• Safety and Health at Work
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• v.3 no.1
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• pp.11-16
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• 2012

Lead poisoning is one of the earliest identified and most known occupational disease. Its acute effects have been recognized from antiquity when this condition principally afflicted manual workers and slaves, actually scarcely considered by the medicine of that time. The Industrial Revolution caused an epidemic of metal intoxication, urging scientists and physician of that period to study and identify specific symptoms and organ alterations related to chronic lead poisoning. During the 20th century, the acknowledgment of occupational and environmental toxicity of lead fostered public awareness and legislation to protect health. More recently, the identification of sub-clinical effects have greatly modified the concept of lead poisoning and the approaches of medicine towards this condition. Nowadays, lead poisoning is rarely seen in developed countries, but it still represents a major environmental problem in certain areas. Consequently, it may appear as a paradigm of "occupational and environmental disease," and the history of this condition seems to parallel the historical development of modern "Occupational and Environmental Health" as a more complete medical discipline.

• The Korean Journal of Physiology
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• v.20 no.1
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• pp.53-63
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• 1986

Carbon monoxide(CO) poisoning has been one of the major environmental problems because of the tissue hypoxia, especially brain tissue hypoxia, due to the great affinity of CO with hemoglobin. Inhalation of the pure oxygen$(0_2)$ under the high atmospheric pressure has been considered as the best treatment of CO poisoning by the supply of $0_2$ to hypoxic tissues with dissolved from in plasma and also by the rapid elimination of CO from the carboxyhemoglobin(HbCO). Hydrogen peroxide $(H_2O_2)$ was rapidly decomposed to water and $0_2$ under the presence of catalase in the blood, but the intravenous administration of $H_2O_2$ is hazardous because of the formation of methemoglobin and air embolism. However, it was reported that the enema of $H_2O_2$ solution below 0.75% could be continuously supplied $0_2$ to hypoxic tissues without the hazards mentioned above. This study was performed to evaluate the effect of $H_2O_2$ enema on the elimination of CO from the HbCO in the recovery of the acute CO poisoning. Rabbits weighting about 2.0 kg were exposed to If CO gas mixture with room air for 30 minutes. After the acute CO poisoning, 30 rabbits were divided into three groups relating to the recovery period. The first group T·as exposed to the room air and the second group w·as inhalated with 100% $0_2$ under 1 atmospheric pressure. The third group was administered 10 ml of 0.5H $H_2O_2$ solution per kg weight by enema immediately after CO poisoning and exposed to the room air during the recovery period. The arterial blood was sampled before and after CO poisoning ana in 15, 30, 60 and 90 minutes of the recovery period. The blood pH, $Pco_2\;and\;Po_2$ were measured anaerobically with a Blood Gas Analyzer and the saturation percentage of HbCO was measured by the Spectrophotometric method. The effect of $H_2O_2$ enema on the recovery from the acute CO poisoning was observed and compared with the room air group and the 100% $0_2$ inhalation group. The results obtained from the experiment are as follows: The pH of arterial blood was significantly decreased after CO poisoning and until the first 15 minutes of the recovery period in all groups. Thereafter, it was slowly increased to the level of the before CO poisoning, but the recovery of pH of the $H_2O_2$ enema group was more delayed than that of the other groups during the recovery period. $Paco_2$ was significantly decreased after CO poisoning in all groups. Boring the recovery Period, $Paco_2$ of the room air group was completely recovered to the level of the before CO Poisoning, but that of the 100% $O_2$ inhalation group and the $H_2O_2$ enema group was not recovered until the 90 minutes of the recovery period. $Paco_2$ was slightly decreased after CO poisoning. During the recovery Period, it was markedly increased in the first 15 minutes and maintained the level above that before CO Poisoning in all groups. Furthermore $Paco_2$ of the $H_2O_2$ enema group was 102 to 107 mmHg and it was about 10 mmHg higher than that of the room air group during the recovery period. The saturation percentage of HbCO was increased up to the range of 54 to 72 percents after CO poisoning and in general it was generally diminished during the recovery period. However in the $H_2O_2$ enema group the diminution of the saturation percentage of HbCO was generally faster than that of the 100% $O_2$ inhalation group and the room air group, and its diminution in the 100% $O_2$ inhalation group was also slightly faster than that of the room air group at the relatively later time of the recovery period. In conclusion, the enema of 0.5% $H_2O_2$ solution is seems to facilitate the elimination of CO from the HbCO in the blood and increase $Paco_2$ simultaneously during the recovery period of the acute CO poisoning.

• Journal of The Korean Society of Clinical Toxicology
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• v.4 no.2
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• pp.170-174
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• 2006

Methylene blue is a basic thiazine dye frequently used for histologic staining. In clinical toxicology settings, it is also used to treat clinically significant methemoglobinemia. It has dose-dependent oxidation or reduction properties, acting as a reducing agent at lower doses and as an oxidizing agent at higher doses. Hemolytic anemia and hyperbilirubinemia are known toxic effects of methylene blue treatment that have been reported clinically. A 42-year-old woman developed significant methemoglobinemia after acute dapsone overdose; she was treated appropriately with intravenous methylene blue in the therapeutic range. The patient's methemoglobin levels returned to normal. However, 2-4 days later she was noted to have rebound methemoglobinemia, hemolytic anemia, and hyperbilirubinemia. A repeat of Coomb's test and other anemia workups were negative. For management of methylene blue-induced hemolytic anemia, she was administered steroid therapy, N-acetylcysteine, and a blood transfusion. She ultimately recovered, and there were no long-term sequelae from the methylene blue poisoning.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.1
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• pp.46-49
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• 2015

Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.

