Definition of the Subject

Solar radiation has both direct and indirect impacts on human health. Only direct effects are described here. (Space is too limited to describe the indirect effects, which are numerous, complex and imbedded into important feedback mechanisms; the most important indirect effects for human health are on the availability and quality of food, effects on aquatic and terrestrial plants and ecosystems, deterioration in air quality, damage to materials, and energy-related issues that drive the world economy.)

While solar energy has been stored in the form of oil and gas for millions of years, it has become evident that these resources are limited and that harnessing renewable energies will be necessary in the future. Closely related are the effects on the environment for food production, which relies on solar energy.

The sun’s spectrum extends over a much-broader range of wavelengths than what is detected by the human eye, which responds only from 380 (violet light) to 780 nm (red light), with a peak response near 550 nm (green light). About 50% of the total solar irradiance originates from the near-infrared region. A relatively small but nevertheless important component is contained in the ultraviolet (UV).

Usually, any effect of solar radiation on biological organisms is wavelength dependent. A frequent concept is to describe these effects by means of biological weighting functions, often called action spectra, which quantify the wavelength dependence of effects introduced by electromagnetic radiation on biological matter. Depending on the effect and the organism involved, different biological weighting functions \( W(\lambda ) \) are used. The biologically effective irradiance, \( {E_{\text{weighted}}} \), is calculated by multiplying the global spectral irradiance, \( {E_G}(\lambda ) \), with the action spectrum \( W(\lambda ) \), and integrating over wavelengths λ:

$$ {E_{\text{weighted}}} = \int\limits {{E_G}(\lambda ) \times W(\lambda )d\lambda } $$

Note that the equation above is applicable for additive effects only (the so-called Bunsen–Roscoe law). Whether the concept is applicable or not must be proven or judged for each individual case. An important weighting function is the action spectrum for erythema (sunburn), as proposed by CIE [1], which describes the wavelength dependence of the reddening of human skin by UV radiation (see also below “erythemally weighted irradiance” E CIE).

Introduction

Humans have long been aware of a close relationship between human health and solar radiation. This is reflected by the fact that in many religions, the sun plays an important role. In many ancient cultures, the sun itself was considered as a god (e.g., in Egypt). The systematic study of the effects of solar radiation progressed in parallel with the evolution of science and medicine. For an assessment of the spectral dependencies of solar radiation, a separation of the different spectra was necessary. A major step was probably the analysis by Joseph von Fraunhofer in the early nineteenth century, who separated the different components of sunlight with high precision using his newly constructed prisms. Later on, the investigations carried out by Carl Dorno, and his publication about “light and air in mountainous regions” that he published in 1911, were other important milestones. For a long time, the UVB radiation was actually called “Dorno radiation.”

In this chapter, the present knowledge of the relationship between solar radiation and human health is described. Historical aspects, which are course interesting in their own right, are not considered further. This chapter is separated into the knowledge of spectral effects (UV, visible, and infrared), followed by a short section that deals with effects for which the spectral dependence is not yet known. Solar radiation has both negative and positive effects on human health. The negative effects of UV radiation have been emphasized in recent decades – on the background that skin cancer has been the cancer with the highest rate of increase. In recent years, however, more attention is being given to the positive side of solar radiation. At the end of this chapter, the benefits and dangers of solar radiation are summarized.

UV Radiation and Health Effects

The atmosphere is largely transparent in the visible region. Conversely, gaseous absorption is important in the UV. The latter is subdivided into three spectral bands: UV-A (315–400 nm) radiation, UV-B (280–315 nm) radiation, and UV-C (100–280 nm) radiation. (some authors still use 320 nm as the boundary between UV-A and UV-B radiation.) This separation has been originally introduced due to its relation with human effects. Nowadays, it is better understood that these effects cannot be strictly separated and, thus, only the general term “UV” is often used. UV-A radiation is largely unaffected by gases in the atmosphere. Conversely, only a small amount of UV-B radiation proceeds to the Earth’s surface because it is strongly absorbed by atmospheric ozone, whose absorption cross section increases rapidly toward shorter wavelengths in this spectral region. UV-C comprises less than 0.6% of the incident solar spectrum at the top of the atmosphere, but none of it reaches the surface. Radiation below 240 nm is absorbed by molecular oxygen (O2, which comprises 20% of the atmosphere). This radiation is capable of photo-dissociating molecules to form two oxygen atoms. The atoms so formed then recombine with another oxygen molecule to form ozone (O3). Under the terms of the Montreal Protocol on Protection of the Ozone Layer, assessments of the knowledge about the science of Ozone Depletion and UV radiation [5, 6] and assessments of the Environmental Impacts of Ozone Depletion [7] are produced regularly.

If human eyes were sensitive to UV radiation rather than to visible radiation, perceptions of the world would be very different. The sky appears blue because air molecules scatter blue light more strongly than red light. This dependence on the wavelength (λ) of light is very strong. Rayleigh scattering theory shows that it varies as λ −4 so, at 300 nm, the strength of this scattering is about 32 times greater than at 600 nm. That is why photographers choose to use blue-blocking filters (i.e., red filters) if they want to obtain dramatic images of cloudy skies in black and white pictures since such filters can greatly enhance the contrast between the bright cloud and dark background.

Because of this wavelength-dependent scattering by air molecules, the UV radiation field is much more diffuse than visible radiation (light). An eye sensitive to UV radiation would therefore perceive a much smaller contrast between clouds and sky, and a smaller contrast between sky and sun. Under clear skies, the diffuse UV component would normally dominate over the direct beam component, whereas in the visible, the diffuse component is typically only 5–15% of the direct. When the sun is low in the sky, Rayleigh extinction becomes so large that the solar disk in the UV region would not even be detectable from the surrounding skylight. The sphere of consciousness would be greatly reduced because objects more distant than even a few kilometers would be completely lost in the gloom of diffuse light. It would be like living in a light fog. Shadows would be less distinct. When the sky is overcast, places normally in the shade would receive more light than under clear skies. One practical implication of this more diffuse field is that any reduction in UV radiation in a shaded area is smaller than the reduction in visible light, as perceived with the eye. Therefore, the protection from the sun offered by shade may be less complete that anticipated from the standpoint of UV effects. The brightness of objects would appear very different too. Most natural surfaces reflect a significant fraction of the incoming visible radiation. But in the UV region, very few surfaces are strongly reflecting. Most natural surfaces would appear quite dark because they reflect less than 5% of the incoming UV-B radiation. Snow and clouds are two of the few exceptions to this rule.

