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  • 51.
    Nordberg, Gunnar F
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Jin, Taiyi
    Wu, Xunwei
    Lu, Jian
    Chen, Liang
    Lei, Lijian
    Hong, Feng
    Nordberg, Monica
    Prevalence of kidney dysfunction in humans - relationship to cadmium dose, metallothionein, immunological and metabolic factors.2009In: Biochimie, ISSN 1638-6183, Vol. 91, no 10, p. 1282-5Article in journal (Refereed)
    Abstract [en]

    Long term cadmium (Cd) exposure in occupational and general environments may give rise to kidney dysfunction. This effect is usually considered to be the critical effect, i. e. the effect that occurs at relatively low level of exposure. The present review focused on studies of the prevalence of cadmium-related kidney dysfunction among population groups residing in cadmium contaminated areas in China. Dose-response relationships were shown between UCd and the prevalence of increased levels of biomarkers in urine of renal tubular dysfunction such as urinary beta-2-microglobulin or N-acetyl-beta-d-glucosaminidase - NAG or urinary albumin, a biomarker of glomerular kidney dysfunction. Factors that influence these dose-response relationships include: 1) Metallothionein mRNA levels in peripheral blood lymphocytes, used as a biomarker of the ability of each person, to synthesize metallothionein (a protein known to provide intracellular protection against cadmium toxicity). 2) The occurrence of increased levels in blood plasma of autoantibodies against metallothionein. 3) Concomitant changes in glucose metabolism i e Type II diabetes. 4) Concomitant exposure to other nephrotoxic agents such as inorganic arsenic. Increased susceptibility in diabetics has been shown also in population groups in Europe. In persons with type II diabetes and increased levels of autoantibodies against metallothionein in blood plasma or in persons with concomitant exposure to environmental inorganic arsenic, indications of Cd-related kidney dysfunction was observed at UCd levels around 1 microg/g creatinine, levels found among "unexposed" population groups in many countries.

  • 52.
    Nordberg, Gunnar F
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Kido, Teruhiko
    Roels, Harry A
    Cadmium-induced renal effects2008In: Clinical Nephrotoxins: Renal Injury from Drugs and Chemicals / [ed] Marc E. De Broe, George A. Porter, William M. Bennett, Gilbert Deray, Springer, 2008, , p. 785-810p. 785-810Chapter in book (Other academic)
  • 53.
    Nordberg, Gunnar F
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lundström, Nils-Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hagenbjörk-Gustafsson, Annika
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lagerkvist, Birgitta J-Son
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nilsson, Johan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Svensson, Mona
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Nilsson, Leif
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Umeå University, Faculty of Science and Technology, Department of Mathematics and Mathematical Statistics.
    Bernard, Alfred
    Dumont, Xavier
    Bertilsson, Helen
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Eriksson, Kåre
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lung function in volunteers before and after exposure to trichloramine in indoor pool environments and asthma in a cohort of pool workers2012In: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 2, no 5, p. e000973-Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Exposure to trichloramine (NCl(3)) in indoor swimming-pool environments is known to cause mucous membrane irritation, but if it gives rise to changes in lung function or asthma in adults is not known. (1) We determined lung function in volunteers before and after exposure to indoor pool environments. (2) We studied the occurrence of respiratory symptoms and asthma in a cohort of pool workers.

    DESIGN/METHODS/PARTICIPANTS: (1) We studied two groups of volunteers, 37 previously non-exposed healthy persons and 14 pool workers, who performed exercise for 2 h in an indoor pool environment. NCl(3) in air was measured during pool exposures and in 10 other pool environments. Filtered air exposures were used as controls. Lung function and biomarkers of pulmonary epithelial integrity were measured before and after exposure. (2) We mailed a questionnaire to 1741 persons who indicated in the Swedish census 1990 that they worked at indoor swimming-pools.

    RESULTS: (1) In previously non-exposed volunteers, statistically significant decreases in FEV(1) (forced expiratory volume) and FEV(%) (p=0.01 and 0.05, respectively) were found after exposure to pool air (0.23 mg/m(3) of NCl(3)). In pool workers, a statistically significant decrease in FEV(%) (p=0.003) was seen (but no significant change of FEV(1))(.) In the 10 other pool environments the median NCl(3) concentration was 0.18 mg/m(3). (2) Our nested case/control study in pool workers found an OR for asthma of 2.31 (95% CI 0.79 to 6.74) among those with the highest exposure. Exposure-related acute mucous membrane and respiratory symptoms were also found.

