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Ultraviolet light was discovered by Johann Wilhelm Ritter in 1801. This form of electromagnetic spectrum with wavelength ranging between 100nm and 400nm can be subdivided into four categories: vacuum UV (<200nm), UVC (200nm - 280nm), UVB (280nm - 315nm) and UVA (315nm - 400nm).
Vacuum UV and UVC with its shorter wavelength property have greater energy levels, therefore may have higher impact on human health and morbidity. However, when emitted from natural source of sunlight, these radiation spectrums are unable to penetrate and get filtered away by ozone layer and environmental atmosphere. Thus, their effects become obstructed and are not studied in detail.
On the other hand, UVA and a portion of UVB reach the earth surface. Although invisible to the human naked eye, UVA and UVB have diverse impacts on human health and morbidity.
Ultraviolet light and vitamin D3 production
A major benefit of UV on human health is the stimulation of vitamin D3 synthesis, a discovery that won Adolf Windaus a Nobel Prize in chemistry in 1928. A study conducted by Kundson and Benford (1938) demonstrated that the effective wavelength for vitamin D production lies between 265.0nm and 313.0nm, and the most effective wavelength was 280.4nm. In a natural environment, a part of this solar energy source gets filtered away, wavelength of approximately 290 to 313nm come into contact with human skin and lead to the synthesis of vitamin D. Figure 1 shows the relation between UV and vitamin D synthesis pathway.
7-dehydrocholesterol in the dermis
Photolysis by UVB (290nm - 315nm)
Vitamin D3 (Cholecalciferol)
Isomerization by heat
Ejected out of cell and binds to
vitamin D binding protein
Hydroxylated in liver by
vitamin D-25 hydroxylase
25 hydroxyvitamin D3 (Calcidiol)
Hydroxylated mainly in kidney by 25OHD-1α-hydroxylase
1, 25 dihydroxyvitamin D3 (Calcitriol)
Figure 1: Vitamin D production pathway in human. Ultraviolet B stimulates the conversion of dermis 7-dehydrochlestrol to previtamin D3 (Holick, 1994, 2002, 2006). Previtamin D3 rapidly isomerizes into vitamin D3 which enters the blood circulation and gets hydroxylated in the liver to 25 hydroxyvitamin D3. Further hydroxylation occurs mainly in the kidney to yield an active vitamin D compound termed 1, 25 dihydroxyvitamin D3.
Studies also claimed that body's vitamin D requirements can be sufficiently attained with 20 minutes of exposure to the ambient sun, three times a week to hands and face (Adams J.S., et al, 1982). Despite the non-fastidious requirements, not every individual is adequately nourished with vitamin D. As the quantity of UVB penetration onto the earth surface is influenced by geographical latitude location (Tisdall and Brown, 1927), cloud cover, environmental air quality (Gorham et al, 1989) etc. UVB penetration in the skin also differs among individuals. Extrinsic factors would depend on the amount of protective wear such as clothing, sunscreen and hats. Intrinsic factors are dependent on skin colour and melanocyte pigmentations. As a result, low levels of vitamin D3, a medical condition known as hypovitaminosis D, may occur in humans and lead to health issues.
Before elaborating on health concerns, some terminology should be discussed. Use of term vitamin D may refer to vitamin D2, vitamin D3 or both. Although calcitriol (1, 25 dihydroxyvitamin D3) is the active form, measurements are often conducted using calcidiol (25 hydroxyvitamin D3) due to their levels in the serum: picogram and nanogram respectively.
Vitamin D, rickets and osteoporosis
Association between UVB and vitamin D3 production was first observed in infants between 6 and 24 months in age where bone deforming disease, rickets was prevalent in the early 1900s. Higher incidence was recorded in winter seasons as compared to summer. This happens when the sun is further away and more UVB photons are lost as they travel a longer distance before reaching the earth. Likewise, countries located at higher geographical latitude are further away from the sun and receives less UVB on a daily basis, hence recorded more cases of rickets (Palm, 1890, Garland and Garland, 1980). Such observations lead to studies and understanding of the nature of disease, which in turn led to awareness and public education on the benefits of vitamin D3.
