• Journal of The Korean Society of Clinical Toxicology
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• v.14 no.2
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• pp.122-128
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• 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.

• 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.

• Carbon letters
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• v.16 no.3
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• pp.198-202
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• 2015

Carbon-supported Pt catalyst systems containing defect adsorption sites on the anode of direct methanol fuel cells were investigated, to elucidate the mechanisms of H₂ dissociation and carbon monoxide (CO) poisoning. Density functional theory calculations were carried out to determine the effect of defect sites located neighboring to or distant from the Pt catalyst on H₂ and CO adsorption properties, based on electronic properties such as adsorption energy and electronic band gap. Interestingly, the presence of neighboring defect sites led to a reduction of H₂ dissociation and CO poisoning due to atomic Pt filling the defect sites. At distant sites, H₂ dissociation was active on Pt, but CO filled the defect sites to form carbon π-π bonds, thus enhancing the oxidation of the carbon surface. It should be noted that defect sites can cause CO poisoning, thereby deactivating the anode gradually.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.2
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• pp.100-109
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• 2021

Purpose: The purpose of this study was to investigate effect of N-acetylcysteine (NAC) on the injury of putative parvalbumin positive interneurons defined by molecular marker and hippocampal long-term potentiation (LTP), a marker of neural plasticity following acute carbon monoxide (CO) poisoning. Methods: Adult Sprague-Dawley rats were exposed to 1100 ppm CO for 40 minutes followed by 3000 ppm CO for 20 minutes. Animals received daily intraperitoneal injection of NAC (150 mg/kg) for 5 days after CO exposure. Changes in learning and spatial memory were evaluated by Y-maze test 5 days after the poisoning. In vivo LTP in hippocampal CA1 area was evaluated by using extracellular electrophysiological technique. Immunohistochemical staining were adopted to observe expressional damages of parvalbumin (PV) immunoreactive interneurons in the hippocampus following the poisoning. Results: Acute CO intoxication resulted in no changes in memory performance at Y-maze test but a significant reduction of LTP in the in hippocampal CA1 area. There was also a significant reduction of PV (+) interneurons in the hippocampal CA1 area 5 days after CO poisoning. Daily treatment of NAC significantly improved hippocampal LTP impairment and reduced immunoreactivity for PV in the hippocampus following the acute CO poisoning. Conclusion: The results of this study suggest that reduction of hippocampal LTP and PV (+) interneurons in the hippocampus is sensitive indicator for brain injury and daily NAC injections can be the alternative therapeutics for the injury induced by acute CO poisoning.

• The Korean Journal of Physiology
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• v.1 no.2
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• pp.185-191
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• 1967

In order to evaluate the elimination of CO through the lung comparing with the decrease of CO content in the blood, authors had induced acute CO poisoning on 9 dogs. Arterial CO-Hb saturation, CO concentration, %, in expired gas and eliminated CO amount through the lung were measured at 1,5,10,30,60, and 120 minutes after acute CO poisoning in 6 dogs breathing room air and 3 dogs breathing room air and oxygen alternately. Results obtained are summarized as follows. In room air breathing group, arterial CO-Hb saturation averaged 50.8% , and 53.67 ml of CO was blew off through the lung during 120 minutes and in alternately air and oBygen breathing group, the arterial CO-Hb saturation averaged 65.6% and 95.6 ml of CO was blew off through the lung. The amount of CO eliminated in expired gas for 120 minute was much less than the amount of decreased CO in arterial blood which was calculated with the decreased CO-Hb content in the estimated circulating blood volume. Such difference between the amount of eliminated CO in expired gas and the decreased CO in blood might be attributed to the oxidation of CO to $CO_2$ in the tissues. Concentration of CO in expired gas was markedly increased and the rate of decrease in arterial CO-Hb saturation is enhanced by oxygen breathing. In early period of recovery from acute CO poisoning, neither the CO concentration in expired gas, nor, the rate of CO elimination (unlit 2 minutes after CO poisoning) showed close correlation with the blood CO-Hb saturation level. The reason seemed to be due to irregularly depressed or unevenly stimulated respiration which were induced by acute CO poisoning.

• Clean Technology
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• v.25 no.4
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• pp.296-301
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• 2019

This study was conducted to investigate the characteristics of CO oxidation by NO poisoning in Pt/TiO₂ catalyst prepared by wet impregnation method and calcined at 400 ℃. In order to confirm the NO poisoning effect of the Pt/TiO₂ catalyst, the change of reaction activity was observed when NO was injected during the CO+O₂ reaction where it was ascertained that the CO conversion rate rapidly decreased below 200 ℃. Also, CO conversion was not observed below 125 ℃. Recovery of initial CO conversion was not verified even if NO injection was blocked at 125 ℃. Accordingly, various analyses were performed according to NO injection. First, as a result of the TPD analysis, it was confirmed that NO pre-adsorption in catalyst inhibited CO adsorption and conversion desorption from adsorbed CO to CO₂. When NO was pre-adsorbed, it was confirmed through H₂-TPR analysis that the oxygen mobility of the catalyst was reduced. In addition, it was validated through FT-IR analysis that the redox cycle (Pt²⁺→Pt⁰→Pt²⁺) of the catalyst was inhibited. Therefore, the presence of NO in the Pt/TiO₂ catalyst was considered to be a poisoning factor in the CO oxidation reaction, and it was determined that the oxygen mobility of the catalyst is required to prevent NO poisoning.