Another aspect of UV radiation is the ratio of diffuse to direct irradiance is much higher in the UV compared to visible wavelengths. Therefore, under clear skies, hazy skies, or very lightly cloudy skies, the diffuse UV irradiance comes from all possible directions, rather than preferentially from around the sun

Fig. 19.1
figure 1

Radiance distribution measured during clear skies in Hannover during noon. The position of the sun – south at noon – is given by the white symbol. Left panel 305 nm, right panel 500 nm. It can be recognized that the spatial distribution is quite different at these two wavelengths and that the distribution of sky radiance is more uniform in the UV, which can be understood as a result of double scattering by Rayleigh scattering

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Fig. 19.2
figure 2

Vitamin D metabolism

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Fig. 19.3
figure 3

Upper panel: UV ir radiance spectra for noon sunlight at midlatitude (45° S) in summer and winter. The grey line shows the erythemal action spectrum. Note the logarithmic scale on the y-axis. Lower panel: The same solar irradiance spectra weighted by the erythemal action spectrum

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Fig. 19.4
figure 4

Approximate exposure times leading to erythema or to sustained adequate vitamin D production, as a function of UVI. Exposure times corresponding to the red-shaded area represent too much UV, leading to erythema (skin reddening- and sunburn). Exposures within the dark blue region represents too little UV to maintain an intake of 1,000 IU with full-body exposure. The unshaded area represents the range of times for optimal exposure, assuming only the hands and face are exposed. The other blue curves give the lower exposure limits for adequate vitamin D for different areas of skin exposed. All times shown are for fair skin (skin type II). For brown skin or black skin (skin types IV and VI), all exposure times should be multiplied by 2 and 5, respectively

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Table 19.1 Relationships between various weightings for a typical dermatological UV-A tanning salon compared with natural sunlight (noon sun in summer and winter at 45° S (Lauder New Zealand) and a powerful 1,000 W quartz halogen lamp at a distance of 0.5 m. UV_Ery and UV-VitD are erythemally weighted and vitamin D-weighted UV radiation, respectively
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Table 19.2 Evidence for association of circulating 25-hydroxyvitamin D level with cardiovascular morbidity and mortality
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Table 19.3 Evidence for association of circulating 25-hydroxyvitamin D level or vitamin D supplementation with all-cause mortality
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disk (Fig. 19.1). This further decreases the effectiveness of partial shading structures.

The variability in UV irradiance between common sources is described in Table 19.1.

Vitamin D

Vitamin D Metabolism

Solar UV-B irradiation (280–315 nm) of the skin is the major source of vitamin D3 for humans, whereas dietary intake of vitamin D2 or vitamin D3 is a second, less important source. The dietary contribution to vitamin D supply usually does not exceed 10–20% in free-living persons. Only few fatty salt water fish such as herring, salmon, and sardines are good sources of vitamin D. Skin synthesis of vitamin D3 is very effective. The relevant quantity is the exposure, as defined above (in units of W). Some authors consider summer exposure of arms and legs for 5–30 min (depending on latitude and skin pigmentation) between the hours of 10 a.m. and 3 p.m. twice a week to be adequate. However, it has been found that the vitamin D action spectrum is more uncertain than previously thought. Consequently, in winter, it may not be possible to gain enough vitamin D by casual exposure to sunlight. Exposure of skin to sunlight at regular intervals results in the photochemical conversion of 7-dehydrocholesterol into previtamin D3, which is rapidly converted to vitamin D3. In the midsummer months (e.g., June and July in the northern hemisphere), the amount of vitamin D3 increases to a maximum of approximately 12% of the amount of 7-dehydrocholesterol at latitudes of 34° and below, to 9% in one hour in Boston (42° N) and 11% in 3 h in Edmonton (52° N). Analyses after exposure of the 7-dehydrocholesterol solution at several places in the southern hemisphere showed concordant results [8]. The sunlight-generated vitamin D3 is a precursor of the active hormonal form of vitamin D3. Because any excess in previtamin D3 or vitamin D3 is destroyed by sunlight, excessive exposure to sunlight does not cause vitamin D intoxication. It has been reported that exposure to one minimal erythemal dose while wearing only a bathing suit is equivalent to ingestion of approximately 500 μg of vitamin D [9]. Because of its skin synthesis, vitamin D3 is not really a vitamin for humans. However, if skin exposure to UV-B radiation is negligible (e.g., in winter) or if people live exclusively indoors (institutionalized people), then there is indeed an absolute regular requirement for the fat soluble vitamin D, which must be met through proper dietary intake.

Once in circulation through the body, vitamin D is metabolized by a hepatic hydroxylase into 25-hydroxyvitamin D (25[OH]D) and by a renal 1α-hydroxylase into the vitamin D hormone 1,25-dihydroxyvitamin D (1,25-dihydroxyvitamin D) (Fig. 19.2). The latter step is under the control of parathyroid hormone (PTH) and serum phosphate. However, in case of vitamin D deficiency/insufficiency, renal synthesis of 1,25-dihydroxyvitamin D becomes substrate dependent, i.e., dependent on the circulating 25(OH)D concentration [10].

The active form of vitamin D, 1,25-dihydroxyvitamin D, is known as a regulator of systemic calcium homeostasis. Together with the parathyroid hormone (PTH) and calcitonin, 1,25-dihydroxyvitamin D carries out the policing job of regulating serum calcium levels in highly evolved mammals. This regulating mechanism is done with astounding efficiency, indicating the importance of serum calcium homeostasis. Serum calcium homeostasis is essential for blood coagulation, activation of various intracellular processes, and bone health. Therefore, serum calcium level of 2.5 mmol/L is maintained in all vertebrate life forms (both aquatic and terrestrial). The regulatory system of calciotropic hormones appears to have developed after transition of life from water (calcium–phosphorus rich environment) to land (environment poor in calcium and phosphorus). This assumption is supported by the fact that, in fish, PTH is missing and calcitonin is inactive [11]. Together with PTH, vitamin D is responsible for maintaining serum calcium levels by increasing intestinal calcium absorption, renal calcium reabsorption, and calcium resorption from bone. Without vitamin D, only 10–15% of dietary calcium and about 60% of phosphorus can be absorbed. vitamin D increases the efficiency of intestinal calcium absorption to 30–40% and phosphorus absorption to approximately 80% [11].

