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      Association of Arsenic and Metals with Concentrations of 25-Hydroxyvitamin D and 1,25-Dihydroxyvitamin D among Adolescents in Torreón, Mexico

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          Abstract

          Background: Limited data suggest that lead (Pb), cadmium (Cd), and uranium (U) may disrupt vitamin D metabolism and inhibit production of 1,25-dihydroxyvitamin D [1,25(OH) 2D], the active vitamin D metabolite, from 25-hydroxyvitamin D [25(OH)D] in the kidney.

          Objectives: We evaluated the association between blood lead (BPb) and urine arsenic (As), Cd, molybdenum (Mo), thallium (Tl), and U with markers of vitamin D metabolism [25(OH)D and 1,25(OH) 2D].

          Methods: We conducted a cross-sectional study of 512 adolescents in Torreón, a town in Mexico with a Pb smelter near residential areas. BPb was measured using atomic absorption spectrometry. Urine As, Cd, Mo, Tl, and U were measured using inductively coupled plasma mass spectrometry. Serum 25(OH)D and 1,25(OH) 2D were measured using a chemiluminescent immunoassay and a radioimmunoassay, respectively. Multivariable linear models with vitamin D markers as the outcome were used to estimate associations of BPb and creatinine-corrected urine As and metal concentrations with serum vitamin D concentrations, controlling for age, sex, adiposity, smoking, socioeconomic status, and time outdoors.

          Results: Serum 25(OH)D was positively associated with urine Mo and Tl [1.5 (95% CI: 0.4, 2.6) and 1.2 (95% CI: 0.3, 2.1) ng/mL higher with a doubling of exposure, respectively]. Serum 1,25(OH) 2D was positively associated with urine As and U [3.4 (95% CI: 0.9, 5.9) and 2.2 (95% CI: 0.7, 3.7) pg/mL higher, respectively], with little change in associations after additional adjustment for serum 25(OH)D. Pb and Cd were not associated with 25(OH)D or 1,25(OH) 2D concentrations.

          Conclusions: Overall, our findings did not support a negative effect of As or metal exposures on serum 1,25(OH) 2D concentrations. Additional research is needed to confirm positive associations between serum 1,25(OH) 2D and urine U and As concentrations and to clarify potential underlying mechanisms.

          Citation: Zamoiski RD, Guallar E, García-Vargas GG, Rothenberg SJ, Resnick C, Rubio Andrade M, Steuerwald AJ, Parsons PJ, Weaver VM, Navas-Acien A, Silbergeld EK. 2014. Association of arsenic and metals with concentrations of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D among adolescents in Torreón, Mexico. Environ Health Perspect 122:1233–1238; http://dx.doi.org/10.1289/ehp.1307861

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          Prospective study of predictors of vitamin D status and cancer incidence and mortality in men.

          Edward L. Giovannucci, Yan Liu, Eric Rimm … (2006)
          Vitamin D has potent anticancer properties, especially against digestive-system cancers. Many human studies have used geographic residence as a marker of solar ultraviolet B and hence vitamin D exposure. Here, we considered multiple determinants of vitamin D exposure (dietary and supplementary vitamin D, skin pigmentation, adiposity, geographic residence, and leisure-time physical activity-to estimate sunlight exposure) in relation to cancer risk in the Health Professionals Follow-Up Study. Among 1095 men of this cohort, we quantified the relation of these six determinants to plasma 25-hydroxy-vitamin D [25(OH)D] level by use of a multiple linear regression model. We used results from the model to compute a predicted 25(OH)D level for each of 47,800 men in the cohort based on these characteristics. We then prospectively examined this variable in relation to cancer risk with multivariable Cox proportional hazards models. From 1986 through January 31, 2000, we documented 4286 incident cancers (excluding organ-confined prostate cancer and nonmelanoma skin cancer) and 2025 deaths from cancer. From multivariable models, an increment of 25 nmol/L in predicted 25(OH)D level was associated with a 17% reduction in total cancer incidence (multivariable relative risk [RR] = 0.83, 95% confidence interval [CI] = 0.74 to 0.92), a 29% reduction in total cancer mortality (RR = 0.71, 95% CI = 0.60 to 0.83), and a 45% reduction in digestive-system cancer mortality (RR = 0.55, 95% CI = 0.41 to 0.74). The absolute annual rate of total cancer was 758 per 100,000 men in the bottom decile of predicted 25(OH)D and 674 per 100,000 men for the top decile; these respective rates were 326 per 100,000 and 277 per 100,000 for total cancer mortality and 128 per 100,000 and 78 per 100,000 for digestive-system cancer mortality. Results were similar when we controlled further for body mass index or physical activity level. Low levels of vitamin D may be associated with increased cancer incidence and mortality in men, particularly for digestive-system cancers. The vitamin D supplementation necessary to achieve a 25(OH)D increment of 25 nmol/L may be at least 1500 IU/day.
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            The influence of smoking on vitamin D status and calcium metabolism.