Besides affecting the young, hypovitaminosis D has also been a health concern in later years where osteoporosis is a condition with reduced bone mineral density (BMD) and increase risk of bone fractures. Osteoporosis has been observed more frequently in elderly people as they are less physically active thus receives less exposure to UVB, have reduced cutaneous synthesis of vitamin D3 and reduced renal function of 1α-hydroxylase; all three factors contributes to lower vitamin D3 metabolites in the system. Besides elderly people, those in residential care, immobilised people, skin cancers patients or those with skin-related condition are also at higher risk to osteoporosis as their exposure to sunlight may be compromised.
Bones are subjected to constant remodelling. 65% of bone contents is constitute of hydroxyapatite crystal [Ca10(PO4)10(OH)2], a compound made up mainly of calcium and phosphate,. The metabolism of calcium in the body is regulated by calcitriol (Reichel et al, 1989, Bushinsky and Monk, 1998). When calcium level in the blood is low, it stimulates the release of parathyroid hormone (PTH), which plays two roles. PTH increases reabsorption of calcium in the kidney's distal convoluted tubule, reducing calcium excretion and lost. It also enhances activity of 1α-hydroxylase for the formation of calcitriol, which then increases calcium resorption from the bones to immediately increase blood calcium levels; this mechanism reduces BMD.
More importantly, calcitriol increases absorption of calcium from small intestine after a meal. Once calcium supply is replenished, spare calcium would be taken in by the bones for storage, thus rebuilding its BMD. Again, calcitriol is involved in mineralization process to increase BMD; it does so by stimulating osteoblasts to undergo cell growth and differentiation (Kream et al, 1977, Chen et al, 1986).
Increase 1, 25 (OH)2D3 production
Increase Ca2+ and PO43-
Low PO43+ in blood
Low Ca2+ in blood
Increase absorption of Ca2+ and PO43-
Increase resorption of
Ca2+ and PO43-
Increase reabsorption of
Ca2+ and PO43-
Mineralization to increase bone density
Figure 2: Metabolism of calcium involving vitamin D (Kolek O et al, 2005)
With the knowledge that humans should not rely solely on UVB for vitamin D3 synthesis, dietary vitamin D has been a useful means for treatment and prevention of rickets (McCollum et al, 1922) and osteoporosis. Dietary vitamin D may come from naturally rich food sources such as cod liver oil (Guy, 1923), or food artificially supplemented with vitamin D like in margarine and milk. Mothers of breast feeding infants should also be supplemented with vitamin D pills.
It should be noted that vitamin D overdose may lead to unnecessary absorption of calcium from small intestine and result in hypercalcemia (British Pediatric Association, 1956), which could in turn lead to other issues such as mental retardation or kidney failure (Bauer and Freyberg, 1946).
Vitamin D and cancer
Similar geographical and seasonal observations had been associated with some cancers, again indicating the effects of UV and vitamin D on health aspect (Lagunova, 2007; Moan et al, 2005; Porojnicu et al, 2007). Measurements of serum calcidiol levels have been found to be inversely related to the incidence and death of these cancers: colon (Garland et al, 1989), breast (Garland et al, 1990; Lowe et al, 2005), ovarian (Tworogger et al, 2007) and prostate (Corder et al, 1993) cancers.
It appears that calcitriol have anticancer properties that have been attributed by its inhibitory effects on cell growth and ability to induce cell differentiation (Suda et al, 1982; Tanaka et al, 1982). When calcitriol enters a cell, it binds to vitamin D receptor (VDR), the complex then translocate into the nucleus and bind with retinoic acid X receptor (RXR). This heterodimer complex then binds to vitamin D response element (VDRE) to initiate transcription of genes (Krishnan, 2003; Stumpf et al, 1979). This can potentially be used as a cancer treatment but side effects of hypercalcemia limit its usage (Koeffler et al, 1985; Osborn 1995).
Ultraviolet light, DNA damage and non-melanoma skin cancer
Despite the numerous benefits received from vitamin D and its metabolites, overexposure to UV is not advisable as adverse effects have also been associated. Indirect damage occurs with increase production of reactive oxygen species (ROS) by longer wavelength, lower energy UVA. Detoxifying enzymes are normally present in keratinocytes to cope with small amounts of ROS (Afaq, 2001). ROS are toxic as they interact with DNA by transferring electron to a guanine base forming 8-hydroxydeoxyguanosine (8-OHdG) (Cadet et al., 2000). If 8-OHdG is not repaired by base excision repair (BER) system, subsequent replication or transcription of this gene would allow incorporation of a mutation as 8-OHdG is structurally recognised as thymine (Cheng et al., 1992).
