Sunlight has a profound effect on the skin that can result in premature aging, skin cancer, and a host of other skin-related conditions. Exposure to ultraviolet (UV) light accounts for around 90% of all symptoms of skin injury.
The Facts About UV Radiation
The sun emits UV radiation that we divide into categories based on their relative wavelength (as measured by a nanometer, or nm):
- UVC radiation (100 to 290 nm)
- UVB radiation (290 to 320 nm)
- UVA radiation (320 to 400 nm)
UVC radiation has the shortest wavelength and is almost completely absorbed by the ozone layer. As such, it doesn’t really affect the skin. However, UVC radiation can be found from such artificial sources as mercury arc lamps and germicidal lamps.
UVB radiation affects the outermost layer of skin (epidermis) and is the primary cause of sunburns. It is most intense between the hours of 10 a.m and 2 p.m. when the sunlight is at its brightest. It is also more intense during the summer months, accounting for around 70 percent of a person’s yearly UVB exposure. Because of is wavelength, UVB does not penetrate glass easily.
UVA radiation, by contrast, was once thought to have only a minor effect on the skin. Studies have since shown that UVA is a major contributor to skin damage. UVA penetrates deeper into the skin with an intensity that doesn’t fluctuate as much UVB. And, unlike UVB, UVA is not filtered by glass.
Damaging Effects of UVA and UVB
Both UVA and UVB radiation can cause a plethora of skin-related abnormalities, including wrinkles, aging-related disorders, skin cancer, and a diminished immunity to infection. While we don’t fully understand the mechanisms for these changes, some believe that the breakdown of collagen and the formation of free radicals can interfere with DNA repair on the molecular level.
UV radiation is known to increase the number of moles in sun-exposed parts of the body. Excessive sun exposure can also lead to the development of premalignant lesions called actinic keratoses. Actinic keratoses are considered precancerous because one in 100 will develop into squamous cell carcinoma. Actinic keratoses “bumps” are often easier to feel than see and will typically appear on the face, ears, and the back of the hands.
UV exposure can also cause seborrheic keratoses, which appear like wart-like lesions “stuck” on the skin. Unlike actinic keratoses, seborrheic keratoses do not become cancerous.
Collagen Breakdown and Free Radicals
UV radiation can cause collagen to break down at a higher rate than normal aging. It does this by penetrating the middle layer of skin (dermis), causing the abnormal buildup of elastin. When these elastins accumulate, enzymes are produced which inadvertently break down collagen and create so-called “solar scars.” Continued exposure only speeds the process, leading to further wrinkling and sagging.
UV radiation is also one of the major creators of free radicals. Free radicals are the unstable oxygen molecules that have only one electron instead of two. Because electrons are found in pairs, the molecule must scavenge its missing electron from other molecules, causing a chain reaction the can damage cells at the molecular level. Free radicals not only increase the number of enzymes that break down collagen, but they can also alter a cell’s genetic material in a way that can lead to cancer.
Immune System Effects
The body has a defensive immune system meant to attack infections and abnormal cell growths, including cancer. This immune defense includes specialized white blood cells called T lymphocytes and skin cells called Langerhans cells. When the skin is exposed to excessive sunlight, certain chemicals are released that actively suppress these cells, weakening the overall immune response.
This is not the only way in which excessive exposure can undermine a person’s immunity. The body’s last line of immune defense is something called apoptosis, whereby severely damaged cells are killed and they cannot become cancerous. (This is one of the reasons why you peel after a sunburn.) While the process is not fully understood, excessive UV exposure appears to prevent apoptosis, allowing precancerous cells the opportunity to become malignant.
Skin Changes Caused by the Sun
UV exposure causes the uneven thickening and thinning of the skin called solar elastosis, resulting in coarse wrinkling and a yellow discoloration. It can also cause the walls of blood vessels to become thinner, leading to easy bruising and spider veining (telangiectasias) on the face.
By far the most common sun-induced pigment changes are freckles. A freckle is caused when the skin’s pigment-producing cells (melanocytes) are damaged, leading to enlargement of the blemish. Another is age spots, which typically appear on the backs of hands, chest, shoulders, arms, and upper back. While age spots are frequently seen in older adults, they are not age-related as their name suggests but a consequence of sun injury.
UV exposure can also lead to the appearance of white spots on the legs, hands, and arms as melanocytes are progressively destroyed by solar radiation.
Skin Cancer and Melanoma
The ability of the sun to cause cancer is well known. The three major types of skin cancer are melanoma, basal cell carcinoma, and squamous cell carcinoma.
Melanoma is the most deadly of the three as it spreads (metastasizes) more readily than the others. Basal cell carcinoma is the most common and tends to spread locally rather than metastasize. Squamous cell carcinoma is the second most common and is known to metastasize, although not as common as melanoma.
Sun exposure is the most important risk factor for developing melanoma. By contrast, the risk of basal cell carcinoma or squamous cell carcinoma is related to both a person’s skin type and the amount of lifetime exposure to UV radiation.
- Narendhirakannan, R. and Hannah, A. “Oxidative Stress and Skin Cancer: An Overview.” Ind J Clin Biochem. April 2013; 28(2):110-115.
- Ratushny, V.; Gober, M.; Hick, R.; et al. “From keratinocyte to cancer: the pathogenesis and modeling of cutaneous squamous cell carcinoma.” Journal of Clinical Investigation. February 1, 2012; 122(2):464-472.
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