Hydrogen sulphide poisoning is an acute poisoning event that occurs frequently in summer. A case of acute hydrogen sulphide poisoning in a confined space in August 2018 was investigated and clinical data were analyzed. This is a typical case of acute hydrogen sulfide gas poisoning in a confined space. The main cause of the accident is the lack of occupational protection and illegal rescue. Among the 5 patients, 3 died, 1 patient had long-term sequelae of nervous system damage such as cortical blindness, and 1 patient was cured.
Accidents ; Accidents, Occupational ; Confined Spaces ; Gas Poisoning ; Humans ; Hydrogen Sulfide ; Poisoning

Hydrogen sulfide is a colorless gas and frequently lethal occupational hazard that causes tissue hypoxia with prominent neurological signs. Depending on the amount of exposure, many neurotoxic effects such as headache, disequilibrium, and loss of consciousness have been reported. However, a few address the brain MRI findings in hydrogen sulfide poisoning. We report serial brain MRI findings in a patient with hydrogen sulfide intoxication.
Anoxia ; Brain ; Headache ; Humans ; Hydrogen Sulfide* ; Hydrogen* ; Hypoxia, Brain* ; Magnetic Resonance Imaging* ; Poisoning ; Unconsciousness

Accidents ; Humans ; Hydrogen Sulfide ; poisoning ; Vegetables

OBJECTIVETo investigate the dynamic changes of oxidative stress and nuclear factor-E2 related factor 2 (Nrf2) expression in the lung tissues of acute hydrogen sulfide (H2S) intoxicated rats and intervention effects of ulinastatin (UTI).

METHODSA total of 96 SD rats of clean grade were divided randomly into four groups: normal control group (n = 8), UTI control group (n = 8), H2S -intoxicated model group (n = 40), and UTI treatment group (n = 40). The H2S-intoxicated model group and UTI treatment group were exposed to H2S (283.515 mg/m3) by inhalation for 1h, then UTI treatment group was intraperitoneally exposed to UTI at the dose of 10(5) U/kg for 2 h. H2S-intoxicated model group and UTI treatment group were sacrificed at 2, 6, 12, 24 and 48 h after exposure, respectively. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione (GSH) in the rat lung tissues were measured. The expression levels of Nrf2 mRNA in the rat lung tissues were detected. Pathological changes of rat lung tissues were observed under a light microscope and the lung injury scores were evaluated.

RESULTSCompared with control group, the pulmonary SOD, CAT and GSH levels at 2,6 and 12 h after exposure and the pulmonary GSH-Px levels at 2, 6, 12 and 24 h after exposure in H2S-intoxicated model group significantly decreased (P < 0.05 or P < 0.01). The levels of pulmonary MDA at 2, 6, 12 and 24 h after exposure in H2S-intoxicated model group were significantly higher than those in normal control group (P < 0.01). As compared with H2S -intoxicated model group, the pulmonary GSH-Px activities at 6 and 12 h after exposure, the pulmonary CAT activities at 2, 6 and 12 h after exposure, the pulmonary GSH levels at 2, 6, 12 and 24 h after exposure and the pulmonary SOD activities at 2, 6, 12, 24 and 48 h after exposure in UTI treatment group significantly increased (P < 0.05 or P < 0.01), the pulmonary MDA levels at 2, 6 and 12 h after exposure in UTI treatment group significantly decreased (P < 0.01). The expression levels of Nrf2 mRNA at 2, 6, 12, 24 h after exposure in H2S-intoxicated model group were 0.314 +/- 0.011, 0.269 +/- 0.010, 0.246 +/- 0.011 and 0.221 +/- 0.018, respectively, which were significantly higher than those (0.149 +/- 0.012) in control group (P < 0.01). As compared with H2S-intoxicated model group, the expression levels (0.383 +/- 0.017, 0.377 +/- 0.014, 0.425 +/- 0.017, 0.407 +/- 0.011 and 0.381 +/- 0.010) of Nrf2 mRNA at 2, 6, 12, 24 and 48 h after exposure in UTI treatment group significantly increased (P < 0.01). The lung injury at 24 h after exposure in H2S-intoxicated model group was higher than that in UTI treatment group. Histopathological examination showed that the scores of lung injury at 12, 24 and 48 h after exposure in UTI treatment group was significantly lower than those in H2S-intoxicated model group (P < 0.01).

CONCLUSIONOxidative stress and Nrf2 activation may be the important factors in rat lung injury induced by H2S-intoxicated, UTI may reduce the rat lung injury and protect the rat lung from damage induced by H2S by inhibiting ROS, improving the imbalance in redox and up-regulating Nrf2 mRNA expression.

