The Journal of Emergency Medicine, Vol. 46, No. 4, pp. 491–494, 2014 Copyright Ó 2014 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter
http://dx.doi.org/10.1016/j.jemermed.2013.08.082
Selected Topics: Toxicology
MULTIPLE POISONINGS WITH SODIUM AZIDE AT A LOCAL RESTAURANT Evan S. Schwarz, MD,* Paul M. Wax, MD,† Kurt C. Kleinschmidt, MD,† Kapil Sharma, MD,† Wendy M. Chung, MD,‡§ Gabriela Cantu, MPH,§ Erin Spargo, PHD,k and Elizabeth Todd, PHDk *Division of Emergency Medicine, Washington University School of Medicine, St. Louis, Missouri, †Division of Emergency Medicine, University of Texas Southwestern School of Medicine, Dallas, Texas, ‡Department of Pediatrics, University of Texas Southwestern School of Medicine, Dallas, Texas, §Dallas County Department of Health and Human Services, Dallas, Texas, and kDallas County Southwestern Institute of Forensic Sciences, Dallas, Texas Reprint Address: Evan S. Schwarz, MD, Division of Emergency Medicine, Washington University School of Medicine, 660 South Euclid, Campus Box 8072, St. Louis, MO 63110
, Abstract—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. Ó 2014 Elsevier Inc.
INTRODUCTION Sodium azide (NaN3) is a colorless, odorless, and tasteless, highly water-soluble crystal or powder that forms hydrazoic acid (HN3) when combined with water (1). It is used as a laboratory preservative and in air bags (2,3). Historically, it was used as an antihypertensive due to its vasodilatory effects (4). Most poisonings from sodium azide (SA) occur during suicide attempts, or are accidental and occur in the laboratory or health care setting, when a vessel containing SA in a clear solution is confused with water and consumed by a victim (4–6). Similar to cyanide, SA inhibits oxidative phosphorylation (3,4,7). However, it is postulated that the formation of nitric oxide from SA may also be responsible for the vasodilatation and central nervous system toxicity (8,9). Standard treatments for cyanide toxicity, such as sodium thiosulfate and sodium nitrite, do not improve outcomes of patients poisoned by SA (4,10). We report a cluster of poisonings that occurred at a public restaurant, and the subsequent investigation that identified iced tea and SA as the foodborne vehicle and agent, respectively (11).
, Keywords—poisoning; sodium azide; hydrazoic acid; terrorism; metabolic inhibitors
RECEIVED: 26 April 2013; FINAL SUBMISSION RECEIVED: 23 July 2013; ACCEPTED: 16 August 2013 491
492
E. S. Schwarz et al.
CASE REPORT In April 2010, a city health department was notified of four people who were transferred to the same Emergency Department (ED) over a period of 4 h after developing similar symptoms while drinking iced tea at a local restaurant. The city health department was notified by the hospital and by the city fire and police departments that originally responded to the scene. Symptoms included lightheadedness, nausea, diaphoresis, headache, syncope, a sense of impending doom, and hypotension (Table 1). All of their symptoms developed within minutes of drinking iced tea at the restaurant. All of the patients arrived at the restaurant separately and did not know one another. They arrived at different times over the 4-h period. The times when they arrived at the restaurant and became symptomatic did not overlap with one another. That evening, city officials conducted a site visit at the restaurant, temporarily suspended further sales of the iced tea, and collected samples of iced tea from restaurant tea urns and from 2 of the patients that brought cups of iced tea with them to the ED. The patients brought iced tea with them due to their suspicion that the tea was responsible for their symptoms. They did not bring samples of any other food items with them. Three of the four patients were examined by the same emergency physician. Due to 2 of the 3 being hypotensive (92/64 and 89/54 mm Hg), he thought that the patients had been poisoned with an antihypertensive agent (Table 1). Laboratory and radiologic diagnostics performed in the ED did not reveal an etiology for their illness; chemistry analysis was normal. ED toxicologic
evaluation consisted of urine drug of abuse screens for all patients and a serum ethanol concentration in one patient. The urine drug screens were negative for all patients, and the one serum ethanol concentration ordered was < 1 mg/dL. All received intravenous fluids and hemodynamic monitoring, and were discharged home either that night, or after an overnight admission (Table 1). Upon learning of the cases, the Dallas County Health and Human Services epidemiology and environmental health staff members (DCHHS) obtained and reviewed medical records, interviewed patients and restaurant staff members, and conducted a site visit. Due to a high suspicion for a chemical etiology, DCHHS consulted multiple agencies, including the county crime laboratory (Dallas County Southwestern Institute of Forensic Sciences [SWIFS]), the Food and Drug Administration, the Texas state health department, and local medical toxicologists at the University of Texas Southwestern School of Medicine (UTSW), regarding testing for possible etiologic agents. A comprehensive list of potential agents was developed. Toxicologists at SWIFS assisted in identification of a laboratory capable of conducting the appropriate testing. A fifth case (Table 1; patient #3) was identified 4 days after the initial health department notification by the Electronic Surveillance System for the Early Notification of Community-based Epidemics (ESSENCE). To assess the extent to which others were affected, ESSENCE was searched for patients presenting to any of 18 area EDs with similar symptoms during that time frame. Of 1827 ED visits recorded in ESSENCE during that time, 81 patients presented with chief complaints of altered mental status, dizziness, syncope, tingling, or hypotension. One
Table 1. Case Patients’ Demographic, Exposure, and Clinical Outcome Data
Age, years Sex Food Drink (iced tea)* Symptoms Headache Syncope Nausea/vomiting Diaphoresis Chest pain Dyspnea Paresthesias Sense of impending doom Heart rate (beats/min)† Blood pressure (mm Hg)† Treatments ED Disposition
Patient #1
Patient #2
Patient #3
Patient #4
Patient #5
46 Male Bite of a sandwich 2 sips
52 Female Cookie 8 ounces
32 Male 1 bite of a sandwich and cookie 1 /4 cup
50 Female Cookie 4 ounces
48 Female 2 bites of a sandwich 2 sips
Yes Yes Yes Yes – Yes – Yes 72 92/64 NS Discharged
– – Yes Yes – – Yes Yes 110 110/68 NS, L, O, P Admitted
Yes Yes Yes Yes Yes – – – 62 84/42 NS, O Discharged
– Yes Yes Yes – Yes Yes Yes 127 89/54 NS, O, P Admitted
– Yes Yes Yes – Yes Yes – 94 86/54 NS, L, O, P Discharged
NS = normal saline; L = lorazepam; O = ondansetron; P = promethazine; ED = emergency department. * None of the patients admitted to drinking anything other than iced tea. † Initial recorded heart rate or blood pressure.
