPF
TREATMENT OF SUNBURN
Scientists have looked for drugs, including certain steroids and an ti- inflammatory agents, that could reduce the inflammatory reaction of UVB and UVA. However, the effectiveness of these agents has not been substantiated in well-controlled studies. Aspirin is an excellent analgesic for early erythema, probably because of its effects on prostaglandin synthesis, but it has not been shown to be effective against the delayed erythema reaction which peaks at 24 hours. l6 Topical indomethaein has been reported to decrease erythema after UVB exposure. 19 However, if heavily applied it could potentially cause systemic toxicity from absorption. For these reasons it seems prudent to treat sunburn with oral aspirin and cool compresses, which will relieve symptoms and not cause excessive toxicity. Topical anesthetics such as benzocaine should be avoided since they have the potential to sensitize the skin, causing allergic eczematous reactions.
Topical aloe vera, jojoba oil, and vitamin E have all been touted by the media to have special powers to alleviate sunburn reactions. The efficacy of these agents has not been well studied. 16 Bland emollients such as petrolatum and cool soaks are good alternatives.
How can we as physicians prevent sun damage in our patients? Making the public more aware of chronic damage from UV light is just the beginning. We must also destroy the misconception that a glowing tan is desirable and healthy. Physicians should realize that a sunburn represents damaged skin, and dispel the myth that only patients with sunburn will develop cancer. Education of our patients should begin early with repeated emphasis on the cumulative effects of the sun. Measures to prevent sun damage should be discussed as part of the health maintenance program at well child examinations. Parents should be encouraged to use sunscreens liberally both on themselves and their children beginning in infancy,17 to wear lightweight protective clothing, and to perform outdoor activities either in the early morning or in the late afternoon. With an intense educational effort the increasing incidence of skin cancer and solar damage may hopefully decrease.
TOPICAL SUNSCREENS WITH SPF 15
1. Willis I, Menici JM, Whyte HJ: The rapid induction of cancers in the hairless mouse utilizing the principle of photoaugmentation. J Iravtt Demuxol 1981; 76:404-408.
2. Black AK, Greaves MW. Hensbv CN, et al: Increased prostaElandins E; and F; in human skin 6 and 24 hours after UVB irradiation (290-Ì20 nm). BrJ Clin Prmrmocni 1978; 5:431-436.
3. Epsrein JH: Adverse cutaneous reactions to the sun. Year Boul· uf Dermatology 1971. Chicago, Year Book Medical Publishers, Inc.. pp 5-43.
4. Wilgam GF. Kidd RL. Kraivczvk WS, et al; Sunburn effect on keratinitsomes. Arch Dermaol 1970; 101:505-519.
5. Rih-FiCpairick MB: The biologic actions of solar radiation on skin with a note on sunscreens. J Dermaial Sun; Oncol 1977; 3(21:199-204.
6. Pathak MA: Sunscreens; Topical und systemic approaches fin protection of human skin against harmful effects of solar radiation. J Am Acod Derma»/ 1982; 7:285-ÌI2.
7. Dobes WLt Public education: An approach. J Am Acad DermonJ 1986; 14:676-679.
8. Kligman AM: Early destructive effect of sunlight on human skin. JAMA 1969; 210:2377-2380.
9. Fisher MS, Kripke ML: Further studies on the tumor-specific suppressor cells induced by ultraviolet radiation. } immutici 1978; 121:1139-1144.
10. Hersey P, Hasic E, Edwards A, et al: Immunologies! effects of solarium exposure. lanca 1983; 1:545-548.
11. Scheibnor A, Mollis DE, McCarthy WH, et al: Effects of sunlight exposure on Langerhans cells and melanocytes in human epidermis. Photodermaiokigy 1986; 3:15-25.
12. Magnus IA: The cutaneous porphyrias. Semin Hemaluì 1968; 5:380-408.
13. Finparrick TB. Sober AJ. Mihm MC, et al: Malignant melanoma of the skin, in ittersdorf RG, Adams R, Braunwald E, et al (eds): Harrison'i Principle! of internal Mediane. New York. McGraw Hill, 1983.
14. Finpatfick TB, Sober AJ: Sunlight and skin cancer. N EngîJMed 1985; 313:818-819.
15. Hanke CW: Skin cancer in the sports world; A study of skin cancers in women golfers. Sun Cancer ftrcndanon J 1985; 15.
16. Pathak MA: Sunscreens. Dermotd Clinics 1986; 4:321-334.
17. Norins AL: Sunscteens for children. .IAMA 1986; 255:2809.
18. Stem RS. "Jfeinstein MC, Baker SG: Risk reduction for nonmelanoma skin cancer with childhood sunscreen use. Arch Dermoidi 1986; 122:537-545.
19. Snyder DS, Eafilstein WH: Topical indomeihacin and sunburn. Br J DermaioJ 1974; 90:91-93.
Figure 1. Energy spectrum of solar energy
SKIN TYPES AND RECOMMENDED SUNSCREEN PROTECTION FACTORS
EXAMPLES OF COMMON SUNSCREENS
TOPICAL SUNSCREENS ARE EVALUATED BY SPF
TOPICAL SUNSCREENS WITH SPF 15