Safe, mild ultraviolet‐B exposure: An essential human requirement for vitamin D and other vital bodily parameter adequacy: A review

Abstract The enigma of skin sunburning, skin ageing and skin cancer and essential vitamin D production both resulting from solar ultraviolet‐B (280‐315 nm) (UVB) exposure has long puzzled photobiologists. Advice to patients by non‐photobiological clinicians is now often to sunbathe to acquire vitamin D adequacy. However, modern work shows only mild UVB exposure is needed to maintain satisfactory levels, which have been demonstrated as very similar in summer and winter from about 25° to 70° north. Even very careful high protection factor 15 sunscreen use does not prevent adequate production, although it is slightly reduced, such that obsessive use of very protective screens of 50 + might. Dark skin pigmentation too usually at most minimally impairs production. However, confinement indoors and widespread clothing cover can, but oral supplementation overcomes any such deficiency. Thus, vitamin D adequacy needs just mild regular UVB skin exposure well under sunburning levels, unlikely to cause significant skin damage. This suggests mild UVB exposure may also be needed for other bodily requirements, which is indeed so. Thus, it also prevents the development of contact dermatitis and polymorphic light eruption through suppressing adaptive immunity. It also prevents the occurrence of multiple skin infections resulting from this suppression through stimulating innate immunity and cutaneous bacterial defensin production. Finally, blood pressure is reduced through low‐dose UVB‐induced production of the vasodilator nitric oxide (though UVA, 315‐400 nm, is more efficient). Thus, mild UVB exposure is important for several aspects of internal health, whereas high‐dose exposure is extremely detrimental to cutaneous health.