    CONCLUSIONS: This is the first study in adults showing statistically significant decreases in lung function after exposure to NCl(3). An increased OR for asthma among highly exposed pool workers did not reach statistical significance, but the combined evidence supports the notion that current workroom exposures may contribute to asthma development. Further research on sensitive groups is warranted.

  • 54.
    Nordberg, Gunnar F.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Environmental Medicine.
    Nogawa, Koji
    Friberg, Lars T.
    Nordberg, Monica
    Cadmium2007In: Handbook on the Toxicology of Metals, 3rd Edition / [ed] Gunnar F. Nordberg, Bruce A. Fowler, Monica Nordberg and Lars T. Friberg, San Diego: Elsevier, 2007, 3, p. 445-486Chapter in book (Other academic)
    Abstract [en]

    Cadmium (Cd) is chemically similar to zinc; it 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, electroplated onto steel, and Cd compounds are used as pigments, often in plastics. Cadmium and its compounds are also used in electric batteries, electronic components, and nuclear reactors. Because some of the applications of Cd can be performed by other less-toxic materials, the use of Cd has, therefore, been restricted by law in some countries. The absorption of Cd compounds through the skin is negligible. Between 10 and 50% of inhaled Cd will be absorbed, with the degree of absorption being greater for smaller particles and fumes than for larger dust particles. Humans absorb 5-10% of ingested Cd. A low intake of calcium, zinc, or iron increases the degree of absorption; for example, in iron-deficient individuals, the gastrointestinal absorption rate may be as high as 20%. Cadmium is transported in plasma when bound to metallothionein-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) having been reported for Cd in muscle, kidney, and liver tissue. Cadmium stimulates metallothionein production in the same manner as other bivalent metals, such as zinc, copper, and mercury. Metallothionein-bound Cd in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released after lysosomal degradation of the protein. The unbound Cd stimulates the production of new metallothionein, which binds the Cd in the renal tubular cells. When not all of this new Cd is bound, toxic effects occur, possibly because of the interference of Cd with zinc-dependent enzymes and/or membrane function. The average amount of Cd ingested in most European and North American countries is approximately 1020 mu g/day. The corresponding average urinary excretion is approximately 0.5-1.0 mu g/day. Most of the Cd in blood is located in the cells. The average blood concentration is approximately 0.5-1.0 mu g/L in nonsmokers; it is twice as high in smokers because of Cd absorption from cigarette smoke. Concentrations of 10-20 mu g/kg are usually found in the kidney cortex of nonsmokers in European countries. Although the intake of Cd through food has been higher in Japan than in Europe, and the reported tissue levels are correspondingly higher, the food intake of Cd has decreased in Japan during the last few decades. Ingestion of highly contaminated food or drink results in acute gastrointestinal effects with concomitant diarrhea and vomiting. 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 lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction. The first sign of damage is a low-molecular-weight proteinuria. This condition is the critical effect of such exposure to Cd and is used in quantitative risk assessment. 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 Cd-polluted areas of Japan; 124 cases were diagnosed up to 1970, and decreasing numbers of clinical cases have been diagnosed later, with 66 cases during the period between 1970 and 2006. In animals exposed to Cd through injection, inhalation, or oral exposure, cancer may develop at the injection site, in the lungs and prostate, or in other organs. Although some epidemiological studies have found an increase in the rates of cancer of the lungs and prostate, other studies have not demonstrated such effects. Cadmium is classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer. Exposure to Cd in the air at concentrations of 5-10 mu g/m(3) during a working life of 45 years may give rise to renal tubular dysfunction in a small proportion of exposed workers. At approximately 100 mu g/m(3), signs of chronic obstructive lung disease may develop even after exposure for a shorter duration. After a lifetime of exposure from food at an average intake of approximately 200 mu g/day, renal effects have been observed at age 50. There is considerable individual variation in the sensitivity of these renal effects. It has been suggested that such effects can be avoided if renal cortex levels are kept <50 mu g/kg and urine levels <2.5 mu g/g CR. Recent reports of low, but statistically significant, increases at even lower levels of urinary Cd are, however, noteworthy. Such increases are observed in the general population, particularly among people with diabetes. 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 in the kidneys, which are the critical organs and the irreversibility of the critical effect, primary prevention is essential. Prevention can be assisted through environmental and biological monitoring. The extensive literature on the toxicological and environmental aspects of Cd has been reviewed in detail by Friberg et al. (1974, 1985, 1986a), Tsuchiya (1978), Nriagu (1980, 1981), the WHO/IPCS (1992), the IARC (1993), Jarup et al. (1998c), the ATSDR (1999), Nordberg and Nordberg (2002), the EU (2003), Satarug and Moore (2004), and the WHO/FAO (2003, 2005).

