Environmental Metals and Cardiovascular Disease in Adults: A Systematic Review beyond Lead and Cadmium

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Abstract

Published systematic reviews concluded that there is moderate to strong evidence to infer a potential role of lead and cadmium, widespread metal exposures, as cardiovascular risk factors. For other non-essential metals, the evidence has not been appraised systematically. Our objective was to systematically review epidemiologic studies on the association between cardiovascular disease in adults and the environmental metals antimony, barium, chromium, nickel, tungsten, uranium, and vanadium. We identified a total of 4 articles on antimony, 1 on barium, 5 on chromium, 1 on nickel, 4 on tungsten, 1 on uranium and 0 on vanadium. We concluded that the current evidence is not sufficient to inform on the cardiovascular role of these metals because the small number of studies. Few experimental studies have also evaluated the role of these metals in cardiovascular outcomes. Additional epidemiologic and experimental studies, including prospective cohort studies, are needed to understand the role of metals, including exposure to metal mixtures, in cardiovascular disease development.

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Estimation of Average Concentration in the Presence of Nondetectable Values

Richard Hornung, Laurence Reed (1990)

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The effects of metals as endocrine disruptors.

Ivo Iavicoli, Luca Fontana, Antonio Bergamaschi (2009)

This review reports current knowledge regarding the roles that cadmium (Cd), mercury (Hg), arsenic (As), lead (PB), manganese (Mn), and zinc (Zn) play as endocrine-disrupting chemicals (EDCs). The influence of these metals on the endocrine system, possible mechanisms of action, and consequent health effects were correlated between experimental animals and humans. Analysis of the studies prompted us to identify some critical issues related to this area and showed the need for more rigorous and innovative studies. Consequently, it was recommended that future studies need to: (1) identify the mechanisms of action, because at the present time only a few have been elucidated-in this context, the possible presence of hormesis need to be determined, as currently this was reported only for exposure Cd and As; (2) study the possible additive, synergistic, or antagonistic effects on the endocrine system following exposure to a mixture of metals since there is a lack of these studies available, and in general or occupational environments, humans are simultaneously exposed to different classes of xenobiotics, including metals, but also to organic compounds that might also be EDCs; (3) assess the potential adverse effects on the endocrine system of low-level exposures to metals, as most of the information currently available on EDCs originates from studies in which exposure levels were particularly high; and (4) assess the effects on the endocrine and reproductive systems of other metals that are present in the general and occupational environment that have not yet been evaluated.

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Cadmium Exposure and All-Cause and Cardiovascular Mortality in the U.S. General Population

Maria Tellez-Plaza, Ana Navas-Acien, Andy Menke … (2012)

Background: Urine cadmium concentrations were associated with all-cause and cardiovascular mortality in men in the 1988–1994 U.S. National Health and Nutrition Examination Survey (NHANES) population. Since 1988, cadmium exposure has decreased substantially in the United States. The associations between blood and urine cadmium and cardiovascular disease (CVD) mortality at more recent levels of exposure are unknown. Objectives: We evaluated the prospective association of blood and urine cadmium concentrations with all-cause and CVD mortality in the 1999–2004 U.S. population. Methods: We followed 8,989 participants who were ≥ 20 years of age for an average of 4.8 years. Hazard ratios for mortality end points comparing the 80th to the 20th percentiles of cadmium distributions were estimated using Cox regression. Results: The multivariable adjusted hazard ratios [95% confidence intervals (CIs)] for blood and urine cadmium were 1.50 (95% CI: 1.07, 2.10) and 1.52 (95% CI: 1.00, 2.29), respectively, for all-cause mortality, 1.69 (95% CI: 1.03, 2.77) and 1.74 (95% CI: 1.07, 2.83) for CVD mortality, 1.98 (95% CI: 1.11, 3.54) and 2.53 (95% CI: 1.54, 4.16) for heart disease mortality, and 1.73 (95% CI: 0.88, 3.40) and 2.09 (95% CI: 1.06, 4.13) for coronary heart disease mortality. The population attributable risks associated with the 80th percentile of the blood (0.80 μg/L) and urine (0.57 μg/g) cadmium distributions were 7.0 and 8.8%, respectively, for all-cause mortality and 7.5 and 9.2%, respectively, for CVD mortality Conclusions: We found strongly suggestive evidence that cadmium, at substantially low levels of exposure, remains an important determinant of all-cause and CVD mortality in a representative sample of U.S. adults. Efforts to further reduce cadmium exposure in the population could contribute to a substantial decrease in CVD disease burden.

