Light

Skin Cancer, Malignant Melanoma and Sunlight

extracted from Dr. Damien Downing's book "Daylight Robbery — The Importance of Sunlight to Health" (Chapter 7: The Melanoma Debate)

1987 saw the most widespread campaign ever to try and persuade us that sunlight is dangerous and we should avoid it. Yet we still go on summer holidays in our millions, and we still come back feeling that it was worthwhile, and that we'll go again next year. Can it be that we are all so foolish that we ignore the medical evidence for the sake of two weeks of sensuality, or might our instincts be telling us the opposite of what the medical profession is telling us?

It is worth looking at the evidence with a fresh eye. For instance, everybody knows that sunlight causes skin cancer. But it is that simple? We know that cancers are much more common in hot, sunny areas such as Queensland, due to solar exposure — or do we? We all know that malignant melanoma is a skin cancer that is caused by sunburn — but is it?

The last two statements are both questionable. The first is half correct — squamous cell and basal cell carcinomas of the skin are more common in white-skinned people living in very sunny areas such as Queensland. This does not apply to cancers anywhere else in the body. The last statement is, at best, misreading of the evidence. Malignant melanoma is more common in people with the sort of skin that burns easily, but we are not in a position to say that the sunburn actually causes the cancer — it may even protect against it.

We have to take all this very seriously, because in the UK one quarter of all deaths are due to cancer. There are about 200,000 new cases of cancer every year, and of these about ten percent are skin cancers. This in turn breaks down to ninety eight per cent squamous and basal cell cancers, and two per cent melanomas.

But — and it's a very big but — the chances of surviving a skin cancer are excellent: ninety five per cent of patients are alive five years after diagnosis. This compares with thirty six per cent survival for cancers in general.[2] So, as we remarked in the previous chapter, if you have to get cancer, then skin cancer is definitely the wisest choice.

The one big exception is melanoma, of course. Although it is very rare — about 0.2 per cent of all cancers — it is the only skin cancer that normally metastasises (spreads to distant parts of the body), and the death rate is much higher. The five-year survival rate is fifty per cent, much poorer than the other skin cancers.

It still doesn't rank in the top ten killers, but if it were avoidable by something as simple as staying out of the sun, this would plainly be a sensible thing for us all to do.

With the common forms of skin cancer, squamous and basal cell, the relationship with sunlight is clear. They occur usually on the exposed surfaces, such as the face, scalp and the back of the hands, [...] in people who have spent many years working out in the sun. They are particularly common in people who have lived for some time in the tropics. In other words, it is long-term steady exposure to sunlight, for several hours a day, over many years, that triggers off these cancers.

Because it is so much less common, it has been much harder to gather sound evidence on melanoma and its relationship to sunlight. But until recently, a single fact was always quoted as proof that it was triggered by sun. This was the particularly high incidence of melanoma in Queensland, in Northern Australia. This is one of the hottest and sunniest places on earth, and it seemed that the link was obvious and inescapable.

Yet when studies were done in Queensland itself, it was found that within the state boundaries, the sunnier the area the fewer melanoma cases occurred. The disease was more common in the coastal areas, which had less sunlight in summer, when the amount of UV was higher. This clearly bemused the doctors doing the research, as they had no other explanation for melanoma than damage from UV.[3]

The next episode in the story also occurred in Australia, with a survey in New South Wales which showed that there was a greater risk of melanoma in women who had been exposed to fluorescent light at work than in those who have not. The longer these women had been working under fluorescent lights, the greater their risk of developing the cancer. Sunlight appeared to play no significant part in causing the problem. [4]

Critics of this study said that this might be a false result due to the fact that people of a higher social class were more prone to melanoma, and also — but incidentally — were more likely to work in offices with fluorescent lighting, But a study in the New York area confirmed the finding in a group who were all predominantly middle class.

With no difference between the social class of the melanoma sufferers and the non-sufferers, fluorescent lights still appeared to increase the risk. [5]

That was in 1982. In 1984 a large study of 507 melanoma cases and 507 matched controls (matched for age, sex and place of residence) was performed in Western Australia.

This one found that, if anything, exposure to sunlight protected against melanoma. People who regularly spent ten hours a week or more in the sun had a lower chance of developing the disease, and the longer time they spent in the sun each week the lower their risk.

