| 1. |
- Aggett, Peter, et al.
(författare)
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Essential metals : assessing risks from dificiency and toxicity
- 2015. - 4
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Ingår i: Handbook on the toxicology of metals. - : Academic Press. - 9780123982926 ; , s. 281-297
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Bokkapitel (refereegranskat)abstract
- Recommendations aimed at protecting the public from toxicity of essential elements including essential metals have usually been developed separately from those recommendations aimed at protection from deficiency. Because of the uncertainties involved in the evaluations, these recommendations have sometimes been in conflict, emphasizing the need for a new approach, including a balanced consideration of nutritional and toxicological data. In developing these new principles of evaluation, some basic concepts based on interindividual variability in sensitivity to deficiency and toxicity must be considered. Such variation translates into one interval of (low) daily intakes, at which there is a risk of developing deficiency, and another interval of (high) dietary intakes at which toxicity may occur. In most instances, there is a third set of intakes in between, which represents the acceptable range of oral intake (AROI), in which no adverse effects occur. It must be noted, however, that a range cannot be found that protects all persons from adverse effects. Those persons with genetically determined sensitivity may require higher intakes to avoid deficiency or lower intakes to avoid toxicity than those defined by the AROI. The AROI is defined as protecting 95% of an unselected human population from minimal adverse effects of deficiency or toxicity.
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| 2. |
- Chen, Xiao, et al.
(författare)
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The association between dietary cadmium exposure and renal dysfunction - the benchmark dose estimation of reference levels : the ChinaCad study
- 2018
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Ingår i: Journal of Applied Toxicology. - : John Wiley & Sons. - 0260-437X .- 1099-1263. ; 38:10, s. 1365-1373
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Tidskriftsartikel (refereegranskat)abstract
- The tolerable dietary intake of cadmium was recommended at provisional tolerable monthly intake of 25gkg(-1) body weight. However, several studies indicated that this tolerable level should be re-evaluated for sufficient health protection. In this study, we show the reference levels of dietary cadmium intake for renal dysfunction by using a benchmark dose (BMD) approach. A total of 790 subjects (302 men and 488 women) living in control and cadmium-polluted areas were included. The dietary cadmium intake was estimated by a food survey. Blood cadmium, urinary cadmium and renal function markers (microalbuminuria, N-acetyl--d-glucosaminidase [NAG] and its isoform B [NAGB], (2)-microglobulin and retinol binding protein) in urine were measured. We calculated the 95% lower confidence bounds of BMD (BMDLs) of cumulative cadmium intake. In control and two polluted areas, the median cumulative cadmium intake was 0.5, 2.1 and 11.1g. The odds ratio of the intermediate (1.0-3.0g), second highest (3.0-11.0g) and the highest cumulative cadmium intake (>11.0g) compared with the lowest cumulative cadmium intake (<1.0g) were 2.8 (95% CI: 1.4-5.8), 8.1 (95% CI: 3.8-17.2) and 11.4 (95% CI: 6.5-26.4) for urinary NAG and 6.6 (95% CI: 3.2-13.8), 14.8 (95% CI: 6.8-32.2) and 22.5 (95% CI: 10.7-47.5) for urinary NAGB. The BMDLs of cumulative cadmium intake were 1.1-1.2g (benchmark response [BMR]=5%) for urinary NAG, and were 0.7-0.9g (BMR=5%) for urinary NAGB, and were 1.3-1.4g (BMR=5%) for urinary (2)-microglobulin. The BMDLs of cumulative cadmium intake in a Chinese population were lower than the critical standard previously reported. Further evaluations are needed for sufficient health protection. Several studies indicated that the tolerable dietary intake of cadmium should be re-evaluated for sufficient health protection. In this study, we show the reference levels of dietary cadmium intake for renal dysfunction by using benchmark dose (BMD) approach. The lowest BMD lower bound confidence limits of cumulative cadmium intake were 0.7-0.9g (benchmark response=5%). The BMD lower bound confidence limits of cumulative cadmium intake were lower than the critical standard previously reported. Further evaluations are needed for sufficient health protection.
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| 3. |
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| 4. |
- Littorin, Margareta, et al.
(författare)
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Kemiska bekämpningsmedel
- 2019. - Fjärde upplagan
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Ingår i: Arbets- och miljömedicin : - en lärobok om hälsa och miljö - - en lärobok om hälsa och miljö. - 9789144127460 ; , s. 339-350
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Bokkapitel (refereegranskat)
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| 5. |
- Nordberg, Gunnar F, et al.
