Ultraviolet Radiation

Solar radiation spans the spectrum of wavelengths between 200 and 4000 nm, including ultraviolet, visible, and infrared radiation. Ultraviolet radiation is divided into ultraviolet A (UVA),

ultraviolet B (UVB), and ultraviolet C (UVC); 3% to 5% of the total solar radiation that penetrates the earth's surface is ultraviolet radiation. Ozone in the atmosphere is an important

protective agent against ultraviolet radiation because it completely absorbs all UVC and partially absorbs UVB. Chlorofluorocarbons, used commercially as propellants, as solvents, and in

refrigerators and air conditioners, interact with and deplete ozone. Such depletion is predicted to contribute to an increase in UVB and possibly UVC exposure, thus triggering a 2% to 4%

increase in the incidence of skin cancers. Some protection from the effects of UV light is afforded by window glasses: they absorb UVB radiation, but they transmit UVA radiation.

Sunblocks and sunscreens offer greater protection because they absorb or block UVB and UVA to variable degrees. There are two major health effects of ultraviolet radiation: premature

aging of the skin and skin cancer ( Table 9-19 ). The carcinogenic effects of ultraviolet light are discussed in Chapter 7 . Here we focus on other effects of ultraviolet radiation.

The acute effects of UVA and UVB are short-lived and reversible. They include erythema, pigmentation, and injury to Langerhans cells and keratinocytes in the epidermis. The kinetics

and chemical mediators of these reactions differ in response to UVA and UVB. Depending on the intensity and length of exposure, erythema, edema, and acute inflammation are mediated

by release of histamine from mast cells in the dermis, synthesis of arachidonic acid metabolites, and the production of pro-inflammatory cytokines like IL-1. UVA produces oxidation of

melanin with transient, immediate

darkening, especially in individuals with darker skin. Tanning induced by UVA and UVB is due to a delayed increase in the number of melanocytes, elongation and extension of dendritic

processes, and transfer of melanin to keratinocytes. Tanning induced by UVB is protective against subsequent exposures; tanning induced by UVA provides limited protection. Both UVA

and UVB deplete Langerhans cells and thus reduce the processing of antigens introduced through the epidermis. UVB causes apoptosis of keratinocytes in the epidermis, resulting in

dyskeratotic, sunburn cells.

Repeated exposures to ultraviolet radiation give rise to changes in the skin that are characteristic of premature aging (e.g., wrinkling, solar elastosis, and irregularities in pigmentation). In

contrast to ionizing radiation that increases deposition of collagen in the dermis, ultraviolet radiation causes degenerative changes in elastin and collagen, leading to wrinkling, increased

laxity, and a leathery appearance. These connective tissue alterations accumulate over time and are largely irreversible. They are caused by increased expression of the elastin gene,

increased expression of matrix metalloproteinases that degrade collagen, and induction of a tissue inhibitor of matrix metalloproteinase. The end result of these changes in connective tissue

enzymes is degradation of type I collagen fibrils and disorganization and degeneration of the dermal connective tissue[61] ( Fig. 9-16 ).

Skin damage induced by UVB is believed to be caused by the generation of reactive oxygen species and by damage to endogenous chromophores such as melanin. Ultraviolet radiation

also damages DNA, resulting in the formation of pyrimidine dimers between adjacent pyrimidines on the same DNA strand. Other forms of DNA damage, for example, formation of

pyrimidine-pyrimidone (6-4) photoproducts, single-stranded breaks, and DNA-protein cross-links, are also noted.[61] A unique spectrum of mutations has been identified in premalignant

and malignant skin lesions in humans,

Figure 9-16Solar elastosis with basophilic degeneration of the connective tissue in the upper layer of the dermis. (American Registry of Pathology © 1990.)

TABLE 9-20-- Adult Mortality Rates in the United States, Ages 25–44, in 1998

Date: 2016-04-22; view: 1272