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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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