There was an increase of melanoma in people who went boating or fishing twice a week, but this was more than the increase in those who sunbathed — hardly strong evidence of a sunlight link.

In fact, the worse a person's history of sunburn in the past, the less the chance of their developing at least one type of the cancer, known as nodular melanoma. [6]

The final piece of research, which looks as though it may have made sense of the whole conundrum, was conducted in Canada in 1985. This showed that the real risk came not from sunburn, but from having the type of skin that burnt easily.

Whether or not a person actually got sunburned was not important in comparison to their tendency to burn easily and tan poorly. Those with the most sensitive skin had twice the risk of melanoma of those who never burned. [7]

Despite all this, the Royal College of Physicians Report published in April 1987 still said that sunlight was the culprit in melanomas. The conclusion was largely based on the research of one doctor in Glasgow who found a high proportion of people with a history of bad sunburn in her study.

She took no account, however, of the point made by the Canadian study, that people who burn badly are likely to have sensitive skin — and of course in Scotland a very high proportion of the population has Type One, or Celtic, skin. They may never tan, only develop freckles, and the lack of melanin in their skin makes them susceptible to sunburn.

There are several small points that round out this argument. Firstly, studies in the laboratory show that vitamin D suppresses malignant melanoma — and also leukemia — in test tube experiments. [9] Understandably, no one is attempting to reproduce this in humans, but it does offer a possible explanation for the apparent protective effect of regular sunlight against melanoma.

Secondly, the ultraviolet wavelengths that produce vitamin D [in] the skin are entirely absent from normal fluorescent light - and the total UV exposure from working under fluorescent lights for a year has been calculated to be equivalent to forty minutes of autumn sun.[10] So how can UV be the culprit?

Thirdly, the incidence of malignant melanoma is going up most rapidly in some far from tropical areas such as Scandinavia and Scotland. It has been estimated to be doubling approximately every ten to twenty years. [11] Nobody has yet shown how this increase could be due to exposure to sunlight. But it could very well be due to increasing exposure to indoor lighting.

Finally, despite the recommendations in the RCP report there is evidence that sunscreens make no difference to the incidence of melanoma. Indeed, there has been for some time proof that they may even contribute to causing skin cancer, as well as certainly helping to trigger off photosensitivity - skin rashes in response to sunlight. [12]

When Apperley, who showed that cancers in general decreased with sunlight exposure, looked at the incidence of skin cancer throughout the continental USA, he found the relationship with sunlight depended on the average temperature.

Over a critical level of 42°C, increases in exposure to sunlight clearly caused an increase in the rate of development of skin cancers — of all types. Below that temperature, however, the rate decreased with increasing exposure to sun.[13]

It would appear, then, that in hot, tropical countries there is a risk of sunlight causing skin cancer, particularly in white skins, of course. In temperate climates such as northern Europe, on the other hand, sunlight is likely to protect.

This would also tie in with the finding that, in contrast to Panner's figures mentioned in the last chapter, English researchers have found that rates of skin cancer and total cancers vary together.[14]

In temperate climates such as ours, sunlight may protect us from both skin cancers and cancers in general, while in hot climates it may encourage skin cancers (basal cell and squamous cell), but still protect against other cancers.

The overall picture, then, seems to be that sunlight in large doses for long periods may cause skin cancer, particularly in the tropical heat, but sunlight at any dose level protects from cancers in general. The more sunlight you receive, the better protected you are.

We know that sunburning with its production of free oxidising radicals is the factor that encourages the development of skin cancer. There is no reason to think that this is the protective factor against other cancers, so the way to take your sunlight as a cancer protection is in frequent small doses, insufficient to burn you.

The secretary who slips out of the office at lunchtime and sunbathes in the park for forty minutes has the right idea. As well as gorgeous brown legs, she is giving herself protection against cancer.

Atmospheric filter

The wavelengths that are responsible for sunburn are those with the highest energy content — ultraviolet. Because their wavelength is shorter, there are more waves per metre of length, or per second, hitting the skin, and therefore more energy is transferred.

Compared to ultraviolet, infra-red has a very low energy content. The whole of our biology is based round the fact that there is a very sharp cut-off point for ultraviolet transmission through the atmosphere.

There are two gateposts framing the narrow inlet for solar radiation. On the low frequency, long wavelength side, much of the solar spectrum is absorbed by carbon dioxide and water, while on the short wavelength side the most important absorber is ozone.

