CIESIN Reproduced, with permission, from: Prawer, S. E. 1991. Sun-related skin diseases. Postgraduate Medicine 89 (8): 51-66.

Sun-related skin diseases


Persons who avoid the sun often reach old age with relatively smooth, unblemished skin, whereas those who are repeatedly exposed to ultraviolet light risk sunburn, premature aging of the skin, and cancer. Dr Prawer explains the deleterious effects of sunlight on the skin and recommends that methods of photo-protection be explained to all patients.

Steven Earl Prawer, MD

Ultraviolet (UV) radiation affects human skin continuously from birth to death. In addition to acute adverse effects such as sunburn, chronic exposure may cause premature aging of the skin, actinic keratoses, and basal and squamous cell carcinoma.

To compound the problem, the "perfect tan" can now be maintained all year by visiting commercial tanning salons. (Adolescent girls and young women are the most frequent patrons.) The equipment in tanning booths can emit five times more ultraviolet A (UVA) radiation per unit of time than solar radiation measured at the equator.[1] This may result in damaging biologic effects on the skin. Even an ultraviolet B (UVB) emission of 1% from the equipment used at tanning salons can significantly increase the potential for skin cancer.[1]

Acute effects of sun exposure

The acute adverse effects of sun exposure on the skin include phototrauma (sunburn), photosensitivity, and tanning.

PHOTOTRAUMA--This is the initial actinic or solar insult to the skin. Redness is produced by vasodilation and increased blood flow in the dermis. Biochemically, it is a manifestation of (1) damage to membranes and to DNA, (2) transient disturbances in protein synthesis, and (3) elaboration of many cytokines and inflammatory mediators.[2] Pain and itching are produced by the effect of chemical mediators on the nerve endings.

All three wavelengths of UV radiation (see box on page 54)[14] cause phototrauma. The epidermis absorbs ultraviolet C (UVC) and UVB radiation, but UVA radiation penetrates into the dermis,[5] where the potential for damage is greater.

Sunburn is delayed in its onset, usually becoming evident 2 to 6 hours after exposure and reaching maximum intensity after 15 to 24 hours.[2] It is less severe in persons over age 60 than in those under age 30. However, redness persists longer in older persons.[5]

PHOTOSENSITIVITY--This refers to an abnormal response of the skin to sun exposure.[2] It includes phototoxic and photoallergic reactions and polymorphous light eruption.

PHOTOTOXIC REACTION--This reaction presents as an exaggerated sunburn (ie, far more severe than expected from the length of exposure) after ingestion of or contact with a photosensitizer.[6] Because this reaction is not mediated immunologically, it may occur in anyone.[6]

Photosensitizers are usually polycyclic compounds capable of absorbing UVA radiation; therefore, most phototoxic reactions are caused by UVA exposure.[6] The drugs most commonly implicated in phototoxic reactions are thiazides (figure 1), sulfonylureas, sulfonamides, tetracyclines, phenothiazines, psoralens, nalidixic acid, and coal tar.[2] Exposure to sunlight after skin contact with plants containing psoralens or furocoumarins (eg, limes, parsley, celery, bishop's-weed, figs) can cause topical photosensitivity.[2,6]

PHOTOALLERGIC REACTION--This abnormal response of chemically exposed skin to sunlight occurs when the immune system is involved.[6] The reaction appears more as a rash than as a sunburn. Essentially, all phototoxins are also photo-allergens.[6]

POLYMORPHOUS LIGHT ERUPTION--This is the most common abnormal response of skin to sunlight and may affect up to 10% of the population.[6] The response is often triggered by the first intense exposure to the sun in the spring or during a southern midwinter vacation. Patients usually call it "sun poisoning" or "sun allergy."[6] Within hours after the patient sunbathes, itchy papules and plaques occur over some, but not all, exposed areas (figure 2). They gradually subside 1 to 2 weeks later if the patient avoids further exposure to the sun. There is no systemic involvement.[6]

TANNING--This form of sun exposure can be divided into two types:

  1. Immediate pigmented darkening. Exposure to UVA radiation results in photo-oxidation of preformed melanin. Darkening lasts only a few minutes after short exposure to UVA radiation but can remain for 36 hours after longer, high-intensity exposure.[4] This darkening does not protect the skin from UVB erythema.1

  2. Delayed pigmented darkening.

This occurs 48 to 72 hours after exposure to either UVA or UVB radiation, peaks in 7 to 10 days, and may persist for weeks to months. It results from an increase both in the production of new melanin (melanogenesis) and in the size of melanocytes.[4]

