Solar ultraviolet-B Exposure Research Articles

Responses to Solar UV-B Exclusion and Drought Stress in Two Cultivars of Chestnut Rose with Different Leaf Thickness

Plants adopt a series of strategies to tolerate solar UV-B radiation (with the side effects of growth reduction), but the positive effects of solar UV-B radiation have not been yet clarified. In this study, two cultivars with different leaf thickness for Chestnut rose (Rosa roxburghii Tratt), a pioneering species for ecological restoration in Karst region of Southwest China, were employed to investigate its responses to ultraviolet-B (UV-B) exclusion, moderate drought, and their combination in an outdoor experiment. Thin-leaf cultivars (Gui 2) adopt an opportunistic growth strategy, growing better than Gui 7 under UV-B exclusion combined with well-watered conditions. To avoid the penetration of solar UV-B wavelengths into the underlying leaf tissues, Gui 2 exhibited higher enhancements in leaf thickness, palisade/spongy tissue ratio, antioxidant responses such as the leaf concentration of flavonols compounds catalyse activity under solar UV-B exposure. Moreover, ambient solar UV-B radiation alleviated the adverse impact caused by drought in both cultivars, improving total biomass and reducing membrane penetration. This alleviation may be related with two potential explanations. First, solar UV-B radiation primes chestnut rose plants with increased antioxidative capacity against drought stress, shown in both antioxidative enzyme activity and non-enzyme antioxidants (in particular, with total flavonols and flavonol ratio [(quercetin+myricetin)/kaempferol]). Second, to avoid nutrition insufficiency, solar UV-B radiation and drought endows chestnut rose plants with complementary effects on nutrition balance. Overall, solar UV-B radiation helps the chestnut tolerate drought stress that occurs frequently in the Karst region by modulating its antioxidative capacity and nutrition balance.

Solar ultraviolet B exposure and global variation in tuberculosis incidence: an ecological analysis.

Epidemiological evidence supports vitamin D deficiency as a risk factor for tuberculosis. Differences in solar ultraviolet B (UV-B) exposure, the major source of vitamin D, might therefore partially explain global variation in tuberculosis incidence.In a global country-based ecological study, we explored the correlation between vitamin D-proxies, such as solar UV-B exposure, and other relevant variables with tuberculosis incidence, averaged over the period 2004-2013.Across 154 countries, annual solar UV-B exposure was associated with tuberculosis incidence. Tuberculosis incidence in countries in the highest quartile of UV-B exposure was 78% (95% CI 57-88%, p<0.001) lower than that in countries in the lowest quartile, taking into account other vitamin D-proxies and covariates. Of the explained global variation in tuberculosis incidence, 6.3% could be attributed to variations in annual UV-B exposure. Exposure to UV-B had a similar, but weaker association with tuberculosis notification rates in the multilevel analysis with sub-national level data for large countries (highest versus lowest quartile 29% lower incidence; p=0.057).The potential preventive applications of vitamin D supplementation in high-risk groups for tuberculosis merits further investigation.

