• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.21 no.4
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• pp.215-221
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• 2011

Objectives: This study was conducted to evaluate the exposure level of hazardous chemical agents for dental technicians in Ulsan. Methods: We measured airborne total dusts and metals such as Nickel, Manganese, Cobalt, and Chromium in 10 dental laboratories by the NIOSH Methods 0500 and 7300, respectively. Methyl methacrylate (MMA), a key ingredient in acrylic resin, was also monitored using passive samplers for long-term sampling and Tenax tubes for short-term sampling. Results: Measured levels of all items were below 10% of the Korean exposure limit except for Nickel. The geometric mean concentration and geometric standard deviation of total dust, Nickel, and MMA were $0.14mg/m^3$ (2.16), $165.3{\mu}g/m^3$ (3.31), and 0.2 ppm (2.5) respectively. Airborne Nickel concentration of two dental laboratories exceeded the exposure limit ($1000{\mu}g/m^3$). The major emission sources of Nickel were metal trimming and casting processes. Conclusions: We found that Nickel, a carcinogen, should be controled most urgently to protect dental technicians.

• Toxicological Research
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• v.22 no.2
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• pp.95-102
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• 2006

Exposure to soluble nickel compound produces toxic effects on immune system, but the mechanism of action remains to be elucidated. Differential gene expression was studied to understand the potential molecular mechanism responsible for acute toxicity induced by nickel acetate in spleen cells. We exposed mouse spleen cells to nickel acetate with a nontoxic dose ($40{\mu}M$) and then extracted total RNA at 6 h and 12 h after exposure. The RNA was hybridized onto 10K mouse oligonucleotide microarrays, and data were analyzed using GeneSpring 7.1. Nickel had a modest effects on expression of many genes, in the range of 1.3-3 fold. The expression profile showed time-dependent changes in expression levels of differentially expressed genes, including some important genes related to cell cycle, apoptosis and DNA repair. In hierarchical cluster analysis of duplicate experiments, 111 genes were screened out. Out of these, 44 genes showing time- dependent up-regulation (>1.5 fold) and 38 genes showing down-regulation (>1.5 fold) at all time points were chosen for further analysis. The change in the expression of three genes (GPX1, GADD45B and FAIM) after nickel treatment was validated using RT-PCR. As a rule, a number of genes appear to be coordinately regulated between cell survival and cell death from nickel toxicity. In conclusion, changes in the gene profile in the spleen after nickel treatment are complex and genes with diverse functions are modulated. These findings will be contributed to the understanding of the complicated biological effects of nickel.

• The Korean Journal of Malacology
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• v.31 no.2
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• pp.143-150
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• 2015

This study was conducted to find out accumulated concentration of nickel, survival rate and falling rate, structural changes of abalone, Haliotis discus hannai exposed to nickel chloride. Experimental groups were composed of one control condition and five nickel chloride exposure conditions (5.9, 8.8, 13.3, 20.0, 30.0 mg/L). The accumulation of nickel in abalone was significantly increased all exposure group. Though the exposure groups had lower survival rate than the control group, higher falling rate than the control group. Histopathological changes in the foot, gill and hepatopancreas of abalone revealed obvious with exposure group than control group.

• Toxicological Research
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• v.27 no.1
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• pp.19-23
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• 2011

It has been proposed that acute phase response can be a mechanism by which inhaled particles exert adverse effects on the cardiovascular system. Although some of the human acute phase proteins have been widely studied as biomarkers of systemic inflammation or cardiovascular diseases, there are only a few studies that investigated the role of serum amyloid P (SAP), a major acute phase protein in mice. In this study, we investigated the changes in SAP, following inhalation exposure to nickel hydroxide nanoparticles (nano-NH). We conducted 1) acute (4 h) exposure to nano-NH at 100, 500, and $1000\;{\mu}g/m^3$ and 2) sub-acute (4h/d for 3d) exposure at $1000\;{\mu}g/m^3$, then measured serum SAP protein levels along with hepatic Sap mRNA levels. The results show that inhaled nano-NH can induce systemic acute phase response indicated by increased serum SAP levels and hepatic Sap mRNA levels. To the best of our knowledge, this is the first study showing induction of SAP in response to repeated particle exposure, and the results suggest that SAP can be used as a biomarker for systemic inflammation induced by inhaled particles.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.1 no.2
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• pp.117-127
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• 1991

