Sodium azide ingestion and secondary contamination risk in healthcare workers

Downes, Michael A.; Taliana, Katrina E.; Muscat, Tracy M.; Whyte, Ian M.

doi:10.1097/mej.0000000000000244

Cited by 6 publications

(7 citation statements)

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“…Ten medical workers were likely exposed to azide from a suicidal patient who was not decontaminated prior to hospitalization ( Table 1(C) [ 58 ]). Three non-hospital staff who either provided prehospital care or transported the patient to the hospital were admitted to the emergency room for evaluation and were subsequently discharged, presumably without symptoms.…”

Section: Resultsmentioning

confidence: 99%

“…Suicide in a laboratory setting: peer-reviewed papers Of 13 people who intentionally ingested NaN 3 , two were found dead, and the remaining 11 were hospitalized, of whom six later died, leaving five survivors (Table 1(B-1) [49][50][51][52][53][54][55][56][57][58][59][60]). Many of the patients were hypotensive with metabolic acidosis, consistent with high-dose azide exposure.…”

Section: Intentional Exposure To Azidementioning

confidence: 99%

“…Twenty-three patients presented with hypotension [2,36,39,47,53,54,[57][58][59][60]64,73,74]. They received intravenous fluids and/or vasopressors, with some patients requiring large amounts of fluids, e.g., up to 32 L over 12 h [36].…”

Section: Treatmentmentioning

confidence: 99%

“…The hypotension was presumably secondary to azide conversion to nitric oxide. Fifteen patients presented with metabolic acidosis, likely due to profound hypotension and anaerobic metabolism to compensate for mitochondrial inhibition [2,36,47,49,50,[52][53][54][55][57][58][59][60]63]. In some cases, acidosis was severe enough that sodium bicarbonate was administered [36,50,53,54].…”

Section: Treatmentmentioning

confidence: 99%

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Sodium azide poisoning: a narrative review

Tat

Heskett

Satomi

et al. 2021

Clinical Toxicology

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Context: Sodium azide is a highly toxic chemical. Its production has increased dramatically over the last 30 years due to its widespread use in vehicular airbags, and it is available for purchase online. Thus, accidental exposure to azide or use as a homicidal or suicidal agent could be on the rise, and secondary exposure to medical personnel can occur. No antidote exists for azide poisoning. We conducted a systematic review of azide poisoning to assess recent poisoning reports, exposure scenarios, clinical presentations, and treatment strategies. Methods: We searched both medical and newspaper databases to review the literature between 01/ 01/2000 and 12/31/2020, pairing the controlled vocabulary and keyword terms "sodium azide" or "hydrazoic acid" with terms relating to exposures and outcomes, such as "ingestion," "inhalation," "exposure," "poisoning," and "death." We included all peer-reviewed papers and news articles describing human azide poisoning cases from English and non-English publications that could be identified using English keywords. Data abstracted included the number, age, and gender of cases, mode of exposure, exposure setting, azide dose and route of exposure, symptoms, outcome, and treatment modalities. Results: We identified 663 peer-reviewed papers and 303 newspaper articles. After removing duplicated and non-qualifying sources, 54 publications were reviewed describing 156 cases, yielding an average of 7.8 reported azide poisoning cases per year. This rate is three times higher than in a previous review covering the period of 1927 to 1999. Poisoning occurred most commonly in laboratory workers, during secondary exposure of medical personnel, or from a ripped airbag. Hypotension occurred commonly, in some cases requiring vasopressors and one patient received an intra-aortic ballon pump. Gastric lavage and/or activated charcoal were used for oral azide ingestion, and sodium nitrite, sodium thiosulfate, and/or hydroxocobalamin were used in severely poisoned patients. Conclusions: Recent increases in azide poisoning reports may stem from greater commercial use and availability. Treatment of systemic poisoning may require aggressive hemodynamic support due to profound hypotension. Based on mechanistic considerations, hydroxocobalamin is a rational choice for treating azide poisoning.

