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Nordberg, Gunnar
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Publications (10 of 57) 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
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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
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
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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
Aggett, P., Nordberg, G. F. & Nordberg, M. (2015). Essential metals: assessing risks from dificiency and toxicity (4ed.). In: Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg (Ed.), Handbook on the toxicology of metals: Volume I: General considerations (pp. 281-297). Academic Press
Open this publication in new window or tab >>Essential metals: assessing risks from dificiency and toxicity
2015 (English)In: Handbook on the toxicology of metals: Volume I: General considerations / [ed] Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg, Academic Press, 2015, 4, p. 281-297Chapter in book (Refereed)
Abstract [en]

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.

Place, publisher, year, edition, pages
Academic Press, 2015 Edition: 4
Keywords
critical effect, critical endpoint, acceptable range of oral intake (AROI), upper level (UL), requirements for individuals, homeostatic mechanisms, bioavailability, speciation, biomarkers of deficiency, biomarkers of toxic effects
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-112398 (URN)10.1016/B978-0-444-59453-2.00014-7 (DOI)9780123982926 (ISBN)
Available from: 2015-12-07 Created: 2015-12-07 Last updated: 2018-06-07Bibliographically approved
Nordberg, G. F., Fowler, B. A. & Nordberg, M. (Eds.). (2015). Handbook on the toxicology of metals (4ed.). Academic Press
Open this publication in new window or tab >>Handbook on the toxicology of metals
2015 (English)Collection (editor) (Refereed)
Place, publisher, year, edition, pages
Academic Press, 2015. p. 1385 Edition: 4
National Category
Pharmacology and Toxicology Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-112305 (URN)9780444594532 (set) (ISBN)9780123982926 (vol. 1) (ISBN)9780123982933 (vol. 2) (ISBN)
Note

Två vol. med löpande paginering:

Vol. 1: General considerations

Vol. 2: Specific metals

Available from: 2015-12-04 Created: 2015-12-04 Last updated: 2018-06-07Bibliographically approved
Nordberg, G. F., Gerhardsson, L., Mumtaz, M. M., Ruiz, P. & Fowler, B. A. (2015). Interactions and Mixtures in Metal Toxicology (4ed.). In: Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg (Ed.), Handbook on the Toxicology of Metals: Volume I: General considerations (pp. 213-238). Academic Press
Open this publication in new window or tab >>Interactions and Mixtures in Metal Toxicology
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2015 (English)In: Handbook on the Toxicology of Metals: Volume I: General considerations / [ed] Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg, Academic Press, 2015, 4, p. 213-238Chapter in book (Refereed)
Abstract [en]

Human exposures to metals, metalloids, and their compounds frequently occur as mixtures, and hence it is important to consider the joint action of these elements in terms of both mechanisms of action and risk assessment purposes. The joint action of these elements may produce additive, synergistic/potentiating, or antagonistic effects that may be manifested as direct cellular toxicity (necrosis or apoptosis) or carcinogenicity. Dose-response relationships may be further influenced by constitutive factors such as age, sex, and the expression of specific proteins. Mechanisms of importance for the development of potentiated or antagonistic toxicity are the expression of metal-binding proteins (metallothioneins or lead-binding proteins) and interference with metal transporters such as DMT-1 and ZIP. Compared to men, women of childbearing age absorb more Cd from the gastrointestinal tract because they have lower iron stores than men. Another example of synergism that occurs in humans is the one between inorganic arsenic and cadmium in inducing kidney toxicity. In many cases, however, direct primary data on the joint action of toxic or essential elements are lacking, and so innovative derivative methods such as the binary weight-of-evidence method have been used to predict potential interactions among groups of metals and metalloids. At present, there is much to be learned about the joint action of both toxic and essential elements, and this is clearly a critical area of research.

Place, publisher, year, edition, pages
Academic Press, 2015 Edition: 4
Keywords
joint metal-metal actions, arsenic-cadmium interactions, lead-arsenic interactions, joint action of lead, cadmium and arsenic, biomarkers, porphyrins, heme biosynthetic pathway alterations, mercury-selenium interactions, molybdenum-copper interactions, cadmium-zinc interactions, lead-zinc interactions, ALA dehydratase, metallothionein induction, genetic polymorphisms, synergistic interactions, additive joint action, antagonistic interactions, metallic mixtures risk assessments, sensitive sub-populations
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-98660 (URN)10.1016/B978-0-444-59453-2.00011-1 (DOI)9780123982926 (ISBN)
Available from: 2015-01-26 Created: 2015-01-26 Last updated: 2018-06-07Bibliographically approved
Nordberg, G. F., Fowler, B. A. & Nordberg, M. (2015). Metal Exposures in Occupational and Environmental Settings. International Commission on Occupational Health Newsletter, 13(1), 12-14
Open this publication in new window or tab >>Metal Exposures in Occupational and Environmental Settings
2015 (English)In: International Commission on Occupational Health Newsletter, ISSN 1795-0260, Vol. 13, no 1, p. 12-14Article in journal (Other academic) Published
Abstract [en]

The use of metals has expanded substantially in the last century and gives rise to widespread exposure of humans. It has long been recognized that metals are important toxic agents that may cause acute and chronic poisoning in metal workers and population groups with high exposures. In recent years evidence has been presented indicating that low level exposures to metallic compounds contribute to the occurrence of several common diseases. The World Health Organization (WHO, 2009) has estimated that on a Global basis, 143,000 deaths and nearly 9 million disability-adjusted life years (DALYs; i.e. years of healthy life lost) were caused by lead exposure in 2004. Although lead exposure in the general population of many countries has decreased since 2004 because of the continued phase-out of lead in gasoline, several recent epidemiological studies support the notion that low-exposure effects of lead occur in addition to those considered by the WHO (2009). It is therefore quite possible that the present global burden of disease caused by lead exposure is the same or greater than the one estimated in 2004.

In addition to the estimates of lead-related disease and mortality, there are other well documented effects that were not included in the WHO estimates of the global burden of disease. This organization further summarized data indicating 9100 deaths and 125,000 DALYs per year in Bangladesh from arsenic in drinking water and that mercury exposure (mainly methylmercury) through fish consumption causes cognitive deficits and mild retardation in a considerable number of children. An increased incidence of myocardial infarction has been reported in populations with a high intake of methylmercury from fish and a low intake of polyunsaturated fatty acids. The public health impact of this observation of interaction between a nutritional factor and a toxic metal compound may be considerable. There is evidence for a role for relatively low occupational exposure to manganese as well as exposure in the general environment as a contributory factor to the increasing prevalence of Parkinson disease and there is a potentially great importance of metal exposure in early life as a risk factor for neurodegenerative disorders later in life. Recent epidemiological evidence indicates a role for cadmium in the general environment in increasing the occurrence of renal effects and osteoporosis, as well as cardiovascular diseases. There is no doubt thus that exposure to toxic metals and their compounds represents important causal factors contributing to the global burden of disease. Deficient dietary intake of essential metals in food in a global perspective was estimated by the WHO (2009) to cause 433,000 deaths and 15,580,000 DALYs from zinc deficiency and 273,000 deaths and 19,734,000 DALYs per year from iron deficiency.

In view of the considerable global burden of disease caused by metals there is an obvious need for preventive action.

National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-111655 (URN)
Available from: 2015-11-19 Created: 2015-11-19 Last updated: 2018-06-07Bibliographically approved
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