Multiple poisonings with sodium azide at a local restaurant.

BACKGROUND: Sodium azide is a chemical with a mechanism similar to cyanide. There is concern that it could be used as a chemical warfare agent. OBJECTIVES: We report a cluster of poisonings that occurred at a public restaurant and the subsequent investigation that identified iced tea contaminated with sodium azide (NaN3) and hydrazoic acid, as the foodborne vehicle and agents, respectively. CASE REPORT: Five patients became ill within minutes of drinking iced tea at a restaurant. They all presented to the same Emergency Department with similar symptoms, and improved with fluids, antiemetics, and supportive care. A joint investigation by the Dallas County Department of Health and Human Services, the Texas State Health Department, the Dallas County Southwestern Institute of Forensic Sciences, and the medical toxicologists at the University of Texas Southwestern School of Medicine identified iced tea, contaminated with sodium azide (NaN3) and hydrazoic acid, as the foodborne vehicle and agents, respectively. CONCLUSION: The recurrence, and seriousness, of these events suggests a need for continued education of emergency providers. Emergency physicians should consider exposures to toxic chemicals in their differential when a cluster of patients presents with similar symptoms over a short period of time.

Toxicological analysis of azide and cyanide for azide intoxications using gas chromatography.

Azide is a highly toxic chemical agent to human being. Accidental, but also intentional exposure to azide occurs. To be able to confirm azide ingestion, we developed a method to identify and quantify azide in biological matrices. Cyanide was included in the method to evaluate suggested in vivo production of cyanide after azide ingestion. Azide in biological matrices was first derivatized by propionic anhydride to form propionyl azide. Simultaneously, cyanide was converted into hydrogen cyanide. After thermal rearrangement of propionyl azide, ethyl isocyanate was formed, separated together with hydrogen cyanide by gas chromatography (GC) and detected using a nitrogen phosphorous detector (NPD). The method was linear from 1.0-100 µg/mL for both analytes, and azide was stable in human plasma at -20°C for at least 49 days. Azide was measured in the gastric content of two cases of suspected azide ingestion (case 1:1.2 mg/mL, case 2:1.5 mg/mL). Cyanide was only identified in the gastric content of case 1 (approximately 1.4 µg/mL). Furthermore, azide was quantified in plasma (19 µg/mL), serum (24 µg/mL), cell pellet (21 µg/mL) and urine (3.0 µg/mL) of case 2. This method can be used to confirm azide and cyanide exposure, and azide concentrations can be quantified in several biological matrices.

Two cases of sodium azide poisoning by accidental ingestion of Isoton.

Accidental ingestion of sodium azide in 0-1% solution by a patient and a laboratory technician in a haematological laboratory has demonstrated that very small quantities of sodium azide can give rise to toxic symptoms and that Isoton should be handled with care.

Analytical findings in a suicide involving sodium azide.

A 47-year-old laboratory assistant ingested approximately 9 g of sodium azide powder and died 4 h later at a hospital. A high-performance liquid chromatographic method using diode-array detection has been developed for the determination of an azide benzoyl derivative in blood (after a simple deproteinization) and in several tissues (after homogenization in a neutral buffer and deproteinization of the supernatant). The blood concentration in this case was lower than those previously published. The highest azide concentration was found in lung tissue. A complete toxicological screening revealed the presence of cyanide in blood, which has been previously reported twice, but for the first time, it was confirmed by mass spectrometry. Whether the production of cyanide in the presence of azide took place in vivo or postmortem remains unknown; the nature of the metabolic pathway involved also remains unknown.

Application of high-performance liquid chromatography to a fatality involving azide.

We describe a fatality resulting from the ingestion of sodium azide. Initial routine toxicological screening of the blood showed a negative result, but pathological findings as well as findings at the scene itself led to the search for azide. The azide was quantitated in all available postmortem samples (blood, stomach contents, liver, kidney, and bile) and was present in all of these matrices in the following concentrations (micrograms per milliliter or micrograms per gram): 262, 754, 14, 205, and 1283, respectively. The method is based on precolumn derivatization with 3,5-dinitrobenzoyl chloride followed by isocratic high-performance liquid chromatography and photodiode array detection. Methemoglobin and cyanide content in the blood were also elevated.

Detection of azide in forensic samples by capillary electrophoresis.

Azide salts are highly toxic compounds that have been difficult to detect in forensic samples. Here, anion analysis by capillary electrophoresis with indirect spectrophotometric detection was applied to detect azide in forensic specimens from two suicide victims. Gastric specimens from the victims were shown to have high azide concentrations; azide represented one of the major anionic components and no corresponding component occurred in normal gastric juice. Samples of blood and bile had low concentrations of azide near the limits of detection. The method described for azide analysis used simple steps for sample preparation and analysis time was less than 10 min per sample. It offers a simple and reliable method for detecting azide in biological fluids.

Death following accidental sodium azide ingestion.