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Section: Resultsmentioning

confidence: 99%

Section: Intentional Exposure To Azidementioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

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Sodium azide poisoning: a narrative review

Tat

Heskett

Satomi

et al. 2021

Clinical Toxicology

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show abstract

“…In recent years, cases involving sodium azide poisonings were still reported in the literature, despite limited access to chemicals of this type ( 4 – 8 ). Various reports have demonstrated that sodium azide poisoning causes severe hypoxemia ( 9 – 11 ), and extensive damage in the nervous ( 10 , 12 ) and cardiac systems ( 11 , 13 , 14 ). A previous study demonstrated that sodium azide also causes acute kidney injury ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

Mdivi-1 attenuates sodium azide-induced apoptosis in H9c2 cardiac muscle cells

Luo

Zhang

et al. 2017

Molecular Medicine Reports

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The aim of the current study was to investigate the effect of mitochondrial division inhibitor 1 (Mdivi-1) in sodium azide-induced cell death in H9c2 cardiac muscle cells. Mdivi-1 is a key inhibitor of the mitochondrial division protein dynamin-related protein 1 (Drp1). Mdivi-1 was added to H9c2 cells for 3 h, after which, the cells were treated with sodium azide for 24 h. Cell viability was measured by Cell Counting kit-8 assay. DAPI staining was used to observe nuclear morphology changes by microscopy. To further investigate the role of mitochondria in sodium azide-induced cell death, mitochondrial membrane potential (ΔΨm) and the cellular ATP content were determined by JC-1 staining and ATP-dependent bioluminescence assay, respectively. Reactive oxygen species (ROS) production was also assessed by use of the specific probe 2′,7′-dichlorodihydrofluorescein diacetate. In addition, the expression of Drp1 and of the apoptosis-related proteins BCL2 apoptosis regulator (Bcl-2), and BCL2 associated X (Bax) was determined by western blotting. The present findings demonstrated that pretreatment with Mdivi-1 attenuated sodium azide-induced H9c2 cell death. Mdivi-1 pretreatment also inhibited the sodium azide-induced downregulation of Bcl-2 expression and upregulation of Bax and Drp1 expression. In addition, the mitochondrion was revealed to be the target organelle of sodium azide-induced toxicity in H9c2 cells. Mdivi-1 pretreatment moderated the dissipation of ΔΨm, preserved the cellular ATP contents and suppressed the production of ROS. The results suggested that the mechanism of sodium azide-induced cell death in H9c2 cells may involve the mitochondria-dependent apoptotic pathway. The present results indicated that Mdivi-1 may have a cardioprotective effect against sodium azide-induced apoptosis in H9c2 cardiac muscle cells.

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Alkylpyridines and Miscellaneous Organic Nitrogen Compounds

Peterson

2023

Patty's Toxicology

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This chapter provides a broad overview of topics related to the occupational use and exposure to a variety of miscellaneous nitrogen‐containing compounds. Topics addressed include chemical/physical properties, uses, exposure assessment, and toxic effects, as well as standards, regulations, and guidelines for exposure. Some of the chemicals and classes represented in this chapter include pyridine, alkylpyridines, vinylpyridines, aminopyridines, aminopicolines, pyridinethione compounds (pyrithiones), nicotine, the substituted uracils, quaternary herbicides, s ‐triazine herbicides, propazine, cyanazine, ametryn, prometryn, simazine, hexazinone, azides, and hydrazine and its derivatives.

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Sodium azide ingestion and secondary contamination risk in healthcare workers

Cited by 6 publications

References 0 publications

Sodium azide poisoning: a narrative review

Sodium azide poisoning: a narrative review

Mdivi-1 attenuates sodium azide-induced apoptosis in H9c2 cardiac muscle cells

Alkylpyridines and Miscellaneous Organic Nitrogen Compounds

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