PCBs are classified as B2 (Probable human carcinogen) based on the induction of hepatocellular carcinomas in rats and mice from IRIS (Integrated Risk Information System). About 20 years ago, PCBs were phased out for electrical use in Korea, but PCBs were continuously used in the other field. Lately, there has been increasing concern on possible effects of contaminated soil to the other environment and human health. The purpose of this study is to determine PCBs level in soil at some site and to assess the human exposure doses according to exposure routes for people living within sites which expected to be exposed to PCBs. Pollution level of PCBs on the site was monitored using gas liquid chromatography. To assess the transport of PCBs in soil to plant and to air, various transfer factors(diffusion coefficient, bioconcentration factor etc.) were considered in simple calculations. To calculate the residential exposure doses by routes, some equations were considered using assumption value, which define inhalation, ingestion (soil, plant) and derreal uptake pathway. Computated results will be used as risk assessment information for human health evaluation on contaminated soil.
Respiratory effects in full time welders include bronchitis, airway irritation, lung function changes, and lung fibrosis. Welder's pneumoconiosis has been generally determined to be benign and not associated with respiratory symptoms based on the absence of pulmonary function abnormalities in welders with marked radiographic abnormalities. Accordingly, to investigate pulmonary function changes during 60 days induced by welding-fume exposure, male Sprague-Dawley rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes with concentrations of 64.8$\pm$0.9 mg/$m^3$ (low dose) and 107.8 $\pm$ 2.6 mg/$m^3$ (high dose) total suspended particulates for 2 hr/day, 5 days/week in an inhalation chamber for 60 days. Pulmonary function was measured every week with whole body plethysmograph compensated (WBP Comp, SFT38116, Buxco Electronics, Sharon, CT). The rats exposed to the high dose of welding fumes exhibited statistically significant (p<0.05~0.01) body weight decrease as compared to the control whereas cell number increase of the bronchoalveolar lavage fluid (BALF) (total cell, macrophage, polymorphonuclear cell and lymphocyte) during the 60 days exposure period. And only tidal volume was significantly decreased in dosedependantly during 60 days of MMA-SS welding fume exposure. This pulmonary function change with inflammatory cell recruitment confirms the lung injury caused by the MMA-SS welding fume exposure.
The preventive effects of ginseng and aloe extract on cigarette smoke-induced hepatotoxicity to Spague-Dawley rats were investigated. The experimental rats were exposed smoke by inhalation for 5 weeks, 3 times per day, and 15 minutes each time. Also ginseng and aloe extract (Group G+A), aloe (Group A) or ginseng (Group G) were administered to each group, but the positive control rats (Group C) were exposed smoke without any other special treatments. Group C showed decreased food intake and increased water consumption. Also the reduction of body weight and the increase in serumAST, ALT, triglyceride and alkaline phosphatase were observed. The relative liver weights of group C were increased and the hepatic parenchyma revealed light brownish red grossly. On histopathologic observation, the hepatocytes of group C animals exhibited diffuse swelling which narrowed the, sinusoidal lumen and disarrayed the hepatic cord-like arrangement. Diffuse necrosis of the hepatocytes was also observed. However, degeneration and necrosis of the hepatocytes were milder in group G+A. In the case of group A, the damage was moderate, while the group G showed marginal improvement from group C. Electronmicroscopically, peroxisome increased and mitochodria decreased in group C. Various hepatic damages related to smoking in group C revealed recovering tendency in group G+A. This study indicated that daily administration of ginseng and aloe could decrease and even prevent cigarette smokeinduced hepatotoxicity.
Chul-Min Park;Oh Jin Min;Min-Seok Kim;Bhesh Raj Sharma;Dong Wook Kim;Dong Young Rhyu
Natural Product Sciences
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v.28
no.4
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pp.161-167
/
2022
Obesity is a complex metabolic disorder that increases the risk for type 2 diabetes, hyperlipidemia, hypertension, and atherosclerosis. In this study, we evaluated the anti-obesity effects of Nelumbo nucifera leaf (NL) extract in 3T3-L1 adipocytes and obese db/db mice. NL extract among various parts (leaf, seed, and root) of N. nucifera most effectively reduced adipogenesis via inhibiting CCAAT enhancer binding protein α (C/EBPα) and peroxisome proliferator activated receptor γ (PPARγ) expression in 3T3-L1 adipocytes. The addition of NL extract enhanced the protein expression of uncoupling protein 2 (UCP2) as compared to untreated 3T3-L1 adipocytes. The oral administration of NL extract (100 mg/kg BW) significantly reduced food efficacy ratio, body weight, and face or total cholesterol level in obese db /db mice. Also, administration of NL extract significantly decreased adipocyte size and C/EBPα or PPARγ expression in the adipose tissues as compared with control (obese db/db mice). Therefore, our results suggest that NL extract among various parts of N. nucifera could be used as a functional food ingredient for the prevention and treatment of metabolic diseases including obesity and diabetes.