After exposure to sunlight, the skin acclimatizes; that is, it is less sensitive to sunburn on subsequent exposure. Acclimatization results from both pigmentation and gradual thickening of the stratum corneum (uppermost layer of the epidermis). It is lost after 1 to 2 months of non-exposure.[2]

UVA radiation from tanning booths provides less protection against future sunburn than natural sunlight. Artifical sunlight stimulates melanogenesis without appreciable thickening of the stratum corneum.[2]

Long-term effects of sun exposure

Prolonged exposure of the skin to sunlight may lead to both photoaging and photocarcinogenesis.

PHOTOAGING--Premature aging of the skin, or photoaging, has unique clinical and histologic features and should be differentiated from true chronologic or intrinsic aging. Because UVB radiation is responsible for erythema, DNA damage, and skin cancer, it has also been implicated as a cause of connective tissue damage that results in photoaging.[7] However, when the total dose of UVA radiation is at least 1,000 times higher than that of UVB radiation, it can be both erythemogenic and carcinogenic. If multiple exposures to UVA radiation from sunlight, fluorescent lamps, and tanning in salons are added together, the result may be 100 to 1,000 times that of UVB radiation.[8] Also, as noted previously, the longer wavelength of UVA penetrates more deeply into the dermis.[7]

Clinically, photoaging can be classified as mild, moderate, or severe (figures 3 through 7). Mild damage is characterized by dryness, roughness, pigmentary abnormalities (eg, irregular hyperpigmentation, solar lentigines, guttate hypopigmentation), and fine lines or wrinkles. Moderate damage is manifested by deep wrinkles (eg, cutis rhomboidalis nuchae, or deep folds and wrinkles on the back of the neck), sallowness, vascular lesions (telangiectases, ecchymoses, purpura, venous lakes), laxity (loss of elasticity), and thickened, leathery skin or, conversely, atrophic skin. Severe damage ultimately results in both actinic keratoses and skin cancers.[2,7-9]

Photoaging can be striking, especially when the skin of outdoor workers, such as farmers and sailors, is compared with that of indoor workers.[7] Even in darkly pigmented individuals, such as South American blacks, photodamage can develop when exposure to sunlight is prolonged and intense.[8]

Age, however, may have no bearing on the amount of photodamage seen. Sun worshippers in their 30s and 40s may have rough, leathery, mottled skin as well as actinic keratoses and carcinomas.[9] In contrast, persons who avoid the sun most of their lives can reach their 80s and 90s with smooth, unblemished skin that has sustained only deepening of the surface markings and some loss of elasticity.[4,9] This intrinsic aging contrasts strikingly with photoaging, especially histologically.

The most dramatic feature of severely photodamaged skin is massive accumulation of thickened, degenerated elastic fibers in the dermis. Mature collagen decreases, whereas ground substance, which is composed of proteoglycans, greatly increases. Capillaries become dilated and tortuous, producing clinically visible telangiectases.[7] The epidermis is generally thickened but eventually may become atrophic and display cellular atypia.[9]

Cigarette smoking has been associated with premature skin aging, which is most noticeable in sun-exposed areas.[2] Taking sun exposure into consideration, investigators have found that persons who smoke 10 or more cigarettes a day for at least 10 years are more likely than nonsmokers to have leathery, atrophic, and deeply wrinkled skin. These changes may be the result of reduced cutaneous oxygenation.[2]

PHOTOCARCINOGENESIS--Extensive evidence supports the role of exposure to direct sunlight in the development of common precancerous and cancerous skin lesions. A large number of these lesions are caused by UVB radiation.

ACTINIC (SOLAR) KERATOSES--These precancerous lesions consist of clones of anaplastic keratinocytes within the epidermis.[4] Actinic keratoses eventually develop in about 75% of the white population.[10] One study[11] found that 50% of whites over age 40 are affected.[11] Investigators showed that the presence of actinic keratoses is a far more sensitive indicator of long-term accumulation of sunlight than the development of true invasive skin cancer.[11]

The prevalence of actinic keratoses increases with age, irrespective of the amount of sun exposure.[4] Celtic (Scottish, Irish, Welsh) males who have blonde or red hair, fair skin, blue or green eyes, freckles, and the tendency to sunburn easily are particularly prone to the development of large numbers of actinic keratoses (figure 8).

