Low-intensity UV still damaged skin DNA in a lab study of 58 people: what low-level sun exposure does

Sun safety advice rests on a simple idea: the sun is dangerous when it is strong. Avoiding it at midday, the thinking goes, makes time outdoors early or late close to harmless. An experiment in Australia has tested part of that idea on human skin, using a lamp that imitates sunlight. A dose delivered at low intensity damaged DNA as much as the same dose delivered at high intensity.

Researchers at QIMR Berghofer, a medical research institute in Brisbane, shone measured doses of ultraviolet (UV) light on a patch of skin on 58 volunteers. The doses were small, too small to cause any reddening. Some were delivered at the strength of midday sun and some at the strength of mid-morning sun. The damage to DNA in the skin was the same either way.

The study, published in the journal Photochemistry and Photobiology, measured early molecular changes over a few days. It did not measure skin cancer, and earlier work suggests that part of this kind of damage is repaired within a day.

What the low-dose UV study did

The question the team asked concerns ultraviolet radiation (UVR), the invisible part of sunlight that tans, burns and makes vitamin D. Small doses are known to be enough for vitamin D. But, as the authors put it, whether delivering these doses at naturally occurring UVR indices causes DNA damage in humans is unknown.

The Low-Dose UV Study included 58 people with light to olive skin. In the six-step classification dermatologists use, which runs from lightest to darkest, these were skin types I to III. Participants received solar-simulated UVR on the lower back on four consecutive days.

Two things were varied. The first was dose, the total amount of ultraviolet energy received. The two doses used were 0.7 and 1.6 standard erythemal doses, a standard unit of sunburn-causing UV. The amount of UV exposure was not high enough to make participants’ skin turn pink, the institute’s account says.

The second was intensity, measured by the UV index, a scale of the sun’s UV strength. The World Health Organization (WHO) describes it as a measure of the level of UV radiation, with values that start at zero and rise with intensity. On the WHO’s chart, 0 to 2 is the lowest band and 8 and above the highest. Doses were delivered at either UVI 2.8 or UVI 8.0, UVI being the abbreviation for the index. The institute likens the lower setting to mid-morning sun and the higher to lunchtime sun. The same dose simply took longer to deliver at the lower setting.

The researchers then looked inside the skin. Skin biopsies were collected at baseline, and from exposed sites at 15 min, 24, and 72 h. A biopsy is a small sample of tissue.

What low-intensity UV did to skin DNA

They measured three things in the cells of the outer skin.

The first was a type of DNA lesion with the chemical name cyclobutane pyrimidine dimer, a spot where UV has fused two neighboring letters of the genetic code. These lesions are the signature of UV damage, and those that persist can lead to the mutations found in skin cancers.

Both doses produced them, and the larger dose produced more. Fifteen minutes after exposure at the higher intensity, 3.67% of cells showed the lesions after the larger dose and 0.89% after the smaller one. A dose a little more than twice as big left about four times as many damaged cells.

The second was p53, a protein that cells produce when their DNA has been damaged and that halts cell division while repairs are made. It rose too. At 72 hours, the level was 2.5 to 3 times higher in skin given the larger dose than in skin given the smaller.

The third was a marker of a different kind of harm, chemical damage from reactive oxygen. It showed minimal, nonsignificant changes over time.

The authors’ conclusion is that UVR delivered at doses that can maintain adequate vitamin D status, and at naturally occurring irradiance, leads to measurable DNA damage. Irradiance is the technical word for intensity.

Why low-intensity UV did as much damage as strong

The central result is what did not make a difference. UVR irradiance did not affect the lesion counts or the p53 response, the authors report. A given dose did the same damage whether it arrived quickly under strong light or slowly under weak light.

Co-lead Rachel Neale spelled out what that means outdoors. “You can get the same dose of UV radiation in a short time in the middle of the day or a longer time earlier or later in the day. Our research has shown it is the total dose that is important - it doesn’t matter how long it takes to get it,” Neale said.

That cuts against a common reading of the UV index. Current guidance recommends sun smart measures when the UV index reaches 3 or higher, the release notes. The WHO’s own page says that even for very sensitive fair-skinned people, the risk of short-term and long-term UV damage below a UVI of 2 is limited.

The Australian result does not contradict that statement so much as add a condition to it: at a low index the risk is limited for a given length of time. Given enough time outdoors, the dose catches up. “People potentially get lulled into a sense of security when the intensity of sunlight is weak and they spend too long outdoors without adequate protection,” Neale said.

