WebMD Medical News
Brenda Goodman, MA
Laura J. Martin, MD
Oct. 6, 2011 -- Ultraviolet A radiation, which can pass through window glass and clouds, causes changes to skin cells that may lead to cancer, a new study shows.
Experts once thought that UVA rays, sometimes called "aging rays" because they penetrate skin most deeply and lead to wrinkles, were less dangerous than UVB, or "burning rays," which act primarily on the outermost layers of the skin where most cancers occur.
UVA rays are further divided into UVA1, the rays with the lowest energy that account for about 75% of visible sunlight, and UVA2. UVA is also the main kind of radiation used in tanning beds.
"People have really not been that concerned with UVA1 in the past. They've been more concerned, in the UVA spectrum, UVA2, which is closer to UVB," says Darrell S. Rigel, MD, a clinical professor of dermatology at New York University Medical Center.
The new study shows that "with the UVA1 they were able to produce the same types of DNA damage that you see in early skin cancer, and that's actually interesting because that hasn't really been shown before," says Rigel, who was not involved in the research.
The new findings make it even more important, experts say, for people to regularly use broad spectrum sun protection, from hats, sun-protective clothing, and sunscreen.
That isn't always an easy task since the sun protection factor (SPF) listed on sunscreen labels only measures how well the product blocks UVB, not UVA.
"The issue right now is that there's no easy way for me to tell my patients how to get good UVA protection in sunscreen," Rigel tells WebMD.
Changes mandated by the FDA are due to go into effect next year, which should make it easier for people to find sunscreen with broad-spectrum sun protection.
For the study, which is published in the Journal of Investigative Dermatology, researchers recruited 12 volunteers who had never sunbathed or used tanning beds while naked.
They exposed skin on their buttocks, which tends to be the least sun-exposed part of the body, to UVB and UVA1 radiation. The light was applied just long enough, in each case, to cause the skin to burn.
Researchers then cut away a small area of the burned skin and looked for DNA damage in the cells.
The kind of damage they saw in UVA exposed skin has been shown in other studies to lead to skin cancer.
UVA causes these changes at a larger incidence than has been expected or predicted, researchers say.
"These particular lesions are repaired quite slowly. And so even if you get small doses, but get them on a daily basis, the damage builds up," says study researcher Antony R. Young, professor of experimental photobiology at St. John's Institute of Dermatology at Kings College London.
"The amount of damage with UVA actually increases as you go more deeply into the skin, and I think that's due to some kind of reflection process of UVA so it goes in and then it's sent back," he says.
"I see this as a marker of UVA penetration," Young says. If it's that deep in skin "it may cause other types of damage, like oxidative damage, which we didn't measure but which are thought to be important in cancer in general."
His findings, Young says, "support a role for UVA protection in sunscreen."
Right now, he says, sunscreens in the U.S. don't protect as well against UVA as they do against UVB.
But new FDA regulations set to go into effect next summer could spur sunscreen makers to increase UVA protection in their products.
"It will still say SPF 30, but in the same-sized letters it will also say broad spectrum if it protects against UVA," says Melody Eide, MD, a dermatologist at Henry Ford Health System, in Detroit.
To claim broad-spectrum protection, sunscreens will have to pass a standardized test that demonstrates that the product blocks a certain amount of UVA.
Currently, products that say broad spectrum offer varying amounts of UVA protection.
SOURCES:Tewari, A. Journal of Investigative Dermatology, Oct. 6, 2011.Darrell S. Rigel, MD, clinical professor of dermatology, New York University Langone Medical Center.Antony R. Young, professor of experimental photobiology, St. John's Institute of Dermatology, Kings College London.Melody Eide, MD, dermatologist, Henry Ford Health System, Detroit
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