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• W2016221502 abstract "Recommendations on limitation of summer sunlight exposure to prevent skin cancer may conflict with requirements to protect bone health through adequate vitamin D levels, the principal source being UVB in summer sunlight. We determined whether sufficient (≥20ngml−1) and proposed optimal (≥32ngml−1) 25(OH)D levels are attained by following UK guidance advising casual short exposures to UVB in summer sunlight, and performed the study under known conditions to enhance the specificity of future recommendations. During wintertime, when ambient UVB is negligible, 120 white Caucasians, aged 20–60 years, from Greater Manchester, UK (53.5°N) received a simulated summer's sunlight exposures, specifically 1.3 standard erythemal dose, three times weekly for 6 weeks, while wearing T-shirt and shorts. The baseline winter data predict that 5% (confidence interval (CI): 2.7–8.6) of Greater Manchester white Caucasians have deficient (<5ngml−1) 25(OH)D, 62.5% (CI: 55.2–69.4) have insufficient, and only 2.9% (CI: 1.4–5.6) have proposed optimal levels. After the simulated summer exposures, 90 (CI: 84.9–93.7) and 26.2% (CI: 20.1–33.2) reached 20 and 32ngml−1 25(OH)D, respectively. Assuming midday UVB levels, sufficient but suboptimal vitamin D status is attained after a summer's short (13minutes) sunlight exposures to 35% skin surface area; these findings will assist future public health guidance on vitamin D acquisition. Recommendations on limitation of summer sunlight exposure to prevent skin cancer may conflict with requirements to protect bone health through adequate vitamin D levels, the principal source being UVB in summer sunlight. We determined whether sufficient (≥20ngml−1) and proposed optimal (≥32ngml−1) 25(OH)D levels are attained by following UK guidance advising casual short exposures to UVB in summer sunlight, and performed the study under known conditions to enhance the specificity of future recommendations. During wintertime, when ambient UVB is negligible, 120 white Caucasians, aged 20–60 years, from Greater Manchester, UK (53.5°N) received a simulated summer's sunlight exposures, specifically 1.3 standard erythemal dose, three times weekly for 6 weeks, while wearing T-shirt and shorts. The baseline winter data predict that 5% (confidence interval (CI): 2.7–8.6) of Greater Manchester white Caucasians have deficient (<5ngml−1) 25(OH)D, 62.5% (CI: 55.2–69.4) have insufficient, and only 2.9% (CI: 1.4–5.6) have proposed optimal levels. After the simulated summer exposures, 90 (CI: 84.9–93.7) and 26.2% (CI: 20.1–33.2) reached 20 and 32ngml−1 25(OH)D, respectively. Assuming midday UVB levels, sufficient but suboptimal vitamin D status is attained after a summer's short (13minutes) sunlight exposures to 35% skin surface area; these findings will assist future public health guidance on vitamin D acquisition. 25 hydroxyvitamin D body mass index Health Protection Agency minimal erythemal dose parathyroid hormone standard erythemal dose Policy recommendations to limit summer sunlight exposure to prevent skin cancer have generated considerable international debate in recent years (Gillie, 2006Gillie O. A new government policy is needed for sunlight and vitamin D.Br J Dermatol. 2006; 154: 1052-1061Crossref PubMed Scopus (36) Google Scholar; Wolpowitz and Gilchrest, 2006Wolpowitz D. Gilchrest B.A. The vitamin D questions: how much do you need and how should you get it?.J Am Acad Dermatol. 2006; 54: 301-317Abstract Full Text Full Text PDF PubMed Scopus (286) Google Scholar). Skin cancer has high incidence in countries with large populations of white Caucasians, including the United Kingdom, United States of America, and Australia, and incidence continues to rise, with UVR being the principal etiological agent in the majority (Elwood and Jopson, 1997Elwood J.M. Jopson J. Melanoma and sun exposure: an overview of published studies.Int J Cancer. 