Besides indirect photoinduced DNA damage, direct photoinduced DNA damage has been observed when UVB induces covalent bonds between two adjacent pyrimidines to form pyrimidine dimers. Dimers may exist as cyclobutane pyrimidine dimers (CPDs) or 6,4 photoproducts. Fortunately, 90% of 6,4 photoproducts is restored to its original state by nucleotide excision repair (NER) system 3hours after UV exposure, thus not causing much damage (Nakagawa et al., 1998). CPDs are however poorly repaired; subsequent deamination of cytosine yields uracil. Thymine-cytosine (TC) and cytosine-cytosine (CC) dimers would thus be misinterpreted as thymine-thymine (TT).
UVB-induced point mutations in p53 proteins have been found in basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). In a cell with DNA damage, normal tumour suppressor p53 protein induces cell cycle arrest, allowing more time for DNA repair and prevents replication of error to the next generation. Another important role of p53 is the triggering of apoptosis when the damage is beyond repair. When a cell loss both copies of P53 gene (loss of heterozygosity), mutated p53 protein would be unable to carry out the above protective functions and defective cells would multiply without control.
BCC and SCC together form a class of non-melanoma skin cancers (NMSC) which accounts for majority of skin cancers cases. Being a skin surface disease, it has an advantage of allowing symptomatic lesions to be sighted. Early detection with early treatment increases the rate of cure, thus giving a low mortality rate.
Ultraviolet light and malignant melanoma
Ultraviolet light, protein damage and cataracts
UV ray has been linked with protein in a number of ways: inhibition uptake of nitrogen hence affecting the rate of protein synthesis, disruption of covalent sulphur bond in protein tertiary structure and oxidation of free tryptophan metabolites. Tryptophan metabolites oxidation has been observed to bind to eye lens causing opacification and resulting in formation of age related cataract (Truscott, 2005). Cataract impacts on one's visual capabilities and has been the leading cause of blindness worldwide (Evans et al., 2004). With no preventive measures available and no therapeutic treatment available, the only way around the health issue is surgical removal of the affected lens to restoration of visual status.
Ultraviolet light and immunosuppression
Besides causing NMSC, pyrimidine dimers appear to play a role in immunosuppression. The mechanism is unclear but appears to involve the release of cytokine interleukin 10 (IL-10) which induces humoral immunity and suppresses cellular response. Immunosuppression can be used to our advantage
Ultraviolet light in medical therapy
More or less ultraviolet light exposure
As a summary, exposure to UV light emits advantages to mankind in the form of vitamin D to reduce the risk of rickets, osteoporosis, bone fractures and provide some protection against varies internal cancers. On the other hand, UV light causes photo ageing of the skin, sunburn, cataracts, skin cancer and immunosuppression. A balance ought to be established to avoid any potential health problems.
In order to overcome the tricky task of balancing the pros and cons of UV exposure, most individuals consciously or subconsciously practice reduce outdoor activities and increase their vitamin D levels with dietary supplements. Recommendations of 1000 IU and 2000IU of vitamin D supplements on a daily basis should be given to children and adults respectively. As previously cautioned, overdose of vitamin D, although a rare incident to occur could result in unwelcome side effects. Such an incident would not have occurred with excessive UV exposure as the human system naturally controls the amount of vitamin D metabolism. High level of vitamin D in the dermis is regulated by auto-destruction by the amazing diverse powers of UV. Therefore it would be better to take vitamin D supplements for minimum body requirements and allow natural UV exposure to regulate the remaining body needs.
To complicate the already complicated situation, UV radiation response between each individual differs greatly. This may be attributed by geographical location, season, ozone layer, air cleanness and to a small extend cloud cover, all of which vary the quantity of UV measured at earth's surface. Thus, clean, equatorial Singapore would receive more UV as compared to winter months of Bradford, located at 45o north latitude. It's also influenced by occupational requirements and recreational preferences which vary the amount of time spend under the sun. For example a farmer and a golf lover would have more UV exposure as compared to a banker or a book lover respectively. Religious believes where females Muslims are required to be covered up also reduces their contact with UV rays. Last but not least, skin colour and melanocyte pigmentation has an impact on the outcome.