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  • 1. Chen, Xiao
    et al.
    Zhu, Guoying
    Wang, Zhongqiu
    Liang, Yihuai
    Chen, Bo
    He, Ping
    Nordberg, Monica
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Nordberg, Gunnar
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Ding, Xiaoqiang
    Jin, Taiyi
    The association between dietary cadmium exposure and renal dysfunction - the benchmark dose estimation of reference levels: the ChinaCad study2018In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 38, no 10, p. 1365-1373Article in journal (Refereed)
    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.

  • 2.
    Gustafsson, Åsa
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Svensson-Elfsmark, Linda
    Lorentzen, Johnny C
    Bucht, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Strain differences influence timing and magnitude of both acute and late inflammatory reactions after intratracheal instillation of an alkylating agent in rats2014In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 34, no 3, p. 272-280Article in journal (Refereed)
    Abstract [en]

    The acute pulmonary responses after exposure to sulfur and nitrogen mustards are well documented whereas the late pulmonary effects are not. With a novel focus on the immune system this paper investigate whether late phase pulmonary effects developed in rats exposed to the nitrogen mustard melphalan are linked to the acute responses and whether the reactions are genetically regulated. The DA rat strain was used to establish a lung exposure model. Five other inbred rat strains (PVG, PVG.1AV1, LEW, WF and F344) were compared within the model at selected time points. All rat strains displayed a biphasic pattern of leukocyte infiltration in the lungs, dominated by neutrophils 2days after exposure and a second peak dominated by macrophages 29days after exposure. The number of macrophages was higher in the DA rat compared with the other strains. The infiltration of lymphocytes in the lungs varied in both time of appearance and magnitude between strains. The quantity of collagen deposition in the lungs varied between strains at day 90; LEW and WF displayed high collagen content which coincided with an increased level of cytotoxic T cells. LEW further displayed an increased number of T helper cells and natural killer (NK) T cells in the lungs. The results in this study suggest there is a link between the development of lung fibrosis and high cytotoxic cell responses and that there is a genetic influence, as there are variations in acute and late adverse reactions between rat strains in both timing and magnitude.

    Copyright (c) 2013 John Wiley & Sons, Ltd.

  • 3. Li, Zhi-Hua
    et al.
    Zlabek, Vladimir
    Velisek, Josef
    Grabic, Roman
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Machova, Jana
    Randak, Tomas
    Physiological condition status and muscle-based biomarkers in rainbow trout (Oncorhynchus mykiss), after long-term exposure to carbamazepine2010In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 30, no 3, p. 197-203Article in journal (Refereed)
    Abstract [en]

    Recently, residual pharmaceuticals are generally recognized as relevant sources of aquatic environmental pollutants. However, the toxicological effects of these contaminants have not been adequately researched. In this study, the chronic toxic effects of carbamazepine (CBZ), an anticonvulsant pharmaceutical commonly present in surface and ground water, on physiological condition status and muscle-based biomarkers of rainbow trout were investigated. Fish were exposed at sublethal concentrations of CBZ (1.0 microg l(-1), 0.2 mg l(-1) and 2.0 mg l(-1)) for 42 days. Compared with the control, there was a significant lower (P < 0.05) condition factor in fish exposed at the highest concentration of CBZ (2.0 mg l(-1)), but the hepatosomatic indices in all groups were not significant changes. At lower CBZ concentration (1.0 microg l(-1), 0.2 mg l(-1)), the antioxidant enzyme activities were induced slightly, except catalase, while at the highest concentration (2.0 mg l(-1)) oxidative stress was apparent as reflected by the significant higher lipid peroxidation and protein carbonyls in the fish muscle, associated with a significant inhibition of antioxidant enzymes activities. Moreover, energy metabolic parameters (RNA-DNA ratio, Na(+)-K(+)-ATPase) were significantly inhibited in muscle of the fish exposed at the highest concentration (2.0 mg l(-1)), compared with the control. In short, CBZ-induced physiological and biochemical responses in fish were reflected in parameters measured in this study, which suggest that these biomarkers could be used as potential indicators for monitoring residual pharmaceuticals present in aquatic environment.