1997; 73: 198-203Crossref PubMed Scopus (585) Google Scholar; National Radiological Protection Board, 2002National Radiological Protection Board Health Effects from Ultraviolet Radiation. Report of an advisory group on Non-ionising Radiation. vol. 13.. NRPB, Didcot2002Google Scholar). It is important that national and international authorities advise summer sunlight limitation in these populations (Ziegelberger et al., 2006Ziegelberger G. Repacholi M. McKinlay A. International commission on non-ionizing radiation protection.Prog Biophys Mol Biol. 2006; 92: 1-3Crossref PubMed Scopus (2) Google Scholar). However, UVB in sunlight triggers cutaneous synthesis of pre-vitamin D from 7-dehydrocholesterol, and this is the body's principal vitamin D source because usually only small amounts are obtained from diet (Hollis, 2005Hollis B.W. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D.J Nutr. 2005; 135: 317-322PubMed Google Scholar). Thus, public health policy on sunlight exposure should also consider vitamin D requirements. Historically, vitamin D deficiency was defined as the circulating level of 25 hydroxyvitamin D (25(OH)D) associated with the development of the severe bone disorders, rickets, and osteomalacia, that is, <5–10ngml−1 (Berry et al., 2002Berry J.L. Davies M. Mee A.P. Vitamin D metabolism, rickets, and osteomalacia.Semin Musculoskelet Radiol. 2002; 6: 173-182Crossref PubMed Google Scholar). The value 5ngml−1 is still used as the deficiency cutoff by national agencies such as the United Kingdom's Health Protection Agency and Department of Health (Great Britain), 1998Department of Health (Great Britain) Nutrition and bone health with particular reference to calcium and vitamin D: report of the Subgroup on Bone Health, Working Group on the Nutritional Status of the Population of the Committee on Medical Aspects of Food and Nutrition Policy. London, Stationery Office1998Google Scholar, although this is under reevaluation. Strong evidence exists showing that 25(OH)D levels <20ngml−1 are associated with secondary hyperparathyroidism, bone loss, fractures, muscle weakness, and reduced calcium absorption (Bischoff et al., 2003Bischoff H.A. Stahelin H.B. Dick W. et al.Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial.J Bone Miner Res. 2003; 18: 343-351Crossref PubMed Scopus (757) Google Scholar; Heaney et al., 2003Heaney R.P. Dowell M.S. Hale C.A. et al.Calcium absorption varies within the reference range for serum 25-hydroxyvitamin D.J Am Coll Nutr. 2003; 22: 142-146Crossref PubMed Scopus (729) Google Scholar; Zittermann, 2003Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence?.Br J Nutr. 2003; 89: 552-572Crossref PubMed Scopus (683) Google Scholar; Bischoff-Ferrari et al., 2004Bischoff-Ferrari H.A. Dietrich T. Orav E.J. et al.Positive association between 25-hydroxy vitamin D levels and bone mineral density: a population- based study of younger and older adults.Am J Med. 2004; 116: 634-639Abstract Full Text Full Text PDF PubMed Scopus (607) Google Scholar). Parathyroid hormone (PTH) is suppressed as the 25(OH)D level rises (Hollis, 2005Hollis B.W. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D.J Nutr. 2005; 135: 317-322PubMed Google Scholar), with a plateau being reached between 20 (Malabanan et al., 1998Malabanan A. Veronikis I.E. Holick M.F. Redefining vitamin D insufficiency.Lancet. 1998; 351: 805-806Abstract Full Text Full Text PDF PubMed Scopus (908) Google Scholar) and 40ngml−1 (Chapuy et al., 1997Chapuy M.C. Preziosi P. Maaner M. et al.Prevalence of vitamin D insufficiency in an adult normal population.Osteoporosis Int. 1997; 7: 439-443Crossref PubMed Scopus (1210) Google Scholar; Thomas et al., 1998Thomas K.K. Lloyd-Jones D.M. Thadhani R. et al.Hypovitaminosis D in medical inpatients.N Engl J Med. 1998; 338: 777-783Crossref PubMed Scopus (1230) Google Scholar). On the basis of these associations, some researchers now believe that 25(OH)D levels ≥20ngml−1 are required to avoid vitamin D deficiency (Malabanan et al., 1998Malabanan A. Veronikis I.E. Holick M.F. Redefining vitamin D insufficiency.Lancet. 1998; 351: 805-806Abstract Full Text Full Text PDF PubMed Scopus (908) Google Scholar; Wolpowitz and Gilchrest, 2006Wolpowitz D. Gilchrest B.A. The vitamin D questions: how much do you need and how should you get it?.J Am Acad Dermatol. 