umu.sePublications
Change search
Link to record
Permanent link

Direct link
BETA
Nordberg, Gunnar
Alternative names
Publications (10 of 61) Show all publications
Andersson, M., Backman, H., Nordberg, G., Hagenbjörk, A., Hedman, L., Eriksson, K., . . . Rönmark, E. (2018). Early life swimming pool exposure and asthma onset in children: a case-control study. Environmental health, 17, Article ID 34.
Open this publication in new window or tab >>Early life swimming pool exposure and asthma onset in children: a case-control study
Show others...
2018 (English)In: Environmental health, ISSN 1476-069X, E-ISSN 1476-069X, Vol. 17, article id 34Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Trichloramine exposure in indoor swimming pools has been suggested to cause asthma in children. We aimed to investigate the risk of asthma onset among children in relation to individual trichloramine exposure.

METHODS: A longitudinal nested case-control study of 337 children with asthma (cases) and 633 controls aged 16-17 years was performed within a population-based cohort from The Obstructive Lung Disease in Northern Sweden studies (OLIN). Year of asthma onset and exposure time at different ages were obtained in telephone interviews. Trichloramine concentrations in the pool buildings were measured. Skin prick test results for inhalant allergens were available from previous examinations of the cohort. The risk for asthma was analyzed in relation to the cumulative trichloramine exposure before onset of asthma.

RESULTS: Swimming pool exposure in early life was associated with a significantly higher risk of pre-school asthma onset. A dose-response relationship between swimming pool exposure and asthma was indicated in children with asthma onset at 1 year of age. Children who were both sensitized and exposed had a particularly high risk.

CONCLUSIONS: Early life exposure to chlorinated swimming pool environments was associated with pre-school asthma onset.

Place, publisher, year, edition, pages
BioMed Central, 2018
Keywords
Asthma, Children, Swimming, Trichloramine
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-146654 (URN)10.1186/s12940-018-0383-0 (DOI)000429733700001 ()29642932 (PubMedID)
Available from: 2018-04-16 Created: 2018-04-16 Last updated: 2018-06-09Bibliographically approved
Nordberg, G. & Fowler, B. (2018). Risk Assessment for Human Metal Exposures:: Mode of Action and Kinetic Approaches. Academic Press
Open this publication in new window or tab >>Risk Assessment for Human Metal Exposures:: Mode of Action and Kinetic Approaches
2018 (English)Book (Other academic)
Abstract [en]

Description

Risk Assessment for Human Metal Exposures: Mode of Action and Kinetic Approaches examines the current principles of risk assessment in human metal exposures, with a focus on Mode of Action(MOA), Toxicokinetic and Toxicodynamic (TKTD) considerations, and computer models. Derived from the highly respected Handbook on the Toxicology of Metals, Fourth Edition(2014), the book summarizes principles and methods and provides examples of how MOA –TKTD can be used. In addition, it presents tactics on how information generated by such methods can be confirmed by epidemiological data. Furthermore, it demonstrates how epidemiological data can be confirmed and evaluated by the examined models and considerations.

This resource uniquely integrates several important topics, such as risk assessment, characterization, management and communication—the classic risk assessment paradigm—with mode of action, TKTD, and epidemiology, all topics related to human exposure. Written by pioneers in the field, this book is an essential reference for researchers, students and technicians in toxicology and risk assessment.