1,25-dihydroxyvitamin D also plays a pivotal role in the intracellular calcium homeostasis and has pleiotropic effects in various tissues. The biological actions of 1,25-dihydroxyvitamin D are mediated through the vitamin D receptor (VDR). In this context, 1,25-dihydroxyvitamin D functions as a steroid hormone that binds to a cytosolic VDR, resulting in a selective demasking of the genome of the nucleolus. The vitamin D receptor is nearly ubiquitously expressed, and almost all cells respond to 1,25-dihydroxyvitamin D exposure. About 3% of the human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system [12]. Apart from the kidney, 1,25-dihydroxyvitamin D can be locally produced in several tissues. These tissues include monocytes, dendritic cells, B lymphocytes, colonocytes, vascular smooth muscle cells, and endothelial cells. Consequently, for 1,25-dihydroxyvitamin D, a paracrine role separate from its calcium-regulating function has been proposed.

Reference Values

There is general agreement that the measurement of 25(OH)D is the appropriate tool for the assessment of vitamin D status. Nevertheless, there is currently no consensus on adequate/optimal circulating 25(OH)D concentrations. Cutoff values range between 50 nmol/L [13], 90–100 nmol/L [14], and more than 100 nmol/L [15]. This inconsistency is in part due to different criteria of defining inadequacy. Many researchers do not differentiate between different stages of vitamin D status. However, similar to other vitamins, it is possible to categorize the stages of vitamin D status into deficiency, insufficiency, hypovitaminosis, adequacy, and intoxication. In the deficiency range, severe vitamin D-specific clinical symptoms such as rickets, osteomalacia, calcium malabsorption, severe hyperparathyroidism, low 1,25-dihydroxyvitamin D concentrations, impaired immune system, and ultimately death can occur. In the insufficiency range, reduced bone mineral density, impaired muscle function, low intestinal calcium absorption rates, elevated PTH levels, and slightly reduced 1,25-dihydroxyvitamin D concentration are encountered. In the stage of hypovitaminosis, the body’s vitamin reserves are already low, and slightly enhanced PTH levels may be present, although the corresponding concentrations are usually still in the reference range. In the stage of adequacy, no disturbances in vitamin D-dependent body functions do occur. Only excessive oral intake can lead to vitamin D intoxication, resulting in intestinal calcium hyperabsorption, hypercalcemia, soft tissue calcification, and death. On an individual basis, the consequences of an insufficient vitamin D status may be mild, but the consequences on a population scale may be more important because of the large number of people who are affected. People with long-lasting vitamin D insufficiency may have the highest risk to develop vitamin-D-related chronic diseases.

Unfortunately, insufficient vitamin D status is prevalent around the world. Over the six regions Asia, Europe, Middle East and Africa, Latin America, North America, and Oceania, it has been found that between 50% and more than 90% of people have 25(OH)D concentrations below 50 nmol/L [16]. Low vitamin D status is most common in South Asia and the Middle East. Insufficient vitamin D status and even vitamin D deficiency is widespread, and is actually reemerging as a major health problem globally. Urbanization is an important risk factor for vitamin D insufficiency/deficiency in large parts of the adult population. Other factors include short daylight periods, long cold or hot seasons – or strict cultural traditions – imposing extensive clothing, modern and also traditional lifestyles such as indoor working, predominantly indoor leisure time activities, and the aging factor (institutionalization of elder persons). In a British study in the 1958 birth cohort, for example, 25-hydroxyvitamin D concentrations below 40 nmol/L were more prevalent in Scotland than in the South of England [17]. In highly urbanized or polluted areas, individual daily sun exposure is usually too low to achieve a 25(OH)D level of 75 nmol/L. Without food supplementation, the diet is then not able to close the gap in vitamin D supply. There have been studies linking vitamin D deficiency to latitude [18–21], but there are also studies that could not confirm such correlations [22].

Musculoskeletal Disease

Urbanization and industrialization (with their associated air pollution problems) have long been known as a major cause of childhood rickets in western countries. Rickets is now on the increase in many developing countries and is also reemerging as an important health problem in countries with strong sun avoidance policies, or in cultures requiring strictly modest dressing codes. In adults, severe vitamin D deficiency causes osteomalacia, a disease resulting in bone demineralization and muscle weakness.

Due to low calcium absorption rates, vitamin D insufficiency can also contribute to the bone disease osteoporosis. It is estimated that up to 50% of women and more than 20% of men 50 years of age or older will sustain an osteoporotic fracture in their remaining lifetime. A meta-analysis of randomized clinical trials that evaluated the effect of vitamin D supplementation came to the conclusion that the fracture preventing effect of vitamin D is approximately 20% when serum 25(OH)D levels of 75–80 nmol/L are achieved [23]. Another meta-analysis of randomized controlled trials (RCTs) came to the conclusion that daily doses of 17.5–20 μg supplemental vitamin D are able to prevent elderly adults to fall down by improving muscle function [24]. The relative risk of falls was reduced by approximately 20% when serum 25(OH)D concentrations of 60 nmol/L or more could be maintained. In contrast to “high-dose” supplemental vitamin D, low-dose daily supplemental vitamin D (5–15 μg) is not able to prevent falls.

Cancer

Since vitamin D is a key regulator of various cellular metabolic pathways, it is important for cellular maturation, differentiation, and apoptosis [25]. In 2008, the WHO published a report from the International Agency for Research on cancer [26] that came to the conclusion that there is (1) consistent epidemiological evidence for an inverse association between 25(OH)D and colorectal cancer and colorectal adenomas, (2) suggested epidemiological evidence for an inverse association between 25(OH)D and breast cancer, (3) insufficient evidence for an inverse association between 25(OH)D and other types of cancer, and (4) the need for new RCTs. One such RCT has recently been published [27]: In a 4-year, population-based study, where the primary outcome was fracture incidence and the principal secondary outcome was cancer incidence, 1,179 community-dwelling women were randomly assigned to receive 1,500 mg supplemental calcium/day alone (Ca-only), supplemental calcium plus 27.5 μg vitamin D/day (Ca + D), or placebo. The cancer incidence was 60–77% lower in the Ca + D women and 43% lower in the Ca-only group than in the placebo control subjects (P < 0.03).