The exposure level of chromium and nickel for chrome and nickel plating workers were evaluated. Chromium and nickel concentrations in serum from 82 exposed workers and 66 controls, who were not exposed occupationally to metals, were analyzed by flameless atomic absorption spectrophotometry. The results were as follows : 1. The recovery percent of chromium and nickel concentrations in personal air samples were 95-108.2%, 88.0-107.7%, precisions (C.V., %) were 2.7-3.1%, 2.1-4.4%. respectively. 2. The recovery percent of chromium and nickel concentrations in serum were 93.6-106.4%, 91.3-107.9% and precisions (C.V. %) were 1.1-7.6%, 2.4-5.4% respectively. 3. The exposure level of chromium and nickel concentrations in the place of preparation process were $2.0{\pm}2.00{\mu}g/m^3$, chromplating were $35.7{\pm}53.07{\mu}g/m^3$, $2.8{\pm}3.42{\mu}g/m^3$, nickelplating were $4.6.0{\pm}5.8{\mu}g/m^3$, $18.62{\pm}4.41{\mu}g/m^3$, and covering were $2.9{\pm}2.02{\mu}g/m^3$, $1.1{\pm}0.47{\mu}g/m^3$ respectively. There were significant difference of concentrations for chromium and nickel in workplaces by groups statistically. 4. Chromium concentrations in serum of exposed group and control were $0.68{\pm}0.399{\mu}g/l$, $1.41{\pm}0.748{\mu}g/l$, respectively. There were significant difference of concentrations for chromium and nickel in serum by groups statistically. 5. Chromium and nickel concentrations in serum of exposed group were not significant by workplaces.

• The Korean Journal of Malacology
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• v.32 no.2
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• pp.111-118
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• 2016

This study was conducted to find out concentration of trace metal, survival rate, falling rate and structural changes of the abalone Haliotis discus hannai exposed to nickel chloride. Experimental groups were composed of one control condition and four nickel chloride exposure conditions (7.0, 12.0, 17.0 and $22.0\;NiCl_2\;mg/L$). The concentration of nickel in abalone was significantly increased all exposure groups. Though the exposure groups had lower survival rate than the control group, falling rate higher than the control group. Histopathological changes in the foot, gill and hepatopancreas of abalone was revealed prominently with exposure group than control group.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.10 no.1
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• pp.93-103
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• 2000

The purpose of this case study is to report a case of lung cancer with exposure to welding fumes of welders in Korea and to demonstrate the causal relationship with exposure to welding fumes, especially with nickel and hexavalent chromium. The case is 47 years old, and had been engaged in welding, gas cutting, grinding and gousing on mild, stainless steel and nickel steel for 11 years from 1982 to 1993, and have been engaged in cleaning steel rollers with a cleaning oil in the same work shop since 1993. The level of welding fume exceeded the occupational exposure limit of $5mg/m^3$ established by the Korean Ministry of Labor and American Conference of Government Industrial Hygienists (ACGIH). Especially, detectable hexavalent chromium and nickel was generated during welding, gousing on stainless and nickel steel. However, there was no ventilation systems(local and dilution) and no personal protection. There is several evidence that the past (1983-1993) exposure would be higher than the present. In conclusion, the lung case could be associated with his task including welding, gousing, and this association could be attributed to carcinogenic potential of the nickel and chromium in the fume.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.3 no.1
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• pp.68-77
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• 1993

