The sun’s emission spectrum is extremely broad, whereas the spectrum that reaches earth is limited to the wavelengths of ultraviolet radiation (UVR), visible light, and infrared radiation. UVR can be further subdivided into three categories:

1. UVA (A-I 340 to 400 nm, A-II 320 to 340 nm) constitutes over 90% of the UVR that reaches earth and penetrates deeply to the dermis contributing to immediate and long-term cutaneous damage by degenerating collagen.¹ UVA may induce severe phototoxicity in combination with some medications such as psoralens, doxycycline, sulfonamides, phenothiazines, and sulfonylureas.

2. UVB (290 to 320 nm) is the primary cause of cutaneous erythema and edema. Chronic exposure to UVB leads to aging and carcinogenesis.

3. UVC (200 to 290 nm) wavelengths are blocked by the ozone layer and do not reach earth’s surface. They can also be found in commercial germicidal lamps and can cause mild conjunctivitis or sunburn.

Sunburn is an acute inflammatory reaction of the skin that results from overexposure to UVR. Upon exposure to UVR, cutaneous blood vessels in the upper dermis vasodilate, resulting in a subsequent increase in vascular permeability, edema, and erythema. Mast cells then release mediators such as histamine, serotonin, and tumor necrosis factor, which stimulate prostaglandin and leukotriene production. Cytokines are released, further stimulating inflammation and an increase in neutrophil and T-cell migration. This cascade results in the production of reactive oxygen species which damage DNA leading to the formation of pyrimidine dimers and subsequent mutations.¹ This can result in the inactivation of tumor suppressor genes, e.g., p53, which has been shown to eventuate in the development of non-melanoma skin cancers.² UVR exposure has also been shown to suppress cutaneous cell-mediated immunity with altered response to antigens, release of immunosuppressive factors such as interleukins, and inhibition of natural killer cells, resulting in an increased risk for the development of non-melanoma skin cancers and infectious disease. Finally, a number of diseases known as photodermatoses may be caused or exacerbated by UVR exposure (Table 42-1).

UVR exposure leads to an increase in skin pigmentation, or suntan, which offers some protection against further sun exposure. This process occurs in two ways:

1. Immediate pigment darkening (IPD) begins 2 to 24 hours after exposure to UVA, which causes metabolic alterations and redistribution of existing melanin. IPD is not photoprotective.

2. Delayed pigment darkening begins 2 to 3 days after exposure to UVB, which causes DNA damage and gene alterations leading to the synthesis of melanin.³ This increase in pigment typically lasts a few weeks and offers some natural protection from further UVR exposure. However, because
it is associated with underlying damage, tanning is not recommended for photoprotection.

A variety of factors influence the likelihood of developing a sunburn. Natural sun-protective mechanisms include thickness of the epidermis, natural antioxidants, melanin, urocanic acid (natural UV absorber), DNA repair mechanisms, and Fas ligand signaling.¹ Tolerance to sunlight is based on the amount of melanin in the skin and an individual’s genetic capacity to produce melanin, or tan, following exposure to UVR. Hydrated skin absorbs a larger percentage of UVR and is therefore more easily damaged. Additionally, a significant proportion of UVR reaches the skin through reflection from snow, sand, or sidewalks. Exposure to UVR is greatest from 10 am to 4 pm and increases at higher altitudes and latitudes closer to the equator.

Fitzpatrick developed a classification system for the response of different skin types to UVR (Table 42-2). The minimal dose of UVR necessary to produce erythema of an unprotected site is known as the minimal erythema dose (MED). This dose varies based on skin type which is categorized on the basis of the sun-reaction response to the first 30-minute exposure to summer sun. People with type I and II skin will exceed their sunburn threshold tolerance
in 10 to 20 minutes of noontime temperate summer sunlight. Three to eight times the MED will produce a moderate-to-severe burn.

The diminishing ozone layer has been a concern over the past 40 years. Regulations to limit production of ozone-depleting materials have slowed its destruction, but there has been no regeneration. As a consequence, more UVB can now reach earth’s surface. The impact of climate changes caused by the stratospheric ozone depletion on skin cancer incidence remains uncertain. To help people better understand the intensity of UV light in their area, the Environmental Protection Agency and the National Weather Service developed the UV Index (Table 42-3), a program that informs the public about the amount of harmful UVR reaching the earth on a particular day. The National Meteorological Center determines the index daily, and it is a recognized part of the weather report in many cities.