Aluminum nanoparticles (Al-NPs) are one of the most widely used nanomaterial in cosmetics and medical materials. For this reason, Al-NP exposure is very likely to occur via inhalation in the environment and the workplace. Nevertheless, little is known about the mechanism of Al-NP neurotoxicity via inhalation exposure. In this study, we investigated the effect AL-NPs on the brain. Rats were exposed to Al-NPs by nasal instillation at 1 mg/kg body weight (low exposure group), 20 mg/kg body weight (moderate exposure group), and 40 mg/kg body weight (high exposure group), for a total of 3 times, with a 24-hr interval after each exposure. Inductively coupled plasma mass spectrometry (ICP-MS) analysis indicated that the presence of aluminum was increased in a dose-dependent manner in the olfactory bulb (OFB) and the brain. In microarray analysis, the regulation of mitogen-activated protein kinases (MAPK) activity (GO: 0043405), including Ptprc, P2rx7, Map2k4, Trib3, Trib1, and Fgd4 was significantly over-expressed in the treated mice than in the controls (p = 0.0027). Moreover, Al-NPs induced the activation of ERK1 and p38 MAPK protein expression in the brain, but did not alter the protein expression of JNK, when compared to the control. These data demonstrate that the nasal exposure of Al-NPs can permeate the brain via the olfactory bulb and modulate the gene and protein expression of MAPK and its activity.
Objectives: The objectives of this study are to estimate the inhalation exposure level of benzene for workers using Tier 1 exposure models ECETOC TRA (European Center for Ecotoxicology and Toxicology of Chemicals Target Risk Assessment) and Stoffenmanager, and to investigate their reliability for exposure assessment in K-REACH. Methods: Two exposure scenarios, 'manufacture of benzene' and 'use as solvents,' were developed for assessment of workers' exposure to benzene. The Process Category (PROC) for ECETOC TRA was collected from the European Chemical Agency (ECHA) registration dossier, and the Activity for Stoffenmanager was converted from PROC using translation of exposure models (TREXMO). The information related to exposure, such as working duration, Respiratory Protective Equipment (RPE), Local Exhaust Ventilation (LEV), and Risk Management Measure (RMM) were classified into high, medium, and low exposure conditions. The risk was determined by the ratio of the estimated exposure and occupational exposure limits of benzene. Results: Under high exposure conditions, the worker exposure level calculated from all PROCs and Activities exceeded the risk level, with the exception of PROC 1 and Activity 1. In the medium exposure condition, PROC 8a, 8b, and 9 and Activity 3, 7, and 8 all exceeded the risk, whereas in the low condition, all PROCs and Activities were determined to be safe. As a result, action corresponding with the low exposure condition is required to reduce the risk of exposure among workers in workplaces where benzene is manufactured or used as a solvent. In addition, the predicted exposure levels derived from the exposure models were lower than measured levels. The exposure levels estimated from Stoffenmanager were more conservative than those from ECETOC TRA. Conclusions: This study demonstrates the feasibility of exposure models for exposure assessment through the example of occupational inhalation exposure assessment for benzene. For more active utilization of exposure models in K-REACH, the exact application of collected information and accurate interpretation of obtained results are necessary.
Kim, Min-Young;Song, Kyung-Suk;Park, Gun-Ho;Kim, Hyun-Woo;Park, Jin-Hong;Kim, Jun-Sung;Jin, Hwa;Kook-Jong, Eu;Cho, Hyun-Sun
Toxicological Research
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v.20
no.1
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pp.71-82
/
2004
Changes in cell cycle control in the lungs and liver of the B6C3F1 mice (20 males per each group) exposed to ozone (0.5 ppm), 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK, 1.0 mg/kg), and dibutyl phthalate (DBP, 5,000 ppm) after 52 weeks were examined through Western, Northern blot, and immunohistochemistry based on alterations in protein expression levels of G1/S checkpoints (cyclin D1, cyclin E, and PCNA), G2/M checkpoints (cyclin B1, cyclin G, and cyclin A), negative regulators (p53, p21, GADD45, and p27), and positive regulator (mdm2). Expression levels of cyclins D1, E, G, PCNA, mutant p53, and mdm2 proteins were higher in the lungs and livers treated with combination of toxicants than in those treated with ozone only. Expression levels of the wild-type and mutant p53, p21, GADD45, p27, and mdm2 proteins and mRNAs were higher in toxicant-treated groups than those of the control. Immunohistochemical analysis revealed staining intensities of the PCNA, cyclin D1, c-myc and mdm2 protein- treated lungs and livers were stronger than those of the control group. Our results showed that combined treatment of ozone with NNK/DBP altered the cell cycle control through instability of the wild-type p53 gene. Such pivotal p53-mediated cell cycle alterations may be responsible for the toxicity observed under our experimental condition. These results may be applied to risk assessment of mixture-induced toxicity.
