Wet detoxification has traditionally been seen as the most promising technology for treating chromium-contaminated sites. However, the addition of chemicals in the wet detoxification process not only increases the cost but also introduces extra pollutants. Moreover, the chromium-containing slag may be re-dissolved in the form of Cr(VI), and the increased concentration of Cr(VI) results in a serious "returning to yellow" phenomenon in the chromium-contaminated sites, causing undesirable secondary pollution. Microbial remediation is a promising technology to address the re-dissolution of chromium-containing slag after wet detoxification, and this article reviews the advances in this area. Firstly, the toxicity, current situation and conventional technologies for treating the chromium-containing slag were briefly summarized. The mechanisms of the inevitable re-dissolution of chromium-containing slag after wet detoxification were summarized. Three main mechanisms, namely bioreduction, biosorption and biomineralization, which are involved in the environmental-friendly and efficient microbial remediation technology, were reviewed. The variation of microbial species and the succession of microbial community during the bioremediation of chromium-contaminated sites were discussed. Finally, future research directions were prospected with the aim to develop long-term, stable and sustainable technologies for remediating the chromium-contaminated sites.
Biodegradation, Environmental ; Chromium/toxicity* ; Environmental Pollutants/toxicity*

OBJECTIVEThis paper aims to elucidate the combined toxicity of magnetite nanoparticles/Chromium [MNPs/Cr(VI)] adducts.

METHODSThe HEK293 cell was exposed to either Cr(VI) or MNPs, or their adducts MNPs/Cr(VI). The cytotoxicity was evaluated by assessing the cell viability, apoptosis, oxidative stress induction, and cellular uptake.

RESULTSThe toxicity of formed adducts is significantly reduced when compared to Cr(VI) anions. We found that the cellular uptake of MNPs/Cr(VI) adduct was rare, only few particles were endocytosed from the extracellular fluid and not accumulated in the cell nucleus. On the other hand, the Cr(VI) anions entered cells, generated oxidative stress, induced cell apoptosis, and caused cytotoxicity.

CONCLUSIONThe results showed minor effects of the nanoadducts on the tested cells and supported that magnetite nanoparticles could be implemented in the wastewater treatment process in which advantageous properties outweigh the risks.

Chromium ; chemistry ; toxicity ; Environmental Restoration and Remediation ; methods ; Ferrosoferric Oxide ; chemistry ; toxicity ; HEK293 Cells ; Humans ; Metal Nanoparticles ; chemistry ; toxicity

Cobalt or chromium alloys are the most common clinical materials of prosthesis and there have been some investigators at home and abroad have done related researches about the genotoxic effects of cobalt and chromium ions and nanoparticles. People have certain understanding about the mechanism of production of ions as well as their influence on cells. However, chromium or cobalt nanoparticles genotoxicity related research is still in its preliminary stage. In each stage, the mechanisms, from creating of the particles, through entering cells, until finally causing genotoxic, are still contained many problems to be solved. This article reviews the research progress in mechanisms of production and genotoxic effects of cobalt, chromium ions and nanoparticles.
Chromium ; toxicity ; Cobalt ; toxicity ; DNA Damage ; Humans ; Ions ; Nanoparticles ; toxicity ; Prostheses and Implants

OBJECTIVETo reveal the role of poly-ADP-ribosylation and DNA methylation in carcinogenic process induced induced by Cr (VI), and to discuss the relations between them.

METHODSThe pre-established Poly (ADP-ribose) glycohydrolase (PARG) deficient cells and 16HBE cells were treated with different concentrations of Cr (VI), and the changes of total genomic DNA methylation level in different groups were detected by methylation immunofluorescent detection, as well as the changes of the activity of methyltransferases. Moreover, RT-PCR and western blotting method were applied to analyze the changes of expression of DNMT1, DNMT3a, DNMT3b and MBD2, upon the protein level.