Diabetes Mellitus

In vitro and in vivo studies suggest that vitamin D can prevent pancreatic beta-cell destruction and reduce the incidence of autoimmune diabetes. This may be due, at least in part, to a suppression of proinflammatory cytokines such as the tumor necrosis factor (TNF)-α. Recently, the relationship between UVB irradiance and age-standardized incidence rates of type-1 diabetes mellitus in children aged 14 years or less was analyzed according to 51 regions of the world [28]. Incidence rates were generally greater at higher latitudes and were inversely associated with UV-B irradiance. As early as 2001, Hyppönen et al. [29] demonstrated, in a birth cohort study, that vitamin D supplementation was associated with a decreased frequency of type-1 diabetes. In contrast, children suspected of having rickets during the first year of life had a three times higher relative risk compared with those without such a suspicion. A meta-analysis of four case-control studies has shown that the risk of type-1 diabetes is reduced by 29% in infants who are supplemented with vitamin D compared to those who are not supplemented [30]. There is also some evidence of a dose-response effect, with those using higher amounts of vitamin D being at lower risk of developing type-1 diabetes.

Observational studies, e.g., Pittas et al. [31], show a relatively consistent association between low vitamin D status and prevalent type-2 diabetes, with an odds ratio of 0.36 for highest vs. lowest 25-hydroxyvitamin D among nonblacks. Evidence from RCTs with vitamin D and/or calcium supplementation suggests that combined vitamin D and calcium supplementation may have a role in the prevention of type-2 diabetes only in populations at high risk (i.e., individuals with glucose intolerance). Whereas vitamin D supplementation did not improve glycemic control in diabetic subjects with initial serum 25(OH)D levels above 50 nmol/L [32], administration of 100 μg vitamin D3 improved insulin sensitivity in vitamin D deficient and insulin-resistant South Asian women [33]. Insulin resistance was most improved when endpoint serum 25(OH)D reached at least 80 nmol/L. Optimal vitamin D concentrations for reducing insulin resistance were shown to be 80–119 nmol/L.

Cardiovascular Disease

Globally, cardiovascular disease (CVD) is the number one cause of death. In 2005, it was responsible for approximately 30% of deaths worldwide. CVD includes various illnesses such as coronary heart disease, peripheral arterial disease, cerebrovascular disease such as stroke, and congestive heart failure. There is accumulating evidence that the vitamin D hormone 1,25-dihydroxyvitamin D exerts important physiological effects in cardiomyocytes, vascular smooth muscle cells, and the vascular endothelium. The mechanisms have been reviewed in detail elsewhere [34]. Hypertension is a key risk factor for CVD. A recently published systematic review and meta-analysis came to the conclusion that vitamin D produces a fall in systolic blood pressure of −6.18 mmHg and a nonsignificant fall in diastolic blood pressure of −2.56 mmHg in hypertensive patients. No reduction in blood pressure is seen in studies examining patients who are normotensive at baseline [35].

Several large prospective observational or cohort studies have demonstrated that a higher vitamin D status is associated with approximately 50% lower cardiovascular morbidity and mortality risk compared with low vitamin D status (Table 19.2).

Mortality

In 2007, a meta-analysis was published, including RCTs on vitamin D and mortality that were not primarily designed to assess mortality [29]. The authors concluded that vitamin D supplementation is linked to lower all-cause mortality rates in middle-aged and elderly patients with low serum concentrations of 25(OH)D than in unsupplemented subjects. Daily doses of vitamin D ranged between 10 and 50 μg. Risk reduction was 7% during a mean follow-up of 5.7 years. Several large prospective cohort studies published in 2008 and 2009 have provided further evidence for association of low circulating 25(OH)D levels with enhanced all-cause mortality (Table 19.3). However, there is some concern that vitamin D has a biphasic effect on mortality with an enhanced risk at deficient 25(OH)D levels but also at levels above 125 nmol/L [41]. The scientific background of this point of view has recently been questioned [42].

Sunburn (Erythema)

Since UV radiation is not detected by the human eye, or by usual light meters, a different standard is needed to quantify how much of it is present at any time. The erythemally weighted irradiance is defined as above, in units of W m−2. For health purposes, the erythemally weighted UV irradiance is generally reported to the public in terms of a dimensionless number called the UV Index (i.e., UVI, – see below). Rather than referring to the response of the human eye (i.e., the “photopic” response) for light, it refers to the response of human skin to sunburn (i.e., the “erythemal” response), which has no contribution from visible radiation but increases rapidly toward shorter wavelengths within the UV range.

Although UVI was developed to represent damage to human skin, it may be applied to other processes because many biological UV effects have similar action spectra. Since UVI is based on the erythemal action spectrum, its sensitivity to ozone change is the same as for erythema. For a 1% reduction in ozone, UVI increases by approximately 1.1%. The UVI is an open-ended scale. In the British Isles, it peaks at ∼6, whereas at northern midlatitudes, it peaks at ∼10. Peak values are higher in the southern hemisphere because of the lower ozone amounts, closer summertime Sun–Earth separation, and generally cleaner air. For example, the peak UVI in New Zealand is approximately 40–50% larger than at corresponding northern latitudes, and it often exceeds 12 [46]. In the tropics, it is even much higher. The highest values on Earth occur in the Peruvian Andes at latitudes 10–15° S, where UVI can reach 25 [47]. Outside the Earth’s atmosphere, the UVI would be ∼300.

The relatively high UV levels in New Zealand and Australia [46, 48] are a contributing factor to the high rates of skin cancer in those countries. There are other factors, however. For those of European extraction, skin types are better adapted to the lower UV levels in Europe, especially in the north [48]. Outdoor lifestyle choices can also be important. In temperate climates, it is quite comfortable to spend long periods of time in direct sunlight. The folly of that behavior manifests itself only later – when the discomfort of sunburn is felt, and much later when skin cancer is experienced.

UV Index

Sunburning UV is often reported to the public in terms of UVI. The upper panel in Fig. 19.3 shows the spectral UV irradiance for two sun angles and an ozone column of 300 Dobson Units (DU) (Note the log scale for the y-axis). The erythemal (i.e., the “skin-reddening,” or “sunburning”) weighting function is shown on the right axis. The lower panel shows the corresponding spectra of erythemally weighted UV irradiance (UVEry).