Journal of The Korean Society of Clinical Toxicology
/
v.14
no.2
/
pp.122-128
/
2016
Purpose: This study was conducted to describe the characteristics of patients with carbon monoxide (CO) poisoning. Methods: We retrospectively surveyed data from the Emergency Department based Injury In-depth Surveillance of 20 hospitals (2011-2014). We included patients whose mechanism of injury was acute CO poisoning caused by inhalation of gases from charcoal or briquettes. We surveyed the annual frequency, gender, age, result of emergency treatment, rate of intensive care unit (ICU) admission, result of admission, association with alcohol, and place of accident. We also surveyed the cause and experience of past suicide attempts by intentional poisoning. Results: A total of 3,405 patients were included (2,015 (59.2%) and 1,390 (40.8%) males and females, respectively) with a mean age of $39.83{\pm}18.51$ year old. The results revealed that the annual frequency of CO poisoning had increased and the frequency of unintentional CO poisoning was higher than that of intentional CO poisoning in January, February and December. The mean age of intentional CO poisoning was younger than that of unintentional CO poisoning ($38.41{\pm}13.03$ vs $40.95{\pm}21.83$) (p<0.001). The rates of discharge against medical advice (DAMA), ICU care and alcohol association for intentional CO poisoning were higher than for unintentional CO poisoning (36.4% vs 14.0%, 17.8% vs 4.7%, 45.2% vs 5.6%) (p<0.001). The most common place of CO poisoning was in one's residence. Conclusion: The annual frequency of total CO poisoning has increased, and unintentional CO poisoning showed seasonal variation. DAMA, ICU care, and alcohol association of intentional CO poisoning were higher than those of unintentional CO poisoning.
Lead (Pb) is ubiquitous in the urban environment and is a well-known toxic element. It may cause adverse health effects on hematopoietic system, peripheral and central nervous systems, kidney functions, and others. In recent decades, lead concentration in blood has been widely used one of indicators for lead exposure and risk evaluation. In this study, we determined the blood-lead levels in general populations of Korea, and investigated the relationship among blood-lead levels, sociobehavioral factors, and lead concentrations in the contacted environments such as ambient air, drinking water, and foods. The study subjects consisted of volunteers who had lived in the residential or industrial area in Korea. Information about gender, age, living area, occupation, smoking, heat system, and dietary habits, etc was collected using a self-reported questionnaires. The lead concentrations of environments were collected by literature search to the study area. Participated subjects in industrial area were 726 and their blood-lead levels were 8.58 $\mu\textrm{g}$/dl for males and 6.26 $\mu\textrm{g}$/dl for female in average. The other subjects in residential area were 317 and their blood-lead levels were 4.58 $\mu\textrm{g}$/dl for males and 3.49 $\mu\textrm{g}$/dl for female in average. The distribution of blood-lead level in the industrial subjects was well fitted to the log -normal distribution and that in the residential subjects was well fitted to the normal distribution. Blood-lead levels in both area were affected by gender, smoking habit, age and residence duration except age in industrial area and residence duration in residential area. It was identified that 30% of blood-lead level was contributed from the inhalation of ambient air in the industrial area, and 8.4% of blood-lead level was from that in the residential area. from this study, it would be suggested for the health risk assessment and management of lead pollution concerns in urban, industrial and rural areas.
Kim, Dae Hyun;Chung, Jae Heun;Yoon, Ji Sung;Ha, Young Mi;Bae, Sungjin;Lee, Eun Kyeong;Jung, Kyung Jin;Kim, Min Sun;Kim, You Jung;Kim, Mi Kyung;Chung, Hae Young
Journal of Ginseng Research
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v.37
no.1
/
pp.54-63
/
2013
Ginsenoside Rd is a primary constituent of the ginseng rhizome and has been shown to participate in the regulation of diabetes and in tumor formation. Reports also show that ginsenoside Rd exerts anti-oxidative effects by activating anti-oxidant enzymes. Treatment with ginsenoside Rd decreased nitric oxide and prostaglandin $E_2$ ($PGE_2$) in lipopolysaccharides (LPS)-challenged RAW264.7 cells and in ICR mouse livers (5 mg/kg LPS; LPS + ginsenoside Rd [2, 10, and 50 mg/kg]). Furthermore, these decreases were associated with the down-regulations of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 and of nuclear factor (NF)-${\kappa}B$ activity in vitro and in vivo. Our results indicate that ginsenoside Rd treatment decreases; 1) nitric oxide production (40% inhibition); 2) $PGE_2$ synthesis (69% to 93% inhibition); 3) NF-${\kappa}B$ activity; and 4) the NF-${\kappa}B$-regulated expressions of iNOS and COX-2. Taken together, our results suggest that the anti-inflammatory effects of ginsenoside Rd are due to the down-regulation of NF-${\kappa}B$ and the consequent expressional suppressions of iNOS and COX-2.
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