(författare)
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Cadmium
- 2015. - 4
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Ingår i: Handbook on the toxicology of metals. - : Academic Press. - 9780123982933 ; , s. 667-716
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Bokkapitel (refereegranskat)abstract
- Cadmium (Cd) occurs naturally with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to industrial emission sources, particularly those of nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries and as pigments. Cd is increasingly used in solar panels. Dispersive use of Cd is restricted by law in the European Union. Absorption of Cd compounds through the skin is negligible. Between 10% and 50% of inhaled Cd will be absorbed. Humans absorb 5-10% of ingested Cd. A low intake of calcium, zinc, or iron increases the degree of absorption. Cadmium is transported in plasma when bound to metallothionein (MT), a low molecular weight protein, and/or to certain high molecular weight proteins. The accumulation of Cd occurs in many tissues, with particularly long half-lives (10-30 years) in muscle, bone, kidney, and liver. MT-bound Cd in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released. When not all Cd is bound, toxic effects occur. The average amount of Cd ingested in European and North American countries is 10-20 μg/day. The corresponding average urinary excretion is 0.5-1.0 μg/day and the blood concentration is 0.5-1.0 μg/L in nonsmokers; it is twice as high in smokers. The intake of Cd through food used to be higher in Japan than in Europe, but it has decreased and is currently similar to levels reported in European countries with high intakes. Acute inhalation of Cd in air, for example from soldering or welding fumes, may lead to severe chemical pneumonitis. Long-term exposure to low air levels may lead to chronic obstructive lung disease and possibly to lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction. The first sign of damage is low molecular weight proteinuria. Long-term exposure from food, often combined with other means of delivery, may also lead to disturbance of calcium metabolism, osteoporosis, and osteomalacia, mainly among postmenopausal women. A disease exhibiting these features—called itai-itai disease—occurred in the 1950s in a Cd-polluted area of Japan: 124 cases were diagnosed up to 1970, and 196 cases in total were diagnosed up to 2011. In laboratory animals, Cd has been shown to induce cancer of the lungs, prostate, and other organs. Epidemiological studies have found increased rates of cancer of the lungs and in some studies also in other organs. Cadmium is classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer (IARC). Exposure to Cd in the air at concentrations of 5-10 μg/m3 during a working life of 45 years may give rise to renal tubular dysfunction in a small proportion of exposed workers. At approximately 100 μg/m3, signs of chronic obstructive lung disease may develop. Epidemiological data shows that adverse kidney effects occur in sensitive occupational groups, as well as in general population groups, after lifelong exposures giving rise to urinary Cd (UCd) of 4 μg/g creatinine. At such exposures, bone effects including osteoporosis and increased risk of fractures may also occur in sensitive groups, mainly among postmenopausal women. Adverse bone and kidney effects may occur in a small but sensitive population group as a result of lifelong cadmium exposure with UCd of approximately 1 μg/g creatinine and higher, but the evidence is still inconclusive. Such exposure occurs in general population groups in many countries. There is no specific treatment for Cd poisoning. When there are signs of osteomalacia, large doses of vitamin D should be given. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects primary prevention is essential.
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| 6. |
- Nordberg, Gunnar F, et al.
(författare)
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Toxicology of metals : overview, definitions, concepts, and trends
- 2015. - 4
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Ingår i: Handbook on the toxicology of metals. - : Academic Press. - 9780123982926 ; , s. 3-14
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Bokkapitel (refereegranskat)abstract
- Metals and their compounds have long been recognized as important toxic agents, causing acute and chronic poisoning cases in occupational settings and in environmental high-exposure situations. In recent years it has been demonstrated in epidemiological studies that exposures in the general environment to low levels of toxic metals may make an important contribution to the global burden of disease. Furthermore, deficient intakes of essential metals through food give rise to a considerable burden of disease from a global perspective. There is an obvious need for preventive action to decrease this global burden of disease. It is also important to address current concerns for possible increases of metal exposures. This chapter highlights such concerns in relation to the current status of the scientific understanding of the metals included and discussed fully in the relevant chapters of this Handbook. Furthermore, it draws attention to future directions for generating new knowledge to fill gaps in the continued quest to assemble the knowledge base necessary for the protection of human health from adverse consequences related to exposure to metals.
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| 7. |
- Nordberg, Gunnar, et al.
