Biomedical subjects

Il Je Yu

Publications and source records attributed to Il Je Yu.

14 recordsLinked to original sources

PubMed2007

Changes in blood manganese concentration and MRI t1 relaxation time during 180 days of stainless steel welding-fume exposure in cynomolgus monkeys.

Welders are at risk of being exposed to high concentrations of welding fumes and developing pneumoconiosis or other welding-fume exposure-related diseases. Among such diseases, manganism resulting from welding-fume exposure remains a controversial issue, as although the movement of manganese into specific brain regions has been established, the similar movement of manganese presented with other metals, such as welding fumes, has not been clearly demonstrated as being similar to that of manganese alone. Meanwhile, the competition between Mn and iron for iron transporters, such as transferrin and DMT-1, to the brain has also been implicated in the welding-fume exposure. Thus, the increased signal intensities in the basal ganglia, including the globus pallidus and subcortical frontal white matter, based on T1-weighted magnetic resonances in welders, require further examination as regards the correspondence with an increased manganese concentration. Accordingly, to investigate the movement of manganese after welding-fume exposure, 6 cynomolgus monkeys were acclimated for 1 mo and assigned to 3 dose groups: unexposed, low dose of (total suspended particulate [TSP] 31 mg/m3, 0.9 mg/m3 of Mn), and high dose of total suspended particulate (62 mg/m3 TSP, 1.95 mg/m3 of Mn). The primates were exposed to manual metal-arc stainless steel (MMA-SS) welding fumes for 2 h/day in an inhalation chamber system equipped with an automatic fume generator for 6 mo. Magnetic resonance imaging (MRI) studies of the basal ganglia were conducted before the initiation of exposure and thereafter every month. During the exposure, the blood chemistry was monitored every 2 wk and the concentrations of metal components in the blood were measured every 2 wk and compared with ambient manganese concentrations. The manganese concentrations in the blood did not show any significant increase until after 2 mo of exposure, and then reached a plateau after 90 days of exposure, showing that an exposure period of at least 60 days was required to build up the blood Mn concentration. Furthermore, as the blood Mn concentration continued to build, a continued decrease in the MRI T1 relaxation time in the basal ganglia was also detected. These data suggested that prolonged inhalation of welding fumes induces a high MRI T1 signal intensity with an elevation of the blood manganese level. The presence of a certain amount of iron or other metals, such as Cr and Ni, in the inhaled welding fumes via inhalation was not found to have a significant effect on the uptake of Mn into the brain or the induction of a high MRI T1 signal intensity.

Air Pollutants, Occupational↗

PubMed2006

Effects of repeated welding fumes exposure on the histological structure and mucins of nasal respiratory mucosa in rats.

To investigate the effects of welding fumes on the histological structure and properties of mucins of the nasal respiratory mucosa, Sprague-Dawley rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes at a concentration of 56-76 mg/m3 total suspended particulates for 2 h per day in an inhalation chamber for 90 days. Experimental animals were sacrificed at 2 h, 15, 30, 60 and 90 days after exposure. Loss of cilia, desquamation of epithelial cells, mucigenous epithelial cells and destruction of nasal septal glands were observed frequently in the welding fumes-exposed groups. These changes became more severe as the exposure continued. The amount of neutral mucins in goblet cells in the welding fumes-exposed group had a tendency to increase, the amount of sulfomucins decreased, while the sialomucins increased as the exposure continued. Mucinogenic epithelial cells, not visible in the control group, contained minimal to small amounts of neutral mucins. In the dorsal septal glands, neutral mucins not visible in the control group appeared, and neutral mucins in the ventral septal glands increased slightly. These results indicate that the observed changes in the properties of mucins due to inhalation of welding fumes may play roles in protection against toxicants.

Animals↗

PubMed2005

Respiratory effect of acute and subacute exposure to endotoxin-contaminated metal working fluid (MWF) aerosols on Sprague-Dawley rats.

