Everyone should avoid overexposure to the sun’s rays. But the desire for the “perfect tan,” the belief that a tan enables one to spend more time in the sun, and a lack of awareness about the dangers of ultraviolet (UV) radiation are factors that contribute to UV-induced skin damage and to an increased risk of skin cancer. Physicians need to be prepared to counsel patients on why and how to avoid damaging UV radiation.
Some measures are straightforward, such as wearing protective clothing, limiting sun exposure during the peak daylight hours, and avoiding tanning booths. The issue of which sunscreen to use can be more difficult, given the quantity of sunscreen products and the confusing claims made on product labels.
In this article, we review UV radiation, the consequences of increased exposure to different parts of the UV spectrum, tanning, and the fundamentals of sunscreens. We also briefly review current guidelines from professional organizations and rulings on sunscreen products by the US Food and Drug Administration (FDA).
FACTORS AFFECTING UV EXPOSURE
UV radiation from the sun is strongest between 10:00 am and 4:00 pm at equatorial latitudes and during summer months.1 Certain wavelengths of UV radiation have long been known to contribute to skin cancer in humans: the wavelengths considered most damaging are those from 320 to 400 nm, referred to as UV-A, and from 290 to 320 nm, referred to as UV-B.1,2 The UV spectrum also includes UV-C and other subdivisions, but in this article we are mainly concerned with UV-A and UV-B. From 90% to 95% of UV radiation that reaches the earth’s surface is UV-A, and most of the rest is UV-B.
The different wavelengths of UV-A and UV-B have different effects on the skin. Much of the shorter-wavelength UV-B radiation is scattered by the atmospheric ozone layer, by clouds, by air pollution, and by glass; on the other hand, UV-B rays are the main cause of sunburn in humans. The longer-wavelength UV-A radiation penetrates more deeply into the skin and so may have greater destructive potential.1,3
The daily UV index
The daily UV index of the US National Weather Service and the US Environmental Protection Agency (EPA) (www.epa.gov/sunwise/uvindex.html) offers a direct measurement of the level of UV radiation on a scale of 1 (low) to 11+ (extremely high). The higher the number, the greater the risk of sunburn for a fair-skinned person, even after allowing for cloud cover.
UV EXPOSURE RISKS ARE WELL KNOWN
The American Cancer Society has estimated that the annual incidence of nonmelanoma skin cancer is greater than 2 million, and the incidence of melanoma is from 65,000 to 70,000.4 The incidence of all types of skin cancer has been increasing for the last 30 years.4,5
Exposure to UV radiation is the major environmental risk factor for nonmelanoma skin cancer.6 It is also believed to be a major risk factor for melanoma; although definitive evidence is still lacking, research is beginning to uncover mechanisms linking UV-related gene damage to melanoma.7
UV LIGHT’S EFFECTS ON THE SKIN
The effects of UV light on the skin can be immediate (eg, erythema) and long-term (eg, photoaging, immunosuppression, carcinogenicity).1
Excessive UV damage creates a biochemical milieu that manifests grossly on the skin as a “sunburn.” Excessive UV exposure is damaging regardless of whether a sunburn occurs. Intensive intermittent UV exposure in childhood and teen years leading to blistering sunburn is a risk factor for basal cell carcinoma and malignant melanoma, whereas excessive chronic cumulative exposure is a risk factor for squamous cell carcinoma. In addition, both types of exposure can lead to photoaging.
Sunburn is noticeable 3 to 4 hours after exposure, peaking at around 24 hours.
A long-term effect of UV exposure is photoaging. Although how photoaging occurs is unclear, studies suggest that UV-A contributes more to photoaging, while UV-B contributes to burning, which results in extracellular matrix degradation and dysregulation of collagen metabolism. These changes in matrix and collagen may cause wrinkles and loss of skin turgor; increases in vascular growth factors may induce telangiectasia. All of these effects are characteristic of photoaging.8,9
Immunosuppression, sun exposure, cancer
Profound systemic immunosuppression, such as in organ transplantation patients, can lead to an increased risk of skin cancer, as evidenced by the frequent development of nonmelanoma skin cancers in patients who have undergone organ transplantation, with reported incidence rates of 21% to 50%.6,10
But sun exposure itself can also cause both local and systemic immunosuppression depending on the area of exposure and the dosage of UV radiation. The immunosuppressive and carcinogenic effects of UV light on the skin are complex, involving a variety of cell types, including antigen-presenting cells, lymphocytes, and cytokines. UV radiation can cause dysregulation of antigen-presenting cells such as Langerhans cells and dermal dendritic cells, which in turn can activate regulatory T cells to suppress the immune system. UV radiation can also induce keratinocytes to produce immunosuppressive cytokines that inhibit the production of a number of “repair cytokines” that fix UV-induced DNA damage. The repair cytokines can mitigate UV-induced immunosuppression.6,11 These effects can suppress the induction of local, systemic, and memory immunity.
Both UV-A and UV-B interact to enhance UV-induced immunosuppression, and this can occur even at doses that do not cause erythema.12 Profound immunosuppression—whether UV-induced or due to HIV infection or immunosuppressive drugs—can lead to an increased risk of skin cancer, as evidenced by the frequent development of nonmelanoma skin cancers in patients who have undergone organ transplantation, with reported incidence rates of 21% to 50%.6,10
Animal studies linking UV-B exposure to skin cancer found that UV-B energy is directly absorbed by DNA, resulting in the formation of cyclobutane pyrimidine dimers and pyrimidine-pyrimidone photoproducts in the DNA, which block replication and transcription.6 The resulting mutations specifically occur in the tumor suppressor gene p53, and these mutations have been linked to squamous cell carcinoma.13,14
UV-A light has also been reported to induce cyclobutane dimers, but via an indirect mechanism, since DNA does not directly absorb UV-A. Dimers induced by UV-A light are apparently cleared at a slower rate than those induced by UV-B, suggesting that UV-A may have a greater potential for carcinogenesis.15 UV-A light can also directly induce carcinogenesis through reactive oxygen species that cause tumorogenic modified bases in the DNA. These modified bases can be misread, leading to decreased DNA integrity.6