Marta Galvez-Fernandez1, Maria Grau-Perez2, Tamara Garcia-Barrera3, Sara Ramirez-Acosta3, Jose L Gomez-Ariza3, Beatriz Perez-Gomez4, Iñaki Galan-Labaca5, Ana Navas-Acien6, Josep Redon7, Laisa S Briongos-Figuero8, Antonio Dueñas-Laita8, Jose Luis Perez-Castrillon8, Maria Tellez-Plaza9, Juan Carlos Martin-Escudero8. 1. Department of Preventive Medicine and Microbiology, Universidad Autonoma de Madrid, Calle Arzobispo Morcillo, 4, 28029, Madrid, Spain; Department of Preventive Medicine, Hospital Severo Ochoa, Avenida de Orellana, 28914, Madrid, Spain; Department of Chronic Diseases Epidemiology, National Center for Epidemiology, Carlos III Health Institute, Calle de Melchor Fernández Almagro, 5, 28029, Madrid, Spain. 2. Department of Preventive Medicine and Microbiology, Universidad Autonoma de Madrid, Calle Arzobispo Morcillo, 4, 28029, Madrid, Spain; Area of Renal Risk and Cardiometabolic Disease, Instituto de Investigación Sanitaria Hospital Clinic de Valencia (INCLIVA), Avinguda de Menéndez y Pelayo, 4, 46010, Valencia, Spain; Department of Statistics and Operational Research, University of Valencia, Calle Dr. Moliner, 50, 46100, Valencia, Spain. 3. Department of Chemistry, University of Huelva, Avenida de las Fuerzas Armadas, 21007, Huelva, Spain. 4. Department of Chronic Diseases Epidemiology, National Center for Epidemiology, Carlos III Health Institute, Calle de Melchor Fernández Almagro, 5, 28029, Madrid, Spain. 5. Department of Preventive Medicine and Microbiology, Universidad Autonoma de Madrid, Calle Arzobispo Morcillo, 4, 28029, Madrid, Spain; Department of Chronic Diseases Epidemiology, National Center for Epidemiology, Carlos III Health Institute, Calle de Melchor Fernández Almagro, 5, 28029, Madrid, Spain. 6. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722W, 168th Street, NY, 10032, USA. 7. Area of Renal Risk and Cardiometabolic Disease, Instituto de Investigación Sanitaria Hospital Clinic de Valencia (INCLIVA), Avinguda de Menéndez y Pelayo, 4, 46010, Valencia, Spain. 8. Departments of Internal Medicine and Toxicology, University Hospital Rio Hortega, Calle Dulzaina, 2, 47012, Valladolid. University of Valladolid, Spain. 9. Department of Preventive Medicine and Microbiology, Universidad Autonoma de Madrid, Calle Arzobispo Morcillo, 4, 28029, Madrid, Spain; Department of Chronic Diseases Epidemiology, National Center for Epidemiology, Carlos III Health Institute, Calle de Melchor Fernández Almagro, 5, 28029, Madrid, Spain; Area of Renal Risk and Cardiometabolic Disease, Instituto de Investigación Sanitaria Hospital Clinic de Valencia (INCLIVA), Avinguda de Menéndez y Pelayo, 4, 46010, Valencia, Spain. Electronic address: m.tellez@isciii.es.
Abstract
BACKGROUND AND OBJECTIVES: Experimental data suggest that trace elements, such as arsenic (As), cadmium (Cd), and selenium (Se) can influence the bone remodeling process. We evaluated the cross-sectional association between As, Cd, and Se biomarkers with bone mineral density (BMD) measured at the calcaneus, in a representative sample of a general population from Spain. As secondary analyses we evaluated the associations of interest in subgroups defined by well-established BMD determinants, and also conducted prospective analysis of osteoporosis-related incident bone fractures restricted to participants older than 50 years-old. METHODS: In N = 1365 Hortega Study participants >20 years-old, urine As and Cd were measured by inductively coupled-plasma mass spectrometry (ICPMS); plasma Se was measured by atomic absorption spectrometry (AAS) with graphite furnace; and BMD at the calcaneus was measured using the Peripheral Instaneuous X-ray Imaging system (PIXI). As levels were corrected for arsenobetaine (Asb) to account for inorganic As exposure. RESULTS: The median of total urine As, Asb-corrected urine As, urine Cd, and plasma Se was 61.3, 6.53 and 0.39 μg/g creatinine, and 84.9 μg/L, respectively. In cross-sectional analysis, urine As and Cd were not associated with reduced BMD (T-score < -1 SD). We observed a non-linear dose-response of Se and reduced BMD, showing an inverse association below ~105 μg/L, which became increasingly positive above ~105 μg/L. The evaluated subgroups did not show differential associations. In prospective analysis, while we also observed a U-shape dose-response of Se with the incidence of osteoporosis-related bone fractures, the positive association above ~105 μg/L was markedly stronger, compared to the cross-sectional analysis. CONCLUSIONS: Our results support that Se, but not As and Cd, was associated to BMD-related disease. The association of Se and BMD-related disease was non-linear, including a strong positive association with osteoporosis-related bone fractures risk at the higher Se exposure range. Considering the substantial burden of bone loss in elderly populations, additional large prospective studies are needed to confirm the relevance of our findings to bone loss prevention in the population depending on Se exposure levels.
BACKGROUND AND OBJECTIVES: Experimental data suggest that trace elements, such as arsenic (As), cadmium (Cd), and selenium (Se) can influence the bone remodeling process. We evaluated the cross-sectional association between As, Cd, and Se biomarkers with bone mineral density (BMD) measured at the calcaneus, in a representative sample of a general population from Spain. As secondary analyses we evaluated the associations of interest in subgroups defined by well-established BMD determinants, and also conducted prospective analysis of osteoporosis-related incident bone fractures restricted to participants older than 50 years-old. METHODS: In N = 1365 Hortega Study participants >20 years-old, urine As and Cd were measured by inductively coupled-plasma mass spectrometry (ICPMS); plasma Se was measured by atomic absorption spectrometry (AAS) with graphite furnace; and BMD at the calcaneus was measured using the Peripheral Instaneuous X-ray Imaging system (PIXI). As levels were corrected for arsenobetaine (Asb) to account for inorganic As exposure. RESULTS: The median of total urine As, Asb-corrected urine As, urine Cd, and plasma Se was 61.3, 6.53 and 0.39 μg/g creatinine, and 84.9 μg/L, respectively. In cross-sectional analysis, urine As and Cd were not associated with reduced BMD (T-score < -1 SD). We observed a non-linear dose-response of Se and reduced BMD, showing an inverse association below ~105 μg/L, which became increasingly positive above ~105 μg/L. The evaluated subgroups did not show differential associations. In prospective analysis, while we also observed a U-shape dose-response of Se with the incidence of osteoporosis-related bone fractures, the positive association above ~105 μg/L was markedly stronger, compared to the cross-sectional analysis. CONCLUSIONS: Our results support that Se, but not As and Cd, was associated to BMD-related disease. The association of Se and BMD-related disease was non-linear, including a strong positive association with osteoporosis-related bone fractures risk at the higher Se exposure range. Considering the substantial burden of bone loss in elderly populations, additional large prospective studies are needed to confirm the relevance of our findings to bone loss prevention in the population depending on Se exposure levels.
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