UV from sun and sunbeds

The sun and sunbeds emit UVB and ultraviolet A (UVA). Sunbed tubes with high fluence rates of UVA are allowed for two reasons: (i) UVA wavelengths are not significantly absorbed by DNA and do not affect DNA directly⁽Reference Von Thaler, Kamenisch and Berneburg⁸⁾; and (ii) UVA produces skin tanning, both immediate pigment darkening (IPD) and delayed tanning. Tanning is thought to protect DNA and reduce carcinogenesis as indicated by the low skin cancer risk of dark-skinned people⁽Reference Marks⁹⁾. The positive effects of UVB are not known, only its carcinogenetic potential. Thus, UVB levels are restricted to those in solar radiation which are sufficient to increase the vitamin D levels in the blood⁽Reference Cicarma, Porojnicu and Lagunova^10–Reference Thieden, Jorgensen and Jorgensen¹³⁾: 10 min of exposure to sunbeds, twice weekly, give similar vitamin D levels as a daily intake of 50 μg of vitamin D⁽Reference Moan, Lagunova and Cicarma¹¹⁾, or 5 teaspoons (25 ml) of cod-liver oil, and can bring a winter level of vitamin D up to a summer level (70–90 nmol/l), which may be optimal⁽Reference Holick, Binkley and Bischoff-Ferrari³⁾.

Sun and cutaneous malignant melanoma

Sun exposure is commonly supposed to be the main cause of cutaneous malignant melanoma (CMM) in most populations⁽Reference Marks⁹⁾. However, the matter is disputed⁽Reference Shuster¹⁴⁾, and we have reviewed the arguments for and against a causation⁽Reference Moan, Porojnicu and Dahlback⁷⁾. Several factors are probably involved, as exemplified by a relationship sometimes found between gross domestic product and CMM incidence⁽Reference Moan, Porojnicu and Dahlback⁶⁾.

Intermittent sun exposure and severe sunburn in childhood are associated with an increased risk of CMM⁽Reference Leiter and Garbe¹⁵⁾. CMM incidence rates per unit skin area are larger on trunk (intermittently exposed) than on head and neck, while the opposite is true for basal cell and squamous cell carcinomas⁽Reference Moan, Porojnicu and Dahlback⁷⁾. Occupational exposure (farmers, fishermen) and regular weekend sun exposure are associated with decreased risk of CMM⁽Reference Newton-Bishop, Chang and Elliott^16, Reference Pukkala, Martinsen and Lynge¹⁷⁾. Sun exposure may even protect against CMM on shielded skin sites⁽Reference Cicarma, Juzeniene and Porojnicu^18, Reference Moan, Cicarma and Setlow¹⁹⁾, and CMM arising on skin with signs of large UV exposure has the best prognosis⁽Reference Berwick, Armstrong and Ben-Porat²⁰⁾. UV exposure earlier in life is related to reduced overall and breast cancer⁽Reference Yang, Veierod and Lof²¹⁾. It has also been observed that patients with the highest blood levels of vitamin D have thinner CMM and better survival prognosis from CMM⁽Reference Newton-Bishop, Beswick and Randerson-Moor²²⁾.

Sunbeds and cutaneous malignant melanoma

A number of publications show conflicting results concerning the risk of CMM developing after sunbed use. Recent studies found that exposure to sunbeds has increased CMM risks⁽Reference Moan, Lagunova and Cicarma^{11, 23–}Reference Walter, King and Marrett²⁹⁾. These studies show that the use of sunbeds before 35 years of age significantly increases CMM risk. Some other studies show no increased CMM risk associated with sunbed use⁽Reference Bataille, Boniol and De^30–Reference Zanetti, Rosso and Faggiano³⁴⁾.

Discrepancies between different studies may be related to differences between UVA/UVB ratios and intensities of the sunbeds. People who are using sunbeds frequently may also have higher than average sun exposure and it may be difficult to separate the effects of the two factors. There has been a significant increase in the number of sunbed exposures in Norway after 1990, but CMM incidence rates among persons younger than 50 years have stabilized⁽Reference Moan, Porojnicu and Dahlback^6, Reference Moan, Porojnicu and Dahlback^7, Reference Moan, Baturaite and Porojnicu^35, Reference Moan, Porojnicu and Dahlback³⁶⁾.

Figure 1 is an updated summary of the published studies on sunbed use and risk of CMM^(23, Reference Cust, Armstrong and Goumas^25, Reference Elliott, Suppa and Chan^31, Reference Fears, Sagebiel and Halpern^37–Reference Westerdahl, Ingvar and Masback⁴⁰⁾. Some of the studies give conflicting results, such as an increased risk for women but not for men⁽Reference Fears, Sagebiel and Halpern³⁷⁾. A recent study, including persons who were 18 years or younger between 1957 and 1977, gave among the highest odds ratios⁽Reference Veierod, Weiderpass and Thorn^28, Reference Veierod, Adami and Lund³⁹⁾. However, in this period there were very few sunbeds in Norway, so sunbed exposure cannot be the only risk factor for the increasing rates of CMM.

