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Skin (Nonmelanoma) Cancer

Jospeh Scotto, M.S.*

Nonmelanoma skin cancer is the most common cancer among whites in the United States. Because most nonmelanoma skin cancer patients are treated in doctors' offices, population-based estimates of skin cancer incidence are fairly difficult to obtain. More than 600,000 new cases of nonmelanoma skin cancer may occur in the United States each year, and this number is rising (Glass and Hoover, 1989; NIH Consensus Development Conference, 1989). The fatality rate from nonmelanoma skin cancer is less than 1 percent (Marks, 1988).

The incidence of nonmelanoma skin cancer varies directly with exposure to ultraviolet (UV) light from the sun and, indirectly, with the degree of skin pigmentation. Thus, nonmelanoma skin cancer is most common among fair-skinned whites who live in sunny locales. The highest rates in the past have been recorded among Caucasians in South Africa and Australia (Marks et al., 1989). Ireland, despite its rain and mist, has had a high incidence because of the susceptibility of persons of Celtic ancestry (Urbach, 1971).

Nonmelanoma skin cancer occurs less often in Hispanics and Orientals, and least often among blacks. In the United States, for example, a National Cancer Institute survey (Scotto, 1983) showed that the age-adjusted incidence rate was only 3.4 per 100,000 among blacks, or about 80 times less than the rate observed among whites.

Most nonmelanoma skin cancers are of two types--squamous cell carcinoma and basal cell carcinoma. The basal cell type is more common, but the squamous cell type is more invasive, and may account for about three-fourths of all deaths from nonmelanoma skin cancer (Dunn et al., 1965).

Several studies have shown that basal cell skin cancer occurs about one and one-half to two times more often in white men than in white women, and squamous cell skin cancer occurs two to three times more often in men. Both types occur most often on the face, head and neck (about 80 percent for both types combined). Women have higher rates than men for both types of cancers on the legs (Scotto, 1982), consistent with their greater sun exposure at this anatomical site. White men have more squamous cell carcinoma of the lip, in line with their risks from tobacco and outdoor work (Lindqvist, 1979).

Skin cancer incidence in the United States is positively correlated with annual dosages of surface solar ultraviolet radiation (UVB) received at each geographic location (Fears and Scotto, 1983). The direct relationship is most clearly seen with squamous cell carcinoma of the skin (Scotto and Fraumeni, 1982), and varies according to cell type. A 1 percent increase in UVB exposure may result in incidence increases of 4, 2, and 1 percent for squamous cell, basal cell, and malignant melanoma of the skin, respectively. This is consistent with the evidence that factors other than sunlight also contribute to the development of melanoma (Greene and Fraumeni, 1979).

There are other risk factors for nonmelanoma skin cancers. They were, for example, the first type of cancer related to ionizing radiation exposure, with reports as early as 1902 among radiation workers (Martin, 1970). Other studies have shown an excess risk associated with radiotherapy for a number of diseases (Matanoski, 1975). Excess risks have also been noted among radiologists and uranium miners (Sevcova, 1978).

Exposure to a number of chemicals may also induce skin cancer in animals, particularly squamous cell carcinoma. Epidemiologic studies substantiate their associated risk in humans. Polycyclic aromatic hydrocarbons induce cancers in animals and are found in coal tars, pitch, asphalt, soot, creosote, and lubricating and cutting oils (Kipling, 1976). Skin and other forms of cancer have been found in various worker groups exposed to these substances. Though Orientals rarely develop sun-induced skin cancer, arsenic exposure (e.g., from artesian well water) may result in excess risk for skin cancer (EPA, 1988).

Studies have shown an excess risk of skin cancer among psoriasis patients treated with crude tar ointments and UVA, i.e., ultraviolet wavelengths of 330 to 400 nm, (Stern, 1980), and there has been increased concern about the possible hazards of other photosensitizers found in tanning aids, cosmetics, and medicines (NIH Consensus Development Conference, 1989).