Two college students developed symptoms of poisoning following ingestion of a salt solution during a college physiology laboratory exercise. Symptoms included nausea, vomiting, diarrhea, and altered consciousness. The ingested solution was identified as isotonic buffered saline containing sodium azide in a concentration of 1.0 g/L. The solution was commercially prepared for instrumentation use only and was used inadvertently for the exercise instead of freshly preparing sodium chloride in water. One student drank three sips of the solution and survived. The other student drank 700 to 800 mL and over several days became progressively ill, suffering myocardial damage and cardiac dysrhythmias, and, finally, died. Toxicologic studies confirmed the presence of azide in an antemortem urine sample from the deceased. Sodium azide is an uncommon but potent poison which can cause serious illness and death.

[Acute poisoning caused by sodium azide]. / Akute Vergiftungen durch Natriumazid.

Until now, only few cases of intoxication with sodium azide have been published. The case of suicidal sodium azide ingestion reported here and a survey of the relevant literature serve to demonstrate the pharmacological mode of action and the symptoms of acute poisoning, as well as the diagnostic proof of the toxic agent. Only symptomatic treatment can be implemented at present. Due to the restricted accessibility of the azide there is a close connection in the known cases of intoxication to the patient's profession or his (her) place of work: 17 out of 20 cases involved persons working in laboratories, whilst in 2 cases sodium azide was administered to patients by mistake. Knowledge of this connection may be of great help in making the diagnosis of acute sodium azide poisoning.

[Fatal sodium azide poisoning in a hospital: a preventable accident]. / Tödliche Natriumazid-Vergiftung im Krankenhaus: ein vermeidbarer Zwischenfall.

A case of fatal sodium azide poisoning is reported. From the hospital staff, a 57 year old patient had obtained 1 g of sodium azide in order to put it as a preservative, in his 24 hour urinal. Probably due to an error, he swallowed the total dose. A cardiovascular collapse was cause of the death after five hours of intensive treatment and reanimation. Azide anions were found in blood (traces, less than 0.5 mg/L), vitreous (10 mg/L) and cerebrospinal fluid (20 mg/L). The use of sodium azide for disinfection of urine samples should be regarded as obsolete. Less toxic substances for disinfection are available. To avoid chemical disinfection, urine samples can be kept at 4-8 degrees C prior to rapid analysis.

Fatal self-administration of sodium azide.

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.

[Suicide with sodium azide]. / Suizid mit Natriumazid.

A case report is presented of the suicide of a 27-year-old female laboratory assistant by means of sodium azide. Simple colorimetric and volumetric methods are present to detect and estimate the salt.

Suicidal sodium azide ingestion.

Sodium azide (NaN3) is a highly reactive, toxic, widely used chemical. Although industrial exposure is common, fatal ingestion is rare. We describe the case of a 30-year-old man who ingested 15 to 20 g of sodium azide. He became comatose within two hours and eventually expired from a combination of acidosis, respiratory depression, and ventricular fibrillation. In sufficient doses, sodium azide is rapidly fatal and there is no effective treatment.

Three fatal sodium azide poisonings.

We report 3 cases and review the published literature on sodium azide ingestion. A 38-year-old man intentionally ingested 2 tablespoonsful of sodium azide in water and developed seizures, coma, hypotension and fatal ventricular arrhythmias within 2 hours. A 33-year-old male ingested an unknown quantity of sodium azide. In the emergency department he was unconscious and underwent immediate intubation and gastric lavage. Nitrite therapy was instituted without improvement. He remained acidotic despite bicarbonate therapy and developed hypotension which was unresponsive to pressor agents. He died approximately 8 hours after admission despite resuscitative efforts. A 52-year-old male ingested 1.5 to 2g of sodium azide and survived for 40 hours. Nitrite therapy was ineffective. The role of sodium nitrite in treating sodium azide toxicity by producing methaemoglobin which complexes with azide is discussed.

A case of fatal sodium azide ingestion.

A fatal case of sodium azide poisoning in which exchange blood transfusions, charcoal hemoperfusion, hemodialysis and potent vasopressor agents failed to prevent the development of circulatory collapse associated with a wide complex cardiac rhythm is presented. The cellular toxin sodium azide resulted in the development of an altered mental status, profound metabolic acidosis, cardiac arrhythmia (atrial fibrillation and terminal wide complex arrhythmias), a relative decrease in cardiac output, hypotension and non-cardiogenic pulmonary edema. Further animal studies are needed to gain new approaches for the treatment of this rare cause of human poisoning.

Poisonings in laboratory personnel and health care professionals.

A case report of an unresponsive chemist presenting to the emergency department is presented; in retrospect, the patient was discovered to have intentionally ingested cyanide. A review of literature regarding ingestions in laboratory and health care personnel reveals five common points encountered in these personnel: barbiturates, carbon monoxide, cyanide, azides, and methemoglobin-inducing chemicals. Key diagnostic findings, in the absence of history of exposure, are discussed for these five agents.