• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.424-428
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• 1994

Many organic and nonorganic agents can cause chemical pneumonitis. Chemical pneumonitis induced by inhalation of acetic acid is a rare clinical condition. As acetic acid is a water soluble agent, it causes chemical irritation to respiratory tract and causes variable symptoms. We experienced a case of acute lung injury due to inhalation of acetic acid fume. A 56-year-old male patient was admitted due to dyspnea with vomiting for one day. After he inhaled acetic acid fume in occupational situation, he had chest tightness, chilling sense, and productive cough. Our case was good response to oxygen inhalation, antibiotics, and systemic steroids.

• Tuberculosis and Respiratory Diseases
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• v.60 no.5
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• pp.564-570
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• 2006

Toxic gases and soot deposition as a consequence of smoke inhalation can cause direct injury to the upper and lower airways and even to the lung parenchyma. A delay in proper and prompt therapy can be detrimental to critically ill burn patients with an inhalation injury. Therefore, serial chest radiography is an important diagnostic tool for pulmonary complications during treatment. The radiographic findings of the chest include normal, consolidation, interstitial and alveolar infiltrates, peribronchial thickening, atelectasis, cardiogenic and non-cardiogenic pulmonary edema, and a pneumothorax as acute complications of smoke inhalation. In addition, bronchiectasis, bronchiolitis obliterans and pulmonary fibrosis can occur as late complications. We encountered a case of 44-year-old male who presented with acute lung injury after an inhalation injury. He required endotracheal intubation and mechanical ventilation due to respiratory failure. He was managed successfully with conservative treatment. Later, a cavitary lesion of the left upper lobe was observed on the chest radiography and computed tomography, which was complicated by massive hemoptysis during the follow-up. However, the cavitary lesion disappeared spontaneously without any clinical consequences.

• The Journal of Pediatrics of Korean Medicine
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• v.33 no.3
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• pp.82-102
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• 2019

Objectives The purpose of this study is to investigate clinical studies on the efficacy and safety of herbal medicine inhalation therapy in children by analyzing recent randomized controlled trials conducted in China. Methods We searched the clinical studies from the China Academic Journal (CAJ) in China National Knowledge Infrastructure (CNKI) using a by key word '霧化吸入' and specific criteria from 1st January 2010 to 2nd July 2019. Data regarding years of publication, demographic information, target diseases or symptoms, treatment methods, outcome measure, results and adverse events are collected for this study. Results Total of 44 randomized controlled trials were selected and analyzed. Respiratory diseases and symptoms (84.1%) were the most frequent target diseases that herbal medicine inhalation therapy was used. Acute stomatitis was another disease state that the therapy was used. In most of the studies, the herbal medicine inhalation in children showed significant efficacies. The most commonly used herbal medicines were Ephedrae Herba (麻黃), Lonicera Flos (金銀花), Armeniacae Semen (杏仁), Glycyrrhizae Radix et Rhizoma (甘草), Scutellaria Radix (黃芩), Forsythia Fructus (連翹) etc. Hardly any adverse effects were reported from the trials selected. Conclusions Based on the results of the clinical studies from China, herbal medicine inhalation therapy in children can be an effective and safe option for treatment and symptom improvement.

• Journal of The Korean Society of Clinical Toxicology
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• v.4 no.2
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• pp.161-165
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• 2006

Organophosphate insecticides, commonly used in agriculture, are a gradually increasing cause of accidental and suicidal poisoning. Intoxication can occur by ingestion, inhalation or dermal contact. Exposure to organophosphorus agents causes a sequentially triphasic illness consisting of the cholinergic phase, the intermediate syndrome, and organophosphate-induced delayed polyneuropathy. Acute pancreatitis as a rare complication of organophosphate intoxication has also been infrequently observed. We report a case of intoxication with organophosphate (phos-phamidon) by parenteral exposure (inhalation and/or dermal contact). A 34-year-old male patient was transferred to our Emergency Medical Center and was intubated due to a progressive respiratory failure. He presented with meiotic pupils, cranial nerve palsies, weak respiration, and proximal limb motor weaknesses without sensory changes. He had been employed in filling syringes with phosphamidon during the previous month. Because the patient's history and symptoms suggested organophosphate intoxication with intermediate syndrome, he was mechanically ventilated for 18 days with continuous infusion of atropine and pralidoxime (total amounts of 159 mg and 216 g, respectively). During his admission, hyperamylasemia and hyperli-pasemia were detected, and his abdominal CT scan showed a finding compatible with acute pancreatitis. He was administered a conservative treatment with NPO and nasogastric drainage. The patient was discharged and showed neither gastrointestinal nor neurologic sequelae upon follow up at one week and three months.