  • 55.
    Nordberg, Gunnar F
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nogawa, Koji
    Nordberg, Monica
    Cadmium2015In: 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.

  • 56.
    Nordberg, Gunnar
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Jin, Taiyi
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Wu, Xunwei
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lu, Jian
    Chen, Liang
    Liang, Yihuai
    Lei, Lijian
    Hong, Feng
    Bergdahl, Ingvar A.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nordberg, Monica
    Kidney dysfunction and cadmium exposure: Factors influencing dose-response relationships2012In: Journal of Trace Elements in Medicine and Biology, ISSN 0946-672X, E-ISSN 1878-3252, Vol. 26, no 2-3, p. 197-200Article in journal (Refereed)
    Abstract [en]

    Our early toxicological studies showed that metallothionein (MT) is a protein that carries cadmium (Cd) to the kidney, explaining why Cd exposures during long time periods may give rise to kidney dysfunction. This dysfunction is usually considered to be the critical effect, i.e. the adverse effect that occurs at the lowest exposure level. MT also provides intracellular protection against cadmium toxicity. In studies of population groups in cadmium contaminated areas in China, we investigated factors that affected the relationship between internal dose of Cd, as indicated by blood Cd (BCd) or urinary Cd (UCd), and the prevalence of kidney dysfunction. We found dose-response relationships between UCd and the prevalence of increased levels of biomarkers of renal tubular dysfunction (urinary beta-2-microglobulin, B2M, or N-acetyl-beta-D-glucosaminidase - NAG) or urinary albumin (UAlb), a biomarker of glomerular kidney dysfunction. Two years after Cd intake from contaminated rice was diminished, renal tubular dysfunction appeared unchanged or aggravated among those with higher UCd; Another 8 years later, i.e. 10 years after Cd intake was decreased, the prevalence of renal tubular dysfunction was still increased but UAlb had returned to normal. Factors that influenced the dose-response relationships were: (1) time after maximum exposure. (2) Concomitant exposure to other nephrotoxic agents such as inorganic arsenic. (3) Cd induced metallothionein mRNA levels in peripheral blood lymphocytes, used as a biomarker of the ability of each person, to synthesize MT. (4) The occurrence of increased levels in blood plasma of autoantibodies against MT. The two last points further support a role in humans of MT as a protective protein against tissue damage from cadmium and gives support to previous ideas developed partly in experimental systems.

  • 57.
    Nordberg, Gunnar
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lundström, Nils-Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hälsoeffekter av svaveldioxid: en litteraturstudie med betoning på de senaste årens publikationer2009Report (Other academic)
    Abstract [sv]

    Föreliggande rapport sammanfattar WHO:s senaste riktlinjer (WHO 2006) för luftkvalitet.Vidare redovisas en litteraturstudie rörande publikationer under de senaste åren angåendeexponering för SO2 och olika hälsoeffekter särskilt astma.

    Bakgrunden till rapporten är det beslut angående Boliden AB´s verksamhet vidRönnskärsverken som träffades i Koncessionsnämnden 1998 06 16. I det kontrollprogramsom föreskrevs av Koncessionsnämnden skall ingå undersökningar hur korttidsvärden avsvaveldioxid varierar samt en karaktärisering av stoftutsläpp från verksamheten.

    Utförda mätningar av SO2 under slutet av 1990-talet och början av 2000-talet innebär intenågot överskridande av gällande miljökvalitetsnorm. Eftersom denna norm bygger på tidigarepublicerad vetenskaplig litteratur är det angeläget att undersöka om nyare studier geranledning till större restriktivitet angående utsläpp av SO2.

    WHO har uppdaterat sina riktlinjer för luftkvalitet (WHO 2006). Enligt de nya riktlinjernarekommenderas gräns för luftföroreningar (SO2) till 20 μg/m3 som 24 timmars medelvärdeoch 500 μg/m3 som tio minuters medelvärde.

    Det är väl känt sedan tidigare att det finns ett samband mellan astmasymtom och exponeringför SO2 i luftföroreningar. Det har dock rått oklarhet om SO2 kan förorsaka astma eller om detär så att astmaanfall utlöses av förhöjda SO2 nivåer i luften hos personer som fått astma avandra anledningar.

    En rad epidemiologiska studier, som delvis omnämns i föreliggande rapport, har visat påsamband mellan korttidshalter av SO2 och andra luftföroreningar och sjukhusinläggningar.