(författare)
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Preface
- 2015. - 4
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Ingår i: Handbook on the toxicology of metals. - : Elsevier. - 9780123973399 - 9780444594532 ; , s. v-vi
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Bokkapitel (refereegranskat)
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| 8. |
- Nordberg, Gunnar, et al.
(författare)
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Risk assessment of effects of cadmium on human health (IUPAC Technical Report)
- 2018
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Ingår i: Pure and Applied Chemistry. - : Walter de Gruyter GmbH. - 0033-4545 .- 1365-3075. ; 90:4, s. 755-808
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Tidskriftsartikel (refereegranskat)abstract
- Chemistry and Human Health, Division VII of the International Union on Pure and Applied Chemistry (IUPAC), provides guidance on risk assessment methodology and, as appropriate, assessment of risks to human health from chemicals of exceptional toxicity. The aim of this document is to describe dose-response relationships for the health effects of low-level exposure to cadmium, in particular, with an emphasis on causation. The term "cadmium" in this document includes all chemical species of cadmium, as well as those in cadmium compounds. Diet is the main source of cadmium exposure in the general population. Smokers and workers in cadmium industries have additional exposure. Adverse effects have been shown in populations with high industrial or environmental exposures. Epidemiological studies in general populations have also reported statistically significant associations with a number of adverse health effects at low exposures. Cadmium is recognized as a human carcinogen, a classification mainly based on occupational studies of lung cancer. Other cancers have been reported, but dose-response relationships cannot be defined. Cardiovascular disease has been associated with cadmium exposure in recent epidemiological studies, but more evidence is needed in order to establish causality. Adequate evidence of dose-response relationships is available for kidney effects. There is a relationship between cadmium exposure and kidney effects in terms of low molecular mass (LMM) proteinuria. Long-term cadmium exposures with urine cadmium of 2 nmol mmol(-1) creatinine cause such effects in a susceptible part of the population. Higher exposures result in increases in the size of these effects. This assessment is supported by toxicokinetic and toxicodynamic (TKTD) modelling. Associations between urine cadmium lower than 2 nmol mmol-1 creatinine and LMM proteinuria are influenced by confounding by co-excretion of cadmium with protein. A number of epidemiological studies, including some on low exposures, have reported statistically significant associations between cadmium exposure and bone demineralization and fracture risk. Exposures leading to urine cadmium of 5 nmol mmol-1 creatinine and more increase the risk of bone effects. Similar associations at much lower urine cadmium levels have been reported. However, complexities in the cause and effect relationship mean that a no-effect level cannot be defined. LMM proteinuria was selected as the critical effect for cadmium, thus identifying the kidney cortex as the critical organ, although bone effects may occur at exposure levels similar to those giving rise to kidney effects. To avoid these effects, population exposures should not exceed that resulting in cadmium values in urine of more than 2 nmol mmol(-1) creatinine. As cadmium is carcinogenic, a 'safe' exposure level cannot be defined. We therefore recommend that cadmium exposures be kept as low as possible. Because the safety margin for toxic effects in kidney and bone is small, or non-existent, in many populations around the world, there is a need to reduce cadmium pollution globally.
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| 9. |
- Nordberg, Monica, et al.
(författare)
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Trace element research-historical and future aspects
- 2016
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Ingår i: Journal of Trace Elements in Medicine and Biology. - : Elsevier BV. - 0946-672X .- 1878-3252. ; 38, s. 46-52
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Tidskriftsartikel (refereegranskat)abstract
- During the last 30 years the International Society for Trace Element Research and the Nordic Trace Element Society has been active . During this period the importance of these elements for human diseases has been increasingly recognized, including their contribution to the global burden of disease. New analytical methods allow biomonitoring data to be related to health outcome. Future research using modern chemical methods will focus more on elemental speciation and on measuring lower concentrations leading to further identifying adverse effects and critical organs. Extensive knowledge about essentiality and toxicity of trace elements in humans has emerged during the last two decades and at present the difficulties in defining a range of acceptable oral intakes for essential elements has largely been overcome. Biological monitoring of trace element concentrations in various media such as blood or urine is of great importance and an overview is given. As an example, a more detailed description of biological monitoring of cadmium is given, explaining biokinetics including the role of metallothionein in modifying kinetics and toxicity. Finally future challenges related to risk assessment of newly developed metallic nanomaterials and metal containing medical devices are discussed.
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| 10. |
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