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Sun and Active Patients

Preventing Acute and Cumulative Skin Damage

Jaime L. Davis, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 7 - JULY 2021


In Brief: Damage from long-term, cumulative effects of sun exposure, while slow to develop, can become life-threatening. The cutaneous effects of ultraviolet light include sunburn, photosensitivity, immunosuppression, premature aging, and several types of skin cancer. Clinicians need to know the characteristic appearance of premalignant lesions, basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Also, patients who are active outdoors need education about sun protection, including avoidance at peak hours, clothing, sunglasses, and sunscreens. Care for sunburn may involve cool compresses, corticosteroid cream, oral antihistamines, and anti-inflamatory drugs.

Sports-related injury to the skin can be immediately apparent, such as a hematoma, laceration, or sunburn at the end of a long day of competition. However, subtle but cumulative cutaneous injury from repeated sunlight exposure over time can be far more damaging. Knowledge of these harmful effects and techniques to prevent them should be indispensable components of every outdoor athlete's sports strategy.

Photobiologic Principles

The solar radiation spectrum spans wavelengths from 270 to 5,000 nm. The study of cutaneous photobiology primarily involves wavelengths from 270 to 800 nm. These wavelengths are subdivided into several classifications (figure 1: not shown).

Visible light (400 to 800 nm) is the white light we can see. It can be separated into the seven familiar colors of a rainbow by passing a beam of white light through a prism. Visible light is poorly absorbed by the ozone layer; therefore, most of it reaches the earth's surface.

Ultraviolet A (UVA) (320 to 400 nm) is most familiar as "black light." The characteristic blue-black color is seen when all other wavelengths are filtered out. UVA rays, however, are not visible when they occur naturally as part of the solar radiation spectrum. Like visible light, UVA is poorly absorbed by the ozone layer and therefore reaches the earth's surface in abundance. This wavelength is mainly responsible for cutaneous aging changes (think "A" for aging) (1).

Ultraviolet B (UVB) (290 to 320 nm) is moderately well absorbed by the ozone layer, but significant amounts reach our skin. UVB is mainly responsible for cutaneous carcinogenesis and sunburn (think "B" for burn) (2). It is important in cutaneous vitamin D metabolism, especially if dietary vitamin D intake is poor.

Ultraviolet C (UVC) (200 to 290 nm) is well absorbed by atmospheric ozone, so relatively little reaches our skin. A source of UVC that does reach our skin is from halogen lightbulbs. This wavelength has a role in the development of sunburn and leads to a protective thickening of the epidermis with chronic exposure, as does UVB (3).

Infrared radiation (above 800 nm) is felt as heat when it reaches the skin. Vasodilation causes mild, transient erythema as the skin attempts to cool down. Infrared radiation is absorbed by the water droplets in clouds, so on a cloudy day, its heating effect is attenuated. UVA and UVB, however, are not well absorbed by clouds and though the skin will not feel as hot on a cloudy day, it is still susceptible to the effects of ultraviolet light.

Cutaneous Effects of Ultraviolet Light

Sunburn. When the shorter-wavelength UVB light is absorbed by the vulnerable upper layers of the epidermis, it causes redness of the skin via direct damage to keratinocytes and subsequent release of inflammatory mediators (4,5). In contrast, the longer-wavelength UVA penetrates the skin more deeply and is absorbed by melanocytes, elastin, and collagen. UVA contributes relatively little to sunburn erythema.

The skin is exposed to greater amounts of UVA and UVB radiation at higher altitudes, where less atmospheric ozone filtration of UV rays occurs. This is also true when the sun is directly overhead; therefore, exposure between 10 am and 2 pm can be particularly intense. Equatorial latitudes are especially vulnerable to this effect. On hot, humid days, the effect of UV light is likewise magnified, since the air density is lower, thus reducing UV filtration (6,7).

Tanning. UV light causes both an immediate and a delayed protective response. Immediate pigment darkening occurs via oxidation of preexisting melanin and redistribution of preexisting melanosomes within melanocytes. This effect fades within minutes after exposure. The delayed-onset and longer-lasting tanning effect begins 48 to 72 hours after exposure to UVA and UVB. The UV-stimulated melanocytes divide, increase their synthesis of melanin (8), and distribute melanosomes to epidermal keratinocytes (9). This tan may remain visible from several days to a few weeks. Darker skin has more abundant melanin, giving it more natural protection from UV than lighter skin.

