Boronic Acids ; adverse effects ; Bortezomib ; Humans ; Peripheral Nervous System Diseases ; chemically induced ; Pyrazines ; adverse effects

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 ; Adult ; Central Nervous System Diseases/chemically induced/epidemiology ; Female ; Humans ; Male ; Middle Aged ; Nervous System Diseases/chemically induced/*epidemiology/etiology ; Neurodegenerative Diseases/chemically induced/epidemiology ; Neurotoxicity Syndromes/*epidemiology/*etiology ; Occupational Diseases/chemically induced/*epidemiology/etiology ; Parkinsonian Disorders/chemically induced/epidemiology ; Peripheral Nervous System Diseases/chemically induced/epidemiology ; Republic of Korea

Antineoplastic Agents ; adverse effects ; Humans ; Integrative Medicine ; Organoplatinum Compounds ; adverse effects ; Peripheral Nervous System Diseases ; chemically induced

OBJECTIVETo observe the peripheral neurotoxicity of 1-bromopropane (1-BP) by developing an animal model of peripheral neuropathy through oral administration of 1-BP.

METHODSForty male Wistar rats were randomly and equally divided into low-dose group (200 mg/kg), medium-dose group (400 mg/kg), high-dose group (800 mg/kg), and control group. The rats in the low-dose, medium-dose, and high-dose groups were orally given 1-BP (dissolved in corn oil), while the rats in the control group were orally given an equal volume of corn oil. The oral administration (0.2 ml/100 g BW) was performed once per day, 5 days per week, for 16 consecutive weeks. Neurobehavioral indices including gait score, hindlimb grip strength, and hindlimb landing foot splay were recorded periodically. Hematological and biochemical parameters were also measured during and after 1-BP exposure.

RESULTSThe gait scores were significantly higher in the high-dose group (after 8 ∼ 16 weeks of 1-BP exposure), medium-dose group (after 14 ∼ 16 weeks of 1-BP exposure), and low-dose group (after 15 ∼ 16 weeks of 1-BP exposure) than in the control group (P < 0.05, P < 0.01). Compared with the control group, the high-dose group showed significantly decreased hindlimb grip strength after 9, 12, and 14 weeks of 1-BP exposure (P < 0.05, P < 0.01), with the hindlimbs paralyzed after 16 weeks of 1-BP exposure. After 16 weeks of 1-BP exposure, the hindlimb grip strengths of rats in the medium-dose and low-dose groups were decreased to 72.6% and 91.2% of the control value (P < 0.01, P < 0.05). Compared with the control group, the high-dose group showed significantly increased hindlimb landing foot splay after 12, 14, and 16 weeks of 1-BP exposure, and the medium-dose group showed significantly increased hindlimb landing foot splay after 14 and 16 weeks of 1-BP exposure (P < 0.05, P < 0.01). The high-dose and medium-dose groups showed significantly higher serum alanine aminotransferase (ALT) activity than the control group after 8 weeks of 1-BP exposure, and so did the low-dose group after 16 weeks of 1-BP exposure (P < 0.01).

CONCLUSIONThe nervous system is sensitive to the toxic effect of 1-BP, and 1-BP exposure can induce peripheral neuropathy in rats.

Animals ; Disease Models, Animal ; Hydrocarbons, Brominated ; administration & dosage ; toxicity ; Male ; Peripheral Nervous System Diseases ; chemically induced ; physiopathology ; Rats ; Rats, Wistar

OBJECTIVE: To compare the effects of intravenous and subcutaneous injection of bortezomib on incidence and relative risk of peripheral neuropathy in patients with multiple myeloma(MM). METHODS: The electronic database of PubMed, Embase, Cochrance library, CNKI and related meeting records were searched by computers. The data were derived all from a matched randomized controlled studies. The incidence, relative risk(RR) and 95% confidence interval of peripheral neuropathy caused by intravenous and subcustaneous injections were calculated by the statistical methods. RESULTS: Four RCT studies were selected for meta-analysis, with a total of 911 patients (479 cases and 432 cases in the subcutaneous injection and intravenous injection groups, respectively). The incidence of peripheral neuropathy in the intravenous injection group was 41.4% (95% CI=0.137-0.692, P=0.003), and the incidence of >2 grade of peripheral neuropathy was 15.6% (95% CI=0.005-0.308, P=0.043). The corresponding incidence rates of the subcutaneous injection group were 16% (95% CI=0.021-0.299, P=0.024) and 3.4% (95% CI=-0.011-0.080, P=0.141) respectively. Compared with the intravenous injection group, the RR of peripheral neuropathy and the relative risk of peripheral neuropathy above grade 2 were 0.525, 95% CI=0.297-0.928 (P=0.027) and 0.376, 95% CI=0.196-0.722 (P=0.003) respectively. CONCLUSION Subcutaneous injection of bortezomib at therapeutic doses significantly reduces the incidence of peripheral neuropathy compared with intravenous injection.
Antineoplastic Agents ; Bortezomib ; adverse effects ; Humans ; Incidence ; Injections, Subcutaneous ; Multiple Myeloma ; Peripheral Nervous System Diseases ; chemically induced

OBJECTIVETo analyze the cause of misdiagnosis of occupational chronic n-hexane poisoning and to investigate the diagnosis and differential diagnosis of this disease.

METHODSThe clinical data of 16 patients with occupational chronic n-hexane poisoning who had been misdiagnosed with other diseases were collected. The hospital they first visited, cause of misdiagnosis, clinical features, and the misdiagnosis rate among inpatients during the same period were retrospectively analyzed.