Male Sprague-Dawley rats were exposed to a water-soluble metal working fluid (MWF) (5% v/v) contaminated with endotoxins (10,000 eu/ml or 100,000 eu/ml) at 10 mg/m3 for six hours per day for three days (acute exposure) or two weeks (subacute exposure). The geometric mean diameter of the MWF aerosols was 1.56 microm, and the airborne endotoxin concentrations ranged from 1,231 to 2,173 eu/m3 (10,000 eu/ml in the bulk MWF) for the low dose and 19,263-27,386 eu/m3 (100,000 eu/ml in the bulk MWF) for the high dose. Minimal effects were observed after exposure to 10 mg/m3 of the MWF without endotoxins for three days or two weeks. However, an increase in the number of polymorphonuclear cells (PMNs) and the level of protein was noted in the bronchoalveolar lavage (BAL) fluid from the rats acutely exposed to the MWF with endotoxins. The acute exposure produced a greater increase in the number of PMNs and total cell number in the BAL fluid than the subacute exposure. The number of white blood cells in the peripheral blood and the weight of the lungs both increased after the subacute exposure to the MWF aerosol with endotoxins, indicating increased vascular permeability in response to the endotoxin exposure. The levels of cyotokines such as IL-4, INF-gamma, and IL-1beta in the BAL fluid from the rats exposed to the MWF with or without endotoxins remained unchanged. Although the level of nitric oxide (NO(x)) in the BAL supernatant did not show any change, the induction of NO(x) from the alveolar macrophages increased in the rats acutely or subacutely exposed to the MWF contaminated with endotoxins. The ConA-induced proliferation response showed no change, yet the LPS-induced proliferation response was significantly increased in the splenocytes from the rats subacutely exposed to the MWF with and without endotoxins. The level of TNF-alpha in the spleen cell culture obtained from the rats exposed to the MWF with or without endotoxins increased without changing the levels of IL-1beta, IL-4, and INF-gamma. The level of endotoxin-specific IgE in the serum obtained from the rats exposed to the MWF with endotoxins increased dose-dependently, while the levels of total immunoglobulins (IgG(1), IgG(2a) and IgE) and endotoxin-specific IgG(1) and IgG(2a) remained unchanged. Accordingly, the current results indicate that lung inflammation can be immediately induced by acute or subacute exposure to an MWF contaminated with endotoxins, and macrophages would appear to play a role in the induction of inflammation along with B-cell functions rather than T-cell functions, after subacute exposure to an MWF with endotoxins. In addition, endotoxin-specific IgE is an early marker for endotoxin exposure in the workplace.

Aerosols↗

PubMed2005

Inflammatory and immunological responses to subchronic exposure to endotoxin-contaminated metalworking fluid aerosols in F344 rats.

Rats were exposed for 6 h per day in inhalation chambers to a 10 mg/m(3) concentration of metalworking fluid (MWF) contaminated with endotoxin at concentrations of 1813 (low dose) and 20,250 eu/m(3) (high dose) 5 days per week for 8 weeks. It was found that 94.7% of the MWF aerosol particles had diameters in the range of 0.42-4.6 microm, with geometric mean diameter of 1.56 microm. The body weight and pulmonary function parameters were measured every week during the 8 weeks of exposure, whereas bronchoalveolar lavage (BAL) fluid was prepared to measure the inflammatory markers and cytokines after the 8 weeks of exposure. There were no changes in body weight and respiratory function (tidal volume and respiratory frequency) during the 8 weeks of exposure to the MWF containing endotoxins, yet lung weight increased significantly (P < 0.05) in the rats exposed to the MWF both with and without endotoxins. The number of polymorphonuclear (PMN) cells in the BAL fluid increased significantly (P < 0.05) in the rats exposed to MWF with endotoxins, and the levels of cytokines such as IL-4, INF-gamma, IL-1beta, and TNF-alpha also were significantly increased (P < 0.05) compared to the control. The NOx production activity of the BAL cells increased significantly (P < 0.05) in the rats exposed to the MWF with and without endotoxins. Increases in lung weight, number of PMN cells, and levels of extracellular cytokines and NOx were all more significant in the rats exposed to the MWF with endotoxins rather than in those exposed to MWF without endotoxins. In spleen cell cultures, T-cell proliferation activity was decreased, yet cytokine levels (INF-gamma, IL-1beta, IL-4, and TNF-alpha) remained unchanged after repeated exposure to MWF with and without endotoxins. Although the levels of total IgG(1), IgG(2a), and IgE antibodies in the serum were not changed, the levels of endotoxin-specific antibodies, including IgG(2a) and IgE, were increased significantly (P < 0.05) in the rats exposed to endotoxins, but there was not a significant increase in endotoxin-specific IgG(1). When taken together, the results indicate that lung inflammatory responses can be induced without changing pulmonary function after repeated exposure to MWFs contaminated with endotoxins. In addition, endotoxin-specific IgG(2a) and IgE may be effective biomarkers for workers exposed to MWFs contaminated with endotoxins in the workplace.