Acute Lung Injury ; chemically induced ; metabolism ; Animals ; Glycoproteins ; pharmacology ; Hydrogen Sulfide ; poisoning ; Lung ; metabolism ; Male ; NF-E2-Related Factor 2 ; metabolism ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.
Arsenic ; Ataxia ; Carbon Disulfide ; Carbon Monoxide ; Cerebellar Diseases ; Delivery of Health Care ; Developing Countries ; Dimethylamines ; Disease Outbreaks ; Electrophysiology ; Gases ; Hexanes ; Hydrogen Sulfide ; Manganese ; Metals, Heavy ; Nervous System ; Neuroimaging ; Neurologic Manifestations ; Neuromuscular Junction Diseases ; Neurotoxins ; Occupational Diseases ; Occupational Health ; Organophosphate Poisoning ; Organophosphates ; Parkinsonian Disorders ; Polychlorinated Biphenyls ; Quaternary Ammonium Compounds ; Semiconductors ; Sodium Fluoride ; Solvents ; Taiwan ; Thallium ; Tin ; Toluene ; Urethane

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.
Arsenic ; Ataxia ; Carbon Disulfide ; Carbon Monoxide ; Cerebellar Diseases ; Delivery of Health Care ; Developing Countries ; Dimethylamines ; Disease Outbreaks ; Electrophysiology ; Gases ; Hexanes ; Hydrogen Sulfide ; Manganese ; Metals, Heavy ; Nervous System ; Neuroimaging ; Neurologic Manifestations ; Neuromuscular Junction Diseases ; Neurotoxins ; Occupational Diseases ; Occupational Health ; Organophosphate Poisoning ; Organophosphates ; Parkinsonian Disorders ; Polychlorinated Biphenyls ; Quaternary Ammonium Compounds ; Semiconductors ; Sodium Fluoride ; Solvents ; Taiwan ; Thallium ; Tin ; Toluene ; Urethane

OBJECTIVETo discuss the clinical manifestations and CT features of acute moderate or severe hydrogen sulphide poisoning fishermen.

METHODSThe clinic and CT datas of 8 acute moderate or severe hydrogen sulphide poisoning cases were retrospectively analysed.

RESULTSThe lesions located at two pulmonary each leaf in 3 cases, located at both lower lungs in 3 cases and asymmetry leaves in 2 cases. Lesions form: little patchy shadow in 8 cases (8/8), fibrous band shadow in 4 cases (4/8), ground glass shadow in 3 cases (3/8), peripheral fuzzy interlobular nodule in 4 cases (4/8); 5 cases complicated with pleural effusion; After treatment 6 ∼ 10 days, the pulmonary shadows were absorbed obviously; Fibrous band shadow was residual in a case after a follow-up of 2 months.

CONCLUSIONWith definite history of hydrogen sulphide inhalation and the corresponding clinical manifestations, and if fishermen contacted for a long time, who would be made chemical pulmonary damage; Combined with the imaging manifestations, the diagnosis as well as the severity of pulmonary damage could be made.

Adult ; Fisheries ; Humans ; Hydrogen Sulfide ; poisoning ; Lung ; diagnostic imaging ; Male ; Middle Aged ; Retrospective Studies ; Tomography, X-Ray Computed

OBJECTIVETo establish health protection zone standards for petroleum processing industry.

METHODSThe intensity of characteristic pollutants from fugitive emission were estimated by the inverse method of ground concentration through field survey and monitoring for representative petroleum processing industry, which was calculated health protection zone by using the model of atmospheric diffusion.

RESULTSCharacteristic pollutant of fugitive emission source from petroleum processing industry was confirmed as hydrogen sulfide. When local average wind speed in the past five years was less than 2, 2-4 m/s and more than 4 m/s respectively and meanwhile the scale of petroleum processing industry was less than 8 million tons, the recommended value of health protection zone were 900, 800, 700 m respectively. Besides, when the scale of petroleum processing industry was more than 8 million tons and in the same wind speed level, the recommended value of health protection zone were 1200, 1000, 900 m respectively.

CONCLUSIONSRecommended value of health protection zone for petroleum processing industry was reasonable and feasible through revising and improving of the version of 1987's standard.

Environmental Monitoring ; Extraction and Processing Industry ; Hydrogen Sulfide ; poisoning ; Occupational Diseases ; prevention & control ; Occupational Health Services ; standards ; Petroleum

Humans ; Hydrogen Sulfide ; poisoning ; Male ; Methylene Blue ; therapeutic use ; Poisoning ; therapy ; Young Adult

OBJECTIVETo evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication.

METHODSOne hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3), the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope.

RESULTSThe results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E.

CONCLUSIONHydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria, alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.

Animals ; Hydrogen Sulfide ; poisoning ; Hyperbaric Oxygenation ; Liver ; pathology ; Lung ; pathology ; Male ; Myocardium ; pathology ; Oxygen Inhalation Therapy ; Pulmonary Alveoli ; pathology ; Rats ; Rats, Wistar