RESULTSSixteen of 62 patients hospitalized during the same period were misdiagnosed at the first visit; 11 cases were in the upper first-class hospitals, and 5 cases in the upper second-class hospitals; 5 cases were misdiagnosed as Green Barry syndrome, 2 cases as motor neuron disease, 2 cases as drug-induced peripheral neuropathy, 3 cases as periodic paralysis, and 4 cases had uncertain diagnosis.

CONCLUSIONMost doctors who work in ordinary hospitals do not know occupational chronic n-hexane poisoning, which is often misdiagnosed as general neuropathies or difficult diseases. The key to correct diagnosis is to know the patient's occupational history and clinical features.

Chronic Disease ; Diagnosis, Differential ; Diagnostic Errors ; Hexanes ; poisoning ; Hospitals ; Humans ; Peripheral Nervous System Diseases ; chemically induced ; Retrospective Studies

Bortezomib ; adverse effects ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Peripheral Nervous System Diseases ; chemically induced ; drug therapy

OBJECTIVETo summarise the clinical features of 18 cases with acute trichloropropane (TCP) poisoning for improving the diagnosis and treatment of the disease.

METHODSExposure history, clinical manifestations, laboratorial examinations, poisoning causes and treatment were retrospectively reviewed in 18 cases with acute TCP poisoning. The results of peripheral lymphocyte micronucleus tests were compared with the healthy control group (n = 33).

RESULTSThe common clinical symptoms were as following: respiratory symptoms were the earlier one set, such as chest tightness in 13, dry and sore throat in 7, cough and runny nose in 2. Gastrointestinal symptoms were more common, such as abdominal pain in 18, nausea and vomit in 14. Only 1 out of 18 patients was found with liver injury. The major manifestation was the increase in ALT and AST, which was returned to normal after treatment. ALL of the 18 patients were found TCP in their serum which concentration was from 39.0 to 310.0 ng/ml, and the average was (68.9 ± 42.1) ng/ml. The symptoms of toxic peripheral neuropathy were typical in all the patients, such as fatigue and numb limb in 18, burning pain of the distal lower limbs in 14, the symmetrical sock-like sensory dysfunction of pain, touch and vibration of the lower limbs in 13, muscle strength reduced in 7, hyporeflexia knee-jerks in 4, hyporeflexia ankle-jerks in 3. The peripheral nerve conduction velocity (NCV) examinations were as followed: the (sensore-nerve conduction velocity) SCV of peroneus super nerve in 18 and the (motor-nerve conduction velocity) MCV of tibial nerve in 8 was slowed down and the distal latency in 18 was prolonged. Micronucleus were found in all 18 cases. The micronucleus rate was 10.06‰ ± 2.80‰ and 8.24‰ ± 2.67‰ in acute TCP poisoning group and healthy control group, respectively. The difference was significant (P < 0.05).

CONCLUSIONThe common clinical manifestations of respiratory exposure of TCP poisoning patients were respiratory symptoms, gastrointestinal symptoms and the symptoms of toxic peripheral neuropathy. Liver injury in those 18 cases was not obvious. Lymphocyte micronucleus of peripheral blood were found in all 18 cases.

Adolescent ; Adult ; Case-Control Studies ; Female ; Gastrointestinal Diseases ; chemically induced ; diagnosis ; therapy ; Humans ; Male ; Neural Conduction ; Peripheral Nervous System Diseases ; chemically induced ; diagnosis ; therapy ; Respiratory Tract Diseases ; chemically induced ; diagnosis ; therapy ; Retrospective Studies ; Trichloroepoxypropane ; poisoning ; Young Adult

OBJECTIVES: Rodenticide Vacor causes a severe peripheral neuropathy in humans. Electrophysiologic studies on a peripheral motor nerve-skeletal system of Vacor-treated rat showed decreased amplitude of muscle action potential without conduction velocity abnormalities. The ultrastructural studies of the neuromuscular junction were performed to clarify the anatomic site of the Vacor-induced peripheral neuropathy in male Wistar rats. METHODS: After oral administration of a single dose of Vacor, 80 mg/kg of body weight, to the experimental animals, neuromuscular junctions within the interosseous muscles of the hind foot were observed in time. RESULTS: No axon terminal change was noted until 24 hours after the administration of Vacor. Remarkable loss of presynaptic vesicles and swollen endoplasmic reticulum in the axon terminal were developed at 3 days after Vacor treatment. Progressive degenerative changes consisting of marked loss of presynaptic vesicles, focal disruption of membrane in the axon terminal with disappearance of the number of the damaged axon terminal appeared, and flattening of postsynaptic folds was also seen. CONCLUSIONS: These results suggest that degenerative changes in axon terminal at neuromuscular junction may contribute to the peripheral neuropathy developed in the early phase of Vacor poisoning.
Animal ; Diabetic Neuropathies/physiopathology ; Diabetic Neuropathies/pathology* ; Diabetic Neuropathies/chemically induced* ; Human ; Male ; Microscopy, Electron ; Neuromuscular Junction/ultrastructure ; Neuromuscular Junction/physiopathology ; Neuromuscular Junction/drug effects ; Peripheral Nervous System Diseases/physiopathology ; Peripheral Nervous System Diseases/pathology ; Peripheral Nervous System Diseases/chemically induced ; Phenylurea Compounds/toxicity* ; Rats ; Rats, Wistar ; Rodenticides/toxicity*

Adolescent ; Adult ; Female ; Hexanes ; poisoning ; Humans ; Male ; Nerve Growth Factor ; blood ; Occupational Diseases ; blood ; Peripheral Nervous System Diseases ; blood ; chemically induced