Cambios en los niveles de vitamina D después de Climatoterapia en el Mar Muerto

Background: The Dead Sea region in Israel is the deepest spot on earth, 422 meter beneath sea level. The atmosphere layer overhanging this region is larger than in any other place on earth, allowing a filtration effect on sunshine beams and leading to their moderate attenuation in the Ultraviolet B (UVB) spectrum. The question was raised whether exposure to this sunshine may increase serum Vitamin D levels of patients treated at the Dead Sea. Objectives: To assess, in Norwegian patients suffering from joint disease and chronic pain syndromes, the magnitude of change in 25-Hydroxyvitamin D levels (25-OH-D) after Dead Sea Climatotherapy (DSC). Methods: 117 Norwegian patients received regular DSC procedures during their 3 weeks visit, which includes sun exposure (60 to 90 minutes), Dead Sea bath and outdoor physical activities. The cumulative solar UVB exposure was calculated in Minimal Erythema Doses (38.3 ±12.8 MEDs). Blood sampling for measurements of 25-OH-D levels were performed upon arrival and on the last day of their stay. Data were evaluated by statistical analysis using paired t test. Results: Following the DSC serum 25 OH Vitamin D levels were increased from 51.9 ± 2.7 nano mol per liter (nM), to 64.2 ± 3.1 nM (p &lt;0.001, 23.8% increase). The rate of increase in serum 25-OH-D was found to be age related with the highest increase in the youngest group. Variations in response were found between patients with different diseases). The highest increase in serum 25-OH-D was obtained in patients with Post Polio Syndrome (36.7%) and only 16.5% increase was measured in Fibromyalgia patients. Conclusions: Even in the attenuated sunshine existing in the Dead Sea region, a daily sun exposure for 3 weeks induces significant increases in serum 25-OH-D levels by Caucasian patients suffering from musculoskeletal and joint diseases. Changes in 25-OH-D after sun exposure were found to be related to initial value of serum 25-OH-D, to age, and disease.

Low vitamin D status likely contributes to the link between periodontal disease and breast cancer

The recent article by Soder et al. [1] found a statistically significant correlation between periodontal disease, related tooth loss and incidence of breast cancer. Periodontal disease with any missing molar teeth was associated with nearly a 12-fold increased risk of breast cancer than no missing molars. It was suggested that the bacterial infection associated with periodontal disease was the risk factor for breast cancer through effects of infection and inflammation. Overlooked from the article as a risk factor for both periodontal disease and breast cancer was inadequate vitamin D repletion. Low solar ultraviolet-B (UVB) doses have been associated with increased risk of tooth loss since 1865 [2]; a role of vitamin D in reducing risk of dental caries was known in 1928 [3] and, by 1935, increased solar UVB exposure was associated with reduced risk of dental caries [4]. Vitamin D deficiency has also been linked to periodontal disease risks [5, 6]. The likely mechanisms by which vitamin D reduces risks of dental caries and periodontal disease include induction of cathelicidin and defensins, which have antibacterial properties [7, 8] and reduced production of matrix metalloproteinases [9, 10]. Furthermore, vitamin D deficiency has also been linked to increased risk of breast cancer [11–15]. An additional benefit of vitamin D is reduced inflammation, primarily through modifying the production of cytokines from proto anti-inflammatory factors [16] and inflammation is a risk factor for breast cancer [17]. Thus, this interesting study of Soder et al. [1] supports the need for further research to examine the role of vitamin D deficiency, as an avoidable risk factor, in those with periodontal disease and breast cancer.

Similarities in solar ultraviolet irradiance and other environmental factors may explain much of the family link between uveal melanoma and other cancers

Sir: The recent paper [1], exploring the family history of cancer for persons diagnosed with uveal melanoma (UM) was aimed at elucidating a hypothesis that there may increased risk for some cancers in carriers of yet unidentified UM predisposition genetic alteration. While that is certainly a hypothesis worthy of further study, it has to be acknowledged that a familial predisposition can also be due to shared environmental factors. Dietary factors play a major role in cancer risk in general [2]. In the case of UM it seems that dietary factors may improve the survival rate [3]. Smoking and alcohol consumption increase cancer risk, and the same has recently been found to be true for a low serum concentration of 25-hydroxyvitamin D [25(OH)D]. Solar ultraviolet-B (UVB) radiation is the primary human source of vitamin D [4], and solar UVB dose has been found to be inversely correlated with risk of uveal melanoma based on an ecological study [5]. Nearly all of the cancers among those diagnosed with UM and their first and second degree relatives listed in Table 3 of Abdel-Rahman[1] are vitamin D sensitive [6–10], possibly with the exception of prostate cancer in terms of incidence [11, 12], although vitamin D status plays a role in survival for this cancer [13]. Still, diet and genetics certainly play important roles in risk for prostate cancer risk [12, 14]. Related to this study [1] are investigations of second cancers for persons diagnosed with non-melanoma skin cancer (NMSC). At latitudes below about 35–40 , NMSC is generally inversely correlated with risk of second cancer [8, 15], while at higher latitudes, NMSC seems to be positively correlated with risk of many types of cancer [15]. This finding was tentatively explained in terms of the skin surface exposed to the sun: At lower latitudes, larger skin surfaces are probably exposed, so that more vitamin D is produced [16]. In addition, diet and smoking are risk factors for both NMSC and many internal cancers, further explaining the correlations at higher latitudes [16]. Thus, any study looking for genetic risk factors for a cancer based on second primary cancers or cancers in first and second degree relatives, should also take into account whether environmental risk factors such as diet, smoking, and solar UVB exposure (producing vitamin D) might, at least partly, explain the links.