Immunosuppressed individuals who have had renal transplantation have a higher incidence of actinic keratoses and nonmelanoma skin cancers.[12] This may be due to a defect in immune surveillance and tumor rejection capability.[10]

There are four clinical types of actinic keratoses: atrophic, hypertrophic, bowenoid, and pigmented. Atrophic actinic keratoses are red, scaly, nonindurated lesions with indistinct borders. Hypertrophic actinic keratoses are thicker-scaled lesions, which may become cutaneous horns (figure 9). Bowenoid actinic keratoses are red plaques with sharply distinct borders. Pigmented actinic keratoses are smooth, brown plaques that may become larger than 1 cm in diameter (figure 10).[10]

These lesions may be treated with liquid nitrogen cryosurgery or, alternatively, by electrodesiccation with or without curettage. Multiple lesions (figure 11) are best treated with topical fluorouracil (Efudex, Fluoroplex).

NONMELANOMA SKIN CANCERS--The incidence of these lesions, which comprise both squamous and basal cell carcinoma, has increased dramatically. A 1978 estimate[4] predicted that 500,000 new cases would be diagnosed each year, which may be due in part to increasing exposure to both natural and artificial UV light.

These cancers commonly occur on the head, neck, arms, and hands.[4] Risk factors are essentially the same as those for actinic keratosis: age, sex occupation (indoors or outdoors), tanning ability, propensity to sunburn, and location of residence in relation to the equator.[11]

SQUAMOUS CELL CARCINOMA--This accounts for about 20% of all skin cancers, with 100,000 new cases occurring each year in the United States. Squamous cell carcinoma is more common than basal cell carcinoma in blacks, although its overall incidence in this group is low.[4]

One study[13] showed that, in 60% of cases, squamous cell carcinoma arose from a lesion diagnosed clinically as an actinic keratosis. In 40% of cases, it developed on skin that had been clinically normal 12 months previously. The risk of transformation of an actinic keratosis to squamous cell carcinoma within a year was less than 1 in 1,000.

Squamous cell carcinoma occurs as a painless, scaly, crusted, or verrucous indurated red plaque on sun-exposed areas, especially the lower lip, helix of the ear (figure 12), and bald scalp. Lesions may also arise in scars caused by thermal burns and in cases of chronic stasis dermatitis or chronic radiation dermatitis. They have a tendency to bleed and grow fairly rapidly, attaining a size of 1 cm in diameter or more. Those that occur in scar tissue or mucous membrane or in black or immunosuppressed patients tend to metastasize.[14]

Surgical excision and histologic examination of margins are recommended because of the potential for metastasis. Mohs' technique is indicated for recurrent or large lesions, those arising in the posterior auricular sulcus, and those in irradiated or scarred skin.[15]

BASAL CELL CARCINOMA--This is the most common skin cancer in the white population. It accounts for about 75% of all malignant lesions of the skin, or approximately 400,000 new cases each year in the United States. About one third occur on areas of limited sun exposure. This type of cancer is rare in blacks.

If left untreated for 10 to 20 years, 1% to 3% of lesions around the eyes, nose, or ears become aggressive and invade bone, nerves, and cartilage, which can result in death. Metastasis is rare.[4]

Several different types have been described. Nodular basal cell carcinoma is the most common. It occurs as a pearly, waxy, telangiectatic nodule that is 0.5 to 1 cm in diameter (figure 13). As it enlarges, it outgrows its blood supply, resulting in central ulceration, and takes on a rodent ulcer appearance (figure 14).[14] Occasionally, when brown or black pigmentation is present in this lesion (pigmented basal cell carcinoma, figure 15), it can be misdiagnosed as a mole or even a melanoma.

A superficial multicentric type grows as multiple buds of basal cells extending centrifugally under the epidermis (figure 16). It can reach several centimeters in diameter and commonly occurs on the trunk as a scaly, red plaque with an elevated, threadlike border.[14]

A morpheaform (sclerotic, fibrosing) type occurs as an indurated, thickened, ill-defined invasive plaque. It is typically seen on the face (figure 17).[14]