The internationally agreed UVI is defined in terms of UVEry. The weighting function involves an arbitrary normalization to unity at wavelengths shorter than 298 nm, so UVEry is not strictly an SI unit. Furthermore, when UV information was first provided to the public, another normalization was applied to give a maximum UVI of ∼10 in Canada, where it was first used. The UVI is therefore a unitless number corresponding to the integral under the curves in the lower panels, multiplied by 40 m2/W. Mathematically,

$$ {\text{UVI}} = {4}0\int {\text{I}}(\lambda ){\text{ w}}(\lambda ){ }d\lambda, $$

where

  • λ is the wavelength in nm

  • I(λ) is the irradiance in W m−2 nm−1 and

  • w(λ) is the erythemal weighting function, defined as:

    • w(λ) = 1.0 for 250 < λ ≤ 298 nm

    • w(λ) = 100.094(298 − λ) for 298 < λ ≤ 328 nm

    • w(λ) = 100.015(139 − λ) for 328 < λ ≤ 400 nm

    • w(λ) = 0.0 for λ > 400 nm

Exposure Times to Optimize Health Effects of UV Radiation

Attempts have been made to estimate the exposure times from sunlight to optimize health [49]. Results are given in terms of UVI (Fig. 19.4). The exposure times also depend on skin type and possible application of any sunscreens. In the case of vitamin D production, the optimal exposure time also depends on the area of skin exposed. There is a huge variation between the optimal exposure times in summer and winter at midlatitude sites. There is no simple relationship between UVI and visible radiation. In the case of sunlight, it is true that as light levels increase, so does UV radiation, but the relationship is complex and nonlinear.

The large seasonal variations are also a health risk. In winter, the UV irradiation may not be high enough to maintain adequate vitamin D. The problem is exacerbated because the skin becomes tanned to protect the body from further damage in summer, and this tan persists into the winter, therefore inhibiting the ability to absorb further UV radiation. Those with darker skins (e.g., Africans, many Maoris, Pacific Islanders, and Asians) are at greater risk.

Some published weighting functions for vitamin D production are similar to that for erythema but do not extend as far into the UV-A region. Consequently, it is a stronger function of ozone amount and sun angle. Nevertheless, the minimum exposure time for sufficient vitamin D production may still be estimated in terms of UVI. It also depends on the skin type, the SPF of any sunscreen applied, and the area of skin that is exposed to sunlight. The estimated exposure times for sufficient vitamin D production are compared with the exposure times for erythema in Fig. 19.2 [49].

In summer, when UVI can exceed 10, skin damage occurs in about 15 min for fair-skinned people, whereas for full-body exposure sufficient vitamin D can be produced in less than 1 min. In winter, when the maximum UVI is ∼1, skin damage occurs in 150 min, and even with full-body exposure (unlikely in winter), it would take at least 20 min to produce sufficient vitamin D. If only the hands and face are exposed, there is only a small margin between receiving too little or too much UV; and in winter, it would be impossible to receive sufficient vitamin D without skin damage. For darker skins, or if sunscreens are applied, these exposure times must be increased.

Note that there are large uncertainties in these relationships. Firstly, the action spectra may not be correct; secondly, the relevant quantity is really the irradiance on the surface of the body, rather than on the assumed horizontal surface; and thirdly, both the sensitivity of skin to damage and its ability to synthesize vitamin D depend on previous exposure and on the anatomical site [50, 51].

Skin Cancer

Three types of skin cancer, basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and malignant melanoma (MM), sum up to the most frequent type of cancer in the white population worldwide. For MM, the incidence increases more rapidly than for any other type of cancer. Data for the non-melanocytic skin cancers, NMSCs (BCC and SCC), for e.g., USA and Germany show incidences in the range of 1,000,000 new cases per year (USA, 2005) [52] and about 100,000 new cases per year (Germany, 2003) [53]; 80% of these are found on sun-exposed areas of the human body [54].

Corresponding numbers for MM (the most deadly skin cancer, 20–25% of diagnosed patients die) are about 62,000 new cases per year (USA, 2006) [55] and about 15,000 (Germany, 2004, Robert-Koch-Institut: http://www.rki.de). Most of melanoma cases occur on sun-exposed areas of the body. The estimated 10-year survival rates for patients without evident metastases range from 88% for those patients with tumors smaller than 1mm without ulceration, to 32% for those patients with tumors larger than 4 mm with ulceration [56].

The skin cancer incidence is still increasing in most countries [57, 58], although some stabilization has been observed for parts of western Europe and Scandinavia [59, 60]. Nevertheless, being the most frequent cancer, skin cancer represents a huge problem for the public. The personal, medical, clinical and, last but not least, the final burden of skin cancer has therefore to be reduced by means of primary prevention and early detection.

Environmental Risk Factor(s)

Although environmental arsenic exposure [60] or certain types of human papillomaviruses (as cofactors in association with UV) [61], as well as ionizing radiation [62] have been considered to play a role during the pathogenesis of NMSC, the overwhelming number of epidemiological and experimental investigations recognize UV-radiation as the main environmental risk factor [63–68]. The role of UV-radiation in melanogenesis has been discussed in past decades because the MM etiology strongly depends on genetic predispositions (e.g., allelic variances in the melanocortin 1 receptor [69]). However, recent epidemiological and experimental investigations, which are mainly dealing with UV-associated induction of benign nevi and the UV-induced mutation patterns, e.g., in the BRAF – gene (in nevi), clearly underline once more the important role of UV-radiation as a risk factor for malignant melanoma [63, 70–74]. It is furthermore important to consider that different types of skin cancer have a different dependence on UV-exposure patterns. Whereas MMs are mainly induced by intermittent UV-exposure (e.g., sunburns) [63, 71, 72], SCC-induction is highly dependent on cumulative UV-exposure, and BCC-induction depends on both cumulative and intermittent exposure patterns [63].

Because the main environmental risk factor in the etiology of skin cancer – UV-radiation (regardless of natural (sun) or artificial (sunbeds) origin) – is known, skin cancer is one of the key cancers that can be prevented by means of primary prevention (i.e., avoiding or reducing risks).

The importance of UV-radiation as the environmental (and artificial) risk factor for the induction of skin cancer has recently been underscored by the International Agency for the Research of Cancer (IARC) which characterized UV-radiation from the sun (and from sunbeds) as a group-1 carcinogen (“carcinogenic to humans”) [75]. IARC has also been able to show in a meta-analysis that regular use of sunbeds before the age of 35 increases melanoma risk later in life by 75% [76].