It may also be obtained much less easily from the diet (particularly in cheese, fish, eggs and beef liver), if parathormone, calcitonin and dietary calcium are normal. 2 It is also conveniently available as an oral supplement if natural measures are inadequate.
Such vitamin D is known to be absolutely necessary for bone health, particularly by virtue of its enhancement of calcium and phosphate absorption. 2 However, in recent years, claimed rickets increases and questionably the occurrence of other major health issues from insufficiency have resulted from major sunlight avoidance to prevent darkening of the skin in some groups, photodermatoses in others, and particularly ultraviolet radiation-induced skin cancer. 3 In an effort to clarify this apparent conflict of evolutionary outcomes from exposure to the same radiation, this review now considers this and related matters in detail. Since sunlight exposure has incontrovertibly been shown to induce the unpleasant, damaging, and sometimes fatal effects of skin sunburn, skin ageing and skin cancer, in addition to production of the essential vitamin D hormone, further investigation of the precise mechanisms of production of these different outcomes is necessary in an attempt to explain the clearly illogical conflict of evolutionary advantage and disadvantage.
This aim must inevitably involve consideration of the following issues. First, careful assessment of the exact wavelengths causing the genetic and related damage potentially leading to skin ageing and skin cancer, and those producing vitamin D, is needed to determine if they might perhaps be separable, just conceivably enabling the use of an appropriately filtered sunscreen.
Next, if the wavelengths producing both effects are similar, it is necessary to determine the amount of exposure needed to cause the unwanted genetic damage, and the amount required to maintain human vitamin D sufficiency, to assess if the amounts are significantly different.
Finally, it is necessary to determine the differential effect on genetic damage and vitamin D production, if any, of any form of photoprotection (whether from a life indoors, widespread clothing, sunscreen use, or particularly constitutional skin colour, as darkskinned races now live in weak solar ultraviolet radiation (UVR) areas), to see if these may contribute partly or completely to vitamin D deficiency.
Once these factors have been carefully assessed, as now to be discussed, a strategy to maintain vitamin D sufficiency without significant genetic and associated damage may conceivably be achievable. Figure 2 shows that the solar wavelengths causing genetic damage and vitamin D production are somewhat different, the UVB region causing both, with the UVA segment also causing some skin F I G U R E 1 Ultraviolet radiation conversion of 7-dehydrocholesterol to previtamin D3 before thermal conversion to vitamin D3 and chemical modification in the liver and kidney to 1, 25  damage but not producing vitamin D. However, these spectra are not sufficiently different for any refined sunscreen or other wavelength dissociation strategy to be effective at preventing genetic damage, while still enabling vitamin D production. Figure 2 also shows that 300nm radiation is optimal in producing vitamin D, confirmed artificially in practice with UVB lamps. 5 Figure 3 demonstrates that high UVR exposure as often advocated by non-photobiological clinicians for best vitamin D production is clearly effective at producing vitamin D but also much increases genetic damage and its associated skin sunburn, skin ageing and skin cancer risks. 6 This however as shown too in Figure 2 is not the case for minimally exposed Danish skiers. In these subjects, increased vitamin D levels without significant thymine dimer production importantly suggest that the major clothing cover of skiers protects against skin damage while still permitting vitamin D production. 6 Apart from in the mostly protected skiers, this situation of increasing genetic damage with only somewhat increasing vitamin D production is not ideal in evolutionary terms, so further consideration is necessary to decide what situation if any is ideal, as indeed foreshadowed by the situation in the skiers.
In pursuit therefore of the aim of dissociating vitamin D production from significant skin damage, as seen in the just mentioned skiers, it has been shown that a mere half artificial UVB white skin Telling other support for the suggestion that vitamin D homeostasis is maintained with just moderate ultraviolet exposure and not significantly increased with high exposure is shown by the fact that it is adequate under normal circumstances worldwide at latitudes with hugely varying solar intensities, in that mean vitamin D levels remain essentially similar from 25° to 70° North. 11 They are therefore not apparently dependent on the availability of heavy sun exposure, being slightly higher in summer and lower in winter everywhere, at about 35-100 nmol/L ( Figure 4). This is best explained overall by vitamin D having a long three-month or so half-life, 12 with small regular exposures maintaining vitamin D levels, or else raising low vitamin D levels to normal rapidly, intense exposures doing this to only a minor amount more. 8,9 Further strong evidence that marked sun exposure is not essential for adequate vitamin D production is that normal hair-covered cows make sufficient amounts of the compound, 13 with the response being proportionately reduced if the hide is partly covered, showing the area of exposed hide is responsible (not just the bare nose for example), as is also the case with the skin in man.
Normal cows though do not suffer skin sunburn or cancers under their coats despite constant sun exposure, 14 indicating adequate sun protection against those disorders while permitting sufficient vitamin D production, while human hair has also been shown to produce useful sun protection, varying between sun protection factors (SPFs) of 5 and 17, more if the hair is short (as in cows). 15 This therefore provides yet further evidence that just mild regular solar exposure is all that is needed to maintain adequate vitamin D levels.
Vitamin D deficiency does of course occur and is greatest in the housebound, particularly in the older or disabled, in those in residential care, in subjects nearly fully covered by clothing, and in others who regularly avoid sun exposure or else work indoors. 16  In addition, the effects of regular, careful sunscreen use have been of major concern as a possible significant cause of vitamin D deficiency. However, heavily sun-exposed groups using a sun pro- broad spectrum screen UVB screen no screen Polish winter just the maximal vitamin D producing UVB spectrum ( Figure 5). This result somewhat resembles that shown in previous work, in which a white skin artificial UVB sunburning dose four times at two-to three-day intervals to the whole body covered with SPF 8 sunscreen at different thicknesses generally maintained adequate vitamin D levels. 20 However, the full recommended sunscreen thickness of 2 mg/cm 2 led to no increase, almost certainly because the UVB was very efficiently absorbed by the sunscreen used. Further proof that sunscreen application only mildly reduces vitamin D production is that double applications in another study before solar exposure for more reliable, overall skin protection had no more effect on reducing vitamin D production than just one application. 21 Given that some reduction in vitamin D production did occur with an SPF 15 sunscreen during heavy ultraviolet exposure in Tenerife, as described above, it does seem very likely that obsessively careful, very high SPF sunscreen use, say 50+, would prevent solar vitamin D production. However, non-obsessional use as generally occurs in normal subjects achieves only a third or often less of the SPF, strongly suggesting that significantly reduced production does not often happen, even SPF 50 seeming safe. 22 Further, and perhaps unexpectedly, even marked skin pigmentation generally appears as shown by two separate research groups to have at most a minor effect on ultraviolet radiation-induced vitamin D production. 9,23 This would appear likely to be because the cholesterol-derived vitamin D precursor is present in high enough concentrations superficially to permit vitamin D production, especially as the melanin is concentrated near the epidermal basal layer In overall summary, therefore, higher average summer and lower average winter vitamin D levels worldwide are similar everywhere, and only mild, regular ultraviolet-B exposure seems necessary to maintain these satisfactory levels. This is largely because low vitamin This overall vitamin D sun exposure situation seems best to fit with a putative mammalian need, briefly considered previously, 1 for minimal, largely harmless, regular sun exposure as an evolutionary advantage, not a drawback, in several ways, as below.
First, it avoids constant delayed type hypersensitivity reactions inducing the sun rash, polymorphic light eruption, as supported by the fact that very low doses of UVB phototherapy are needed to give months of relief from the condition, 28 and that immunological tolerance or "hardening" frequently develops during the summer. It also F I G U R E 6 This shows the minor differences in vitamin D production in the volunteer subjects tested, of skin types I to VI, irradiated all over with solar simulated radiation, apart from under their underwear, indicating skin pigmentation does not inhibit production to a significant degree 23  immunity. [29][30][31] Secondly, it induces bactericidal defensins by activating innate immunity, to prevent skin infection likely with the ultraviolet-reduced adaptive immunity just mentioned. [29][30][31] Thirdly, it somewhat helps reduce blood pressure, although UVA is more efficient at this, 32 reducing the likelihood of myocardial infarctions and cerebrovascular accidents, by increasing cutaneous production of the vasodilator, nitric oxide. 33 And finally, it avoids vitamin D deficiency, as fully discussed in this review.
In addition, as if to confirm the need for only minimal human UVR exposure, excessive ambient UVR produces an unpleasant warning through the eye leading sufferers to shun such exposure by seeking shade or going indoors, unless wearing sunglasses. 34 Therefore, a safe and convenient strategy for maintaining adequate vitamin D status and receiving the other advantages mentioned above would seem to be to live normally, using photoprotection as suggested to minimize skin ageing and cancer risks, but if in at risk group, take vitamin D supplementation.
The exact, putative amount and frequency of low-dose ultraviolet exposure needed to achieve these very useful aims without significant genetic damage remains to be assessed, and this matter should now be addressed as a follow-up to the items addressed in this review.

CO N FLI C T O F I NTE R E S T
None declared.