2006; 54: 301-317Abstract Full Text Full Text PDF PubMed Scopus (286) Google Scholar; Norman et al., 2007Norman A.W. Bouillon R. Whiting S.J. et al.13th Workshop consensus for vitamin D nutritional guidelines.J Steroid Biochem Mol Biol. 2007; 103: 204-205Crossref PubMed Scopus (191) Google Scholar; Holick, 2009Holick M.F. Vitamin D status: measurement, interpretation and clinical application.Ann Epidemiol. 2009; 19: 73-78Abstract Full Text Full Text PDF PubMed Scopus (954) Google Scholar), whereas it is proposed that an optimal level for health is reached at 30–32ngml−1 or higher (Hollis, 2005Hollis B.W. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D.J Nutr. 2005; 135: 317-322PubMed Google Scholar; Bischoff-Ferrari et al., 2006). Significant percentages of populations at northerly latitudes fall short of these levels (Webb and Engelsen, 2006Webb A.R. Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status.Photochem Photobiol. 2006; 82: 1697-1703Crossref PubMed Scopus (243) Google Scholar; Hypponen and Power, 2007Hypponen E. Power C. Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors.Am J Clin Nutr. 2007; 85: 860-868Crossref PubMed Scopus (592) Google Scholar; Hirani et al., 2009Hirani V. Mosdøl A. Mishra G. Predictors of 25-hydroxyvitamin D status among adults in two British national surveys.Br J Nutr. 2009; 101: 760-764Crossref PubMed Scopus (40) Google Scholar). Evidence continues to grow of wider health benefits conveyed by vitamin D, with much of this being indirect in nature. Mortality from prostate, colon, and breast cancers is inversely associated with ambient UVB, and this has been attributed to low vitamin D status (Berwick and Kesler, 2005Berwick M. Kesler D. Ultraviolet radiation, vitamin D and cancer.Photochem Photobiol. 2005; 81: 1261-1266Crossref PubMed Scopus (33) Google Scholar; Garland et al., 2006Garland C.F. Garland F.C. Gorham E.D. et al.The role of vitamin D in cancer prevention.Am J Public Health. 2006; 96: 252-261Crossref PubMed Scopus (763) Google Scholar; Holick, 2006Holick M.F. Vitamin D: its role in cancer prevention and treatment.Prog Biophys Mol Biol. 2006; 92: 49-59Crossref PubMed Scopus (199) Google Scholar), whereas the International Agency for Research on Cancer, 2008International Agency for Research on Cancer Vitamin D and Cancer. IARC Working Group Reports. vol. 5.. International Agency for Research on Cancer, World Health Organisation, Lyon2008Google Scholar supports a protective role for vitamin D in colon cancer. Further evidence exists for a beneficial effect of vitamin D on other diseases, including multiple sclerosis, tuberculosis, diabetes, hypertension, and other cancers (Zittermann, 2003Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence?.Br J Nutr. 2003; 89: 552-572Crossref PubMed Scopus (683) Google Scholar; Holick, 2004Holick M.F. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.Am J Clin Nutr. 2004; 79: 362-371PubMed Google Scholar; Vieth, 2006Vieth R. What is the optimal vitamin D status for health?.Prog Biophys Mol Biol. 2006; 92: 26-32Crossref PubMed Scopus (165) Google Scholar; Lipworth et al., 2009Lipworth L. Rossi M. McLaughlin J.K. et al.Dietary vitamin D and cancers of the oral cavity and esophagus.Ann Oncol. 2009; 20: 1576-1581Crossref PubMed Scopus (43) Google Scholar), although epidemiological data are conflicting regarding protection against melanoma (Millen et al., 2004Millen A.E. Tucker M.A. Hartge P. et al.Diet and melanoma in a case–control study.Cancer Epidemiol Biomarkers Prev. 2004; 13: 1042-1051PubMed Google Scholar; Ingraham et al., 2008Ingraham B.A. Bragdon B. Nohe A. Molecular basis of the potential of vitamin D to prevent cancer.Curr Med Res Opin. 2008; 24: 139-149Crossref PubMed Scopus (147) Google Scholar; Asgari et al., 2009Asgari M.M. Maruti S.S. Kushi L.H. et al.A cohort study of vitamin D intake and melanoma risk.J Invest Dermatol. 