Pigment darkening because of UVA and UVB light imparts protection from subsequent exposure. The relative protection, however, is greater from UVB-induced darkening. This is because the tan from UVA primarily affects the basal layer, whereas the UVB tan occurs throughout the epidermis (10). This "protection," however, comes at the cost of an increased risk of photoaging and carcinogenesis. The pigment darkening from tanning beds (artificial UVA sources) is not only inadequate sun protection, but the gratuitous radiation contributes to photoaging and skin cancer risk. Tanning beds should therefore be avoided unless specifically recommended by a dermatologist for medical purposes.

Photoinduced pigment darkening may occur unevenly and is commonly seen as freckling, melasma, "liver spots," or other blotchy discoloration in areas subject to long-term sun exposure, such as the face, dorsal hands, and forearms.

Photosensitivity. Many skin diseases are aggravated or triggered by sunlight exposure. These include metabolic and genetic abnormalities such as porphyrias, oculocutaneous albinism, and xeroderma pigmentosum. Various immunologic diseases with cutaneous manifestations, such as lupus erythematosus, solar urticaria, and polymorphous light eruption are also included in this group (11,12).

Photosensitivity may also be induced by oral medication. Common culprits are diuretics, tetracycline antibiotics (particularly doxycycline), sulfa drugs, and nonsteroidal anti-inflammatory agents such as naproxen sodium. The reaction resembles a sunburn and involves direct cell damage, independent of immunologic mechanisms, and is most commonly due to UVA wavelengths (13).

Photoimmunosupression. Exposure to UVA and UVB light can suppress certain delayed-type hypersensitivity responses, such as allergic contact dermatitis (14). Therapeutic use of light (natural or artificial) is based on this effect. These wavelengths can also generate suppressor T-lymphocytes, which have been shown to inhibit tumor rejection (15). This phenomenon is believed to play a role in the development of cutaneous malignancy. The immunosuppressive effect of UV rays also accounts for sun-induced recurrences of herpes simplex labialis (cold sores).

Photoaging. The damaging effects of UVA on collagen and elastin are manifested as premature aging and wrinkling of chronically sun-exposed skin. Collagen and elastin fibers lose their resilience over time and appear thickened and clumped on biopsy specimens of photoaged skin. This "solar elastosis" accounts for the leathery appearance of exposed skin and is also termed "dermatoheliosis."

Photoaged skin also demonstrates epidermal thinning, irregular pigmentation, and telangiectasia (16). Collectively, these changes are referred to as poikiloderma and are commonly seen on the sides of the neck, while the skin in the shadow of the chin is characteristically spared.

Premalignant lesions. Actinic keratosis or solar keratosis is a common precancerous change consisting of rough red patches, most commonly on the exposed skin of the scalp, face, upper back, hands, or forearms (figure 2: not shown). These are easily treated with liquid nitrogen cryotherapy and daily sun protection. If left untreated, actinic keratosis can evolve into squamous cell carcinoma. The lower lip is another area susceptible to precancerous actinic damage. This leads to a progressive white discoloration of labial skin (leukoplakia), which, like actinic keratoses elsewhere, can evolve into squamous cell carcinoma.

Photocarcinogenesis. Development of skin cancer is largely an effect of UVB radiation. Cumulative unprotected sun exposure increases the risk of developing premalignant and malignant cutaneous lesions, especially in lighter skin types that have less natural protection from melanin. UV-induced carcinogenesis is believed to result from pyrimidine dimer formation leading to damage of nuclear DNA (17,18). In most instances, the damage is spontaneously repaired by endonucleases; however, when DNA repair mechanisms fail (eg, because of genetic defects or immunosuppression), abnormal cell proliferation can occur, leading to tumor formation (19).

Malignant Lesions

There are three main types of cutaneous carcinoma.

Basal cell carcinoma is the most common skin cancer. It typically appears as a slow-growing, pink to red, pearly, translucent papule. Carcinomas of this type typically involve the face (particularly the nose) or ears but can occur elsewhere (figure 3: not shown). Treatment involves complete surgical excision, daily sun protection, and close follow-up by a dermatologist. If left unattended, a basal cell carcinoma can cause disfiguring local tissue destruction, but this type of carcinoma rarely metastasizes.

Squamous cell carcinoma is the second most common skin cancer. It typically appears as a keratotic or crusted erythematous nodule on a background of sun-damaged skin, most commonly on the scalp, face, upper back, hands, or forearms (figure 4: not shown). As with basal cell carcinomas, treatment involves complete surgical excision, daily sun protection, and close follow-up by a dermatologist. If left untreated, a squamous cell carcinoma can invade deeply, resulting in fixation of the skin to the underlying tissues, and it may metastasize, especially if the tumor develops on a mucous membrane.

