Sensitive electrochemical detection of sodium azide based on the electrocatalytic activity of the pasting liquid of a carbon paste electrode.

Sodium azide (NaN3) is highly toxic and widely used in, for example, automobile airbags and biochemical laboratories. The electrochemical detection of sodium azide on commonly used electrodes is challenging due to sluggish electron transfer, but it has been achieved using a boron-doped diamond thin-film electrode and a highly oriented pyrolytic graphite electrode. Utilizing the electrocatalytic activity of the pasting liquid of a carbon paste electrode, we developed an effective method for the electrochemical detection of sodium azide in which silicone oil was employed as the pasting liquid of the carbon paste electrode. This simple and cheap silicone-oil-based carbon paste electrode exhibited comparable sensitivity to the boron-doped diamond thin-film electrode and highly oriented pyrolytic graphite electrode. The limit of detection for sodium azide at the silicone-oil-based carbon paste electrode was found to be 0.1 µM. Recoveries from diluted human serum samples were between 97.2 and 101.3%. Graphical abstract ᅟ.

Clinical and analytical problems of sodium azide poisonings as exemplified by a case of fatal suicidal poisoning.

AIM OF THE STUDY: To present clinical and analytical aspects associated with sodium azide poisoning. The problems were verified on the basis of a case of sodium azide poisoning which was unique due to its circumstances and the development of an analytical method applied for medico-legal practice. MATERIAL AND METHODS: The object of the study was a toxicological analysis of biological specimens collected from a woman who ingested two doses of sodium azide purchased over the Internet, in a suicide attempt. After the ingestion of the first dose, the clinical management in the form of symptomatic treatment indicated a possibility of recovery. However, the ingestion of a second dose of the xenobiotic, already in the hospital, caused death. Toxicological findings were obtained with the dedicated technique of gas chromatography-mass spectrometry (GC-EI-MS-MS) after extraction combined with derivatization using pentafluorobenzyl bromide (PFBBr). RESULTS: Post-mortem toxicological studies demonstrated sodium azide in the blood (0.18 mg/l) and urine (6.50 mg/l) samples collected from the woman. CONCLUSIONS: Cases of sodium azide poisoning are rare and difficult to treat, but a review of the literature over a longer interval of time shows that they continue to occur. Therefore, case studies of sodium azide poisoning, together with descriptions of research methodology, can be useful both in clinical terms and in the preparation of toxicological expert opinions for medico-legal purposes.

Convenient headspace gas chromatographic determination of azide in blood and plasma.

Azide in human blood and plasma samples was derivatized with propionic anhydride in a headspace vial without prior sample preparation. The reaction proceeds quickly at room temperature to form propionyl azide. A portion of the headspace was assayed by gas chromatography with a nitrogen-phosphorus detector. In the heated injector of the gas chromatograph, the propionyl azide undergoes thermal rearrangement, forming ethyl isocyanate, which is subsequently chromatographed and detected. Propionitrile was used as the internal standard. The method is linear to at least 20 microg/mL. Limit of quantitation was 0.04 microg/mL, and the within-run coefficient of variation was 5.6% at 1 microg/mL. There was no interference from cyanide. A fatality report in which blood and plasma azide concentrations from a 59-year-old man were monitored for 24 h following the ingestion of an unknown amount of sodium azide is presented. The patient became critically ill after his self-inflicted sodium azide ingestion. He was intubated and treated with vasopressors and aggressive supportive care, including extracorporeal membrane oxygenation therapy, in the intensive care facility but died from neurological brain damage secondary to anoxia. On admission, 1.4 h after ingestion, his azide level was 5.6 microg/mL (blood); shortly thereafter, it had risen to 13.7 microg/mL (plasma) and, subsequently, was projected to have been eliminated by 16.7 h. No azide was detected in the postmortem blood and vitreous humor.

[A case of fatal acute sodium azide poisoning].

A case of fatal sodium azide poisoning induced by suicidal ingestion was reported. When the patient arrived, her vital signs such as consciousness and blood pressure, were normal. But 25 hours after ingestion, she died from metabolic acidosis, ARDS (acute respiratory distress syndrome) and acute cardiac failure. We detected the azide ion in patient's serum using GCMS method and measured the blood concentration of sodium azide using the GC/NPD method. The half-life period of sodium azide in blood was calculated as about 2.5 hours.

Determination of azide in blood and urine by gas chromatography-mass spectrometry.

A sensitive and simple method for determining azide in blood and urine using an extractive alkylation technique was devised. This inorganic anion was alkylated with pentafluorobenzyl bromide using tetradecyldimethylbenzylammonium chloride as the phase-transfer catalyst. 1,3,5-Tribromobenzene was used as an internal standard. The obtained derivative was analyzed by gas chromatography-mass spectrometry using the negative ion chemical ionization mode with isobutane as the reagent gas. The calibration curves for azide were linear over the concentration range from 1 to 200 nmol/mL in blood and urine, and the lower limit of detection was 0.5 nmol/mL for blood and urine. The accuracy and precision of the method were evaluated, and the coefficients of variation were found to be lower than 10%.

The catalase inhibitor sodium azide reduces ethanol-induced locomotor activity.

The involvement of brain catalase in modulating the psychopharmacological effects of ethanol was investigated by examining ethanol-induced locomotor activity in sodium azide-treated mice. Mice were pretreated with i.p. injections of the catalase inhibitor sodium azide (5, 10, or 15 mg/kg) or saline. Following this treatment, animals received i.p. injections of ethanol (0.0, 1.6, 2.4, or 3.2 g/kg). Ten minutes after ethanol administration, locomotor activity was recorded during a 10-min testing period in open-field chambers. The time effect between the two treatments (0, 30, 60, or 90 min) was also evaluated. Results indicated that sodium azide alone did not change spontaneous locomotor activity. However, this catalase inhibitor significantly reduced ethanol-induced locomotor activity when it was injected simultaneously or 30 min before ethanol injections. Moreover, perfused brain homogenates of mice treated with sodium azide also showed a significant reduction of catalase activity. No differences in blood ethanol levels were observed between sodium azide and saline pretreated animals. Results of an additional experiment showed that sodium azide (10 mg/kg, at 30 min) did not produce an effect on d-amphetamine- (2 mg/kg) or tert-butanol- (0.5 g/kg) induced locomotor activities. A specific interaction between ethanol and sodium azide at the level of the central nervous system is suggested. These results provide further support for the involvement of brain catalase in ethanol-induced behavioral effects. They also support the notion that acetaldehyde may be produced directly in the brain by catalase and that it may be an important regulator of ethanol's locomotor effects.

Determining sodium azide concentration in blood by ion chromatography.

We describe a simple method for measuring sodium azide concentrations in aliquots of blood and other tissues. Aliquots are acidified, converting azide to volatile hydrazoic acid (HN3) which is then trapped in sodium hydroxide. We analyze the resulting aliquots by ion chromatography, using a sodium tetraborate eluent and suppressed conductivity detection. The method is sensitive to at least 100 ng/mL.