Aerosols↗

PubMed2005

Effect of water-soluble metal working fluid aerosols on respiratory system after 13 weeks of repeated inhalation exposure in F344 rats.

Three groups of male F344 rats were exposed to a water-soluble metal working fluid (MWF) aerosol at concentrations of 20, 60 or 180 mg/m3 for 6 h/day, five days a week, for 13 weeks in inhalation chambers. The aerosol particles were normally distributed and the mass median aerodynamic diameter was 1.56 microm. Despite the absence of clinical findings or significant changes in body weight during the 13-week exposure period, the numbers of white blood cells and lung weights were significantly higher at the end of the 13-week exposure period. Exposure to 20 mg/m3 of the MWF aerosol was found to have an effect on the respiratory system, including an accumulation of foamy macrophages in the bronchoalveolar lavage (BAL) fluid and thickening of the alveolar walls in the histopathology. The level of histamine and number of polymorphonuclear (PMN) cells were also higher in the BAL fluid from the rats exposed to 60 mg/m3 of the MWF aerosol, while the respiratory inflammation was most pronounced in the rats exposed to 180 mg/m3 of the MWF aerosol, including the accumulation of PMNs and foamy macrophages in the BAL cells, lung weight increase and thickening of the alveolar walls. Immunoglobulin IgG2a level was also lower in the sera from the rats exposed to 180 mg/m3 of the MWF aerosol. Therefore, even though no clinical symptoms were observed in the rats exposed to the high MWF concentration, respiratory inflammation was still induced by a relatively low concentration of the MWF, while the immune system was affected by the high MWF concentration.

Administration, Inhalation↗

PubMed2005

Korean initiative of GHS activities.

To implement a globally harmonized system of classification and labelling of chemicals (GHS) in Korea, an interminsterial GHS committee involving 6 ministries established an expert working group composed of 7 experts from relevant organizations and one private consultant to prepare an official Korean GHS version by March, 2005. As such, the translation and review of the official Korean GHS version, including annexes, started in October, 2004 and was completed on March 15, 2005. The official Korean GHS version has now been posted on the websites of the relevant ministries and organizations to solicit public opinions. The official Korean GHS version will be finalized after a public hearing scheduled for May, 2005. Collaborative efforts as regards implementing and disseminating the GHS in Korea will be continued to avoid any confusion or duplication and for effective use of resources.

Consensus↗

PubMed2004

Inflammatory and genotoxic responses during 30-day welding-fume exposure period.