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Author and article information

Journal

Journal ID (nlm-journal-id): 101629387

Journal ID (pubmed-jr-id): 42445

Journal ID (nlm-ta): Curr Environ Health Rep

Journal ID (iso-abbrev): Curr Environ Health Rep

Title: Current environmental health reports

ISSN (Electronic): 2196-5412

Publication date Nihms-submitted: 26 January 2018

Publication date (Print): December 2016

Publication date PMC-release: 07 February 2018

Volume: 3

Issue: 4

Pages: 416-433

Affiliations

[1 ]Department of Environmental Health Sciences Johns Hopkins Bloomberg School of Public Health, Baltimore, US

[2 ]Department Epidemiology Johns Hopkins Bloomberg School of Public Health, Baltimore, US

[3 ]Department of Internal Medicine, Hospital Clínico de Valencia, Valencia, Spain

[4 ]Area of Cardiometabolic and Renal Risk, Institue for Biomedical Research Hospital Clinical of Valencia (INCLIVA)

[7 ]CIBER Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Minister of Health, Madrid, Spain

[10 ]Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD, US

[11 ]Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, US

Author notes

Corresponding author: Maria Tellez-Plaza, Institute for Biomedical Research Hospital Clinico de Valencia - INCLIVA, Av. Menendez Pelayo, 4 accesorio, 46010 Valencia, Spain, Telephone: +34963983060, maria.tellez@ 123456uv.es ; mtellez3@ 123456jhu.edu

Adrian Ruiz-Hernandez, Department of Internal Medicine, Hospital Clinic de Valencia, Avenida Blasco Ibañez, 17, 46010 Valencia, Spain, anruhe@ 123456gmail.com

Anne E Nigra, Department of Environmental Health Sciences, Columbia Mailman School of Public Health, 722 W 168th St, 11 Floor Rm 1105, New York, NY 10032, aen2136@ 123456cumc.columbia.edu

Josep Redon, Institute for Biomedical Research Hospital Clinico de Valencia - INCLIVA, Av. Menendez Pelayo, 4 accesorio, 46010 Valencia, Spain, josep.redon@ 123456uv.es

Ana Navas-Acien, Department of Environmental Health Sciences, Columbia Mailman School of Public Health, 722 W 168th St, 11 Floor Rm 1105, New York, NY 10032, an2737@ 123456cumc.columbia.edu

[*]

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¹Department of Internal Medicine, Hospital Clínico de Valencia, Valencia, Spain; ²Area of Cardiometabolic and Renal Risk and ⁶ Genotyping and Genetic Diagnosis Unit, Institute for Biomedical Research INCLIVA, Valencia, Spain; ³Departments of Environmental Health Sciences and ⁴Epidemiology Johns Hopkins Bloomberg School of Public Health, Baltimore, US; ⁵ Kidney Institute and Division of Nephrology, Department of Internal Medicine, China Medical University Hospital and College of Medicine, China Medical University, Taichung, Taiwan; ⁷CIBER Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Minister of Health, Madrid, Spain; ⁸Nutrition and Genomics Laboratory, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts, USA; ⁹Instituto Madrileño de Estudios Avanzados en Alimentación, Madrid, Spain and ¹⁰Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD, US

Article

Accession ID: PMC5801549 Pmcid ID: PMC5801549 Pmc-uid ID: 5801549 Manuscript ID: nihpa936802

DOI: 10.1007/s40572-016-0117-9

PMC ID: 5801549

PubMed ID: 27783356

SO-VID: 5abcd02d-11f6-4485-b65e-0fc3099238b5

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Environmental Metals and Cardiovascular Disease in Adults: A Systematic Review beyond Lead and Cadmium

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Karger: Cardiovascular System

Most cited references 105

Estimation of Average Concentration in the Presence of Nondetectable Values

The effects of metals as endocrine disruptors.

Cadmium Exposure and All-Cause and Cardiovascular Mortality in the U.S. General Population

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