2009; 129: 1675-1680Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar). Mechanisms may involve immunomodulatory and chemopreventive properties of 1,25-dihydroxyvitamin D, now known to be metabolized from 25(OH)D by many extra-renal tissues (Millen et al., 2004Millen A.E. Tucker M.A. Hartge P. et al.Diet and melanoma in a case–control study.Cancer Epidemiol Biomarkers Prev. 2004; 13: 1042-1051PubMed Google Scholar; Ingraham et al., 2008Ingraham B.A. Bragdon B. Nohe A. Molecular basis of the potential of vitamin D to prevent cancer.Curr Med Res Opin. 2008; 24: 139-149Crossref PubMed Scopus (147) Google Scholar; Asgari et al., 2009Asgari M.M. Maruti S.S. Kushi L.H. et al.A cohort study of vitamin D intake and melanoma risk.J Invest Dermatol. 2009; 129: 1675-1680Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar). The UK Department of Health-funded SunSmart campaign is in line with similar campaigns in many countries in its recommendations to limit personal summer sunlight exposure (http://info.cancerresearchuk.org/healthyliving/sunsmart), whereas the United Kingdom's Health Protection Agency, in keeping with countries positioned at similar latitude, advises that casual exposures to summer sunlight, containing the requisite UVB, are sufficient for attaining vitamin D (National Radiological Protection Board, 2002National Radiological Protection Board Health Effects from Ultraviolet Radiation. Report of an advisory group on Non-ionising Radiation. vol. 13.. NRPB, Didcot2002Google Scholar). However, there is uncertainty regarding the specification and impact of following this guidance, as it is based on data derived from theoretical and in vitro models (National Radiological Protection Board, 2002National Radiological Protection Board Health Effects from Ultraviolet Radiation. Report of an advisory group on Non-ionising Radiation. vol. 13.. NRPB, Didcot2002Google Scholar; Ziegelberger et al., 2006Ziegelberger G. Repacholi M. McKinlay A. International commission on non-ionizing radiation protection.Prog Biophys Mol Biol. 2006; 92: 1-3Crossref PubMed Scopus (2) Google Scholar). To address this, we designed a study to examine the impact of following these recommendations on vitamin D status. A total of 120 white Caucasian subjects received simulated summer sunlight exposures mimicking UK guidance; sample size was selected for estimation of population variation with adequate precision. The aims of this study were to (i) determine whether recommended brief casual summer sunlight exposures can achieve 25(OH)D levels ≥20ngml−1 and the proposed optimal, that is, 25(OH)D ≥32ngml−1, vitamin D status; and (ii) provide specific information to assist future guidance on vitamin D acquisition, by performance under known conditions of UV dose and skin surface area. Of 120 recruited subjects, five were subsequently excluded because of vitamin D supplement use, and six failed to continue UVR treatment, resulting in 109 subjects (68% female, 32% male) completing the study. Baseline characteristics of the 109 volunteers, including minimal erythemal dose (MED), 25(OH)D, PTH, and serum biochemistry values are shown in Table 1. The average daily oral vitamin D intake was low; intakes during the first and last weeks of the study are shown in Table 1.Table 1Participant informationParticipants109Sex: male, female (%)35 (32.1), 74 (67.9)Skin type: I, II, III, and IV (%)8 (7.3), 60 (55.0), 40 (36.7), 1 (0.9)MinimumLower quartileMedianUpper quartileMaximumHeight (m)1.491.631.681.781.98Weight (kg)45.462.672.179.8112.0BMI (kgm−2)17.721.824.527.543.7Age (years)2027354760MED (mJcm−2)16.028.034.051.082.0Serum biochemistryMinimumLower quartileMedianUpper quartileMaximumNormal range25(OH)D (ngml−1)3.111.915.622.338See textParathyroid hormone (pmoll−1)0.61.21.62.77.50.8–3.9Sodium (mmoll−1)133140141143148132–144Potassium (mmoll−1)3.04.14.34.65.53.5–5.5Urea (mmoll−1)2.63.74.55.26.93.5–7.4Creatinine (μmoll−1)4463708012862–106Calcium (mmoll−1)2.092.192.242.282.442.15–2.65Inorganic phosphorus (mmoll−1)0.781.121.211.321.560.7–1.4Alkaline phosphatase (Ul−1)2549576917235–105Albumin (gl−1)404445475334–48Alanine transaminase (Ul−1)491116645–40Total Protein (gl−1)677275779160–80Bilirubin (μmoll−1)2468240–22Iron (μmoll−1)5.41318.523.2597–29Average daily vitamin D intake (μg)0.21.42.23.19.9—Abbreviations: BMI, body mass index; MED, minimal erythemal dose. Open table in a new tab Abbreviations: BMI, body mass index; MED, minimal erythemal dose. The 6 