The trade-off between skin damage and vitamin D

The same rays do two things at once. Ultraviolet light is how the skin makes vitamin D, and it is also what damages DNA. The experiments so far have not found a dose that does the first without the second.

A team at the University of Manchester, independent of the Australian group, looked for one. They exposed volunteers of all six skin types to a series of doses well below each person’s sunburn threshold. Public health guidance recommends limiting sun exposure to sub-sunburn levels, they noted, but whether that avoids DNA damage had not been established. It did not. They found vitamin D and DNA lesions rising together from the very smallest dose tested, a fifth of what it takes to redden skin.

An earlier Manchester experiment asked whether such damage builds up. Ten white (phototype II) and six South Asian volunteers (phototype V), aged 23-59 years, were given simulated summer sunlight three times a week for six weeks. Phototype is another name for skin type. In the white volunteers, lesions appeared after the course, and on average 44% of them had cleared a day later. There was no more damage after six weeks than after a single exposure.

The authors drew a measured conclusion. Low-dose summer sunlight exposures confer vitamin D sufficiency in light-skinned people concurrently with low-level, nonaccumulating DNA damage. Nonaccumulating is the reassuring word: the skin was keeping up with repairs.

The two Manchester results and the Australian one are consistent. All three find damage at doses below the level of a burn. They differ in emphasis, with the British group stressing that the damage is modest and cleared, and the Australian group stressing that it is there at all.

Does skin color change the damage from low UV?

It does, and substantially. The new study enrolled only people with lighter skin, so it cannot speak to this, but the Manchester studies can.

In the six-week experiment, the South Asian volunteers fared differently from the white volunteers. The same exposures produce minimal DNA damage but less vitamin D in brown-skinned people, the authors reported.

The later study showed why. The pattern of damage tracked the amount of melanin, the pigment that darkens skin. In the darkest skin, lesions formed only near the surface and none reached the basal layer, the deepest layer of the outer skin, whose long-lived dividing cells the authors call the most likely site for skin cancer to start. In the lightest skin, lesions were spread evenly through the full depth.

The authors’ conclusions differed accordingly. “People with darker skin can be encouraged to use sub-sunburn UVR-exposure to enhance their vitamin D,” they wrote. In people with lighter skin, basal cell damage occurs concurrent with vitamin D synthesis at exquisitely low UVR levels.

What sun protection has been shown to do

DNA lesions are an early step on a long road. The stronger evidence on preventing skin cancer comes from a trial that counted cancers.

In 1992, 1,621 randomly selected residents of Nambour, a township in Queensland, Australia, were assigned either to apply sunscreen to the head and arms every day or to use it as they pleased. The trial ran for four years and the participants were followed for ten more.

Ten years after trial cessation, 11 new primary melanomas had been identified in the daily sunscreen group, and 22 had been identified in the discretionary group. That is half as many, though with so few cases the result fell just short of the usual statistical threshold. For invasive melanomas, the more dangerous kind, the difference was 3 against 11. The authors concluded that melanoma may be preventable by regular sunscreen use in adults.

The Australian researchers connect their result to that kind of everyday use. The institute argues that the result favors daily sunscreen use to cover the short, unplanned exposures of ordinary life. The study itself did not test sunscreen.

What the low-dose UV study leaves unanswered

It did not measure cancer. The study counted molecular markers in skin samples taken up to 72 hours after exposure. Co-lead David Whiteman acknowledged the gap between the two. The presence of skin damage does not mean cancer has already formed, Whiteman said. “Our lab results show these small, incremental doses of UV have caused some damage to the DNA in the skin cells, enough for the cells to then respond to the damage,” Whiteman said.

His argument is about accumulation over a lifetime. The study itself gave doses on four consecutive days and took its last skin samples 72 hours after exposure. The earlier Manchester work found low-level damage was cleared between exposures and did not build up over six weeks.

The light came from a lamp built to imitate sunlight, and it fell on a small area of the lower back, not on the face, hands or forearms that take most everyday exposure.

Only lighter skin was tested. Nothing in the study applies directly to people with brown or black skin, in whom the earlier experiments found far less damage.

Fifty-eight people is a small group.

The researchers are explicit that their results are not a call for people to avoid sunlight altogether. Their aim, they say, is for guidance to reflect what happens in the skin.

Doses of ultraviolet light too small to redden lighter skin left measurable DNA damage whether they came from weak or strong light, in a short laboratory study that did not measure cancer.