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      Migration of aluminum from food contact materials to food—a health risk for consumers? Part I of III: exposure to aluminum, release of aluminum, tolerable weekly intake (TWI), toxicological effects of aluminum, study design, and methods

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          Abstract

          Background

          In spite of the prevalence of aluminum in nature, no organism has been found to date which requires this element for its biological functions. The possible health risks to human beings resulting from uptake of aluminum include detrimental effects to the hemopoietic system, the nervous system and bones. Aluminum is used in many fields and occurs in numerous foodstuffs. Food contact materials containing aluminum represent an anthropogenic source of dietary aluminum.

          Results

          As a result of their frequent use in private households a study was undertaken to detect migration of this metal to foodstuffs from drink containers, coffee pots, grill pans, and camping cookware made of aluminum.

          Conclusions

          An estimate of the health risk to consumers is calculated, based on the tolerable weekly intake (TWI) specified by the European Food Safety Authority of 1 mg/kg body weight for all groups of people. In some instances the TWI is significantly exceeded, dependent upon the food contact material and the food itself.

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          Human exposure to aluminium.

          Christopher Exley (2013)
          Human activities have circumvented the efficient geochemical cycling of aluminium within the lithosphere and therewith opened a door, which was previously only ajar, onto the biotic cycle to instigate and promote the accumulation of aluminium in biota and especially humans. Neither these relatively recent activities nor the entry of aluminium into the living cycle are showing any signs of abating and it is thus now imperative that we understand as fully as possible how humans are exposed to aluminium and the future consequences of a burgeoning exposure and body burden. The aluminium age is upon us and there is now an urgent need to understand how to live safely and effectively with aluminium.
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            Aluminum as a toxicant.

            A Becaria, G Bondy, Matthew Campbell (2002)
            Although aluminum is the most abundant metal in nature, it has no known biological function. However, it is known that there is a causal role for aluminum in dialysis encephalopathy, microcytic anemia, and osteomalacia. Aluminum has also been proposed to play a role in the pathogenesis of Alzheimer's disease (AD) even though this issue is controversial. The exact mechanism of aluminum toxicity is not known but accumulating evidence suggests that the metal can potentiate oxidative and inflammatory events, eventually leading to tissue damage. This review encompasses the general toxicology of aluminum with emphasis on the potential mechanisms by which it may accelerate the progression of chronic age-related neurodegenerative disorders.
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              Aluminium neurotoxicity: neurobehavioural and oxidative aspects.

              Vijay Kumar, Kiran Gill (2009)
              Aluminium is the most widely distributed metal in the environment and is extensively used in daily life that provides easy exposure to human beings. The exposure to this toxic metal occurs through air, food and water. However, there is no known physiological role for aluminium within the body and hence this metal may produce adverse physiological effects. Chronic exposure of animals to aluminium is associated with behavioural, neuropathological and neurochemical changes. Among them, deficits of learning and behavioural functions are most evident. Some epidemiological studies have shown poor performance in cognitive tests and a higher abundance of neurological symptoms for workers occupationally exposed to aluminium. However, in contrast to well established neurotoxic effects, neurobehavioural studies of aluminium in rodents have generally not produced consistent results. Current researches show that any impairment in mitochondrial functions may play a major role in many human disorders including neurodegenerative disorders. Being involved in the production of reactive oxygen species, aluminium may cause impairments in mitochondrial bioenergetics and may lead to the generation of oxidative stress which may lead to a gradual accumulation of oxidatively modified cellular proteins. In this review, the neuropathologies associated with aluminium exposure in terms of neurobehavioural changes have been discussed. In addition, the impact of aluminium on the mitochondrial functions has also been highlighted.
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                Author and article information

                Contributors
                Thorsten Stahl: +49 561 9888233 , thorsten.stahl@lhl.hessen.de
                Sandy Falk: sandy.falk@lhl.hessen.de
                Alice Rohrbeck: alice.rohrbeck@web.de
                Sebastian Georgii: sebastian.georgii@lhl.hessen.de
                Christin Herzog: christin-herzog@gmx.de
                Alexander Wiegand: alexander.wiegand@lhl.hessen.de
                Svenja Hotz: Svenja.V.Hotz@lc.chemie.uni-giessen.de
                Bruce Boschek: bruce@boschek.de
                Holger Zorn: Holger.Zorn@lcb.Chemie.uni-giessen.de
                Hubertus Brunn: hubertus.brunn@lhl.hessen.de
                Journal
                Journal ID (nlm-ta): Environ Sci Eur
                Journal ID (iso-abbrev): Environ Sci Eur
                Title: Environmental Sciences Europe
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 2190-4707
                ISSN (Electronic): 2190-4715
                Publication date (Electronic): 12 April 2017
                Publication date PMC-release: 12 April 2017
                Publication date (Print): 2017
                Volume: 29
                Issue: 1
                Electronic Location Identifier: 19
                Affiliations
                [1 ]Hessian State Laboratory, Am Versuchsfeld 11, 34128 Kassel, Germany
                [2 ]Hessian State Laboratory, Glarusstr. 6, 65203 Wiesbaden, Germany
                [3 ]GRID grid.8664.c, Institute of Food Chemistry and Food Biotechnology, , Justus Liebig University Giessen, ; Heinrich-Buff-Ring 17, 35392 Giessen, Germany
                [4 ]GRID grid.8664.c, Institute of Medical Virology, , Justus Liebig University, ; Schubertstraße 81, 35392 Giessen, Germany
                [5 ]Hessian State Laboratory, Schubertstr. 60, 35392 Giessen, Germany
                Article
                Publisher ID: 116
                DOI: 10.1186/s12302-017-0116-y
                PMC ID: 5388732
                PubMed ID: 28458989
                SO-VID: 6f507edf-eb63-474e-b18f-5c245ae7d6e5
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 30 December 2016
                Date accepted : 25 March 2017
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                Keywords: aluminum,exposure,migration limit,tolerable weekly intake
                Data availability:
                Keywords: aluminum, exposure, migration limit, tolerable weekly intake

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