UV:harmful effects - School of Public Health
The harmful effects from exposure to ultraviolet (UV) radiation can be classified as acute or chronic. The acute effects of UV-A and UV-B exposure are both short-lived and reversible. These effects include mainly sunburn (or erythema) and tanning (or pigment darkening). The chronic effects of UV exposure can be much more serious, even life threatening, and include premature aging of the skin, suppression of the immune system, damage to the eyes, and skin cancer.
Sunburn (or erythema) is redness of the skin, which is due to increased blood flow in the skin caused by dilatation of the superficial blood vessels in the dermis as a result of exposure to UV radiation. High UV doses may also results in edema, pain, blistering, and peeling of the skin a few days following exposure. UV-B radiation is believed to be mainly responsible for sunburn as it is more erythmogenic by a factor of 1,000, however since there is more UV-A radiation reaching the earths surface, UV-A contributes 15-20% to the sunburn reaction in the summer months. Risk factors for sunburn include fair skin, red or blond hair, blue eyes, and freckles. For people with fair skin, it takes only 15-30 minutes in midday sun to induce erythema. In terms of areas of the body that are more susceptible to sunburn, the face, neck, and trunk are two to four times more sensitive than the limbs. In addition, children and the elderly are believed to be more sensitive to UV radiation and may burn more easily. A sunburn reaches its maximum redness eight to 12 hours after exposure and fades within one to two days (1).
Tanning refers to delayed pigmentation of the skin, or melanin pigmentation. It usually becomes noticeable one to two days after exposure to the sun and gradually increases for several days persisting for weeks or months. Tanning results from an increase in the number of functions melanocytes (pigment cells) resulting in increased activity of the enzyme tyrosinase. This leads to the formation of new melanin and an increase in the number of melanin granules throughout the epidermis (2). Tanned skin need not only be considered a harmful effect as it does confer some protection for subsequent exposure to the sun, but the degree of protection is thought to be moderate and not sufficient as a sunscreen for Caucasian skin. However, there is another mechanism that may provide more protection for subsequent exposures. In addition to tanning and sunburn, thickening (or hyperplasic) of the epidermis also occurs and is thought to be a significant component of a mild sunburn reaction. A single moderate exposure to UV-B radiation is sufficient to induce 3-fold thickening in the stratum cornea that lasts one to two months. This thickening is likely to be more important than tanning for providing endogenous photoprotection for those with Caucasian skin (1).
One of the chronic effects resulting from repeated exposure to UV radiation is premature aging of the skin, which encompasses a number of clinical signs that reflect structural changes in the dermis. These clinical signs include dryness, wrinkles, accentuated skin furrows, sagging, loss of elasticity, and mottled pigmentation, and are the result of degenerative changes in elastin and collagen (1,2). The degenerative changes accumulate over time and are largely irreversible (2). It is believed that as much as 80% of premature aging of the skin may occur within the first 20 years of life. UV-A radiation has been found to be an important contributor to premature aging of the skin. Whereas UV-B is 1,000 to 10,000 times more efficient than UV-A in terms of induction of sunburn and nonmelanoma skin cancer, respectively, with premature aging of the skin UV-B radiation is only 20-50 times more efficient than UV-A (1).
Suppression of the immune system resulting from exposure to UV radiation is believed to be an important contributor to the development of nonmelanoma skin cancers. Put simply, UV radiation induces a state of relative immunosuppression that prevents tumor rejection. This is mainly accomplished by interfering with the normal surveillance function of antigen-presenting Langerhans cells in the epidermis, which are responsible for T-lymphocyte activation in response to foreign antigens (2). The number of Langerhans cells and their characteristics are altered from exposure to UV radiation while similar cells that are responsible for the selective induction of suppressor lymphocyte pathways are resistant to UV damage. This creates an imbalance in the local T-cell function and a shift from helper to suppressor pathways, which ultimately favors tumorigenesis and progression. Grossman and Leffell conclude that the immunosuppressive effects of UV may be as important as the carcinogenic effects of UV radiation in the establishment and progressive growth of UV-induced skin tumors.