Squamous cell skin cancer has also been observed as a complication of tropical ulcers, burns, scars, and chronic infections and wounds (Malik et al., 1974), chiefly among dark-skinned populations in Africa and Asia, but recent studies of black Americans have indicated that burn scars or chronic infections may predispose them to skin cancer also (Fleming, 1975). Actinic keratoses--brownish, hardened areas on skin exposed to excess sunlight--are considered precursor lesions for squamous cell skin cancer (Marks, 1988). Individuals with several rare hereditary diseases, including multiple basal cell carcinoma syndrome, xeroderma pigmentosum, and albinism, are also at heightened risk of developing skin cancer (Kraemer, 1984).

Avoiding overexposure to sunlight is the best way to prevent nonmelanoma skin cancer. In addition to natural sunlight, it is also important to avoid unnecessary X-rays and ultraviolet light exposure from artificial sources such as sunlamps and tanning booths.


REFERENCES

Dunn JE Jr, Levin EA, Linden G, et al.: Skin cancer as a cause of death. Calif Med 102:361-3, 1965.

EPA Risk Assessment Forum: Special report on ingested inorganic arsenic--Skin Cancer; Nutritional essentiality. U.S. Environmental Protection Agency, EPA/625/ 3-87/013, Washington, DC, 1988.

Fears TR and Scotto J: Estimating increases in skin cancer morbidity due to increases in ultraviolet radiation exposure. Cancer Invest 1(2):119-26, 1983.

Fleming ID, Barnawell JR, Burlison PE, et al.: Skin cancer in black patients. Cancer 35:600-5, 1975.

Glass AG and Hoover RN: The emerging epidemic of melanoma and squamous cell skin cancer. JAMA 262 (l5):2097-l00, October 20, l989.

Greene MH and Fraumeni JF Jr: The hereditary variant of malignant melanoma. In Human Malignant Melanoma (Clark WH, Goldman LI, Mastrangelo MJ, eds.). New York: Grune and Strattion, 1979.

Kipling MD and Waldron HA: Polycyclic aromatic hydrocarbons in mineral oil, tar, and pitch, excluding petroleum pitch. Prev Med 5:262-78, 1976.

Kraemer KH, Lee MM and Scotto J: DNA repair protects against cutaneous and internal neoplasia: Evidence from xeroderma pigmentosum. Carcinogenesis 5:511-4, 1984.

Lindqvist C: Risk factors in lip cancer: A questionnaire survey. Am J Epidemiol 109:521-30, 1979.

Malik MOA, Hidyatalla A, Daoud EH, et al.: Superficial cancer in the Sudan--A study of 1225 primary malignant superficial tumours. Br J Cancer 30:355-64, 1974.

Marks R, Rennie G and Selwood TS: Malignant transformation of solar keratoses to squamous cell carcinoma. Lancet l(8589):795-7, April 9, 1988.

Marks R, Jolley D, Dorevitch AP, et al.: The incidence of non-melanocytic skin cancers in an Australian population: Results of a five-year prospective study. Med J Aust 150(9):475-8,1989.

Martin H, Strong E and Spiro RH: Radiation-induced skin cancer of the head and neck. Cancer 25:61-71, 1970.

Matanoski GM, Seltser R, Sartwell PE, et al.: The current mortality rates of radiologists and other physician specialists: Specific causes of death. Am J Epidemiol 101:199-210, 1975.

NIH Consensus Development Conference Statement: Sunlight, Ultraviolet Radiation and the Skin. vol 7, no 8, May 8-10, 1989.

Scotto J, Fears TR and Fraumeni JF Jr: Incidence of Nonmelanoma Skin Cancer in the United States. NCI NIH Publ. No. 83-2433, April l983.

Scotto J and Fraumeni JF Jr: Skin (other than melanoma) In Cancer Epidemiology and Prevention (Schottenfeld D, and Fraumeni JF Jr, eds.). Philadelphia: W.B. Saunders, 1982.

Sevcova M, Sevc J and Thomas J: Alpha irradiation of the skin and the possibility of late effects. Health Physics 35:803-6, 1978.

Stern RS, Zierler S and Parish JA: Skin carcinoma in patients with psoriasis treated with topical tar and artificial ultraviolet radiation. Lancet 1:732-5, 1980.

Urbach F: Geographic distribution of skin cancer. J Surg Oncol 3:219-34, 1971.


* From the Biostatistics Branch, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland

National Cancer Institute

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