• Journal of Veterinary Science
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• v.24 no.2
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• pp.22.1-22.12
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• 2023

Background: Citric acid (CA) and sodium hypochlorite (NaOCl) have been used to disinfect animals to protect them against avian influenza and foot-and-mouth disease. Objectives: We performed a good laboratory practice (GLP)-compliant animal toxicity study to assess the acute toxic effects of CA and NaOCl aerosol exposure in Sprague-Dawley rats. Methods: Groups of five rats per sex were exposed for 4 h to four concentrations of the two chemicals, i.e., 0.00, 0.22, 0.67, and 2.00 mg/L, using a nose-only exposure. After a single exposure to the chemicals, clinical signs, body weight, and mortality was observed during the observation period. On day 15, an autopsy, and then gross findings, and histopathological analysis were performed. Results: After exposure to CA and NaOCl, body weight loss was observed but recovered. Two males died in the CA 2.00 mg/L group and, two males and one female died in the 2.00 mg/L NaOCl group. In the gross findings and histopathological analysis, discoloration of the lungs was observed in the CA exposed group and inflammatory lesions with discoloration of the lungs were observed in the NaOCl exposed group. These results suggest that the lethal concentration 50 (LC50) of CA is 1.73390 mg/L for males and > 1.70 mg/L for females. For NaOCl, the LC50 was 2.22222 mg/L for males and 2.39456 mg/L for females. Conclusions: The Globally Harmonized System is category 4 for both CA and NaOCl. In this study, the LC50 results were obtained through a GLP-based acute inhalation toxicity assessment. These results provide useful data to reset safety standards for CA and NaOCl use.

• Tuberculosis and Respiratory Diseases
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• v.62 no.3
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• pp.223-226
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• 2007

Tetrafluoroethylene is a colorless gas that can be used to synthesize a variety of fluoride compounds by polymerization (e.g., Teflon). Fluoride compounds have many applications in industry. There are several reports of inhalation injury from the pyrolytic product of fluoride compounds. When the polymer is heated under the conditions of inadequate ventilation, the fumes can cause polymer fume fever or pulmonary edema which manifested as symptoms such as fever, chill, profuse sweating, cough and dyspnea. However there are no reports of a direct lung injury caused by tetrafluoroethylene. We report a case of a 27-year-old male presented with acute lung injury after inhaling concentrated tetrafluoroethylene. He complained of cough and dyspnea after the accidental inhalation of tetrfluoroethylene at his workplace. The symptoms improved without any complications after conservative treatment with oxygen and steroid.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.1
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• pp.20-22
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• 2004

Acute mercury inhalation poisoning is a rare cause of acute peripheral neuropathy. A 44-year-old female inhaled the fume from heating mercury to treat her palmar dermatitis. For 4 days, this procedure was done for 2-3 minutes after each meal. She subsequently complained flu like symptoms, such as headache, toothache, myalgia and arthralgia. She was admitted for 9 days and then symptoms disappeared. About 3 weeks after exposure, both knee pain developed and then she could not walk. To treat mercury intoxication, she was referred to our hospital. At that time, initial laboratory data were within normal limits, but blood and urinary mercury level were 5.6 11$\mu$g/dl, 132.8 $\mu$g/L. After treatment with D-penicillamine for 7 days, blood and urinary mercury level were 3.9 1$\mu$g/dl, 177.3 $\mu$g/L. During the following 1 month, both leg symptoms remained. Nerve conduction studies were performed, both leg sensory nerve amplitude decreased. These findings were suggestive of peripheral polyneuropathy.