• Journal of The Korean Society of Clinical Toxicology
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• v.17 no.2
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• pp.86-93
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• 2019

Purpose: The objective was to determine the association between PaCO₂ and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Methods: This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 hours later. The baseline characteristics and clinical course during hospitalization were collected and compared. The mean PaCO₂ during the first 6 hours after presentation was calculated. Results: The incidence rates of moderate (30 mmHg< PaCO₂ <35 mmHg) or severe (PaCO₂ ≤30 mmHg) hypocapnia at presentation after acute CO poisoning were 40.7% and 26.8%, respectively. The mean PaCO₂ during the first 6 hours was 33 (31-36.7) mmHg. The incidence of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total ranges of PaCO₂ variables. In multivariate regression analysis, mean PaCO₂ was independently associated with ACVEs (OR 0.798 (95% CI 0.641-0.997)). Conclusion: Mean PaCO₂ during the first 6 hours was associated with increased ACVEs. Given the high incidence of ACVEs and PaCO₂ derangement and the observed association between PaCO₂ and ACVEs, this study suggests that 1) PaCO₂ should be monitored at the acute stage to predict and/or prevent ACVEs; and 2) further study is needed to validate this result and investigate early manipulation of PaCO₂ as treatment.

• Journal of The Korean Society of Clinical Toxicology
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• v.21 no.2
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• pp.117-127
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• 2023

Purpose: No consensus currently exists regarding the maximal pressure of hyperbaric oxygen (HBO₂) therapy performed within 24 hours of acute carbon monoxide (CO) poisoning. This study aimed to evaluate the difference in therapeutic effects according to the first HBO₂ pressure (3.0 atmospheres absolute [ATA] vs. 2.8 ATA). Methods: We used prospectively collected registry data on CO poisoning at a tertiary academic hospital in the Republic of Korea. Adult patients with acute CO poisoning treated with HBO₂ within 24 hours after arrival at the emergency department and without the use of additional HBO₂ after 24 hours between January 2007 and February 2022 were included. Data from 595 patients were analyzed using propensity score matching (PSM). Patients with mild (non-intubated) and severe (intubated) poisoning were also compared. Neurocognitive outcomes at 1 month after CO poisoning were evaluated using the Global Deterioration Scale combined with neurological impairment. Results: After PSM, the neurocognitive outcomes at 1-month post-CO exposure were not significantly different between the 2.8 ATA (110 patients) and 3.0 ATA (55 patients) groups (p=1.000). Similarly, there was also no significant difference in outcomes in a subgroup analysis according to poisoning severity in matched patients (165 patients) (mild [non-intubated]: p=0.053; severe [intubated]: p=1.000). Conclusion: Neurocognitive sequelae at 1 month were not significantly different between HBO₂ therapy pressures of 2.8 ATA and 3.0 ATA in patients with acute CO poisoning. In addition, the 1-month neurocognitive sequelae did not differ significantly between intubated and non-intubated patients.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.1
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• pp.17-23
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• 2021

Purpose: Alcohol ingestion enhances impulsivity and aggression, and has been proven to have a close relationship with suicide. This study investigates whether alcohol co-ingestion affects the Poisoning Severity Score (PSS) grade in patients with intentional poisoning. Methods: We conducted a retrospective analysis of intentional poisoning patients who visited the emergency department (ED) from January 1 to December 31, 2020. Patients were divided into non-drunken and drunken groups. We collected the data based on the medical records of the patients and serum ethanol level results recorded during initial blood tests at the ED. To grade the PSS, the highest score was assessed through clinical signs and test results during the hospital stay. A comparative analysis was conducted between the two groups. Results: A total of 277 patients were included in the study. 163 (58.8%) were in the non-drunken group, and 114 (41.2%) were in the drunken group. The PSS grade showed a significant difference between the two groups (p=0.002). While grade 1 (mild) was observed more in the non-drunken group, grade 2 (moderate) and grade 3 (severe) were seen more in the drunken group. In an ordinal logistic regression analysis, alcohol co-ingestion (adjusted odds ratio [aOR] 2.557, 95% confidence interval [CI] 1.554-4.208, p<0.001) was considered to be a risk factor for a higher PSS grade. There was no significant correlation between the serum ethanol level and the PSS grade. (p=0.568) Conclusion: Intentional poisoning patients with alcohol co-ingestion had a higher PSS. Hence close observation and aggressive treatment in the ED is warranted in such cases.

• Journal of Environmental Health Sciences
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• v.5 no.1
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• pp.25-39
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• 1978

Carbon monoxide poisoning is one of the most serious health problems in Korea. In this review, the author made a intensive reference review on the causes of carbon monoxide poisoning, the patterns of carbon monoxide poisoning and the prospects of CO poisoning. Following findings were induced through the review. 1. Carbon monoxide poisoning is influenced by variable social factors than any other diseases or accidents and is more closely related with the economical and cultural parameters of the community. 2. The increase of risk in the populatlon is expected by National Energy Policy and the hazards of CO poisoning will rather be increasing as long as no radical control measure will be taken. 3. More practical control measure, including extensive public relation service, should be established to eradicate this serious health hazard in Korea.