            C Brot, O Sørensen, N Jørgensen (1999)
            To assess the influence of smoking on serum parathyroid hormone (PTH), serum vitamin D metabolites, serum ionized calcium, serum phosphate, and biochemical markers of bone turnover in a cohort of 510 healthy Danish perimenopausal women. A cross-sectional study. Copenhagen, Denmark. Five-hundred-and-ten healthy women aged 45-58 y, included 3-24 months after last menstrual bleeding. None were using hormone replacement therapy. The women were grouped according to their current smoking status. The two groups were compared with regard to serum levels of 25-hydroxyvitamin D (25OHD) and 1, 25-dihydroxyvitamin D (1,25-(OH)2D), intact PTH, ionized calcium and phosphate, osteocalcin, as well as urine pyridinolines. Bone mineral density (BMD) was measured with DEXA-scans. Multiple regression analyses were performed to detect the effect of potentially confounding lifestyle factors, such as calcium and vitamin D intakes, alcohol and coffee consumption, sunbathing, and physical exercise. Fifty percent were current smokers. Smokers had significantly reduced levels of serum 25OHD (P=0.02), 1,25(OH)2D (P=0.001), and PTH (P<0.001). There was no difference in serum ionized calcium between smokers and non-smokers. We found a negative effect of smoking on serum osteocalcin (P=0.01), while urinary pyridinolines were similar in the two groups. The small differences in lifestyle between the two groups could not explain these findings. Smokers had small but significant reductions in bone mineral density. Smoking has a significant effect on calcium and vitamin D metabolism, which is not likely to be explained by other confounding lifestyle factors. The depression of the vitamin D-PTH system seen among smokers may represent another potential mechanism for the deleterious effects of smoking on the skeleton, and may contribute to the reported risk of osteoporosis among smokers. Grants from the Karen Elise Jensens Foundation.
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              Seafood intake and urine concentrations of total arsenic, dimethylarsinate and arsenobetaine in the US population.

              Eliseo Guallar, Ana Navas-Acien, E Silbergeld … (2010)
              Seafood is the main source of organic arsenic exposure (arsenobetaine, arsenosugars and arsenolipids) in the population. Arsenosugars and arsenolipids are metabolized to several species including dimethylarsinate (DMA). Evaluate the association of seafood intake with spot urine arsenic concentrations in the 2003-2006 National Health Nutrition and Examination Survey (NHANES). We studied 4276 participants ≥ 6 years. Total arsenic was measured using inductively coupled plasma dynamic reaction cell mass spectrometry (ICPMS). Urine DMA and arsenobetaine were measured by high-performance liquid chromatography coupled with ICPMS. Participants reporting seafood in the past 24-h had higher urine concentrations of total arsenic (median 24.5 vs. 7.3 μg/L), DMA (6.0 vs. 3.5 μg/L), arsenobetaine (10.2 vs. 0.9 μg/L) and total arsenic minus arsenobetaine (11.0 vs. 5.5 μg/L). Participants reporting seafood ≥ 2/wk vs. never during the past year had 2.3 (95% confidence interval 1.9, 2.7), 1.4 (1.2, 1.6), 6.0 (4.6, 7.8) and 1.7 (1.4, 2.0) times higher (p-trend <0.001) concentrations of total arsenic, DMA, arsenobetaine and total arsenic minus arsenobetaine, respectively. In participants without detectable arsenobetaine and in analyses adjusted for arsenobetaine, seafood consumption in the past year was not associated with total arsenic or DMA concentrations in urine. Seafood intake was a major determinant of increased urine concentrations of total arsenic, DMA, arsenobetaine and total arsenic minus arsenobetaine in the US population. Epidemiologic studies that use total arsenic, DMA, the sum of inorganic arsenic, methylarsonate and DMA, and total arsenic minus arsenobetaine as markers of inorganic arsenic exposure and/or metabolism need to address seafood intake. Copyright © 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Journal ID (iso-abbrev): Environ. Health Perspect
                Journal ID (publisher-id): EHP
                Title: Environmental Health Perspectives
                Publisher: NLM-Export
                ISSN (Print): 0091-6765
                ISSN (Electronic): 1552-9924
                Publication date (Electronic): 05 August 2014
                Publication date (Print): November 2014
                Volume: 122
                Issue: 11
                Pages: 1233-1238
                Affiliations
                [1 ]Department of Environmental Health Sciences,
                [2 ]Department of Epidemiology, and
                [3 ]Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA
                [4 ]Facultad de Medicina, Universidad Juárez del Estado de Durango, Gómez Palacio Durango, México
                [5 ]Secretaría de Salud del Estado de Coahuila, Coahuila, Mexico
                [6 ]Instituto Nacional de Salud Pública, Centro de Investigación en Salud Poblacional, Cuernavaca, Morelos, Mexico
                [7 ]Laboratory of Inorganic and Nuclear Chemistry, Wadsworth Center, New York State Department of Health, Albany, New York, USA
                [8 ]Department of Environmental Health Sciences, School of Public Health, University at Albany, Albany, New York, USA
                [9 ]Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
                Author notes
                Address correspondence to E.K. Silbergeld, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe St., E6644, Baltimore MD 21205 USA. Telephone: (410) 955-8678. E-mail: esilberg@ 123456jhsph.edu
                Article
                Publisher ID: ehp.1307861
                DOI: 10.1289/ehp.1307861
                PMC ID: 4216165
                PubMed ID: 25095279
                SO-VID: 6a3f64b8-f1f3-478a-b6fc-a084120d1393
                License:

                Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, “Reproduced with permission from Environmental Health Perspectives”); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.

                History
                Date received : 07 November 2013
                Date accepted : 01 August 2014
                Date: 05 August 2014
                Date: 01 November 2014
                Categories
                Subject: Children's Health

                ScienceOpen disciplines: Public health
                Data availability:
                ScienceOpen disciplines: Public health

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