UV Radiation

How Sunlight Really Affects Your Skin

Woman wears hat in sun
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Sunlight has a profound effect on the skin. It causes premature skin aging, skin cancer and a host of other skin issues. Many changes in the skin that were commonly believed to be due to aging, such as bruising easily, are actually a result of prolonged exposure to UV radiation. Exposure to ultraviolet light - UVA or UVB - from sunlight accounts for 90 percent of premature skin aging symptoms. We know sun exposure is generally a bad thing, but why?

What Is UV?

The sun emits ultraviolet radiation in wavelengths that are measured in nanometers. A nanometer is one-billionth of a meter, which is approximately 39 inches. The wavelengths are divided into three categories:

  • UVA: 320 to 400 nanometers
  • UVB: 290 to 320 nanometers
  • UVC: 100 to 290 nanometers

The UV A's, B's & C's

UVA rays are the rays that age. They are able to penetrate deeper into the dermis - the second layer of the skin - and cause damage that contributes to photoaging and skin cancer. The ozone layer does nothing to weaken the intensity of UVA rays, and they can also penetrate glass. The intensity of UVA radiation is more constant than UVB rays. There are no variations during the day or throughout the year.

UVB rays are the rays that burn. They affect the outermost layer of the skin: the epidermis. About 90 percent of UVB radiation is absorbed by the ozone layer. As the ozone layer becomes more and more depleted, however, we are gradually becoming exposed to more and more UVB radiation.

UVB rays are at their most intense when the sun is at its brightest between 10 a.m. and 2 p.m., and they're even more intense during summer months. In fact, 70 percent of a person's annual UVB dose occurs during the summer. UVB rays can't penetrate glass.

UVC rays are almost completely absorbed by the ozone layer and do not affect the skin.

UVC radiation can be found in artificial light sources such as mercury arc lamps and germicidal lamps.

How UVA & UVB Rays Work Together

Because of the ozone layers and other atmospheric filters, most of the UV radiation that reaches us is UVB. In fact, we're exposed to 20 times more UVB radiation than UVA. We think of UVA and UVB as separate entities - UVA as the wrinkle and skin cancer producer and UVB as the sunburn producer - but they actually work together to cause skin damage, including:

  • Wrinkles
  • A weakened immune system
  • Aging skin disorders
  • Cancer

Both UVA and UVB cause damage to DNA because they affect the dermis and epidermis, respectively. This damage causes mutations in the p53 tumor suppressor gene: a gene responsible for repairing damaged DNA and discarding cells that are damaged beyond repair. If p53 doesn't function properly these highly damaged cells are allowed to continue dividing, creating even more extremely damaged cells. Approximately 50 percent of skin tumors have this mutated p53 gene in them.

UVA penetrates deeper into the skin, reaching the dermis where collagen - the structural scaffolding of the skin - is located. This causes the skin to sag in places where wrinkles appear.

UVA also increases the number of inflammatory cells in the dermis. Both UVA and UVB cause the number of Langerhans cells, an important part of the immune system, to decrease, lowering immunity.

What Does This Mean for Me?

Perhaps the scariest part of all of this is that you can't see of feel any of these mutations happening until the damage is already done. Most of this damage occurs in childhood. This means it's extremely important to use sunscreen and sun-protective clothing at all times. Even young children need to be protected any time they go outside, not just when they're swimming.


Marrot, L, and JR Meunier. “Skin DNA Photodamage and Its Biological Consequences.” Journal of the American Academy of Dermatology 58.5 Suppl 2 (2008): S139-48.

Palm, Melanie, and Marianne O'Donoghue. “Update on Photoprotection.” Dermatologic Therapy 20(2007): 360-76.

Rigel, DS. “Cutaneous Ultraviolet Exposure and Its Relationship to the Development of Skin Cancer.” Journal of the American Academy of Dermatoly 58.5 Suppl 2 (2008): S129-32.

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