  • 4.
    Lin, Xialu
    et al.
    Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Shao, Wanzhen
    Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Yu, Fangfang
    Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Xing, Ke
    Xi'an Hong Hui Hospital, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Liu, Huan
    Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Zhang, Feng'e
    Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Goldring, Mary B.
    Hospital for Special Surgery, Weill Cornell Medical College, New York, NY, USA.
    Lammi, Mikko J.
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Guo, Xiong
    Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Collaborative Innovation Center of Endemic Diseases and Health Promotion in Silk Road Region, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, China.
    Individual and combined toxicity of T-2 toxin and deoxynivalenol on human C-28/I2 and rat primary chondrocytes2019In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 39, no 2, p. 343-353, article id 30251759Article in journal (Refereed)
    Abstract [en]

    Deoxynivalenol (DON) and T-2 toxin are prevalent mycotoxin contaminants in the food and feed stuffs worldwide, with non-negligible co-contamination and co-exposure conditions. Meanwhile, they are considerable risk factors for Kashin-Beck disease, a chronic endemic osteochondropathy. The aim of this study was to investigate the individual and combined cytotoxicity of DON and T-2 toxin on proliferating human C-28/I2 and newborn rat primary costal chondrocytes by MTT assay. Four molar concentration combination ratios of DON and T-2 toxin were used, 1:1 for R1 mixture, 10:1 for R10, 100:1 for R100 and 1000:1 for R1000. The toxicological interactions were quantified by the MixLow method. DON, T-2 toxin, and their mixtures all showed a clear dose-dependent toxicity for chondrocytes. The cytotoxicity of T-2 toxin was 285-fold higher than DON was in human chondrocytes, and 22-fold higher in the rat chondrocytes. The combination of DON and T-2 toxin was significantly synergistic at middle and high level concentrations of R10 mixtures in rat chondrocytes, but significantly antagonistic at the low concentrations of R100 mixtures in both cells and at the middle concentrations of R1000 mixtures in rat chondrocytes. These results indicated that the combined toxicity was influenced by the cell sensitivity for toxins, the difference between the combination ratio and equitoxic ratio, the concentrations and other factors.

  • 5.
    Rankin, Gregory D.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Wingfors, Håkan
    Swedish Defence Research Agency, CBRN Defence and Security, Umeå, Sweden..
    Uski, Oskari
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Hedman, Linnéa
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Department of Health Sciences, Division of Nursing, Luleå University of Technology, Luleå, Sweden..
    Ekstrand-Hammarström, Barbro
    Swedish Defence Research Agency, CBRN Defence and Security, Umeå, Sweden..
    Bosson, Jenny
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lundbäck, Magnus
    Karolinska Institutet, Department of Clinical Sciences, Division of Cardiology, Danderyd University Hospital, Stockholm, Sweden..
    The toxic potential of a fourth-generation E-cigarette on human lung cell lines and tissue explants2019In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 39, no 8, p. 1143-1154Article in journal (Refereed)
    Abstract [en]

    The use of electronic cigarettes (E‐cigs) is rapidly increasing. The latest generation of E‐cigs is highly customizable, allowing for high heating coil temperatures. The aim of this study was to assess the toxic potential of a fourth‐generation E‐cig. Aerosols generated from E‐liquid with (24 mg/mL) and without nicotine, using a fourth‐generation E‐cig, were chemically analysed and compared with cigarette smoke (K3R4F). Human lung epithelial cell lines and distal lung tissue explants were exposed to E‐cig vapour extract (EVE) and cigarette smoke extract for 24 hours and assessed for viability, inflammation, oxidative stress and genotoxicity. E‐cig aerosols contained measurable levels of volatile organic compounds, aldehydes and polycyclic aromatic hydrocarbons, in general, to a much lesser extent than cigarette smoke. Higher levels of certain carbonyls, e.g. formaldehyde, were detected in the E‐cig aerosols. EVEs decreased cell viability of BEAS‐2B cells, whereas little effect was seen in A549 cells and distal lung tissue. The nicotine‐containing EVE caused a greater decrease in cell viability and significant increase in DNA damage than the nicotine‐free EVE. Increased cytotoxicity, reactive oxygen species production and genotoxicity were seen with cells and tissue exposed to cigarette smoke extract compared with EVEs. Although E‐cig aerosols were less toxic than cigarette smoke, it was not benign. Moreover, the EVE containing nicotine was more toxic than the nicotine‐free EVE. More research is needed on the short‐ and long‐term health effects of vaping and the usage of newly emerging E‐cig devices to evaluate better the potential negative effects of E‐cigs on human health.

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