Sunlight is the most visible and obvious source of comfort in the environment. The sun provides the beneficial effects of warmth and vitamin D synthesis; however, acute and chronic sun exposure also have pathologic consequences. Few effects of sun exposure beyond those affecting the skin have been identified, but cutaneous exposure to sunlight is the major cause of human skin cancer and can have immunosuppressive effects as well.
The sun's energy reaching the earth's surface is limited to components of the ultraviolet (UV), the visible, and portions of the infrared spectra. The cutoff at the short end of the UV is at ~290 nm; this is due primarily to stratospheric ozone formed by highly energetic ionizing radiation, preventing penetration to the earth's surface of the shorter, more energetic, potentially more harmful wavelengths of solar radiation. Indeed, concern about destruction of the ozone layer by chlorofluorocarbons released into the atmosphere has led to international agreements to reduce production of those chemicals.
Measurements of solar flux indicate that there is a twentyfold regional variation in the amount of energy at 300 nm that reaches the earth's surface. This variability relates to seasonal effects, the path that sunlight traverses through ozone and air, the altitude (4% increase for each 300 m of elevation), the latitude (increasing intensity with decreasing latitude), and the amount of cloud cover, fog, and pollution.
The major components of the photobiologic action spectrum capable of affecting human skin include the UV and visible wavelengths between 290 and 700 nm. In addition, the wavelengths beyond 700 nm in the infrared spectrum primarily emit heat and in certain circumstances may exacerbate the pathologic effects of energy in the UV and visible spectra.
The UV spectrum reaching the earth represents <10% of total incident solar energy and is arbitrarily divided into two major segments, UV-B and UV-A, constituting the wavelengths from 290–400 nm. UV-B consists of wavelengths between 290 and 320 nm. This portion of the photobiologic action spectrum is the most efficient in producing redness or erythema in human skin and hence sometimes is known as the "sunburn spectrum." UV-A includes wavelengths between 320 and 400 nm and is ~1000-fold less efficient in producing skin redness than is UV-B.
The wavelengths between 400 and 700 nm are visible to the human eye. The photon energy in the visible spectrum is not capable of damaging human skin in the absence of a photosensitizing chemical. Without the absorption of energy by a molecule, there can be no photosensitivity. Thus, the absorption spectrum of a molecule is defined as the range of wavelengths absorbed by it, whereas the action spectrum for an effect of incident radiation is defined as the range of wavelengths that evoke the response.
Photosensitivity occurs when a photon-absorbing chemical (chromophore) present in the skin absorbs incident energy, becomes excited, and transfers the absorbed energy to various structures or to oxygen.
UV Radiation (UVR) and Skin Structure and Function
Skin consists of two major compartments: the outer epidermis, which is a stratified squamous epithelium, and the underlying dermis, which is rich in matrix proteins such as collagens and elastin. Both compartments are susceptible to damage from sun exposure. The epidermis and the dermis contain several chromophores capable of absorbing incident solar energy, including nucleic acids, proteins, and lipids. The outermost epidermal layer, the stratum corneum, is a major absorber of UV-B, and <10% of incident UV-B wavelengths penetrate through the epidermis to the dermis. Approximately 3% of radiation below 300 nm, 20% of radiation below 360 nm, and 33% of short visible radiation reaches the basal cell layer in untanned human skin. In contrast, UV-A readily penetrates to the dermis and is capable of altering structural and matrix proteins that contribute to photoaging of chronically sun-exposed skin, particularly in individuals of light complexion. Thus, longer wavelengths can penetrate more deeply into the skin.
Molecular Targets for UVR-Induced Skin Effects
Epidermal DNA, predominantly in keratinocytes and in Langerhans cells (LCs), which are dendritic antigen-presenting cells, absorbs UV-B and undergoes structural changes between adjacent pyrimidine bases (thymine or cytosine), including the formation of cyclobutane dimers and 6,4-photoproducts. These structural changes are potentially mutagenic and are found in most basal cell and squamous cell skin cancers. They can be repaired by cellular mechanisms that result in their recognition and excision and the restoration of normal base sequences. The efficient repair of these structural aberrations is crucial, since individuals with defective DNA repair are at high risk for the development of cutaneous cancer. For example, patients with xeroderma pigmentosum (XP), an autosomal recessive disorder, are characterized by variably deficient repair of UV-induced photoproducts, and their skin phenotype often manifests the dry, leathery appearance of prematurely photoaged skin as well as basal cell and squamous cell carcinomas and melanoma in the first two decades of life. Studies in mice using knockout gene technology have verified the importance of functional genes regulating these repair pathways in preventing the development of UV-induced cancer. Furthermore, incorporation of a bacterial DNA repair enzyme, T4 endonuclease V, into liposomes in a product applied to the skin of patients with XP selectively removes cyclobutane pyrimidine dimers and reduces the degree of solar damage and skin cancer. This approach also may benefit other patients who are susceptible to skin cancer, such as organ transplant recipients receiving chronic immunosuppressive drug therapy. DNA damage in LCs may contribute to the known immunosuppressive effects of UV-B (see "Immunologic Effects," below).
In addition to DNA, molecular oxygen is a target for incident solar UVR, leading to the generation of reactive oxygen species (ROS). These ROS can damage skin components, such as epidermal lipids, either free lipids in the stratum corneum or cell membrane lipids. UVR also can target proteins, leading to increased cross-linking and degradation of matrix proteins in the dermis and thus to photoaging changes known as solar elastosis.
Cutaneous Optics and Chromophores
Chromophores are endogenous or exogenous chemical components that can absorb physical energy. Endogenous chromophores are of two types: (1) normal components of skin, including nucleic acids, proteins, lipids, and 7-dehydrocholesterol, the precursor of vitamin D, and (2) components that are synthesized elsewhere in the body that circulate in the bloodstream and diffuse into the skin, such as porphyrins. Normally, only trace amounts of porphyrins are present in the skin, but in selected diseases known as the porphyrias (Chap. 358), increased amounts are released into the circulation from the bone marrow and the liver and are transported to the skin, where they absorb incident energy both in the Soret band, around 400 nm (short visible), and to a lesser extent in the red portion of the visible spectrum (580–660 nm). This results in the generation of ROS that ...