Malignant melanoma is less common than the previous two carcinomas, but it is far more dangerous because of its high metastatic potential, so prevention and early detection are critical. The lifetime risk of melanoma is steadily increasing in the US population. The American Academy of Dermatology estimates that there will be about 47,700 new cases diagnosed and 7,700 deaths attributable to melanoma in the United States in 2021 (20).

A malignant melanoma typically appears as an irregularly shaped, asymmetrically shaded brown to black macule on sun-exposed skin (figure 5: not shown). Melanoma can also occur in sun-protected areas. Complete skin screening in high-risk individuals is necessary, including those with light hair and eyes, multiple sunburns, and/or a family or personal history of melanoma. The key clinical features of lesions with a higher likelihood of malignancy are summarized in the ABCD mnemonic. "A" is for asymmetry of shape, "B" for border irregularity, "C" for color change or irregularity, and "D" for diameter greater than 6 mm (21). If any of these features is noted, an examination by a dermatologist is warranted.

Treatment includes a complete history and physical exam incorporating a full skin and lymph node examination and relevant lab tests for staging. Complete surgical excision of the malignant melanoma, appropriate adjunctive therapy, and close follow-up are also essential. It is important that the patient receive education on the necessity of daily sun protection and self examination of the skin.

Sun Protection

Today's options for effective protection from UV damage are numerous. Choosing a combination of at least two modes provides the best protection from short-term burning and long-term photoaging and photocarcinogenesis. Lighter skin has less constitutive protection (melanin) from sunlight than does darker skin; therefore, lighter individuals must be especially meticulous and consistent in using sun protection, but individuals of any skin type should protect their skin from the sun.

Self-tanning preparations darken the skin by staining epidermal keratin, and while this method of acquiring a tan is preferable to UV light exposure, the tan from these products provides little or no photoprotection. Therefore, other methods of sun protection must be used. These options include:

Sun avoidance when possible. Midday (10 am to 2 pm) exposure to sunlight, when UV rays are most intense, should be avoided or minimized. If your shadow is shorter than you are, the damaging rays of the sun are at their strongest, and you're likely to sunburn (20).

Sun-protective clothing, such as long-sleeved shirts and pants made from a tightly woven, lightweight fabric, are excellent adjuncts to topical sunscreens, activity permitting. The fabric should be fast drying because wet clothing is more transparent to UV rays than dry clothing. A wide-brimmed hat adds extra protection for the nose, ears, throat, and neck.

Sunglasses help protect the eyes from UV damage that can result in cataract formation (21). A quality pair of UVA- and UVB-screening sunglasses, preferably in a wraparound style, should be worn outdoors in all daylight hours, activity permitting. Glasses that are merely darkly tinted, but do not screen UVA and UVB rays, should be avoided.

Chemical sunscreens act by chemical absorption of UV light. Newer agents, like benzophenones (including Parsol 1789), absorb both UVA and UVB light and are referred to as "broad spectrum." A broad-spectrum sunscreen with a sun protective factor (SPF) of at least 15 should be worn every day year round, even on cloudy days, to prevent cumulative skin damage from UV rays. To be most effective, these sunscreens should be applied at least 1 hour before sun exposure to be adequately absorbed into the stratum corneum (22). Sunscreens should be reapplied every 2 hours during activity, especially after swimming. A waterproof/sweatproof sunscreen with an SPF of 30 to 45 is optimal for outdoor sporting activities.

Physical sunscreens are broad-spectrum agents that protect the skin from both UVA and UVB rays by scattering UV light. These products typically contain micronized titanium dioxide or zinc oxide. The micronizing process renders the preparations transparent when applied, unlike the older, visibly white formulations. Physical sunscreens are effective immediately when applied since no absorption is necessary, but these must be reapplied during activity and after swimming. The SPF guidelines mentioned above apply for physical sunscreens also.

In Case of Sunburn

If the above measures fail (or are not employed) and sunburn occurs, the discomfort, erythema, and risk of blistering may be reduced with some simple measures. Cool tap water compresses applied over a low- or mid-potency topical corticosteroid cream for 1 hour three times a day for the first 24 to 48 hours are soothing and anti-inflammatory. Oral antihistamines and oral anti-inflammatory agents help counteract the histamines and prostaglandins released in the skin during an acute sunburn. Oral prednisone is rarely necessary, but a short course may be used to help quiet a more severe sunburn.