Welder's pneumoconiosis has generally been determined to be benign and unassociated with respiratory symptoms based on the absence of pulmonary-function abnormalities in welders with marked radiographic abnormalities. In previous studies, the current authors suggested a three-phase lung fibrosis process to study the pathological process of lung fibrosis and found that the critical point for recovery was after 30 days of welding-fume exposure at a high dose, at which point early and delicate fibrosis was observed in the perivascular and peribronchiolar regions. Accordingly, the current study investigated the inflammatory and genotoxic responses during a 30-day period of welding-fume exposure to elucidate the process of fibrosis. As such, rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes at concentrations of 65.6 +/- 2.9 (low dose) and 116.8 +/- 3.9 mg/m3 (high dose) total suspended particulate for 2 h per day in an inhalation chamber for 30 days. Animals were sacrificed after the initial 2 h exposure, and after 15 and 30 days of exposure. The rats exposed to the welding fumes exhibited a statistically significant (P < 0.05) decrease in body weight when compared to the control during the 30-day exposure period, yet an elevated cellular differential count and higher levels of albumin, LDH, and beta-NAG, but not elevated TNF-alpha, and IL-1beta in the acellular bronchoalveolar lavage fluid. In addition, the DNA damage resulting from 30 days of welding-fume exposure was confirmed by a comet assay and the inmmunohistochemistry for 8-hydroxydeoxyguanine (8-OH-dG). Consequently, the elevated inflammatory and genotoxic indicators confirmed the lung injury and inflammation caused by the MMA-SS welding-fume exposure.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2004

Recovery from welding-fume-exposure-induced lung fibrosis and pulmonary function changes in sprague dawley rats.

Welder's pneumoconiosis has generally been determined as benign based on the absence of pulmonary function abnormalities in welders with marked radiographic abnormalities. Yet, there have also been several reports on welders with respiratory symptoms, indicating lung function impairment, X-ray abnormalities, and extensive fibrosis. Accordingly, this study attempted to investigate the inflammatory responses and pulmonary function changes in rats during a 60-day welding-fume-inhalation exposure period to elucidate the process of fibrosis. The rats were exposed to manual metal-arc stainless-steel welding fumes (MMA-SS) with total suspended particulate concentrations of 64.8 +/- 0.9 (low dose) and 107.8 +/- 2.6 mg/m3 (high dose) for 2 h per day in an inhalation chamber for 60 days. Animals were sacrificed after the initial 2-h exposure and after 15, 30, and 60 days, and the pulmonary function was also measured every week after the daily exposure. Elevated cellular differential counts were also measured in the acellular bronchoalveolar lavage fluid of the rats exposed to the MMA-SS fumes for 60 days. Among the pulmonary function test parameters, only the tidal volume showed a statistically significant and dose-dependent decrease after 35 to 60 days of MMA-SS welding-fume exposure. When the rats exposed to the welding fumes were left for 60 days to recover their lung function and cellular differentiation, recovery was observed in both the high and low-dose rats exposed up to 30 days, resulting in the disappearance of inflammatory cells and restoration of the tidal volume. The rats exposed for 60 days at the low dose also recovered from the inflammation and tidal volume loss, yet the rats exposed for 60 days at the high dose did not fully recover even after a 60-day recovery period. Therefore, when taken together, the results of the current study suggest that a decrease in the tidal volume could be used as an early indicator of pulmonary fibrosis induced by welding-fume exposure in Sprague Dawley rats, and fibrosis would seem to be preventable if the exposure is short-term and moderate.

Animals↗

PubMed2004

Asbestos exposure among Seoul metropolitan subway workers during renovation of subway air-conditioning systems.

Air quality in underground spaces has seldom been evaluated in Korea. Accordingly, the current study recently evaluated asbestos exposure among Seoul metropolitan subway workers during the renovation of the subway's air-conditioning system. To identify possible routes of asbestos exposure, suspected sources, including gaskets, ceiling boards, ceiling materials, and dust settled inside ducts, were all sampled. Personal air samples were also taken to evaluate any asbestos exposure during the renovation. The asbestos fibers found in the samples were analyzed using a transmission electron microscope (TEM) equipped with an energy dispersive X-ray analyzer (EDX). Twelve out of eighteen bulk samples contained asbestos, the majority of which was chrysotile fibers. Asbestos was detected in 9 out of 72 personal air samples and the level ranged from 0.003 to 0.02 fibers/cm(3). While asbestos levels were below Korean occupational limit of 2 fibers/cm(3), they were still detectable and therefore further monitoring would be appropriate.