Biological Damage Leading to Skin Cancer

UV-photon absorption of DNA leads to photochemical conversion of absorbed energy into photodimerization between adjacent pyrimidine bases. According to an action spectrum, UVB is about 1,000 times more effective than UVA in inducing this kind of photodimerization [77]. UVB also induces, at a much lower frequency, inter- and intra-strand crosslinks, protein-DNA crosslinks, DNA strand-breaks, and rare base adducts [78–80]. Photodimerizations between adjacent pyrimidine bases are by far the most prevalent photoreactions resulting from the direct action of UV-radiation. Two major photoproducts are formed via this reaction pathway: the cyclobutyl pyrimidine dimer (CPD) and the pyrimidine(6–4)pyrimidone photoproduct (6-4PP). CPDs are formed between adjacent pyrimidines linked by a cyclobutyl ring between the five and six carbons of adjacent thymine (Thy) and/or cytosine (Cyt) bases. The 6-4PP links the 6 carbons on a 3’ Cyt or Thy with the four carbons of a 5’ Cyt. However, using the same wavelength of excitation in the UVB, 6-4PPs are induced only at 15–30% the rate of CPDs [81]. Using fluorescently labeled monoclonal antibodies against CPD and a calibration with a radioimmunoassay (RIA) [82], it was shown that a UVB dose of 300 Jm−2 is able to induce several hundred thousands of CPDs per genome per cell [83]. Both induction of CPDs and repair of these lesions via nucleotide-excision repair (NER) are UV-dose dependent. Increasing both the UVB dose and the amount of premutagenic CPDs leads to a increase of the time constant for NER to remove CDPs [83]. Furthermore, deficiencies in NER of CPDs have been linked with increased risk of cutaneous malignant melanoma and non-melanoma skin cancers [84–86].

When CPDs are not repaired, these DNA lesions can lead to mutations in the DNA sequence. Mutations are in the form of C→T and CC→TT transitions, known as “UV-signature mutations” [87–90]. These mutations have long been believed to be a specific signature for UVB-radiation. However, recent work suggests that UV-A also induces CPDs that lead to UV-signature mutations [91–93]. This view is supported by results showing that UV-A induces mainly CPDs in human skin [94]. A so called “A-rule” has been proposed to explain how these signature mutations arise [95]. According to the A-rule, DNA polymerase (pol η) inserts, in a default-mechanism, adenine (A) residues,opposite to those lesions it cannot interpret. A mutation is then created upon DNA replication of the strand containing base-pair changes. At a CC cyclobutane dimer, therefore, a CC → TT transition occurs because two A-residues are placed opposite the dimer by default, in place of two guanine (G)-residues. A similar default mechanism for 6–4 PPs might be responsible for C→T transitions [95]. Recent findings show that defects in efficiency of translesion polymerase η (despite other polymerases) seem to play an important role in UV-induced mutagenesis [96, 97].

UV-signature mutations have been detected in a number of tumor suppressor genes and oncogenes (including, e.g., patched, p16, ras and p53) in human SCC, BCC, and malignant melanoma [95]. Because the important biological function of p53 results from transcriptional activation of a large number of genes involved in fundamental cellular processes like cell cycle control, apoptosis, DNA replication, repair, genome instability, and senescence, it is not surprising that genetic alterations of the p53 gene have most frequently been found in human tumors [98]: especially in skin cancers like SCC, BCC, and precancerous actinic keratoses [99–103]. Convincing models for the initial steps of UV-carcinogenesis, especially for SCC, already exist [104, 105] based on findings that p53 mutations in non-melanoma skin cancers are detected at higher frequency (50–90%) than those in internal malignancy, and that the predominant alterations are C→T and CC→TT transitions at dipyrimidine sites [103]. Very recent investigations, exploring the melanoma genome, furthermore show that UV-induced signature mutations play the primary role in melanoma induction in humans [106].

Etiology of Skin Cancer

In recent years, a huge amount of information has been obtained in the fields of genetics, molecular pathways, and cellular changes, which are important players in skin cancer induction, promotion, progression, and metastasis. Excellent reviews are now available [107–112]. Very briefly, there is convincing evidence that the BCC etiology is highly dependent on dysregulation of the hedgehog signaling pathway, whereas for the SCC etiology, p53-regulated pathways are of outstanding importance. For malignant melanoma, at least three molecular pathways have been found to be nearly invariably disregulated in melanocytic tumors, including the RAS-RAF-MEK-ERK pathway (through mutation of BRAF, NRAS or KIT), the p16 INK4A-CDK4-RB pathway (through mutation of INK4A or CDK4), and the ARF-p53 pathway (through mutation of ARF or TP53). Less frequently targeted pathways include the PI3K-AKT pathway (through mutation of NRAS, PTEN, or PIK3CA) and the canonical Wnt signaling pathway (through mutation of CTNNB1 or APC) [113].

It is to be expected that future research dealing with biological markers will give further insight into the etiology of skin cancer. Furthermore, very recent findings in the field of stem-cell research very clearly show that epidermal stem cells and their regulation on the genetic and epigenetic levels are the main cell targets involved in skin carcinogenesis [113–120]. Investigating the genetic and epigenetic regulation of (cancer-) stem cell fate, therefore, will enduringly increase knowledge about the etiology, as well as about (bio-) markers indicative for progression, staging, and metastasis of skin cancers.

Immunosuppression

It is now generally accepted that chronic and/or intermittent UV-exposure from the sun or from artificial sources (e.g., sunbeds) can initiate and promote skin cancer development through two major mechanisms: (1) induction of UV-dependent mutations; and (2) UV-induced immunosuppression, which might impair recognition of, e.g., UV-induced tumors (as an antigen source) by immunocompetent cells in the skin [121]. The “skin immune system” (SIS) is composed of several different cell types: keratinocytes (KC), melanocytes (MC), fibroblasts, monocytes, epidermal homing T cells, dermal macrophages, and Langerhans cells. These cells interact in a complex network via a number of soluble mediators like cytokines, interleukines, and prostaglandins and build up immune response and immunosurveillance of the skin [122].

UV-induced immunosuppression has been demonstrated initially by in vivo experiments with mice. These studies were able to show that (UV-induced) skin tumors are not rejected when transplanted to previously UV-irradiated mice. Later on, it was shown that UV-radiation mostly impaired the cellular immune response, leaving humoral immunological pathways almost untouched. The cell-mediated immune response was then studied in a large number of investigations with contact or delayed hypersensitivity reactions (CHS or DTH) as a biological endpoint in human skin [122, 123]. These investigations show that antigenes applied to the skin are taken up by antigen presenting cells (APC), where they are processed and finally presented to T lymphocytes to induce the complex immune response to eliminate the antigen.

