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Skin and sunlight

In this series a GP interviews an expert to get first-hand information that goes beyond the textbook on a topic of current clinical interest

GP Dr Linden Ruckert asks Professor John Hawk about the latest evidence on the risks of prolonged exposure to the sun

Practical points

lSuboptimal use of sunscreens means actual SPF is a

third of that printed on the bottle

lHydroquinone is usually safe and well tolerated for melasma

lSelf-tans are safe and may stop people going in the sun so much

l30 minutes on a sunbed causes the same amount of DNA damage as 10 minutes of Mediterranean sunlight

lA topical NSAID every couple of hours for a day can reduce the effects of sunburn by 30 per cent

UVA, UVB and environmental change

What are the effects of UVA and UVB on the skin?

UVB light is the radiation present when the sun is high in the sky – regardless of the weather, that is in the middle of the day in summer or in the tropics. It is the most damaging radiation, being well absorbed by DNA in the skin. It causes sunburn most readily, as well as promoting tanning and thickening of the skin; the sunburn occurs in the next few hours while the tanning and thickening happens over days to weeks.

DNA damage – tanning is a response to this – leads to ageing of the skin, but strategically important damage can lead to cancer. So, we should minimise exposure between 10-11am and 3-4pm. Cloud has little effect unless it is heavy and low.

UVA is not nearly as well absorbed in skin and has fewer effects than UVB. It probably does cause tanning more readily, but less burning – hence its use in sunbeds. Very large amounts, however, will result in the same damage as UVB, but cancer might be slightly less likely and ageing more likely.

UVA is absorbed by molecules other than DNA, leading to active free radicals, molecular elements that cause secondary damage to DNA. UVA is around most of the time, even in winter, although more in the summer. UVA also passes through windows and many sunscreens unless they are thick and white. The more 'stars' a sunscreen has the greater its protection against UVA.

The sun protection factor of a sunscreen relates to its protection against burning. An SPF of 15 is a figure, not an ingredient as many patients seem to think. In adequate amounts it will reduce the damage by 15 times.

It refers to UVA and UVB effects together. The optional star system for UVA protection is of less relevance than SPF, and it was introduced when the media was making a big fuss about UVA. I personally do not think it is of huge extra value. But it is better to use high star rating than not.

Has environmental change led to an increase in

UV light intensity?

Contrary to popular opinion, essentially not. There are one or two areas where the intensity has increased; this tends to be in specific parts of the world such as Antarctica and to a lesser extent in other countries in that area. It also tends to be in early spring when the UV intensity isn't high anyway.

The fuss being made about ozone layer depletion is relevant in terms of what it may do in the future but not in terms of what it is doing now. Some people insist they can get sunburnt more easily but nowadays there is much more variation from minute to minute, with the coming and going of heavy cloud and the sun dropping in the sky, than there is from ozone layer changes.

Changes in the middle of the day in summer may be 100 per cent but ozone effects only account for 1-2 per cent. The same applies with changes in latitude; sunlight in total throughout the day may be two to three times stronger in Spain, for example.

The damage to DNA is done steadily throughout life. Previous damage cannot be repaired if it is not repaired at the time, although in the 24-48 hours after sun exposure most of it is repaired. Too much damage may entail the DNA strand opposing where the damage occurs – from which the repair is copied – being damaged, leading to permanent mutations which can then lead to ageing and cancer.

Children generally develop more DNA damage in their first 18-20 years because of their outdoor lifestyles.

What advice can I give people on choice of sunscreen?

Sunscreen products work if applied in the concentrations that their test protocol requires (2mg/cm2), which is liberal and much thicker than many people use. It has been shown that the SPF of a product as really used is probably only a third of what is on the bottle, on the areas where you remember to put it – and that's only for the first hour or so if you don't reapply it.

Careful case studies show sunscreens do work but epidemiological studies confirm strongly that people who use sunscreens get more skin cancer than those who don't. This is because people who go in the sun use them but don't use them properly, particularly on beaches. A better approach to protection is sun avoidance in the middle of the day or wearing close-weave protective clothing, such as cotton which you can't see through when it is held up to the light.

White sunscreens give good UVA protection, otherwise there is not much difference between the protectivity of these and clear ones. In the last few years chemicals that absorb UVA have also been developed so there is quite good UVA protection now from non-white sunscreens.

There has been discussion about titanium dioxide in white sunscreens but no adverse effects of the reflectants have ever been shown. There has also been discussion about chemical absorbers being absorbed into the skin and being mutagenic but nothing has come of that either.

P20 is a very old sunscreen – or at least the active ingredient, para-amino benzoic acid (PABA), is. After 20 years of use it was rejected as mutagenic – which it is but it doesn't get through the skin surface so that doesn't matter. It also stains clothing, and protects only against UVB. It does work but it seems to have been marketed again recently without any particular advantages apart perhaps from good skin adhesion.