It is the fact that ozone absorbs best at a wavelength of 260 nanometres, and the absorption then tails off completely above 300, that gives us the cut-off point for solar radiation at around 300 nanometres.

There has been concern among scientists in recent years about the danger that certain environmental pollutants, particularly the propellants in aerosol cans, may destroy the ozone layer in the atmosphere and lead to an increase in the amount of ultraviolet reaching the earth.

However, the ozone level varies greatly from hour to hour and from day to day, in response to normal environmental and weather factors. The level of ozone in the atmosphere has been measured for over fifty years in the Swiss Alps, and in some other places, and no clear trend has been demonstrated so far.

This is true notwithstanding the finding of an apparent 'hole' in the ozone layer above Antarctica. Although such a discovery suggests that our environment is being disturbed by man's activities, it is still a local phenomenon and does not appear to reflect a general reduction in the ozone layer — yet. Indeed, some scientists think that it may always have been there and we have only just noticed it.

Smog

Pollution from car exhausts and industry produces a range of chemicals in the atmosphere, including both the components of acid rain (sulphates and nitrates in particular), and indeed ozone itself.

In this circumstance, with a very high local concentration at just above ground level, ozone is more important as a toxic pollutant than as a sunscreen. In fact, the level of ozone in smog appears to be increased by ionisation triggered by ultraviolet light.

Monitoring of the intensity of sunlight in Washington DC and California has shown a reduction in the sunlight reaching the earth of more than ten per cent over the last fifty years, with a twenty six per cent reduction in the ultraviolet fraction.[1] The only evident cause of this is environmental pollution.

Therefore, if you live under a smog, as many people in cities around the world now do, you receive less ultraviolet light because it is absorbed by the smog. You also breathe less fresh air and more pollution.

Once again, modern life has increased the toxic component of our intake while reducing the nutritional or beneficial component. In this case, it appears that ultraviolet light helps to make the problem worse by interacting with the chemical components of smog.

But the real culprit is not the ultraviolet light, it is the products of fossil fuel combustion that go to make up pollution.

Photoreactivation

It is ultraviolet light of around 295 nanometres wavelength (UVB) which has the potential to cause damage to DNA and other molecules. These are the shortest wavelengths — and therefore have the highest energy — of any light reaching the earth. Thus they have the greatest potential for transferring energy to our bodies — for producing either benefit or damage.

Damaged DNA may lead to a cellular mutation — an abnormal cell which can be the start of cancer, or in the next generation of a genetic change or a congenital abnormality.

Although several people have suggested that this is necessary for evolution, that an element of randomness is needed to keep things changing, it is certain that the process does lead to cancers and deformities. Under normal circumstances, all such genetic mutations are filtered out of the body by the immune system.

When cancer develops this is detected at an early stage by the immune surveillance and the cells are killed and removed. Clinical cancer is therefore more a sign of an immune problem than of something unusual in the way of genetic events.

Transplant patients who have received immunosuppressant drugs so that they will not reject the transplanted heart or kidney have an eighty times greater than normal chance of developing cancer.

AIDS sufferers also have a tendency to develop unusual forms of cancer such as Kaposi's Sarcoma. Both groups have in common a low level of immunity to infections and to cancers.

But it has always been known that some organisms have the ability to repair DNA damage in a manner that is dependent on ultraviolet light. Many micro-organisms have been shown to contain a protein molecule — an enzyme — which absorbs near-ultraviolet light (UVA), and is thereby activated to repair broken strands of DNA. [17]

The chemicals that are measured as an indicator of DNA damage are known as pyrimidine dimers. These are small x molecules of DNA which have been broken free of the chromosome and then joined together in pairs to form dimers (which consist of two identical molecules).

Evidence of repair of DNA damage is obtained if these dimers are split into two monomers again. The process by which this occurs in response to UV light is called photoreactivation. It has always been known that it occurs in small organisms, but until recently it was thought that higher animals did not perform this function.

In the past decade there has been increasing evidence that it occurs in a range of mammals, and the hunt was therefore on for evidence of its occurence in humans.[18]

In 1986 Betsy Sutherland, a researcher at Brookhaven National Laboratory in New York, finally demonstrated that photoreactivation occurred in human skin. She described its parameters quite clearly:

It is light-dependent, being stimulated best by light of wavelength 350 to 400 nanometres, which is in the near ultraviolet range. When such light hits the skin, the process happens very rapidly, clearing most of the dimers out of the tissue within minutes.[19]

There is also some non-enzymatic repair that is still dependent on light, but occurs by chemical reactions that do not depend on human enzymes. Although this can be measured in skin also, it occurs at a much slower rate, taking about an hour to remove half of the dimers. Clearly it is less important than photoreactivation.