• Journal of The Korean Society of Clinical Toxicology
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• v.6 no.2
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• pp.83-90
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• 2008

Organophosphate (OP) pesticides are the most common source of human toxicity globally, causing high mortality and morbidity despite the availability of atropine as a specific antidote and oximes to reactivate acetylcholinesterase. The primary toxicity mechanism is inhibition of acetylcholinesterase (AchE), resulting in accumulation of the neurotransmitter, acetylcholine, and abnormal stimulation of acetylcholine receptors. Thus, the symptoms (muscarinic, nicotinic, and central nervous system) result from cholinergic overactivity because of AchE inhibition. OP can also cause rhabdomyolysis, pancreatitis, parotitis, and hepatitis. OP therapy includes decontamination, supportive therapy, and the use of specific antidotes such as atropine and oximes. However, there has been a paucity of controlled trials in humans. Here we evaluated the literature for advances in therapeutic strategies for acute OP poisoning over the last 10 years.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.2
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• pp.172-175
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• 2018

Acute nicotine poisoning by liquid nicotine for electronic cigarettes is becoming an increasing problem worldwide. On the other hand, there are no regulations regarding its concentration, container or labelling in Korea. This is the first case of a cardiac arrest after liquid nicotine ingestion that was confirmed by plasma nicotine detection in Korea. A 34-year-old male was found with a cardiac arrest at home by the emergency medical services crew, and had a return of spontaneous circulation after 27 minutes of cardio-pulmonary resuscitation. The cause of his cardiac arrest was suspected to be acute nicotine poisoning by the ingestion of liquid nicotine. Toxicology analysis of the National Forensic Service confirmed plasma nicotine, and the pharmacokinetic estimated average concentration of plasma nicotine at the time of the cardiac arrest was 29.7 mg/L, a lethal dose. He was hospitalized for further treatment, but was discharged after 20 days without any improvement. Considering the strong toxicity of nicotine, appropriate policy decisions are required for sales and distribution.

• Korean Journal of Veterinary Research
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• v.7 no.2
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• pp.46-50
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• 1967

The pathologic studies on the cottonseed meal poisoning in chicken were performed by feeding a diet containing 50 per cent cottonseed meal. The results obtained are summarized as follows: The specific effect of cottonseed meal on chicken was apparently limited to the parenchymatous tissue and blood vessels, where its major pathologic manifestations were degenerative changes in acute cases fed for a period of 7 days, while necrosis of portal and central veins of liver and consequent perivascular hemorrhage and coagulative necrosis of liver and intra-glomerular hemorrhage were characteristic lesions in chronic cases fed for a period 20, 40 and 60 days. In addition, specific cottonseed pigment cells were observed in small number in villus of small intestine in acute cases and in large number in villus, liver and spleen in chronic cases.

• Annals of Clinical Neurophysiology
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• v.20 no.1
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• pp.41-43
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• 2018

ntermediate syndrome (IMS) typically occurs at 24-96 hours following organophosphate (OP) poisoning, after an acute cholinergic crisis, but before OP-induced delayed polyneuropathy. It is characterized by proximal muscle weakness and respiratory insufficiency, which is a major contributing factor of OP-related morbidity and mortality. We report an atypical IMS case showing rapid-onset ascending paralysis and respiratory disturbance with an acute cholinergic crisis occurring 4-5 days after skin exposure to OP.

• Journal of Environmental Health Sciences
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• v.37 no.1
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• pp.22-28
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• 2011

This study aimed to determine the feasibility of survey questionnaires for pesticide poisoning. We conducted a pilot study to develop a questionnaire for evaluating pesticide poisoning symptoms and to examine the validity of self-reported information for individual pesticides used. In December 2010 we interviewed 20 farmers with self-reported pesticide poisoning histories residing in Gyeonggi Province. For validity of pesticide information, the purchased pesticide lists from the agricultural cooperative federation were compared with individual self-reported pesticides used. Neurological symptoms were the most common among clinical symptoms related to pesticide poisoning, followed by gastrointestinal, dermal and eye symptoms. Insecticides were the main causative pesticide class for poisoning. Twenty one major symptoms were selected for screening for acute pesticide poisoning in a field study based on the pilot results and literature reviews. Substantial under-reporting was found in data on self-reported individual pesticides used (9.2%), as well as low accuracy (36%) compared with their actual purchase lists. In this pilot study, we suggest the selected symptom lists may apply to a field survey of pesticide poisoning. However, the self-reported information on individual pesticides may not be valid and alternative methods need to be developed.

• Applied Microscopy
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• v.10 no.1_2
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• pp.53-76
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• 1980