Fatal and non-fatal cases of lime sulfide exposure and pathogenetic mechanisms underlying pancreatic injury: Case reports with an animal experiment.

Lime sulfide poisoning by the oral route is rarely encountered in the practice of forensic science, whereas hydrogen sulfide poisoning is seen frequently. We report here two cases of fatal lime sulfide poisoning with several related cases and in addition induced histological damage with acute inflammation in animal models under at similar concentrations. We also evaluated sulfide and thiosulfate concentrations and speculated as to the cause of pancreatic damage in these cases.

Inhalational and dermal injury due to explosion of calcium hypochlorite.

Calcium hypochlorite is a yellow-white powder widely used as a disinfectant in swimming pools. It releases chlorine gas when added to water and can cause respiratory effects. Dermal and eye injury can occur because of the caustic nature of chlorine. We report a case of chlorine toxicity and burns on a man's face due to the explosion of calcium hypochlorite while he was mixing it into the water.

[Fatal calcium polysulfide overdose presenting corrosive chemical injury of esophagus and sulf-hemoglobinemia].

A-79-year-old woman ingested a cup of unknown violet agricultural solution intentionally. She was vomiting and smelt of sulfur. Arterial blood gas showed metabolic acidosis and marked cyanosis regardless of relatively high PaO2, caused by sulfhemoglobinemia. A nasogastric tube could not be inserted because of marked stenosis caused by endoscopically proven severe corrosive chemical injury (burn) of esophagus. Considering the smell and the clinical presentation, we concluded that the causative agent was calcium polysulfide or lime-sulphur solution, a common agricultural product used as a fungicide. Despite supportive therapy including infusion of NaNO2, the patient expired 4.5 hours after ingestion. Calcium polysulfide ingestions cause direct injury to the upper gastrointestinal tract, and react with gastric HCl producing poisonous H2S gas, which interferes cytochrome oxidase activity, developing tissue hypoxia, shock, and metabolic acidosis. Sulfhemoglobin is also produced causing severe cyanosis.

Fibrosis of the lung and pleura and long-term exposure to wollastonite.

OBJECTIVES: The purpose of this study was to determine whether long-term exposure to wollastonite causes fibrosis of the lung and pleura in humans. METHODS: Forty-nine workers (mean exposure 25 years) in a Finnish limestone-wollastonite mine and mill were examined. Their work histories and symptoms of chronic bronchitis were recorded. The chest radiographs were classified according to the classification of the International Labour Office (1980); a radiographic follow-up from 1981 to 1990 was included. Spirometry and diffusion capacity were measured. Four workers underwent high-resolution computed tomography (HRCT) and bronchoalveolar lavage (BAL). Lung tissue specimens were available for 2 workers. Mineral fibers and asbestos bodies were analyzed from the BAL fluid and lung tissue specimens, which were also analyzed for lung fibrosis. RESULTS: Two workers (4%) had small irregular lung opacities (ILO 1/0), 1 worker (2%) ILO 0/1 of the s/t type. HRCT revealed no parenchymal fibrosis in the 2 workers with the ILO 1/0 classification. Of the 9 workers (18%) with pleural plaques, 5 had been exposed to asbestos. Multivariate logistic regression analyses revealed no association of plaques with the duration of wollastonite or asbestos exposure. Wollastonite fibers or bodies were not found in any of the 4 workers who underwent BAL, nor in either of the workers whose lung tissue specimens were available. CONCLUSIONS: No evidence was found that long-term exposure to wollastonite causes parenchymal fibrosis of the lung and pleura. Furthermore, the findings indicate that wollastonite fibers are poorly retained in human lungs.

Calcium polysulfide overdose: a report of two cases.

BACKGROUND: Calcium polysulfide or lime-sulfur solution is a common agricultural product used as a fungicide. Despite its easy availability, only two prior cases of intentional ingestion, both from Japan, have been reported in the literature. CASE REPORTS: Two cases of calcium polysulfide ingestion are presented. In the first case severe acidosis, coma and cardiac arrest occurred. Despite aggressive supportive therapy, the patient expired. Autopsy examination revealed hemorrhagic necrosis of the gastric mucosa. The second patient also exhibited altered mental status and metabolic acidosis. He experienced liver dysfunction, rhabdomyolysis, renal dysfunction, and aspiration pneumonia. He had endoscopically proven esophageal and gastric mucosal burns which developed into esophageal strictures. CONCLUSIONS: Calcium polysulfide ingestions cause direct caustic injury to the upper gastrointestinal tract, coma and severe metabolic acidosis.

How to diagnose polysulphide poisoning from tissue samples.

We carried out animal experiments to toxicologically verify polysulphide poisoning by analyzing tissue samples. A bathing agent containing calcium polysulphides was administered orally to rats, and then polysulphides and sulphide, the decomposed product of polysulphides, were analyzed by GC and GC/MS. The concentrations of polysulphides (mumol/ml or g) were found to be highest in blood (0.196), followed by the liver (0.051), the lungs (0.018) and kidneys (0.013), but were below the detection limit (0.005 mumol/g) in the other tissues tested. Sulphide was detected in all the tissue samples and was found to be highest in the blood (0.518 mumol/ml), this being 40 times higher than that required for fatal poisoning in the case of hydrogen sulphide. Polysulphide poisoning was considered to be confirmatively diagnosed by detecting and measuring polysuphides and supplementarily sulphide in body tissues, most pertinently in the blood. Two practical cases of suspected poisoning by polysulphides are briefly described.