weeks of UVR exposures caused the mean 25(OH)D value to rise significantly by 10.4ngml−1 (95% confidence interval (CI): 9.1–11.8), from 17.6ngml−1 (SD 7.6; range: 3.1–38) before treatment to 28.0ngml−1 (SD 6.3; range: 10.8–50.9) after treatment (Figure 1). The increase in 25(OH)D levels after 6 weeks of UVR treatment varied among individuals (interquartile range: 5.4–14.5; range: 2.1–31.9ngml−1). Multiple linear regression analysis identified that posttreatment 25(OH)D levels were significantly associated with pretreatment 25(OH)D levels (P<0.0001), consistent with the results of a previous study (Moan et al., 2009Moan J. Lagunova Z. Cicarma E. et al.Sunbeds as vitamin D sources.Photochem Photobiol. 2009; 85: 1474-1479Crossref PubMed Scopus (35) Google Scholar), whereas other factors were not significantly associated (Table 2).Table 2Association of post-UV course 25(OH)D levels with participant baseline characteristicsFactorEstimate1Estimates are modeled differences in post-treatment 25(OH)D levels per unit increase in factor.95% CIP-valuePre-treatment 25(OH)D0.410.27–0.55<0.0001Age-0.00-0.10 to 0.100.94Sex (F vs M)0.32-2.02 to 2.650.79BMI-0.18-0.44 to 0.080.16Log MED-0.61-3.15 to 1.930.63Log dietary vitamin D0.37-0.28 to 1.030.22Cohort (1 vs 2)-1.31-3.49 to 0.870.23Abbreviations: BMI, body mass index; CI, confidence interval; MED, minimal erythemal dose.1 Estimates are modeled differences in post-treatment 25(OH)D levels per unit increase in factor. Open table in a new tab Abbreviations: BMI, body mass index; CI, confidence interval; MED, minimal erythemal dose. Assuming normality, the mean and SD values of the study group were used to calculate the percentage of the Greater Manchester population predicted to have 25(OH)D values, indicating deficient, sufficient, and proposed optimal status (Table 3). Baseline winter data predict that 5% (95% CI: 2.7–8.6) of the population has 25(OH)D levels <5ngml−1, 62.5% (CI: 55.2–69.4) has levels <20ngml−1, whereas 37.5% (CI: 30.6–44.8) has levels ≥20ngml−1 and only 2.9% (CI: 1.4–5.6) has levels ≥32ngml−1.Table 3Estimated percentage (95% CI) of the Greater Manchester, UK population exhibiting deficient, sufficient, and the proposed optimal circulating 25(OH)D levelsWeek of studyDeficient <5ngml−1Sufficient ≥20ngml−1Proposed optimal ≥32ngml−105.0 (2.7–8.6)37.5 (30.6–44.8)2.9 (1.4–5.6)10.9 (0.3–2.2)59.0 (51.7–66.0)6.9 (4.0–11.2)20.2 (0.04–0.6)72.7 (65.7–78.9)10.5 (6.7–15.7)30.1 (0.01–0.3)80.8 (74.3–86.1)14.7 (10.1–20.6)40.01 (<0.01–0.1)87.5 (82.0–91.7)19.3 (13.9–25.7)50.01 (<0.01–0.1)89.8 (84.7–93.5)25.4 (19.3–32.3)60.01 (<0.01–0.1)90.0 (84.9–93.7)26.2 (20.1–33.2)Abbreviation: CI, confidence interval. Open table in a new tab Abbreviation: CI, confidence interval. After a summer's short sunlight exposures, 90% (95% CI: 84.9–93.7) of the Greater Manchester, white Caucasian population is predicted to reach sufficient (≥20ngml−1) levels of 25(OH)D, whereas 26.2% (CI: 20.1–33.2) reaches 32ngml−1 or higher (Table 3). Given the same conditions as seen in the volunteers in this study, including white skin, dressed to reveal 35% skin surface area, and receiving a regimen of regular short midday exposures, the exposure time taken to acquire the same vitamin D-weighted dose across a range of European and North American cities is calculated to be 9–16minutes, compared with 13minutes in Manchester, in midsummer (21 June; Table 4).Table 4Estimated time taken to acquire the same vitamin D-weighted dose as used in this study, at different North American and European locations at local noon on June 21 and December 21CityLatitude1Latitude is given in degrees and minutes. (deg, min)Summer2Times are given to the nearest minute; times >1h are not shown. (minutes)Winter2Times are given to the nearest minute; times >1h are not shown. (minutes)New Orleans29, 57939San Diego32, 42949Athens37, 589—Washington38, 539—Boston42, 2110—Vancouver49, 1311—Brussels50, 5212—Manchester53, 3013—Oslo58, 5716—1 Latitude is given in degrees and minutes.2 Times are given to the nearest minute; times >1h are not shown. Open table in a new tab Our data indicate that regular short midday exposures to summer