Air Conditioning↗

PubMed2004

Gene-expression profiling using suppression-subtractive hybridization and cDNA microarray in rat mononuclear cells in response to welding-fume exposure.

Welders with radiographic pneumoconiosis abnormalities have shown a gradual clearing of the X-ray identified effects following removal from exposure. In some cases, the pulmonary fibrosis associated with welding fumes appears in a more severe form in welders. Accordingly, for the early detection of welding-fume-exposure-induced pulmonary fibrosis, the gene expression profiles of peripheral mononuclear cells from rats exposed to welding fumes were studied using suppression-subtractive hybridization (SSH) and a cDNA microarray. As such, Sprague-Dawley rats were exposed to a stainless steel arc welding fume for 2 h/day in an inhalation chamber with a 1107.5 +/- 2.6 mg/m3 concentration of total suspended particulate (TSP) for 30 days. Thereafter, the total RNA was extracted from the peripheral blood mononuclear cells, the cDNA synthesized from the total RNA using the SMART PCR cDNA method, and SSH performed to select the welding-fume-exposure-regulated genes. The cDNAs identified by the SSH were then cloned into a plasmid miniprep, sequenced and the sequences analysed using the NCBI BLAST programme. In the SSH cloned cDNA microarray analysis, five genes were found to increase their expression by 1.9-fold or more, including Rgs 14, which plays an important function in cellular signal transduction pathways; meanwhile 36 genes remained the same and 30 genes decreased their expression by more than 59%, including genes associated with the immune response, transcription factors and tyrosine kinases. Among the 5200 genes analysed, 256 genes (5.1%) were found to increase their gene expression, while 742 genes (15%) decreased their gene expression in response to the welding-fume exposure when tested using a commercial 5.0k DNA microarray. Therefore, unlike exposure to other toxic substances, prolonged welding-fume exposure was found to substantially downregulate many genes.

Air Pollutants, Occupational↗

PubMed2004

Perspectives on new chemical regulatory framework and research direction in Korea.

In response to new information about the health risk of chemical and concern expressed by academia, labor, and industry, chemical regulatory framework under Industrial Safety and Health Act was completely restructured in Year 2003 to be more systematic and to meet the particular needs in Korea. The history and the current status of chemical regulatory framework in the Republic of Korea are reviewed.

Chemical Industry↗

PubMed2003

Recovery from manual metal arc-stainless steel welding-fume exposure induced lung fibrosis in Sprague-Dawley rats.

Welders with radiographic pneumoconiosis abnormalities have exhibited a gradual clearing of the X-ray identified effects following removal from exposure. In some cases, the pulmonary fibrosis associated with welding fumes appears in a more severe form in welders. Accordingly, to investigate the disease and recovery process of pneumoconiosis induced by welding-fume exposure, rats were exposed to welding fumes with concentrations of 63.6+/-4.1 mg/m(3) (low dose) and 107.1+/-6.3 mg/m(3) (high dose) of total suspended particulate for 2 h per day in an inhalation chamber for a total of 2 h or 15, 30, 60 or 90 days. Thereafter, the rats were no longer exposed and allowed to recover from the welding fume-induced lung fibrosis for 90 days. When compared to the unexposed control group, the lung weights significantly increased in both the low- and high-dose rats from day 15 to 90. A histopathological examination combined with fibrosis-specific staining revealed that the lungs from the low-dose rats did not exhibit any significant progressive fibrotic changes. Whereas, the lungs from the high-dose rats exhibited early delicate fibrosis from day 15, which progressed into the perivascular and peribronchiolar regions by day 30. Interstitial fibrosis appeared at day 60 and became prominent by day 90, along with the additional appearance of pleural fibrosis. Recovery, evaluated based on the body and lung weights and a histopathological examination, was observed in both the high and low-dose rats that were exposed up to 30 days. The rats exposed for 60-90 days at the low dose also recovered from the fibrosis, yet the rats exposed for 60-90 days at the high dose did not fully recover. Consequently, recovery from pneumoconiosis induced by welding-fume exposure was observed when the degree of exposure was short-term and moderate.