UV-induced immunosuppression works both locally and systemically. Locally, the site of hapten application corresponds to the UV-irradiated area of skin. Systemic immunosuppression, on the other hand, induces the effect far away from hapten application. Local immunosuppression is mediated by direct UV-induced alterations in APC function, whereas systemic immunosuppresion needs mediators like e.g., Interleukin-1, 10, 12, tumor necrosis factor (TNF-α) or tumor-growth factor β (TGF-β). Furthermore, dose-rate effects of UV-irradiation seem to have an influence on whether immunosuppresion is induced locally or systemically [124].

UV-radiation needs photoreceptors that are able to “translate” UV-interaction into immunomodulatory effects at the cellular level. According to absorption- (and action-) spectra, the most important chromophores involved in immunosuppression are: urocanic acid (UCA) and DNA [123].

UCA is one of the major UV absorbing components in the stratum corneum of human skin and undergoes trans to cis isomerization after UVB irradiation [125]. Cis-UCA then modulates the action of several cytokines, including TNF-α, IL-6, IL-8, IL-12, and others [126, 127], in this way influencing the complex reaction pathways of SIS. It is well accepted now that UV-B-radiation-induced UCA changes, which are involved in immunosuppressive pathways, both work locally and systemically in mice and humans [122, 125, 128], although there exists some evidence that UV-induced production of cis-UCA might be insufficient to suppress CHS [129].

Another, possibly more important molecular target to interact with UV-radiation and to induce immunosuppresion, is DNA [130]. DNA is able to absorb UV-B irradiation directly, which creates cyclobutane pyrimidine dimers (CPD) and (with lower yield) 6–4 photoproducts [90]. These are known to be pre-cancerogenic DNA lesions, giving rise to UV-signature mutations, prominantely involved in the skin cancer etiology. However, these lesions (if not repaired) are also responsible for direct activation of genes involved in immune reactions [131]. CPD play an important role in immunosuppression through alterations of APC function [132], cytokine production, e.g., IL-10, and inhibition of transcription factors [133]. An increase of enzymatic repair activity for CPDs (via support of repair enzymes T4 endonuclease V) restores CHS and DTH response after UV-irradiation [134].

There is convincing evidence that cis-UCA and CPDs mediate their immunosuppressive properties through the impairment of immunocompetent cells populations like APCs, especially Langehans cells [135, 136]. One of the major actions of UV radiation on LC is that it makes them unable to prime Th1 lymphocytes, therefore inducing some tolerance against antigenes [137]. This leads to the hypothesis that UV induced cytokine might affect the critical balance between Th1 and Th2 cells in favor of an (immunosuppressive) Th2 response [138, 139]. There is a convergence of evidence now supporting this hypothesis.

Most of the immunosuppressive effects of UV-radiation have been documented after experimental UV-B irradiation on subjects [122]. However, there is increasing evidence that UVA-radiation (315–400 nm) might also be capable of inducing immunosuppression in human skin [140–143]. From a mechanistic point of view, this seems reasonable because it has recently been shown that UVA (apart from other premutagenic DNA-lesions) predominantly induces CPDs [94] (known to be involved in immunosuppression, see above) in human skin.

Skin Treatments

During the past decade, UV-radiation has been used extensively to cure certain types of skin diseases, especially psoriasis, which is shortly discussed here as an example.

Psoriasis is one of the most frequent inflammatory skin disorders. Its prevalence is estimated to be 2% in the Caucasian population, and it may develop at any age [144]. Immunological mechanisms play an important role, and it is now recognized that psoriasis is the most important T-cell mediated inflammatory disease in humans [145]. The primary immune defect in psoriasis appears to be an increase in cell signaling via chemokines and cytokines that act on upregulation of gene expression and cause hyperproliferation of keratinocytes [146]. There exists, however, strong evidence for an equally important role of polygenetic inheritance in complex genetics of psoriasis [147]. At least eight genetic loci (PSORS1–PSORS8) have been identified so far [147, 148].

Classic psoriarsis treatments use UV radiation. Broadband UV-B, narrowband UV-B (311 nm), as well as psoralen plus UV-A (PUVA) treatments have been used in the past [149]. Among other things, UV radiation reduces the number of antigen presenting cells and affects cell signaling pathways responsible for a decrease of hyperproliferating keratinocytes. UV-B-radiation seems to be less effective than PUVA-therapy. However, the latter carries an elevated risk of skin cancer induction [150–153]. For instance, high-dose PUVA patients (with more than 337 PUVA treatments) carry a 68-fold increase in overall risk of SCC (fourfold increased risk of BCC) [154].

Eye Damage

With the exception of snow- and ice-covered surfaces, most surfaces have a very low UV reflectivity. However, over ice- or snow-covered areas, reflections can directly increase the eye exposure. In some case, this natural reflectance can be as high as 100% [155]. These enhanced radiation fields can contribute to eye damage. Some impacts on the eye are described below. For more details, see [7].

Photoconjunctivitis

Photoconjunctivitis is an inflammation of the conjunctiva of the eye caused by UV radiation. The action spectrum is similar to DNA damaging radiation. The threshold irradiation for photoconjunctivitis is 50 J m−2 [156].

Photokeratitis

Photokeratitis is an inflammation of the cornea’s epithelial layer caused by UV radiation. The action spectrum is again similar to DNA damaging radiation. The threshold irradiation is 50 J m−2 [156].

Cataract

Cataracts are irreversible turbidities of the eye that can be caused by infrared (IR) or UV radiation. IR cataracts are caused by direct absorption of IR radiation or, indirectly, by heat transfer from the iris to the lens. They are usually caused by long-term (many years) exposure to large infrared sources and are therefore rare as a result of sun exposure only. UV cataracts are quite common. However, there is no known action spectrum for IR or UV cataracts [156].

Visible Radiation and Health Effects

Circadian Effects

It is well known that visible radiation has an impact on human health by affecting the eyes. The major task for the eyes is to gather and further process incoming visible radiation. Basically, the eye acts like a camera. In this “picture,” the retina is the film or, more appropriately, the sensitive array that converts incoming photons to electrical signals that are further processed in the brain. For 150 years, it has been known that there are two types of sensors in the retina: the rods and the cones. There is some evidence that visual perception has an indirect impact on human health through psychological effects. However, this is not discussed further here.

In recent years, another photoreceptor, called melanopsin, has been found. It is likely that this photoreceptor has been developed early in the evolution of man. Melanopsin has a lower sensitivity and a coarser spatial resolution compared to the rods and cones. It is “designed” to help synchronizing the inner clock with the solar day.

The inner clock is thought to be essential to human health. The concentrations of many hormones are regulated by the inner clock, and it is known that a long-term disturbance of the inner clock has negative impact on humans [157]. For example, it is known that night-shift workers have a higher incidence of cancer.