UV rays can also damage the eyes as more than 99% of UV radiation is absorbed by the front of the eyes. Corneal damage, cataracts, and macular degeneration are all possible chronic effects from UV exposure and can ultimately lead to blindness. Melanoma, a type of skin cancer, can also develop within the eye. Intraocular melanomas are the most common ocular malignancy in whites. These melanomas originate in the uveal melanocytes, which are found the iris, ciliary body, and choroids of the eye. The annual age-adjusted incidence of non-skin melanomas is 0.7 per 100,000 persons in the U.S. of which ocular melanomas constitute 80%. The risk of intraocular melanomas is 8-fold higher in whites than blacks (2).
Skin cancers are the most commonly occurring cancers in terms of incidence in the world. There are different types of skin cancer including the nonmelanoma skin cancers, basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), and melanoma. Exposure to UV radiation is thought to be an important factor in each of these cancers as it induces DNA damage, however the types of exposure necessary to cause the different types of skin cancer may vary. For the nonmelanoma skin cancers, cumulative sun exposure is believed to be important, whereas for melanoma the intermittent exposure hypothesis has been postulated. This hypothesis proposes that infrequent intense exposure of unacclimatized skin to sunlight is related to the increasing incidence of melanoma and is more important than chronic sun exposure (1). The incidence of all types of skin cancer is increasing. Below is graph with data from nine SEER registries showing the increasing incidence of age-adjusted rates of melanoma in men and women between 1973-2000 ().
Basal Cell Carcinoma
Basal cell carcinomas account for 80% of all nonmelanoma skin cancers. These tumors are slow growing and rarely metastasize. They are commonly found on the head and neck, areas subject to chronic sun exposure. They occur just as frequently in men as in women. In terms of cases, 20% occur in individuals less than 50 years of age while 70% occur in individuals less than 70 years of age. Genetic factors that associated with the development of BCC include light eyes, a fair complexion, light hair color, tendency to sunburn, and poor ability to tan. The incidence also increases with immunosuppression and in persons with inherited defects in DNA replication and repair, namely xeroderma pigmentosum (2). Epidemiological data suggests that for both BCC and SCC that risk also increases with increasing recreational exposure to the sun, but that perhaps more important is exposure to the sun in childhood. Childhood sun exposure leads to higher cancer risks than the same exposure in later life. It is thought that use of high SPF sunscreen during the first 18 years of life can reduce lifetime incidence of nonmelanoma skin can by 70% (1).
Squamous Cell Carcinoma
Squamous cell carcinomas account for the other 20% of nonmelanoma skin cancers. These tumors are the most common skin cancers on sun-exposed sites in older people. Virtually 100% of SCCs occur in individuals who are 50 years of age or older and 50% of these occur in individuals who are 65 years of age or older. SCCs are more common in men than women occurring at a ratio of 4:1 and more lethal than BCCs accounting for 75% of the deaths from nonmelanoma skin cancers. It is important to note here that overall nonmelanoma skin cancers have a cure rate of 96-98% and are the most easily and successfully treated cancers. SCCs have similar genetic risk factors as BCCs. SCCs have precursor lesions called actinic keratoses. These lesions represent dysplasia that occurs as a result of chronic exposure to sunlight with build-up of keratin. They are less than 1 cm in diameter; are tan-brown, red or skin color; and have a rough sandpaper-like consistency (2). According the multistage model of carcinogenesis, these precursor lesions represent the first genetic hit on the pathway to carcinoma development (3).
Melanoma skin cancers are tumors derived from the melanocytes (pigment cells). They have marked tendency to metastasize and therefore are more likely than nonmelanoma skin cancers to cause death. Melanomas are more common in young women and older men. In women, they tend to occur on the back and legs and in men on the upper back. UV radiation appears to play an important role in melanoma development, however melanomas also have a tendency to occur on non-sun-exposed surfaces as well as sun-exposed surfaces and therefore intermittent exposure may be more important than chronic exposure to UV radiation. The most important risk for melanoma is the total number of nevi (moles) that are larger than 2 mm as dysplastic nevi are precursors of malignant melanoma. Dysplastic nevi are usually larger than 5 mm, have variability in pigmentation, and have irregular borders, with the most important clinical sign of disease being a change in color in a pigmented lesion to black, brown, red, dark blue, or gray.