1.Occupational Neurological Disorders in Korea.
Journal of Korean Medical Science 2010;25(Suppl):S26-S35
The purpose of this article was to provide a literature review of occupational neurological disorders and related research in Korea, focusing on chemical hazards. We reviewed occupational neurological disorders investigated by the Occupational Safety and Health Research Institute of Korean Occupational Safety and Health Agency between 1992 and 2009, categorizing them as neurological disorders of the central nervous system (CNS), of the peripheral nervous system (PNS) or as neurodegenerative disorders. We also examined peer-reviewed journal articles related to neurotoxicology, published from 1984 to 2009. Outbreaks of occupational neurological disorder of the CNS due to inorganic mercury and carbon disulfide poisoning had helped prompt the development of the occupational safety and health system of Korea. Other major neurological disorders of the CNS included methyl bromide intoxication and chronic toxic encephalopathy. Most of the PNS disorders were n-hexane-induced peripheral neuritis, reported from the electronics industry. Reports of manganese-induced Parkinsonism resulted in the introduction of neuroimaging techniques to occupational medicine. Since the late 1990s, the direction of research has been moving toward degenerative disorder and early effect of neurotoxicity. To understand the early effects of neurotoxic chemicals in the preclinical stage, more follow-up studies of a longer duration are necessary.
Adolescent
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Adult
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Central Nervous System Diseases/chemically induced/epidemiology
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Female
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Humans
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Male
;
Middle Aged
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Nervous System Diseases/chemically induced/*epidemiology/etiology
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Neurodegenerative Diseases/chemically induced/epidemiology
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Neurotoxicity Syndromes/*epidemiology/*etiology
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Occupational Diseases/chemically induced/*epidemiology/etiology
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Parkinsonian Disorders/chemically induced/epidemiology
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Peripheral Nervous System Diseases/chemically induced/epidemiology
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Republic of Korea
2.Caffeine Exposure Causes Immune Dysfunction and Intrauterine Growth Restriction Retardation in Rats.
Wen Zhong ZHANG ; Na Na SUN ; Yang HU ; Yu CAO ; Sheeks AMBER
Biomedical and Environmental Sciences 2022;35(2):170-173
Animals
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Caffeine/adverse effects*
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Central Nervous System Stimulants/adverse effects*
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Dose-Response Relationship, Drug
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Female
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Fetal Growth Retardation/chemically induced*
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Immune System Diseases/chemically induced*
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Male
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Organ Size/drug effects*
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Pregnancy
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Pregnancy Complications/immunology*
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Rats
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Spleen/growth & development*
3.Clinical Study on Carbon Monoxide Intoxication in Children.
Jung Keun KIM ; Chang Joon COE
Yonsei Medical Journal 1987;28(4):266-273
Carbon monoxide intoxication has long been one of the most serious public health problems in Korea. This is mainly due to the wide use of anthracite coal briquettes as domestic fuel for cooking and under-the floor heating. One hundred and seven cases of CO intoxicated children hospitalized at Yonsei Medical center from January 1970 to December 1986 have been investigated clinically. The sex ratio was 1.3:1 (male 60 cases, female 47 cases) with the peak incidence occuring in patients between 12 and 14 years of age (28%). The most common symptoms were vomiting convulsions and headache; and the most frequent signs were altered mental state, increased deep tendon reflex and a positive Babinski sign. The outcome of patients was as follows: 4 cases (3.7%) expired, 77 cases (72.0%) recovered without neurologic sequelae and 26 cases (24.3%) survived with neurologic sequelae. The neurologic sequelae included persistent convulsions (7 cases), cortical blindness (3 cases), peripheral neuropathy (2 cases) and delayed neurologic sequelae (11 cases). Neurologic sequelae occurred most frequently in comatose patients (45.5%) and least often in mentally alert patients (6.1%), more frequently m patients exposed to CO gas for more than 8 hours than in those exposed for less than 8 hours, and in patients who did not receive hyperbaric oxyen therapy(29.4%) than in those who did(19.6%). Delayed neurologic sequelae were mental retardation (72.7%), epilepsy (36.4%), mutism (18.2%) etc. The lucid interval in 11 cases of delayed neurologic sequelae ranged from 2 to 20 days. The results of this study suggest that every patient exposed to CO gas should receive prompt and efficient oxygenation including hyperbaric oxygen therapy and that expeditious reduction of cerebral edema maybe of value. The importance of providing follow-up facilities in anticipation of a relapse of the delayed neurologic sequelae has been established.
Adolescent
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Carbon Monoxide Poisoning/complications*
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Carbon Monoxide Poisoning/radiography
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Carbon Monoxide Poisoning/therapy
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Central Nervous System Diseases/chemically induced*
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Child
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Child, Preschool
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Female
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Human
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Hyperbaric Oxygenation
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Male
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Tomography, X-Ray Computed
4.Short-term central nervous system symptoms and changes in blood indicators after benzene poisoning in rats.
Qiu-ying LIU ; Xiao-yang LIANG ; Xiu-qin WANG ; Nian-guang CHEN ; Jie SUN ; Guan-chao LAI
Journal of Southern Medical University 2011;31(11):1935-1937
OBJECTIVETo observe the central nervous system symptoms and alterations in the blood indicators in rats within a short term after benzene poisoning.