The remarkable fact is that although ultraviolet stimulates synthesis of DNA, and therefore cell activity and multiplication, it suppresses DNA synthesis during the first hour after exposure.[20] During this hour, the photoreactive enzymes are able to repair most of the damaged DNA in readiness for the burst of cellular activity that then occurs.

Therefore, as well as having a potential for damaging human tissues, ultraviolet light is also essential for the repair of such damage. We are so well adapted to our solar environment that there is a built-in protective mechanism, triggered by sunlight, to protect us against the possible harmful effects of this same sunlight.

The message seems clear. Although some doctors and scientists are still determined to prove that sunlight is damaging and should be avoided, the evidence is mounting in its favour. We are designed to feed on sunlight, and we suffer if starved of it.

But changes in our lifestyle over the past few decades have only advanced a process started by the industrial revolution, driving us indoors and away from the sun.

Attemping to rectify this by brief binges of sunlight for a fortnight in the summer may well have harmful effects that offset their benefits. We should aim to nourish ourselves with sunlight regularly, every week of the year.

Note

"Daylight Robbery" is one of several important books on the link between health and light.

References

1. Cramer, W., 'The Prevention of Cancer', Lancet: 1; 15,1934.
2. Fry, J., Sandier, G., and Brooks, D., Disease Data Book, MTP Press Ltd., Lancaster, 1986.
3. Green, A., and Siskind, V., 'Geographical Distribution of Cutaneous Melanoma in Queensland', The Medical Journal of Australia, April 1983.
4. Beral, V., et al., 'Malignant Melanoma and Exposure to Fluorescent Lighting at Work'. Lancet, 7 August 1982.
5. Pasternak, B.S., 'Malignant Melanoma and Exposure to Fluorescent Lighting at Work', Lancet, 26 March 1983.
6. Holman, C.D.J., and Armstrong, B.K., 'Relationship of Cutaneous Malignant Melanoma to Individual Sunlight Exposure Habits', Journal of the National Cancer institute, Vol 76, No 3, March 1986.
7. Elwood, J.M., et al., 'Sun Exposure and Malignant Melanoma', Br. J. Cancer: 51; 543549, 1985.
9. Colston, K., et al., 1, 25-Dihydroxyvitamin D and malignant Melanoma: The Presence of Receptors and Inhibition of Cell Growth in Culture', Endocrinology: 108;1083-83,1981.
10. Pasternak, B.S., et al., 'Malignant Melanoma and Exposure to Fluorescent Lighting at Work' (Letter) Lancet: 1; 704, 1983.
11. MacKie, R.M., et al., 'Malignant Melanoma in Scotland 1979-1983'. Lancet: 2; 859-862, 1985.
12. Hodges, N.D.M., et al., 'Evidence for Increased Genetic Damage due to the Presence of a Sunscreen Agent', J. Pharm. Pbarmacol: 28; 53, 1976.
13. Apperley, F.L., 'The Relation of Solar Radiation to Cancer Mortality in North America', Cancer Research.
14. Conrad, K.K., and Hill A.B., 'Mortality from Cancer of the Skin in Relation to Mortality from Cancer of Other Sites'. Am. J. Cancer: 36; 8397, 1939.
17. Achey, P.M., et al., 'Photoreactivation of Pyrimidine Dimers in DNA, from Thyroid Cells of the Teleost Poccilia Formosa'. Photochem Pbotobiol: 29; 305-310,1979.
18. Sutherland, B.M., 'Pyrimidine Dimer Formation and Repair in Human Skin'. Cancer Research: 40; 3181-3185, 1980.
19. Sutherland, B.M., 'Photoreactivation and Other Ultraviolet/Visible Light Effects on DNA in Human Skin', Ann. N.Y. Acad. Sci: 453; 73-79, 1985.
20. Pathak, M.A., 'Activation of the Melanocyte System by Ultraviolet-Radiation and Cell Transformation', Ann. N.Y. Acad. Sci: 453; 328-339, 1985.

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