• Journal of Radiation Protection and Research
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• v.38 no.2
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• pp.68-77
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• 2013

Derived Investigation levels(DILs) were calculated to protect the workers from the effects of both radiological hazard and chemical toxicity by uranium intake. Investigation Levels(ILs) of committed effective dose of 2 mSv $y^{-1}-6$ mSv $y^{-1}$ and uranium concentration of 0.3 ${\mu}g$ $g^{-1}$ in kidney, based on Korean Nuclaer Safety Act, Korean Occupational Safety and Health Act and current scientific studies of uranium intake were assumed. DILs of radiological hazard and chemical toxicity were then calculated based on the concentration of uranium in air of workplace, the lung monitoring and urine analysis, respectively. As a result, in case of the nuclear fuel fabrication plant where 3.5% enriched uranium is handled, derived investigation level(DIL) for the control of the concentration of uranium in the air of workplace assumed with 15-min acute inhalation was 0.6 mg $m^{-3}$ for all types of uranium. DILs for the control of the average concentration of uranium in air of workplace, assuming an 8-hour workday, were 15.21 ${\mu}g$ $m^{-3}$ of Type F uranium, 0.41-1.23 Bq $m^{-3}$ and 0.13-0.39 Bq $m^{-3}$ for Type M and Type S uranium, respectively. DILs for the lung monitoring assumed with a period of 6-month interval were 0.37-1.11 Bq and 0.39-1.17 Bq in acute and chronic inhalation for Type M, respectively and 0.30- 0.91 Bq and 0.19-0.57 Bq in acute and chronic inhalation for Type S, respectively. Since a detection limit of typical germanium detector for the measurement of 235U activity is 4 Bq, DILs calculated for the lung monitoring were not appropriate. DILs for urine analysis, for which an interval was assumed to be 1 month, were 14.57 ${\mu}g$ $L^{-1}$ based on chemical toxicity after acute inhalation. In addition, acute and chronic inhalation of Type M were calculated 2.85-8.58 ${\mu}g$ $L^{-1}$ and 1.09-3.27 ${\mu}g$ $L^{-1}$ based on the radiological hazard, respectively.

• Toxicological Research
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• v.14 no.4
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• pp.495-500
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• 1998

The effect of acute toluene exposure on behaviour and monoamine concentrations in the various brain regions were investigated in the rat. Toluene was adminstered via inhalation to rats at concentrations of 0, 1000, 10000, 40000 ppm for 20 min. During exposure to toluene, spontaneous locomotor activity was counted. After exposure, animals were sacrificed instantly and brains were separated. Regional concentratons of brain monoamines (norepinephrine, NE; dopamine, DA; 5- hydroxytryptamine, 5-HT) and its metabolites (3,4-dihydroxyphenylacetic acid, DOPAC; homovanillic acid, HVA; 5-hydroxyindole-3-acetic acid, 5-HIAA) were determined. The changes in locomotor activity during toluene exposure depended on the toluene concentration. At 1000 ppm concentration, spontaneous locomotor activity increased initially and thereafter decreased. At higher concentrations (10000 ppm and 40000 ppm), spontaneous locomotor activity decreased and eventually ceased. A regional analysis of VA, NE, 5-HT, VOPAC, HVA, and 5-HIAA indicated a significant decrease in VA concentrations in cerebellum and striatum while NE and 5-HT concentrations were significantly increased in the cerebellum and cortex. 5-HIAA concentrations were significantly increased in all brain regions. DOPAC concentrations were significantly increased in cerebellum and cortex while decreased in striatum. These results especially indicated that metabolic conversion of DA to HVA in striatum was highly increased by toluene inhalation. However, It remains to elucidate between behavioural responses and monoamine changes.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.2
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• pp.67-71
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• 2004

Arsenic poisoning has three types of poisoning. First, acute arsenic poisoning is usually caused by oral intake of large amount of arsenic compound with purpose of homicide or suicide. Second, chronic arsenic poisoning is caused by inhalation of arsenic in the occupational setting or by long-term oral intake of arsenic-contaminated well water. Third, arsine poisoning occurs acutely when impurities of arsenic in non-ferrous metal react with acid. Clinical manifestation of acute arsenic poisoning is mainly gastrointestinal symptoms and cardiovascular collapse. Those of chronic poisoning are skin disorder and cancer. Arsine poisoning shows massive intravascular hemolysis and hemoglobinuria with acute renal failure. Exposure evaluation is done by analysis of arsenic in urine, blood, hair and nail. Species analysis of arsenic is very important to evaluate inorganic arsenic acid and mono methyl arsenic acid (MMA) separated from dimethyl arsenic acid (DMA) and trimethyl arsenic acid (TMA) which originate from sea weed and sea food. Treatment with dimercaprol (BAL) is effective in acute arsenic poisoning only.