Air Pollutants, Occupational↗

PubMed2003

Manganese distribution in brains of Sprague-Dawley rats after 60 days of stainless steel welding-fume exposure.

Welders working in a confined space, as in the shipbuilding industry, are at risk of being exposed to high concentrations of welding fumes and developing pneumoconiosis or other welding-fume exposure related diseases. Among such diseases, manganism resulting from welding-fume exposure remains a controversial issue, as the movement of manganese into specific brain regions has not yet been clearly established. Accordingly, to investigate the distribution of manganese in the brain after welding-fume exposure, male Sprague-Dawley rats were exposed to welding fumes generated from manual metal arc-stainless steel (MMA-SS) at concentrations of 63.6 +/- 4.1 mg/m(3) (low dose, containing 1.6 mg/m(3) Mn) and 107.1 +/- 6.3 mg/m(3) (high dose, containing 3.5 mg/m(3) Mn) total suspended particulate (TSP) for 2 h per day in an inhalation chamber over a 60-day period. Blood, brain, lung, and liver samples were collected after 2 h, 15, 30, and 60 days of exposure and the tissues analyzed for their manganese concentrations using an atomic absorption spectrophotometer. Although dose- and time-dependent increases in the manganese concentrations were found in the lungs and livers of the rats exposed for 60 days, only slight manganese increases were observed in the blood during this period. Major statistically significant increases in the brain manganese concentrations were detected in the cerebellum after 15 days of exposure and up until 60 days. Slight increases in the manganese concentrations were also found in the substantia nigra, basal ganglia (caudate nucleus, putamen, and globus pallidus), temporal cortex, and frontal cortex, thereby indicating that the pharmacokinetics and distribution of the manganese inhaled from the welding fumes were different from those resulting from manganese-only exposure.

Animals↗

PubMed2002

Potential source of asbestos in non-asbestos textile manufacturing company.

Recently, a worker with lung carcinoma and a metastatic brain tumor was diagnosed as having a work-related disease. He had been employed in a non-asbestos textile company for 25 years. Consequently, to identify and explore possible causative agents for lung cancer in a non-asbestos textile manufacturing company and establish a causal relationship between exposure and lung cancer, an epidemiological investigative study was conducted and the work processes the worker was engaged in were examined. Air samples were taken from the workplace and during the drilling processes, and a suspected causative material was analyzed. The study revealed that the subject had been employed in the non-asbestos textile manufacturing company for 25 years from 1973 and his responsibilities included repairing spinning machines. In particular, the subject was involved in drilling B-bushings that were used to protect against gear abrasion in the spinning machines. An analysis of the B-bushings using a transmission electron microscope equipped with an energy dispersive X-ray analyzer indicated that they contained crocidolite asbestos fibers. Air samples obtained when drilling the B-bushings clearly indicated that the subject had most likely been exposed to crocidolite fibers when installing the B-bushings in the spinning machines. The frequency and duration of the work suggested that there would be a sufficient degree of exposure to crocidolite fibers to cause lung cancer. Except for smoking and asbestos exposure, no other chemical exposure was suspected for developing lung cancer in the workplace. Smoking appeared to be more of a potentiating risk factor in conjunction with the asbestos exposure. Accordingly, this case may provide significant evidence in identifying the cause of the mesothelioma or lung carcinoma found among workers in non-asbestos textile manufacturing companies elsewhere.

Air Pollutants, Occupational↗