RESULTSAfter treated by Cr(VI) for 24 h, the healthy 16HBE cells showed a significant lower level of genomic DNA methylation; however, there was no significant changes (P > 0.05) found in PARG deficient cells by immunofluorescence assay. When the dose of Cr (VI) reached 5.0 µmol/L, the activity of methyltransferases in 16HBE cells and PARG deficient cells (49.33 ± 2.65, 80.05 ± 2.05) decreased by 20% and 50% comparing with contrast group (99.27 ± 1.10, 99.30 ± 0.60) . After treated by Cr (VI) for 24 h, the expression of mRNA and protein level among DNMT1, DNMT3a, DNMT3b and MBD2 decreased significantly in healthy 16HBE cells; and the expression of DNMT1 and DNMT3a decreased in PARG deficiency cells. The relevant expression levels of mRNA of DNMT1 were separately (0.99 ± 0.09), (0.79 ± 0.10), (0.59 ± 0.13) and (0.39 ± 0.02) (F = 247.17, P < 0.01), the expression levels of protein were separately (1.00 ± 0.03), (0.69 ± 0.15), (0.65 ± 0.10) and (0.55 ± 0.13) (F = 214.12, P < 0.01), the expression levels of DNMT3a mRNA were separately (1.00 ± 0.04) , (0.93 ± 0.11) , (0.79 ± 0.07) , (0.59 ± 0.05) (F = 498.16, P < 0.01) , and the expression levels of protein were separately (1.00 ± 0.14) , (0.97 ± 0.11) , (0.79 ± 0.17) , (0.57 ± 0.15) (F = 390.11, P < 0.01) when the dose of Cr (VI) at 0, 0.3, 1.2 and 5.0 µmol/L. However, there were no significant changes of expression found in DNMT3b and MBD2.

CONCLUSIONPoly-ADP-ribosylation could regulate the activity of DNMT3b and MBD2, protect cells against the DNA methylation alteration induced by Cr(VI) and maintain the global genomic DNA methylation level.

Cell Line ; Chromium ; toxicity ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases ; metabolism ; DNA Methylation ; drug effects ; DNA-Binding Proteins ; metabolism ; Epithelial Cells ; metabolism ; Genome ; Humans ; Poly Adenosine Diphosphate Ribose ; metabolism ; RNA, Messenger ; genetics

An understanding of the characteristics of occupational lung cancer is important to establish policies that prevent carcinogen exposure and to compensate workers exposed to lung carcinogens. This study analyzed the characteristics of occupational lung cancers in workers who were compensated under the Industrial Accident Compensation Insurance Law between 1994 and 2011. A total of 179 occupational lung cancers were compensated. The main carcinogenic exposure was asbestos, followed by crystalline silica and hexavalent chromium. The mean exposure duration and latency were 19.8 and 23.2 yr. The most common industry was manufacturing, followed by construction and transportation. The most common occupation was maintenance and repair, followed by foundry work, welding, painting, and spinning or weaving. Although asbestos was predominant carcinogen, the proportion of these cases was relatively low compared to other developed countries. Proper surveillance system is needed to monitor occupational lung cancer and improve prevention measures.
Adult ; Aged ; Asbestos/toxicity ; Chromium/toxicity ; Female ; Humans ; Insurance Benefits/legislation & jurisprudence ; Lung Neoplasms/economics/*epidemiology/etiology ; Male ; Middle Aged ; Occupational Diseases/economics/*epidemiology/etiology ; Occupational Exposure ; Republic of Korea/epidemiology ; Silicon Dioxide/toxicity ; Smoking ; Workers' Compensation/statistics & numerical data

Chromium ; toxicity ; DNA Methylation ; drug effects ; Epigenesis, Genetic ; Humans

Carcinogens ; chemistry ; toxicity ; Chromium ; chemistry ; toxicity ; Chromium Compounds ; chemistry ; toxicity ; Humans ; Occupational Exposure ; analysis

OBJECTIVETo explore the effects of chronic exposure to trace chromium (VI) as a result of metal-on-metal hip arthroplasty on oxidative stress in mouse liver cells.

METHODSEighty NIH mice were randomly divided into 4 groups and subject to intraperitoneal injection of CrO(3) at the dose of 0, 5, 10 or 20 mg/kg every other day for 16 weeks. Five mice from each group were selected every 4 weeks for determining the content of chromium (VI) in the whole blood and the levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR) activity, and glutamate cysteine ligase (GCL) expression in the liver cells. The ultrastructural changes of the liver cells were also observed using transmission electron microscopy.

RESULTSExposure to 5 and 10 mg/kg CrO(3) caused significantly increased blood chromium concentration and ROS level, which reached the peak level at 8 weeks and became stabilized, whereas at the dose of 20 mg/kg, CrO(3) exposure resulted in progressive, time-dependent increase of blood chromium concentration and ROS level. MDA showed no significant changes in the 4 groups. With the prolongation of the exposure time, GSH content and GR activity were decreased in these groups. In 5 and 10 mg/kg CrO(3) groups, GCL expression increased at each time point of measurement, but in 20 mg/kg group, GCL expression decreased gradually with a prolonged exposure. Transmission electron microscopy revealed apoptotic changes of the liver cells in 20 mg/kg group.