Solar ultraviolet-B exposure and cancer incidence and mortality in the United States, 1993–2002

BackgroundAn inverse relationship between solar ultraviolet-B (UV-B) exposure and non-skin cancer mortality has long been reported. Vitamin D, acquired primarily through exposure to the sun via the skin, is believed to inhibit tumor development and growth and reduce mortality for certain cancers.MethodsWe extend the analysis of this relationship to include cancer incidence as well as mortality, using higher quality and higher resolution data sets than have typically been available. Over three million incident cancer cases between 1998 and 2002 and three million cancer deaths between 1993 and 2002 in the continental United States were regressed against daily satellite-measured solar UV-B levels, adjusting for numerous confounders. Relative risks of reduced solar UV-B exposure were calculated for thirty-two different cancer sites.ResultsFor non-Hispanic whites, an inverse relationship between solar UV-B exposure and cancer incidence and mortality was observed for ten sites: bladder, colon, Hodgkin lymphoma, myeloma, other biliary, prostate, rectum, stomach, uterus, and vulva. Weaker evidence of an inverse relationship was observed for six sites: breast, kidney, leukemia, non-Hodgkin lymphoma, pancreas, and small intestine. For three sites, inverse relationships were seen that varied markedly by sex: esophagus (stronger in males than females), gallbladder (stronger in females than males), and thyroid (only seen in females). No association was found for bone and joint, brain, larynx, liver, nasal cavity, ovary, soft tissue, male thyroid, and miscellaneous cancers. A positive association between solar UV-B exposure and cancer mortality and incidence was found for anus, cervix, oral cavity, melanoma, and other non-epithelial skin cancer.ConclusionThis paper adds to the mounting evidence for the influential role of solar UV-B exposure on cancer, particularly for some of the less-well studied digestive cancers. The relative risks for cancer incidence are similar to those for cancer mortality for most sites. For several sites (breast, colon, rectum, esophagus, other biliary, vulva), the relative risks of mortality are higher, possibly suggesting that the maintenance of adequate vitamin D levels is more critical for limiting tumor progression than for preventing tumor onset. Our findings are generally consistent with the published literature, and include three cancer sites not previously linked with solar UV-B exposure, to our knowledge: leukemia, small intestine, and vulva.

The epidemiology of vitamin D and colorectal cancer: recent findings

To highlight the human studies published over the past year examining the influence of vitamin D on risk of colorectal cancer. Studies over the past year have added more support to the idea that higher levels of vitamin D may decrease risk of colorectal cancer. Further, typical dietary intakes such as 200-400 IU/day may be too low to exert appreciable benefits, and protection may occur with higher levels of vitamin D associated with exposure to sunshine. Recent studies also suggest a potential benefit of vitamin D on other digestive-tract cancers, and that vitamin D status at the time of diagnosis and treatment may influence survival of cancer. However, the evidence for these latter findings is based on limited data and needs to be confirmed. Higher vitamin D levels may also be associated with a higher rate of apoptosis in colorectal mucosa. Recent studies add more support to a potential role of vitamin D on risk of colorectal cancer, but suggest that intakes higher than customary are required if solar ultraviolet-B exposure is low. More studies are required to determine the optimal levels and intakes of this vitamin to reduce cancer risk. Potential benefits of vitamin D on other digestive-tract cancers and on survival in patients with colorectal cancer have been suggested by recent studies, but require confirmation.