Key Features

  • Covers fundamental risk assessment concerns for the effects of metals on human health
  • Provides an easy-to-use structure to quickly locate specific methods
  • Uses case studies to illustrate the methods and theories described
  • Written to be understood by students, researchers and industry workers who need to conduct risk assessment in metals and human health
Place, publisher, year, edition, pages
Academic Press, 2018. p. 348
Identifiers
urn:nbn:se:umu:diva-156704 (URN)9780128042274 (ISBN)
Available from: 2019-02-25 Created: 2019-02-25 Last updated: 2019-02-25
Nordberg, G., Bernard, A., Diamond, G. L., Duffus, J. H., Illing, P., Nordberg, M., . . . Skerfving, S. (2018). Risk assessment of effects of cadmium on human health (IUPAC Technical Report). Pure and Applied Chemistry, 90(4), 755-808
Open this publication in new window or tab >>Risk assessment of effects of cadmium on human health (IUPAC Technical Report)
Show others...
2018 (English)In: Pure and Applied Chemistry, ISSN 0033-4545, E-ISSN 1365-3075, Vol. 90, no 4, p. 755-808Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
Walter de Gruyter GmbH, 2018
Keywords
biomarkers, cadmium, cancer, exposure, hazard assessment, kidney, risk assessment, skeleton, xicokinetics, urine, NCKER L, 1975, JOURNAL OF REPRODUCTION AND FERTILITY, V44, P461
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-148635 (URN)10.1515/pac-2016-0910 (DOI)000428802600015 ()
Available from: 2018-06-26 Created: 2018-06-26 Last updated: 2019-02-25Bibliographically approved
Chen, X., Wang, Z., Zhu, G., Nordberg, G. F., Jin, T. & Ding, X. (2018). The association between cumulative cadmium intake and osteoporosis and risk of fracture in a Chinese population. Journal of Exposure Science and Environmental Epidemiology
Open this publication in new window or tab >>The association between cumulative cadmium intake and osteoporosis and risk of fracture in a Chinese population
Show others...
2018 (English)In: Journal of Exposure Science and Environmental Epidemiology, ISSN 1559-0631, E-ISSN 1559-064XArticle in journal (Refereed) Epub ahead of print
Abstract [en]

Bone is one of the target organs for cadmium toxicity. However, few studies have shown the association between cumulative cadmium intake and prevalence of osteoporosis and bone fracture. In the present study, we evaluated the association between cumulative cadmium intake and osteoporosis and risk of fracture in a Chinese population. A total of 790 subjects (488 women and 302 men) living in a control area and two cadmium-polluted areas were included. The cumulative cadmium intake was estimated by a food survey. The bone mineral density was determined by using single-photon absorptiometry. The cumulative cadmium intakes were 0.48, 2.14, and 11.00 g for men, and 0.42, 2.11, and 11.12 g in women in control, and moderately and heavily polluted areas, respectively. In women, the odds ratios (ORs) of subjects with a cadmium intake between 2.21 and 10.63 g and >10.63 g were 1.30 (95% CI: 0.58-2.94) and 2.36 (95% CI: 1.14-5.16), compared with those with a cadmium intake < 0.58 g after adjusting to the confounders for osteoporosis. The ORs of subjects with a cadmium intake >10.63 g were 2.34 (95% CI: 1.23-4.38) for all of the women and 2.62 (95% CI: 1.02-5.58) in women ≥ 60 years old, compared with those with a cadmium intake <10.63 g after adjusting to the confounders for bone fractures. In men, similar trends were observed, but no statistical significance was found. In addition, those subjects with renal tubular dysfunction showed high risk of bone fracture. Our results indicate that a high level of cumulative cadmium intake is associated with an increased rate of osteoporosis and fractures among women.

Place, publisher, year, edition, pages
Springer, 2018
Keywords
Bone, Bone fracture, Cadmium, Cumulative intake, Osteoporosis
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-151968 (URN)10.1038/s41370-018-0057-6 (DOI)30185939 (PubMedID)
Available from: 2018-09-20 Created: 2018-09-20 Last updated: 2019-03-18
Chen, X., Zhu, G., Wang, Z., Liang, Y., Chen, B., He, P., . . . Jin, T. (2018). The association between dietary cadmium exposure and renal dysfunction - the benchmark dose estimation of reference levels: the ChinaCad study. Journal of Applied Toxicology, 38(10), 1365-1373
Open this publication in new window or tab >>The association between dietary cadmium exposure and renal dysfunction - the benchmark dose estimation of reference levels: the ChinaCad study
Show others...
2018 (English)In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 38, no 10, p. 1365-1373Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018
Keywords
benchmark dose, cadmium, dietary exposure, renal dysfunction, the 95% lower confidence limit of the benchmark dose
National Category
Pharmacology and Toxicology Food Science
Identifiers
urn:nbn:se:umu:diva-151516 (URN)10.1002/jat.3647 (DOI)000442215100009 ()29888394 (PubMedID)
Available from: 2018-09-13 Created: 2018-09-13 Last updated: 2019-03-18Bibliographically approved
Chen, X., Wang, Z., Zhu, G., Nordberg, G. F., Ding, X. & Jin, T. (2018). The association between renal tubular dysfunction and zinc level in a Chinese population environmentally exposed to cadmium. Biological Trace Element Research, 186(1), 114-121
Open this publication in new window or tab >>The association between renal tubular dysfunction and zinc level in a Chinese population environmentally exposed to cadmium
Show others...
2018 (English)In: Biological Trace Element Research, ISSN 0163-4984, E-ISSN 1559-0720, Vol. 186, no 1, p. 114-121Article in journal (Refereed) Published
Abstract [en]