CONCLUSIONThe slow accumulation of trace chromium (VI) after metal-on-metal hip arthroplasty may cause oxidative stress and changes in the oxidative stress system in the liver cells.

Animals ; Apoptosis ; Chromium ; administration & dosage ; toxicity ; Environmental Exposure ; Glutathione ; metabolism ; Hepatocytes ; metabolism ; pathology ; Malondialdehyde ; metabolism ; Mice ; Oxidative Stress ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism ; Toxicity Tests, Chronic

OBJECTIVETo detect cobalt chromium alloy antimicrobial coating silver of the surface structure and the cell toxicity in order to provide a theoretical basis for clinical application.

METHODSPlasma spraying technique was adopted to prepare cobalt chromium alloy antimicrobial coating silver. Scanning electron microscopy, energy dispersive analysis and X-ray diffraction analysis were used to evaluate the surface properties. The methyl thiazolyl tetrazolium and flow cytometry method was adopted to test the L929 cell proliferation and the influence of the cell cycle.

RESULTSThe surface of the coating was uniform and compact, combined perfectly with substrate material. The content of the surface was mainly Ag, Cr and a small amount of Ag(2)O, Cr(2)O(3). After cobalt chromium alloy was cultured in leach liquor for 1, 2 and 3 days, the statistical result showed that there was no significant different between the three groups. The cytotoxic level of negative control group was level 0 at each time point and that of other groups was level 1 at each time point. There was no significant difference between cobalt chromium alloy and cobalt chromium alloy antimicrobial coating silver in cell toxicity (P > 0.05). There was no statistical significance of the influence on cell cycle between cobalt chromium alloy with Ag coating [the G2's rate of cell cycle was (8.23 ± 0.39)%] and cobalt chromium alloy group [the G2's rate of cell cycle was (8.70 ± 0.46)%] (P > 0.05).

CONCLUSIONSThe surface of the coating was stable and there was no significant difference between cobalt chromium alloy widely used in clinic and cobalt chromium alloy with Ag coating of the influence on proliferation of L929 cell and cell cycle, the cell compatibility of cobalt chromium with Ag coating is well.

Animals ; Cell Cycle ; drug effects ; Cell Line ; Cell Proliferation ; drug effects ; Chromium Alloys ; chemistry ; toxicity ; Dental Casting Technique ; Fibroblasts ; cytology ; drug effects ; Mice ; Microscopy, Electron, Scanning ; Silver ; chemistry ; toxicity ; Surface Properties ; X-Ray Diffraction

Malignant mesothelioma and lung cancer are representative examples of occupational cancer. Lung cancer is the leading cause of cancer death, and the incidence of malignant mesothelioma is expected to increase sharply in the near future. Although information about lung carcinogen exposure is limited, it is estimated that the number of workers exposed to carcinogens has declined. The first official case of occupational cancer was malignant mesothelioma caused by asbestos exposure in the asbestos textile industry in 1992. Since then, compensation for occupational respiratory cancer has increased. The majority of compensated lung cancer was due to underlying pneumoconiosis. Other main causative agents of occupational lung cancer included asbestos, hexavalent chromium, and crystalline silica. Related jobs included welders, foundry workers, platers, plumbers, and vehicle maintenance workers. Compensated malignant mesotheliomas were associated with asbestos exposure. Epidemiologic studies conducted in Korea have indicated an elevated risk of lung cancer in pneumoconiosis patients, foundry workers, and asbestos textile workers. Occupational respiratory cancer has increased during the last 10 to 20 yr though carcinogen-exposed population has declined in the same period. More efforts to advance the systems for the investigation, prevention and management of occupational respiratory cancer are needed.
Asbestos/toxicity ; Carcinogens/toxicity ; Chromium/toxicity ; Female ; Humans ; Lung Neoplasms/chemically induced/*epidemiology/*etiology ; Male ; Mesothelioma/epidemiology/*etiology ; Occupational Diseases/chemically induced/*epidemiology/etiology ; Occupational Exposure/*adverse effects ; Pneumoconiosis/complications ; Republic of Korea/epidemiology ; Silicon Dioxide/toxicity ; Workers' Compensation