The suppression of melatonin is closely linked with melanopsin concentration. The known action spectrum of melatonin suppression has its maximum in the blue part of the spectrum, at about 460 nm and almost no sensitivity in the red part [156]. Since the spectral transmission of the aging human eye progressively shifts toward longer wavelengths, it is assumed that elderly people have a reduced ability to synchronize the inner clock from blue light.

Since the solar spectrum changes appreciably during the day – certainly much more than the visual impression, which is regulated by the brain to recognize objects regardless of the incoming solar spectrum – it can be assumed that the red-shift of the solar spectrum during mornings and evenings may also have an impact on the melatonin suppression as well. This is an example of impacts of the solar spectrum on human health that is being understood, and that should be regarded when artificial lighting is used.

Damage of the Retina

Radiation (including infrared) that is absorbed by the retina can cause thermal damage. UV does not play a role in this case because it has a relatively low thermal contribution and is mostly absorbed before it reaches the retina. What is relevant to the damage of the retina is not the irradiance but its thermal impact [156].

Infrared Effects

For a long time, infrared radiation was considered as biologically irrelevant for human health. Consequently, the study of the impact of infrared radiation only began relatively recently [158]. Infrared radiation produces a high concentration of reactive oxygen species (ROS), i.e., free radicals, that can damage the skin. It was shown that the generation of free radicals depends not only on the incident irradiance but also on the temperature of the skin, which is increased by infrared radiation [159]. A doubling of the irradiance from 400 to 800 W/m2 can increase the temperature by ∼10°C. Such a temperature change enables biochemical reactions in the skin. There are nonlinear dose-effect relationships. The production of free radicals starts at about 37°C and becomes much stronger at about 41°C. However, further increase in temperature to 43°C causes little additional damage. At low latitude sites or in a likely warmer climate of the near future, increased infrared irradiation will lead to an increased formation of ROS, which is potentially dangerous for human health [159]. As a consequence, infrared protection may be beneficial, in as much as the threshold skin temperature of 41°C is not reached. For example, at a latitude of 43.4° N (corresponding to Monaco), these experiments value can be reached after only 20 min of sun exposure. However, these experiments were made with artificial light (Sullux 500 W), which emits a nearly continuous spectrum, whereas the solar irradiance has absorption bands, especially from water vapor. It is not known to what extent such effects can play a role when evaluating the potential danger of infrared radiation for humans. In addition, the spectral transmittance of infrared radiation must be considered. In the near-infrared (IR-A), the spectral transmittance of the skin varies between 2% and 10%. The maximum transmittance is reached at about 1,150 nm.

Several other studies of infrared affects have been undertaken [160, 161] Schieke 2002 [155]; Jantschitsch 2009 [163]. They use a special infrared light source (called “hydrasun”) that includes a water filter to minimize heating from long-wave radiation. Experiments with this source show that there is a time- and dose-dependent metalloproteinase-1 (MMP-1) that leads to increased skin aging [162], similar to that from UV exposure. The necessary dose may be reached after 2.5 h of exposure at midlatitudes in summer. However, another study [160] found that even with a high irradiance (380 W/cm2), there is no systematic induction of MMP-1, which is clearly in contradiction with the findings in [162]. Another study [161] found that, without increased temperature, there is a protection of infrared radiation to UV exposure – a result confirmed by another study [163].

In summary: there are clear indications for effects of infrared radiation for human health, but the complete process is far from being well understood.

Effects for Which the Spectral Responsivity Is Not Yet Known

Depression

Depression can occur as a result of a lack of light in winter. This is often described as seasonal affective disorder (SAD), also known as winter depression. The U.S. national library of medicine notes that some people experience a serious mood change when the seasons change. They may sleep too much, have little energy, and crave sweets and starchy foods. They may also feel depressed. Though symptoms can be severe, they usually clear up naturally. It has been estimated that 1.5–9% of adults in the U.S. experience SAD [164]. There are many different treatments for classic (winter-based) SAD, usually using artificial bright lights, or a temporary stay at a southern, sunny location. However, the spectral sensitivity of SAD is not known yet. It may be cured just by exposing the eyes with bright light, but it may be also connected to a deficiency in vitamin D.

Human Behavior in Response to Solar Radiation

Humans change their behavior in response to changes in solar radiation. Possible reactions include: avoiding too intense solar irradiation by seeking shadow, or seeking high level of solar irradiance for cultural or cosmetic reasons. As a consequence, human health is not only influenced by changes in solar irradiation (geographically, daily, seasonally), but to a large extent also by human behavior. Of course, such reactions depend on many factors, both socioeconomic and individual, and it is therefore hard to give general statements on the advantages or disadvantages of changes induced by human behavior in response to solar radiation.

Future Directions

The descriptions above clearly show that solar radiation has both positive and negative effects on human health. Positive effects are the synchronization of the inner clock by natural sunlight and avoidance of winter depression, which affects many people at higher latitudes. Another positive effect is the vitamin D production, for which an overdose by natural sunlight is not known. There is clear evidence that high vitamin D levels are very beneficial to humans. The list of the resulting positive effects has increased considerably in recent years.

On the other hand, there is also clear evidence that UV radiation is mainly responsible for skin cancer, for which the incidence rates are rapidly increasing, probably as a result of changed behavior. Also, negative effects of UV radiation on the eyes are well known. Strong indications of negative impacts of infrared radiation have been found recently.

The positive aspects just mentioned have already led to changes in the “sun-smart” recommendations given by some national cancer agencies. In the past, the most frequent recommendation may have been along the lines “avoid the sun as much as possible.” This is now altered to “avoid being sunburnt.” Other suggestions are “avoid the sun in summer, seek it in winter.” Despite the great number of studies and publications on these topics, there seems to be still insufficient scientific knowledge to convey simple messages to the public about the optimum solar exposure. It is clear that overexposure leads to severe negative effects, whereas underexposure has a negative impact on human health. It is concluded that more research is needed to assess under which conditions either overexposure or underexposure occur and must be considered. This is a rather difficult question for which simple answers are not to be expected soon due to the complexity of human health and of varying physical and meteorological conditions [165]. In addition, the relevant quantity to consider in vitamin D studies is not the irradiance on a horizontal surface but the actual exposure, which requires knowledge of the spectral radiance. This quantity, however, is far from being as well known as the widely used irradiance. More studies are required since the solar radiation regime is expected to be modified as a consequence of climate change.