Microglobulin (UBMG) were measured. The median UCd, BCd, SZn, and HZn were 2.8 and 13.6 μg/g cr, 1.3 and 12.2 μg/L, 1.31 and 1.12 mg/L, and 0.14 and 0.12 mg/g in subjects living in control and polluted areas. The UBMG level of subjects living in the polluted area was significantly higher than that of the control (0.27 vs 0.11 mg/g cr, p < 0.01). SZn, HZn, and Zn/Cd ratios were negatively correlated with UBMG (p < 0.05 or 0.01). Subjects with high SZn concentrations (≥ 1.62 mg/L) had reduced risks of elevated UBMG [(odds ratio (OR) = 0.26, 95% confidence interval (CI) 0.07-0.99)] after controlling for multiple covariates compared with those with lower zinc levels. A similar result was observed in subjects with high HZn (OR = 0.09, 95% CI 0.02-0.48). The ORs of the second, third, and fourth quartiles of Zn/Cd ratio were 0.40 (95% CI 0.19-0.84), 0.14 (95% CI 0.06-0.37), and 0.01 (95% CI 0.02-0.18) for renal dysfunction compared with those of the first quartile, respectively. For those subjects with high level of UCd, high level of SZn and HZn also had reduced risks of elevated UBMG. The results of the present study show that high zinc body burden is associated with a decrease risk of renal tubular dysfunction induced by cadmium. Zinc nutritional status should be considered in evaluating cadmium-induced renal damage.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
Cadmium, Renal dysfunction, Zinc, β2Microglobulin
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-147952 (URN)10.1007/s12011-018-1304-3 (DOI)000446972000013 ()29574673 (PubMedID)
Available from: 2018-05-23 Created: 2018-05-23 Last updated: 2018-12-13Bibliographically approved
Elinder, C.-G. & Nordberg, G. F. (2017). Re: Byber et al. in Critical Reviews in Toxicology 2016;46:191-240 [Letter to the editor]. Critical reviews in toxicology, 47(10), 904-905
Open this publication in new window or tab >>Re: Byber et al. in Critical Reviews in Toxicology 2016;46:191-240
2017 (English)In: Critical reviews in toxicology, ISSN 1040-8444, E-ISSN 1547-6898, Vol. 47, no 10, p. 904-905Article in journal, Letter (Refereed) Published
Place, publisher, year, edition, pages
Taylor & Francis, 2017
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:umu:diva-141514 (URN)10.1080/10408444.2017.1377151 (DOI)000418249900006 ()29035126 (PubMedID)
Available from: 2017-11-06 Created: 2017-11-06 Last updated: 2018-06-09Bibliographically approved
Iavicoli, I., Fontana, L. & Nordberg, G. (2016). The effects of nanoparticles on the renal system. Critical reviews in toxicology, 46(6), 490-560
Open this publication in new window or tab >>The effects of nanoparticles on the renal system
2016 (English)In: Critical reviews in toxicology, ISSN 1040-8444, E-ISSN 1547-6898, Vol. 46, no 6, p. 490-560Article, review/survey (Refereed) Published
Abstract [en]