Small basal cell carcinomas on the cheeks and superficial multicentric lesions on the trunk can be satisfactorily treated by curettage and fulguration. Large lesions and those on the scalp, forehead, ear rim, chin, neck, and other body sites can be managed with elliptic excision, followed by histologic examination. The highest cure rate, approaching 99%, is obtained with Mohs' micrographically controlled surgery. This technique is recommended for lesions occurring in the "H zone," or embryonic fusion planes of the face, such as the nasolabial fold, nose, periorbital region, and periauricular area. Mohs' technique is also indicated for aggressive morpheaform or scleroic types of basal cell carcinoma, tumors larger than 2 cm in diameter, lesions in immunosuppressed patients, and recurrent lesions. Radiation therapy offers an excellent alternative for frail, elderly individuals who have multiple medical problems and are unable to tolerate surgery.[15]

CUTANEOUS MALIGNANT MELANOMA--About 5% of all skin cancers are malignant melanoma.[4] In the United States, the incidence has risen by 100% in the past decade, faster than any other cancer except lung cancer. The projected US incidence for 1990 was 27,600 cases with 6,300 deaths. By the year 2000, the lifetime risk of melanoma for whites in the United States is expected to be 1 in 90.[16]

Controversy exists as to whether cutaneous malignant melanoma is related to sunlight exposure. Evidence in support of UVB exposure as a cause includes (1) higher incidence in areas closer to the equator (2) occurrence primarily in lightly pigmented persons, and (3) rare occurrence in heavily pigmented persons. Risk is increased if a person has a past history of severe blistering sunburn or sun sensitivity[16] or several years of exposure to UV lamps and sunbeds.[17]

Evidence against UVB exposure as a cause includes (1) lower rates in outdoor workers, (2) higher rates in white collar groups who work indoors, and (3) uncommon occurrence on the head, neck, and hands.[16]

Men are affected more frequently than women and often have a poorer prognosis. The disease is seen more typically on the trunk and extremities in men and on the lower extremities in women. Survival rates tend to be lower when the disease occurs in the midline of the body and the so-called BANS-HF areas: upper back, lateral upper arms, posterior neck and scalp, hands, and feet.[14]

Several types of cutaneous malignant melanoma have been described. The most common, superficial spreading malignant melanoma (figure 18), accounts for 70% of cases. It appears as an irregular, pigmented plaque with various hues of red, white, and blue.[14]

Nodular melanoma (figure 19) is seen in 15% of patients who have melanoma. It is a highly invasive, violaceous, brown-black nodule with fairly normal surrounding skin. It tends to ulcerate as it outgrows its blood supply.[14]

Acral-lentiginous melanoma presents as an irregularly shaped, deeply pigmented macule on the hands, feet (figure 20), and phalanges and also under the nails. It is associated with accelerated metastasis.[14]

Lentigo maligna melanoma, the least common type, is a palpable black nodule that may ulcerate (figure 21). It usually occurs on the cheek of an elderly person and has a more favorable prognosis than other melanomas of similar thickness.[14]

The mainstays of management of these melanomas are early diagnosis and excision. The classic excision of 5-cm margins is no longer recommended and does not affect survival. Current recommendations for margins are 0.5 to 1 cm for in situ lesions, 1.5 cm for lesions less than 0.85 mm in depth, and 3 cm for lesions deeper than 0.85 mm.[15]

Prognosis is determined by level of invasion. The classification of Clark and colleagues has been replaced by Breslow's measure of invasion in millimeters of thickness. The thicker the lesion, the worse the prognosis. Patients with lesions thicker than 3.64 mm have a 42% five-year survival rate.[15]


All patients, including the elderly, and parents of young children should be counseled on the dangers of all sources of UV radiation. They should also be advised regarding methods of photoprotection.

When applied correctly, sunscreens (see box on page 60)[18,19] can greatly decrease the deleterious effects of UV radiation. The thickness and evenness of application are very important. An adult body can be covered completely with less than 1 oz of sunscreen. This can be accomplished as follows[20]:

Sunscreens should be applied 1 to 2 hours before exposure to allow adequate penetration into the stratum corneum.[18]

The sun protection factor (SPF) is also important. (The following example is a simplified explanation of SPF: If a person's skin normally burns in 15 minutes without a sunscreen, use of an SPF 10 preparation will allow exposure for 10 times longer [150 minutes] before the same degree of erythema is sustained.[19]) A sunscreen with an SPF of 15 or more is recommended for persons with fair skin who often burn and for those who have photosensitivity syndromes or have had radiation therapy or skin cancer. SPF 15 offers 93% protection from UV radiation. SPF 34 only increases this protection to 97%.[20]

How long the sunscreen stays on the skin is as important as its active ingredients. "Sweat resistant" means that the product is protective for up to 30 minutes in persons who perspire heavily and continuously. "Water resistant" means it is protective for up to 40 minutes of continuous water exposure. "Waterproof" products are protective for up to 80 minutes of continuous water exposure.[19]

The Food and Drug Administration (FDA) currently does not recommend sunscreens for use in children who are younger than 6 months of age. Avoidance of the sun or physical protection is advised instead. It is estimated that regular use of SPF 15 sunscreens during the first 18 years of life could reduce a person's lifetime risk of nonmelanoma skin cancer by 78%.[19] Minimizing exposure (see box on page 65) is also helpful.