To evaluate efficiencies of the local exhaust systems installed in chromiun and nickel eletroplating tanks, specifications of each tank and general performances of the local exhaust systems were measured in 16 electroplating plants from July 3 to November 24, 1992. Airborne concentrations of total chromium, hexa-chromium and nickel were also measured, Most of the local exhaust systems installed in electroplating plants were inadequately designed. Average capture velocities of local exhaust systems in chromium and nickel tanks were 0.45 m/sec and 0.29 m/sec. Average slot velocities in chromium and nickel tanks were 7.30 m/sec and 2.87 m/sec repectively. Both average capture and solt velocities were in noncompliance with the standards recommened by American Conference of Governmental Industrial Hygienists (ACGIH) and National Institute for Occupational Safety and Health (NIOSH), Exhausted air volume was insufficient in all local exhaust systems surveyed. Worker exposure levels to total chromium, hexa-chromium and nickel were $43.0{\mu}g/m^3$, $1.7{\mu}g/m^3$ and $9.3{\mu}g/m^3$, which were below the Korean Standard and U.S. Occupational Health and Safety Administration (OHSA) Permissible Exposure Limit(REL). However, Worker exposure level to hexa-chromium exceeded the NIOSH Recommended Exposure Limit(REL) of $1{\mu}g/m^3$. As the result of Scheffee's multiple comparions, worker exposure levels to all metals were significantly different between two groups by the management state of existing local exhaust systems (p<0.05). However, Difference between a group with local exhaust systems which were poorly managed and another group without local exhaust system was satatistically non-significant.

• Environmental Mutagens and Carcinogens
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• v.19 no.1
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• pp.20-27
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• 1999

In order to know the inhibitory effect of magnesium carbonate(MgCO3) on cytotoxicity, DNA damage, mutagenicity, and cell transforming ability of nickel subsulfide, the inhibition of cell proliferation, DNA-protein crosslinks formation (DPC), HGPRT point mutation, and cell transformation were evaluated. Nickel subsulfide(Ni3S2) and magnesium carbonate as insoluble compounds were used for this study. BALB/3T3 cell, CHO-K1 cell, and C3H10T1/2 cell were used in this experiment. Exposure concentration of nickel subsulfide was 1 $\mu\textrm{g}$/ml. The concentrations of magnesium carbonate in this study were 0.6 $\mu\textrm{g}$/ml, 1.2 $\mu\textrm{g}$/ml, 2.4 $\mu\textrm{g}$/ml and the molar ratio of magnesium to nickel when exposed simultanously were 0.5, 1.0 and 2.0 respectively. The results were as follows; 1. Magnesium carbonate reduced the inhibitory effect of nickel subsulfide on cell proliferation. 2. Magnesium carbonate also reduced the effect of nickel subsulfide on DNA-protein crosslinks formation. 3. HGPRT point mutagenicity of nickel subsulfide was reduced when magnesium carbonate treated simultaneously. 4. Magnesium carbonate reduced cell transforming ability of nickel subsulfide. Conclusively, nickel subsulfide showed cytotoxicity, cell transforming ability, and mutagenicity strongly and magnesium carbonate may have protective roles in these nickel effects.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.119-134
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• 2004

Human exposure to highly nickel-polluted environments, such as those associated with nickel refining, electroplating, and welding, has the potential to produce a variety of pathologic effects. Among them are skin allergies, lung fibrosis, and cancer of the respiratory tract. The exact mechanisms of nickel-induced carcinogenesis are not known and have been the subject of numerous epidemiologic and experimental investigations. This review provides the evidence of the current state for the genotoxic and mutagenic activity of Ni (II) particularly at high doses. Such doses are best delivered into the cells by phagocytosis of sparingly soluble nickel-containing dust particles. Ni (II) genotoxicity may be aggravated through the generation of DNA-damaging reactive oxygen species (ROS) and the inhibition of DNA repair by this metal. The epigenetic effects of nickel includes alteration in gene expression resulting from DNA hypermethylation and histone hypoacetylation, as well as activation some signaling pathways and subsequent transcrziption factors.