Through a process of translocation across biological barriers, nanoparticles can reach and deposit in secondary target organs where they may induce adverse biological reactions. Therefore, a correct assessment of nanoparticle-induced adverse effects should take into account the different aspects of toxicokinetics and tissues that may be targeted by nanoparticles. For this reason, a comprehensive evaluation of renal nanotoxicity is urgently needed as kidneys are particularly susceptible to xenobiotics and renal excretion is an expected and possible elimination route of nanoparticles in living organisms. On one hand, summarizing the findings of in vitro and in vivo studies that have investigated the adverse effects of nanoparticles on the kidney, this review intends to provide a thorough insight into the nephrotoxicity of these substances. The evaluation of the in vitro studies revealed that different types of nanoparticles (carbon, metal and/or silica nanoparticles) are able to exert significant cytotoxic effects (i.e., decreased cell viability, induction of oxidative stress, mitochondrial or cytoskeleton dysfunction and cell membrane and DNA damage). On the other hand, in vivo studies demonstrated that nanoparticles exhibited an important nephrotoxic potential both at tubular (i.e., degeneration of tubular epithelial cell, cellular fragments and proteinaceous liquid in tubule lumen, renal interstitial fibrosis) and glomerular level (i.e., swollen glomeruli, changes in Bowman's space and proliferation of mesangial cells). Although the data currently available indicate that nanoparticles may adversely impact the renal system, further studies are needed in order to clarify all the potential molecular mechanisms of nephrotoxicity induced by these xenobiotics, in particular at glomerular level.

Keywords
Glomerular effects, in vitro studies, in vivo studies, kidney, nanoparticles, nanotoxicology, nephrotoxicity, tubular effects
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-121533 (URN)10.1080/10408444.2016.1181047 (DOI)000381399800002 ()27195425 (PubMedID)
Available from: 2016-06-03 Created: 2016-06-03 Last updated: 2018-06-07Bibliographically approved
Nordberg, M. & Nordberg, G. F. (2016). Trace element research-historical and future aspects. Journal of Trace Elements in Medicine and Biology, 38, 46-52
Open this publication in new window or tab >>Trace element research-historical and future aspects
2016 (English)In: Journal of Trace Elements in Medicine and Biology, ISSN 0946-672X, E-ISSN 1878-3252, Vol. 38, p. 46-52Article in journal (Refereed) Published
Abstract [en]

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.

Keywords
Toxicity, Essentiality, Biological monitoring, Biomonitoring, Cadmium, Global burden of disease, Metallothionein
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-121532 (URN)10.1016/j.jtemb.2016.04.006 (DOI)000385473600006 ()27238729 (PubMedID)
Note

Special Issue: SI

Available from: 2016-06-03 Created: 2016-06-03 Last updated: 2018-06-07Bibliographically approved
Nordberg, G. F., Nogawa, K. & Nordberg, M. (2015). Cadmium (4ed.). In: Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg (Ed.), Handbook on the toxicology of metals: Volume II: Specific metals (pp. 667-716). Academic Press
Open this publication in new window or tab >>Cadmium
2015 (English)In: Handbook on the toxicology of metals: Volume II: Specific metals / [ed] Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg, Academic Press, 2015, 4, p. 667-716Chapter in book (Refereed)
Abstract [en]

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.

Place, publisher, year, edition, pages
Academic Press, 2015 Edition: 4
Keywords
cadmium toxicokinetics, biological monitoring of Cd, biological half-life of cd, Itai-Itai disease, kidney effects of Cd, osteomalacia, osteoporosis, bone mineral density and Cd, fractures and Cd, reproductive effects, endocrine disruption, carcinogenesis of Cd, dose-response relationships, risk assessment of Cd
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-112390 (URN)10.1016/B978-0-444-59453-2.00032-9 (DOI)9780123982933 (ISBN)
Available from: 2015-12-07 Created: 2015-12-07 Last updated: 2018-06-07Bibliographically approved
Organisations

Search in DiVA

Show all publications