sunlight while informally dressed would place 90% of the Greater Manchester, UK, white Caucasian nonelderly adult population in the vitamin D sufficiency range (25(OH)D ≥20ngml−1), and 26% in the proposed optimal range (≥32ngml−1), whereas none would be in the range for deficiency that is currently defined by the UK Department of Health (<5ngml−1; 1998). Specifically, 13minutes of midday sunlight exposure on a cloudless day, three times weekly, to 35% skin surface area over a 6-week summer period, is required to achieve these outcomes. These findings will apply across the majority of the UK population and to white Caucasian populations residing in countries positioned at similar latitude (50–60°N) when equivalent summer sunlight conditions prevail. Using knowledge of UVR action spectra for cutaneous vitamin D synthesis and of sunlight emission spectra over different geographical conditions, the equivalent exposures required at a broader range of locations can also be estimated from our data (Table 4; Webb and Engelsen, 2006Webb A.R. Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status.Photochem Photobiol. 2006; 82: 1697-1703Crossref PubMed Scopus (243) Google Scholar). Exposure times in the United Kingdom and elsewhere will vary with people's activities and the presence of shade. An important consideration is the time of day at which individuals are exposed to summer sunlight, as this influences the amount of UVB available to generate vitamin D. Maximal amounts of UVB are available at solar noon, when the sun is directly overhead and solar radiation has the shortest path to the earth's surface, although in countries of mid latitude, such as the United Kingdom, UVB is insufficient to generate appreciable vitamin D even at midday from October to March (Webb and Engelsen, 2006Webb A.R. Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status.Photochem Photobiol. 2006; 82: 1697-1703Crossref PubMed Scopus (243) Google Scholar). Thus, the amount of vitamin D generated from following current recommendations on summer sunlight exposure can range from maximal levels, such as in our study in which midday exposures were simulated, to minimal levels when people are exposed to sunlight only at other times during the day, as could arise depending on an individual's interpretation of the SunSmart advice. The SunSmart campaign, which is aware that UVB is the prime cause of skin cancer but that some exposure is necessary for vitamin D synthesis, does not advocate complete avoidance of sunlight at midday, but rather to “seek shade” between 1100 and 1500 hours (http://info.cancerresearchuk.org/healthyliving/sunsmart/). However, no specific advice is given on skin surface area or duration of exposure. The 2002 Heath Protection Agency report advises that short exposures to summer sunlight containing the requisite UVB (by implication at midday), several times per week, to limited skin areas, are sufficient for avoidance of the vitamin D deficiency complications of rickets and osteomalacia in a fair-skinned person in the United Kingdom (National Radiological Protection Board, 2002National Radiological Protection Board Health Effects from Ultraviolet Radiation. Report of an advisory group on Non-ionising Radiation. vol. 13.. NRPB, Didcot2002Google Scholar). Given more recent definitions of vitamin D status (Malabanan et al., 1998Malabanan A. Veronikis I.E. Holick M.F. Redefining vitamin D insufficiency.Lancet. 1998; 351: 805-806Abstract Full Text Full Text PDF PubMed Scopus (908) Google Scholar; Hollis, 2005Hollis B.W. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D.J Nutr. 2005; 135: 317-322PubMed Google Scholar; Wolpowitz and Gilchrest, 2006Wolpowitz D. Gilchrest B.A. The vitamin D questions: how much do you need and how should you get it?.J Am Acad Dermatol. 2006; 54: 301-317Abstract Full Text Full Text PDF PubMed Scopus (286) Google Scholar), along with suggestions based on theoretical grounds of the greater UVR requirements that may be needed to reach this more elevated status (Holick, 2004Holick M.F. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.Am J Clin Nutr. 2004; 79: 362-371PubMed Google Scholar), agencies are aware of the need to assess the impact of following their general advice on vitamin D status, and to more accurately define how much sunlight exposure is required to achieve vitamin D sufficiency. Thus, our controlled conditions of known UVR dose and skin surface area exposure have provided a quantitative assessment that can more accurately inform future guidance. Although the majority of our population reached 25(OH)D levels designated sufficient immediately after the simulated summer sunlight exposures, only a minority reached the proposed optimal level of 32ngml−1. The increase in 25(OH)D levels was less than that reported in some previous studies involving UVR exposures, but in these studies, volunteers received near total skin surface exposure (Varghese et al., 1989Varghese M. Rodman J.S. Williams J.J. et al.The effect of ultraviolet B radiation treatments on calcium excretion and vitamin D metabolites in kidney stone formers.Clin Nephrol. 1989; 31: 225-231PubMed Google Scholar; Holick et al., 2007Holick M.F. Chen T.C. Lu Z. Vitamin D and skin physiology: a D-Lightful story.J Bone Miner Res. 2007; S2: V28-V33Crossref Scopus (345) Google Scholar; Thieden et al., 2008Thieden E. Jorgensen H.L. Jorgensen N.R. et al.Sunbed radiation provokes cutaneous vitamin D synthesis in humans – a randomized controlled trial.Photochem Photobiol. 2008; 84: 1487-1492Crossref PubMed Scopus (64) Google Scholar), whereas our volunteers wore casual clothing to reveal areas of skin commonly exposed during leisure activities; this is important as it cannot be assumed that different skin sites are equally efficient in synthesizing vitamin D. In addition, both oral vitamin D supplements and ambient UVB exposure were excluded to avoid confounding of UVR treatment outcomes. We observed the weekly incremental increase in mean 25(OH)D levels to reduce steadily during the course, with increases of only 0.8 and 0.2ngml−1 during the last two weeks, suggesting that levels would plateau if UVR exposures continued, in agreement with previous smaller studies (Porojnicu et al., 2008Porojnicu A.C. Bruland O.S. Aksnes L. et al.Sun beds and cod liver oil as vitamin D sources.J Photochem Photobiol B. 2008; 91: 125-131Crossref PubMed Scopus (35) Google Scholar; Thieden et al., 2008Thieden E. Jorgensen H.L. Jorgensen N.R. et al.Sunbed radiation provokes cutaneous vitamin D synthesis in humans – a randomized controlled trial.Photochem Photobiol. 2008; 84: 1487-1492Crossref PubMed Scopus (64) Google Scholar). This may be attributable to photoadaptation through UVR-induced epidermal thickening and melanization. In addition, the sufficient levels attained through summer exposures are anticipated to fall during the UK winter months (Hypponen and Power, 2007Hypponen E. Power C. Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors.Am J Clin Nutr. 2007; 85: 860-868Crossref PubMed Scopus (592) Google Scholar; Hirani et al., 2009Hirani V. Mosdøl A. Mishra G. Predictors of 25-hydroxyvitamin D status among adults in two British national surveys.Br J Nutr. 2009; 101: 760-764Crossref PubMed Scopus (40) Google Scholar). Our study revealed low baseline 25(OH)D levels, with 5% of the population in the deficiency range, and only 37.5 and 3% reaching sufficiency and optimal levels, respectively. Thus, the Greater Manchester population was representative of the wider UK population, a substantial proportion of which does not currently achieve a pattern of UVB exposure and oral intake conferring vitamin D sufficiency during winter (Hypponen and Power, 2007Hypponen E. Power C. Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors.Am J Clin Nutr. 2007; 85: 860-868Crossref PubMed Scopus (592) Google Scholar; Hirani et al., 2009Hirani V. Mosdøl A. Mishra G. Predictors of 25-hydroxyvitamin D status among adults in two British national surveys.Br J Nutr. 2" @default.
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• W2016221502 title "Recommended Summer Sunlight Exposure Levels Can Produce Sufficient (≥20ngml−1) but Not the Proposed Optimal (≥32ngml−1) 25(OH)D Levels at UK Latitudes" @default.
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