    Den genomförda litteraturgenomgången visar att ett avsevärt antal studier finns publiceradeunder de senaste åren angående luftföroreningar, särskilt SO2 och astma. Det framgår i mångaav dessa studier att en ökning av astmasymtom har relaterats till ökande halter avluftföroreningar i städer. Vilken roll olika luftföroreningskomponenter spelar för uppkomstenav symtom framgår dock inte klart i de publicerade studierna.

    WHO 2006 rekommenderade en riktlinje på 20 μg/m3 som dygnsmedelvärde för SO2 och destudier som publicerats 2006-2009 ger ytterligare stöd för denna uppfattning.

  • 58. Nordberg, M
    et al.
    Nordberg, G.F.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    "Metallothioneins and Related Chelators", in Vol. 5 of 'Metal Ions in Life Sciences2009In: "Metallothioneins and Related Chelators", in Vol. 5 of 'Metal Ions in Life Sciences' / [ed] A. Sigel, H. Sigel, R. K. O. Sigel, Eds.; The Royal Society of Chemistry, Cambridge, UK, 2009, p. 1-29Chapter in book (Other (popular science, discussion, etc.))
  • 59. Nordberg, Monica
    et al.
    Nordberg, Gunnar F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Toxicology and biological monitoring of metals2009In: General and Applied Toxicology: volume 6, part thirteen: Toxicology of specific groups of substances / [ed] Bryan Ballantyne, Timothy C. Marrs and Tore Syversen, Wiley , 2009, 3Chapter in book (Other academic)
    Abstract [en]

    There are 67 elements classified as metals and the present chapter presents a review of the toxicology and evidence for useful biological monitoring of 29 of these elements and their various chemical compounds. Introductory sections of the chapter deals with general aspects of metal toxicology. Emphasis is given to the fundamental importance of speciation of metals. The chemical species is defined as the specific form of an element defined as to isotopic composition, electronic or oxidation state and /or complex or molecular structure. Consideration of specific chemical species is of fundamental importance in toxicology and biological monitoring. Advances in chemical analytical methods has made it possible in recent years to use biological monitoring i.e., repeated measurements of metallic compounds in tissues or biological fluids in order to evaluate occupational or environmental exposures and health risks. For all the elements dealt with in this chapter the importance of chemical species is considered when reviewing the uptake, metabolism and excretion; toxic effects and dose-response relationships; carcinogenicity; genotoxicity as well as biological monitoring. The following metals and their compounds are covered in the present chapter: Aluminium, Antimony, Arsenic, Barium, Beryllium, Bismuth, Cadmium, Chromium, Cobalt, Copper, Gallium and Semiconductor compounds, Germanium, Indium, Iron, Lead, Manganese, Mercury, Molybdenum, Nickel, Palladium, Platinum, Selenium, Silver, Tellurium, Thallium, Tin, Titanium, Tungsten and Zinc.

  • 60. Nordberg, Monica
    et al.
    Nordberg, Gunnar F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Trace element research-historical and future aspects2016In: Journal of Trace Elements in Medicine and Biology, ISSN 0946-672X, E-ISSN 1878-3252, Vol. 38, p. 46-52Article in journal (Refereed)
    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.

  • 61. Wu, Xunwei
    et al.
    Liang, Yihuai
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Jin, Taiyi
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Ye, Tingting
    Kong, Qinghu
    Wang, Zaijuan
    Lei, Lijian
    Bergdahl, Ingvar A
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Nordberg, Gunnar F
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Renal effects evolution in a Chinese population after reduction of cadmium exposure in rice.2008In: Environmental research, ISSN 1096-0953, Vol. 108, no 2, p. 233-8Article in journal (Refereed)
    Abstract [en]

    Cadmium is a well-known nephrotoxic agent with extremely long biological half-time of 10-30 years in human. To investigate the evolution of cadmium-induced renal effects in the population, a number of 148 residents who lived in cadmium-polluted area were followed-up for 3 years after the reduction of cadmium exposure in rice. Urinary cadmium (UCd), beta(2)-microglobulin (B2M) and albumin (ALB) were analyzed in 1995 and 1998, respectively. The results demonstrated that the changes of renal effects of residents depended on the levels of UCd before inflow of cadmium to human body declined. In cases where UCd were less than 10 microg/g creatinine in 1995, evidence was found indicating significant decreases in proteinuria (i.e., B2M and ALB) 3 years later, whereas, in cases where the excretion of UCd exceeded 10 microg/g creatinine in 1995, progression was observed. The study of dose-response relationships between UCd and B2M or ALB also showed that the cadmium-induced renal dysfunction might be reversible if UCd concentration was low-level before exposure decreasing, otherwise it might be irreversible or aggravated.

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