METHODTwenty-four female SD rats were randomized into 4 equal groups to receive intraperitoneal injection of low-, medium- or high-dose benzene (39.05, 78.11, and 234.33 mg/kg, respectively) or peanut oil. Blood samples were taken from the rats via the femoral artery 24 h after the injections for routine blood test and liver and kidney function test.
RESULTSIntraperitoneal injection of benzene at a high dose, but not at a low or medium dose, caused obvious symptoms in the central nervous system. Benzene either at a low or medium dose did not produce obvious changes in routine blood test or liver and kidney function test as compared with the control group, but a high dose resulted in significant changes in WBC, PLT, ALT and AST (P<0.05). Abnormalities in the renal function were found in none of the groups (P>0.05).
CONCLUSIONExposure to high-dose benzene can result in abnormalities in the central nervous system, routine blood indicators and liver function, but does not obviously affect the kidney function in rats.
Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Benzene ; toxicity ; Blood Cell Count ; Central Nervous System Diseases ; chemically induced ; Female ; Kidney ; drug effects ; Liver ; drug effects ; Rats ; Rats, Sprague-Dawley
5.Effect of heavy metals exposure on neurobehavioral function in welders.
Xian-Liang WANG ; Yong-Jian YANG ; Ming-Yu DING ; Zhan-Jun QUAN ; Xiu-Ge ZHAO ; Jing NIE ; Yan QIAN ; Jin-Liang ZHANG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2008;26(11):641-644
OBJECTIVETo explore the relationship between heavy metals exposure and neurobehavioral function impairment in welders.
METHODSThe metals exposure in 82 welders and 51 operators were investigated with blood Pb, Cd and Mn via AAS, and the nervous impairment was evaluated with neurobehavioral core test battery (NCTB).
RESULTSPb [(115.49 +/- 79.22) microg/L] and Cd [(3.67 +/- 3.19) microg/L] in welders were significantly higher than operators [(69.32 +/- 50.79) and (0.83 +/- 0.76) microg/L respectively] (P < 0.05). Welders had worse standard scores of NCTB 13 items such as depression-dejection than non-welders (P < 0.05). Significant difference of confusion-bewilderment and forward digit span in welders only existed in different groups of Pb and Mn, respectively. A dose-effect relationship was found between forward digit span and serum Mn level in welders. General linear regression analysis indicated that Pb exposure, Mn exposure and alcohol consume had negative relation with the loss of nervous system function.
CONCLUSIONThe nervous impairment in welders is attributed to occupational exposure to Pb and Mn, concomitantly.
Adult ; Air Pollutants, Occupational ; adverse effects ; Central Nervous System Diseases ; chemically induced ; physiopathology ; Cross-Sectional Studies ; Female ; Humans ; Male ; Metals, Heavy ; adverse effects ; Neuropsychological Tests ; Occupational Exposure ; adverse effects ; Welding ; Young Adult
6.In vitro and in vivo gene therapy with CMV vector-mediated presumed dog beta-nerve growth factor in pyridoxine-induced neuropathy dogs.
Jin Young CHUNG ; Jung Hoon CHOI ; Il Seob SHIN ; Eun Wha CHOI ; Cheol Yong HWANG ; Sang Koo LEE ; Hwa Young YOUN
Journal of Veterinary Science 2008;9(4):367-373
Due to the therapeutic potential of gene therapy for neuronal injury, many studies of neurotrophic factors, vectors, and animal models have been performed. The presumed dog beta-nerve growth factor (pdbeta-NGF) was generated and cloned and its expression was confirmed in CHO cells. The recombinant pdbeta-NGF protein reacted with a human beta-NGF antibody and showed bioactivity in PC12 cells. The pdbeta-NGF was shown to have similar bioactivity to the dog beta-NGF. The recombinant pdbeta-NGF plasmid was administrated into the intrathecal space in the gene therapy group. Twenty-four hours after the vector inoculation, the gene therapy group and the positive control group were intoxicated with excess pyridoxine for seven days. Each morning throughout the test period, the dogs' body weight was taken and postural reaction assessments were made. Electrophysiological recordings were performed twice, once before the experiment and once after the test period. After the experimental period, histological analysis was performed. Dogs in the gene therapy group had no weight change and were normal in postural reaction assessments. Electrophysiological recordings were also normal for the gene therapy group. Histological analysis showed that neither the axons nor the myelin of the dorsal funiculus of L(4) were severely damaged in the gene therapy group. In addition, the dorsal root ganglia of L(4) and the peripheral nerves (sciatic nerve) did not experience severe degenerative changes in the gene therapy group. This study is the first to show the protective effect of NGF gene therapy in a dog model.
Amino Acid Sequence
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Animals
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Base Sequence
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CHO Cells
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Central Nervous System Diseases/chemically induced/therapy/*veterinary
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Cloning, Molecular
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Cricetinae
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Cricetulus
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Cytomegalovirus
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Dog Diseases/*chemically induced/therapy
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Dogs
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Female
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Gene Therapy/*veterinary
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Genetic Vectors
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Male
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Molecular Sequence Data
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Nerve Growth Factor/genetics/*metabolism/*therapeutic use
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Pyridoxine/*toxicity