Are self-tans safe?

Yes. They consist of dihydroxyacetone and have been used for decades with no problems. They bind to the stratum corneum through covalent bonding with amino acids and are part of normal metabolic activity in the body. They also give an SPF of about two against UVB. I encourage them to help stop people going in the sun.

As GPs we don't support sunbeds – but is there anything patients should know about the risks that GPs may be unaware of?

Sunbed manufacturers tried to skirt round the dangers by saying they emitted just UVA before people knew about the dangers of UVA. Since it's been possible to follow people up long enough now, it has been shown that problems from sunbeds are similar to those from sunlight. Half an hour on a sunbed causes the same damage as 10 minutes of Mediterranean sun.

Not much can be done to repair sun damage

Going back to skin repair, are there any treatments that work?

The body has an enzymatic skin repair system and a copy of this has been developed from a bacteriophage repair system and incorporated into liposomes. This treatment – called Dimericine or T4 endonuclease V – has been shown to improve DNA repair by 30 per cent in xeroderma pigmentosum patients, who develop skin cancer easily because their own repair system is genetically impaired.

It is due to be approved by the US Food and Drug Administration. It should also theoretically work in normal subjects and might well be incorporated into sunscreens.

I don't think vitamin A works as a protectant – or if it does its effect is minimal. Most cosmetic creams work purely as moisturisers, which also occlude transpiration so the skin is plumped up for several hours which helps prevent ageing changes to a degree. All the other additives are mostly advertising blurb. Retin A does adjust the growth of skin to a degree and minimises irregular pigmentation so the skin looks marginally better but it can photosensitise and irritate. It needs to be used constantly and its effects are minor.

Topical NSAIDs diminish the effects of sunburn if used from the moment exposure begins – although this suggests you know you are going to get sunburnt. If you find you have overexposed, a topical NSAID applied directly and every couple of hours for a day will diminish the effects by 10-30 per cent. This is not new – I wrote about this in the early 1980s. Hydrocortisone topically has not been shown to work.

Is there anything that really works for melasma, which upsets a lot of women?

There is a genetic predisposition and it's promoted by oestrogen. Irritation by acne or eczema will make it worse. A hydroquinone-containing preparation will dispose of it very gradually over three to six months.

There is a lot of hype about the dangers, which I can't understand because I have used such preparations a lot with no trouble. But they do cause irritation in some people and allergy in a few, but nevertheless 80 per cent of patients can use them. They are said to cause ochronosis, an orangey dermal degeneration, but I've never seen it and I follow people up every three months.

It is possible to prescribe 2 and 4 per cent hydroquinone as Eldoquin through pharmacists.

Intermittent sun exposure and risk of cancer

Exactly how does sunburn relate to melanoma risk? Are dysplastic naevi inevitably melanoma precursors?

People who are fair skinned and get lots of blistering sunburn – especially as children – have a higher chance of melanoma. Skin cancer probably develops through a series of steps, so it seems that if you stop exposing before you get a cancer you won't get one later. Melasma can occur on non sun-exposed parts probably because these are exposed on holiday. The diagnosis is now made more frequently because we have been exposing more and we take more moles off.

It's probable that in the past some early melanomas would have gone back to normal if sun exposure stopped. Dysplastic naevi are not inevitably melanoma precursors but it's probable that they can become melanomas more easily. Many melanomas also probably develop from a melanocyte that grows wrongly rather than from a mole that already exists. If someone has irregular but not enlarging moles I usually take a clinical picture and see them again in four months – if they are growing, getting darker and changing shape this suggests malignancy. Those bigger than the eraser end of a pencil with a clear history of change I remove.

It's quite common to get an irritated mole that you don't remember irritating. If it goes back to normal in one to two weeks it doesn't matter.

Is it the same for BCC and SCC – or is this only cumulative sun exposure?

For BCC the risk is likely to be from intermittent severe exposure as for melanoma; for SCC it is lifetime exposure, especially in fair-skinned people. BCC also often seems to have an extra genetic factor.

What about actinic keratoses?

Solaraze is a topical NSAID, which has been shown to probably improve or dispose of actinic keratoses. It needs to be used over two to three months but irritation can limit its use. Improvement continues for a month after stopping. I tend to use it in patients with constant mild actinic keratoses developing – as well as telling patients to avoid sun exposure.

I also find 5-fluorouracil works well but is so inflammatory that I don't give it to patients – I use liquid nitrogen cryotherapy if they are significant. I haven't noted that affected patients are getting younger.

Linden Ruckert is a GP in central London

John Hawk is a consultant dermatologist at

St Thomas' Hospital, London, and co-author of Understanding your skin: sunlight & skin cancer (Family Doctor Publications, 2003)

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