Complete Skin Care

Complete care of active patients involves care of their skin. Familiarity with the effects of UV light is important for athletes and those responsible for their care. Regular and consistent sun-protection measures help keep the outdoor athlete active by preventing sunburn, photoaging, and photocarcinogenesis. Sunscreens are most effective at preventing premature aging and skin cancer when applied daily, especially to the face. Sunburn is best prevented when sunscreens are applied prior to sun exposure and reapplied frequently during activity. Sunburn, skin cancer, and even photoaging can indeed be treated, but the best treatment is prevention.

References

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  2. de Gruijl FR: Skin cancer and solar UV radiation. Eur J Cancer 1999;35(14):2021-2021
  3. Epstein JH, Fukuyama K, Fye K: Effects of ultraviolet radiation on the mitotic cycle and DNA, RNA and protein synthesis in mammalian epidermis in vivo. Photochem Photobiol 1970;12(1):57-65
  4. Gilchrest BA, Soter NA, Stoff JS, et al: The human sunburn reaction: histologic and biochemical studies. J Am Acad Dermatol 120211;5(4):411-422
  5. Kaidbey KH, Kligman AM: The acute effects of long-wave ultraviolet radiation on human skin. J Invest Dermatol 1979;72(5):253-256
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  7. Owens DW, Knox JM, Hudson HT, et al: Influence of humidity on ultraviolet injury. J Invest Dermatol 1975;64(4):250-252
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  9. Stierner U, Rosdahl I, Augustsson A, et al: UVB irradiation induces melanocyte increase in both exposed and shielded human skin. J Invest Dermatol 120219;92(4):561-564
  10. Gange RW, Blackett AD, Matzinger EA, et al: Comparative protection efficiency of UVA- and UVB-induced tans against erythema and formation of endonuclease-sensitive sites in DNA by UVB in human skin. J Invest Dermatol 120215;85(4):362-364
  11. Cavallo J, DeLeo VA: Sunburn. Dermatol Clin 120216;4(2):181-187
  12. Fitzpatrick TB, Eisen AZ, Wolff K, et al, (eds): Dermatology in General Medicine, ed 4. New York City, McGraw-Hill, 1993, pp 1661-1677
  13. Gonzalez E, Gonzalez S: Drug photosensitivity, idiopathic photodermatoses, and sunscreens. J Am Acad Dermatol 1996;35(6):871-885
  14. Kim TY, Kripke ML, Ullrich SE: Immunosuppression by factors released from UV-irradiated epidermal cells: selective effects on the generation of contact and delayed hypersensitivity after exposure to UVA or UVB radiation. J Invest Dermatol 1990;94(1):26-32
  15. Baadsgaard O, Salvo B, Mannie A, et al: In vivo ultraviolet-exposed human epidermal cells activate T suppressor cell pathways that involve CD4+CD45RA+ suppressor-inducer T cells. J Immunol 1990;145(9):2854-2861
  16. Pearse AD, Gaskell SA, Marks R: Epidermal changes in human skin following irradiation with either UVB or UVA. J Invest Dermatol 120217;88(1):83-87
  17. Tan EM, Stoughton RB: Ultraviolet light induced damage to desoxyribonucleic acid in human skin. J Invest Dermatol 1969;52(6):537-542
  18. Sutherland BM, Harber LC, Kochevar IE: Pyrimidine dimer formation and repair in human skin. Cancer Res 120210;40(9):3181-3185
  19. Hart RW, Setlow RB, Woodhead AD: Evidence that pyrimidine dimers in DNA can give rise to tumors. Proc Natl Acad Sci USA 1977;74(12):5574-5578
  20. American Academy of Dermatology: Melanoma/skin cancer detection and prevention, 2021 melanoma fact sheet. Shaumberg, Illinois, American Academy of Dermatology, 2021
  21. Fitzpatrick TB, Eisen AZ, Wolff K, et al (eds): Dermatology in General Medicine, ed 4. New York City, McGraw-Hill, 1993, pp 1078-1115
  22. Habif TB: Clinical Dermatology: a Color Guide to Diagnosis and Therapy, ed 3. St Louis, Mosby, 1996, pp 603-604

Dr Davis is a consultant in dermatology at Albert Lea Medical Center in Albert Lea, Minnesota. Address correspondence to Jaime L. Davis, MD, Albert Lea Medical Center, 404 W Fountain St, Albert Lea, MN 56007.


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