Fig. 1 Relative risks and 95 % confidence intervals for cutaneous malignant melanoma associated with sunbed use in different studies. For results to 2005, numbers are references from the International Agency for Research on Cancer work⁽²³⁾; for recent results (2010/2011), reference numbers are from the present study⁽Reference Cust, Armstrong and Goumas^25, Reference Elliott, Suppa and Chan^31, Reference Fears, Sagebiel and Halpern^37–Reference Veierod, Adami and Lund³⁹⁾

Ultraviolet A and cutaneous malignant melanoma

UVA was reported to induce CMM with high efficiency in the small swordfish Xiphophorus ⁽Reference Setlow, Grist and Thompson⁴¹⁾. The opossum Monodelphis domestica also develops CMM-like lesions after UVA exposure, but with low potency compared with UVB⁽Reference Robinson, Hill and Kripke⁴²⁾. CMM are induced by UVB in a HGF/SF (hepatocyte growth factors/scatter factor) transgenic mouse model, but not by UVA⁽Reference Noonan, Dudek and Merlino⁴³⁾. Furthermore, it has recently been noted that UVA did not induce melanomas in Xiphophorus ⁽Reference Mitchell, Fernandez and Nairn⁴⁴⁾, so the UVA involvement in CMM generation is not solved experimentally.

Epidemiological investigations suggest that the use of sunscreens that absorb only UVB, but transmit UVA, may contribute to the risk of CMM⁽Reference Gorham, Mohr and Garland^45, Reference Nilsen, Aalerud and Hannevik⁴⁶⁾. Regular use of sunscreens absorbing both UVB and UVA perhaps reduces the CMM risk by approximately 50 %⁽Reference Green, Williams and Logan⁴⁷⁾.

All of these findings have not resulted in any reduction of the allowed UVA fluence rates in sunbeds, which still may emit five to ten times more UVA than noon summer sun in southern Europe⁽Reference Nilsen, Aalerud and Hannevik⁴⁶⁾. Most people get much more UVB and probably also more UVA from the sun than from sunbeds. This may not be true for frequent sunbed users.

The latitude gradient for CMM in Scandinavia, England, New Zealand and Australia is much lower than for non-melanomas⁽Reference Moan, Dahlback and Setlow⁴⁸⁾. Differences between Scandinavia and Australia are a factor of only two for CMM v. a factor of twenty to forty for non-melanomas⁽Reference Moan, Dahlback and Setlow⁴⁸⁾. The fact that the latitude gradient of ambient annual exposures is much smaller for UVA than for UVB (roughly a factor of 1·5 to 2·0 smaller) leads us to suggest that solar UVB is the main cause of non-melanomas and UVA may be CMM generating⁽Reference de Gruijl and Forbes⁴⁹⁾.

Sun and vitamin D

There is a seasonal variation of vitamin D status as the sun is its main source⁽Reference Moan, Porojnicu and Robsahm⁵⁰⁾. Latitude gradients for blood levels of vitamin D have been recorded in the UK⁽Reference Hypponen and Power⁵¹⁾ and in France⁽Reference Chapuy, Preziosi and Maamer⁵²⁾, but international latitude gradients are not clearly documented. The reasons for this include varying methods of measuring vitamin D status⁽Reference Lai, Lucas and Banks⁵³⁾, varying skin types in different populations with less vitamin D produced in dark skin, and differences in intake of vitamin D-rich food in different countries. For example in Norway, people in the north eat more oily fish and consume more cod-liver oil than in the south⁽Reference Johansson and Solvoll⁵⁴⁾.

Young ethnic Norwegians and immigrants from southern countries in Norway have a low vitamin D status, notably in the winter⁽Reference Lagunova, Porojnicu and Lindberg⁵⁵⁾. This may be related to more indoor life. About 70 % of 15-year-old persons spend more than 4 h daily in front of a computer or television⁽⁵⁶⁾. They also spend more time on indoor activities and, therefore, less time out of doors during the day. Immigrants from South Asia usually cover their skin almost completely with clothes, and the women may cover their faces with veils. Compared with indigenous Norwegians they eat less vitamin D-containing oily fish and they have no tradition for cod-liver oil supplementation.

Benefits v. risks of UV exposure

Using the relationship between CMM risk and UV exposure and the results published by Giovanucci et al. ⁽Reference Giovannucci, Liu and Rimm⁵⁷⁾, it can be estimated that increased sun exposure to the Norwegian population might at worst result in 200–300 more CMM deaths per year, but it would elevate the vitamin D status by about 25 nmol/l and might result in 4000 fewer internal cancers and about 3000 fewer cancer deaths overall⁽Reference Moan, Lagunova and Porojnicu⁵⁸⁾. The lack of sunlight exposure leads to more health problems than bone disease and increased risk for cancer⁽Reference Reichrath and Nurnberg⁵⁹⁾. Other benefits include protection against infectious diseases and non-cancerous diseases (diabetes, CVD, multiple sclerosis and mental disorders)⁽Reference Juzeniene, Brekke and Dahlback⁶⁰⁾. New trials assessing higher doses of vitamin D supplementation are in progress and future research may more clearly demonstrate the benefits of vitamin D⁽Reference Reichrath and Nurnberg⁵⁹⁾.