A consumer group has recently charged that sunscreen preparations containing urocanic acid may promote skin cancer by suppressing the immune system and has asked the FDA to ban sales of these products. The FDA is reviewing the petition.


Severe photoaging of the skin, which may be caused by exposure to both natural and artificial ultraviolet light, ultimately results in actinic keratoses and cancer. Cancers are common on the head, neck, arms, and hands. Because of the potential for metastasis, squamous cell carcinomas generally require surgical excision and histologic examination. Although metastasis is rare with basal cell carcinoma, neglected lesions around the eyes, nose, or ears can invade bone, nerves, and cartilage and may cause death. Avoidance of sun, physical protection, and regular use of sunscreens are recommended. PGM


Address for correspondence: Steven Earl Prawer, MD, Associated Skin Care Specialists, PA, 7205 University Ave NE, Fridley, MN 55432-3133.



1. Sunlight, ultraviolet radiation, and the skin. Natl Inst Health consensus Dev conf Consensus Statement 1989;7(8):1-10.

2. Taylor CR, Stern RS, Lyden JL, et al. Photoaging/photodamage and photoprotection. J Am Acad Dermatol 1990;22(1):1-15.

3. Young AR. Cumulative effects of ultraviolet radiation on the skin: cancer and photoaging. Semin Dermatol 1990;9(1):25-31.

4. Odom RB. Focus on photodamage: a medical problem. Parsippany, NJ: Skin Phototrauma Foundation, 1990:1-29.

5. Soter NA. Acute effects of ultraviolet radiation on the skin> Semin Dermatol 1990;9(1):11-5.

6. Glichrest BA. Actinic injury. Annu Rev Med 1990;41:199-210.

7. Kligman LH. Photoaging Naimfestations, prevention, and treatment. Clin Geriatr Med 1989;5(1):235-51.

8. Sams WM Jr. Sun-induced aging: clinical and laboratory observations in humans. Clin Geriatr Med 1989;5(1):223-33.

9. Lober CW; Fenske NA. Photoaging and the skin: differentiation and clinical response. Geriatrics 1990;45(4):36-40, 42.

10. Basler RS, Eberspacher DL. Actinic keratoses. Nebr Med J 1989;74(7):174-7.

11. Narks R, Rennie G, Selwood T. The realtionship of basal cell carcinomas and squamous cell carcinomas to solar keratoses. Arch Dermatol 1988;124(7):1039-42

12. Marks R. Solar keratoses. Br J Dermatol 1990;122(Suppl 35):49-54

13. Marks R, Rennie G, Selwood TS. Malignant transformation of solar keratoses to squamous cell carcinoma. Lancet 1988;1(8589):795-7.

14. Proper SA, Fenske NA. Common skin tumors in the geriatric poplations. Ceriatr Med Today 1985;4(9):17-34

15. Arnold HL, Odom RB, James WD. Sauamous cell carcinoma, basal cell carcinoma, malignant melanoma. In: odom RB, James WD, eds. Andrews' diseases of the skin: clinical dermatology. Philadelphia: WB Saunders, 1990:763-865.

16. Koh HK, Kligler BE, Lew RA. Sunlight and cutaneous malignant melanoma: evidence for and against causation. photochem photobiol 1990; 51(5);765-79

17. Swerdlow AJ, English JS, MacKie RM, et al. Flourscent lights, ultraviolet lamps, and risk of cutaneous melanoma. BMJ 1988;297(6649):647-50 [erratum, BMJ] 1988;297(6657):1172]

18. Rumsfield J. Sunscreens: what you and your patients should know. Dermatol Nurs 1990;2(3):134-47

19. Nicol NH. Actinic Keratosis: preventable and treatable like other precancerous and cancerous skin lesions. Plast Surg Nurs 1989;9(2):49-55

20. Jacob R. Sunscreens: prevention by the ounce. Tex Dent J 1990;107(6):7-11