Sodium Azide Poisonings
additional case belonging to this cluster was identified. The patient was initially taken to the same hospital as the four other cases, but left prior to being evaluated. He was later evaluated at an outpatient clinic, and referred to a different ED with a dysrhythmia. Although patients suspected that the iced tea was responsible, due to the initial absence of laboratory confirmation proving this, DCHHS conducted a casecontrol study to assess the epidemiologic association of the illnesses with specific foods. The case-control study concluded that cases were approximately 65 times more likely to have consumed iced tea compared with controls (odds ratio 65.0; 95% confidence interval 2.4–3292). Testing of tea samples by SWIFS was negative for over 100 different chemicals and drugs (e.g., cyanide, arsenic, metoprolol, verapamil), except for caffeine. SWIFS then referred tea samples to the Federal Bureau of Investigation (FBI) laboratories (Quantico, VA). Almost 5 months after the incident, headspace-gas chromatography/mass spectrometry analysis by the FBI laboratory detected hydrazoic acid. The presence of hydrazoic acid led to the use of infrared spectroscopy to detect SA. Both compounds were found in three samples: two from patients’ cups and one from the tea urn in use at the time of the incident. Neither was found in a control sample from a second tea urn used earlier that day. Neither chemical was used at the FBI laboratory or at the restaurant. Filter lines were not recently changed, and the dried tea used for brewing was distributed in individually sealed packets. The tea and soda were connected to a common water line, but no one drinking soda reported feeling ill. The self-service urns were kept in an open location in the restaurant, accessible by customers, and out of the direct line-of-sight of employees. How the tea became contaminated with SA remains unknown. A police investigation was unrevealing and is now closed. After receiving notification of SA as the etiologic agent, all 5 patients were evaluated in the medical toxicology clinic at UTSW. All had improved and were determined not to have any persistent symptoms due to the effects of SA. DISCUSSION Previous reports of SA poisonings are mainly limited to case reports involving ingestion of SA either accidently or during a suicide attempt, and did not take place at a public venue such as a restaurant. There are two reports of previous SA foodborne poisonings; however, neither included clinical or epidemiological information on the victims or the investigation, making our cases important and unique (5,12). Six workers at Harvard Medical School became ill after drinking from a communal coffee pot that was contaminated with SA (5). They had palpitations and diaphoresis within minutes of the inges-
493
tion. Two fainted, but all their symptoms rapidly resolved, and there were no fatalities. The coffee pot was located in the New Research Building on the campus of a medical school. SA was deliberately added to a teapot in Niigata, Japan in 1998; this prompted five other copycat poisonings (12). Where and why these poisonings took place is not discussed. No further clinical data or any other details concerning the poisonings were mentioned in either report, which makes our cases unique. Toxicity from SA is dose dependent (4). Lower doses cause hypotension, palpitations, tachycardia, dyspnea, headaches, syncope, diaphoresis, and nausea and vomiting, whereas higher doses cause prolonged or recurrent hypotension, seizures, dysrhythmias, acidosis, and death (2–4,10,13–16). Our patients developed symptoms similar to other low-dose exposures. Edmonds and Bourne report five laboratory technicians that drank tea made from water that was accidentally treated with SA (2). Dizziness, headache, and nearsyncope were reported by four people; the fifth patient developed severe chest pain. All recovered within a few hours without long-term sequelae. Two patients accidentally drank laboratory diluting fluid that contained 0.1% SA (16). The diluting fluid was for a hematology blood counter in the hematology laboratory. In both cases, instead of dissolving folic acid in water, the folic acid was accidentally dissolved in the diluting fluid. The first patient drank the solution as part of an evaluation for macrocytosis; the second patient was a laboratory technician who drank the solution because she liked the taste of folic acid. They developed a combination of diaphoresis, headache, nausea, and syncope. Both recovered rapidly. Deaths are reported after poisoning with SA (3,4,10). A 38-year-old man developed seizures followed by hypotension and ventricular fibrillation; he died within an hour and a half of the ingestion (4). Two months later, a 33year-old co-worker ingested SA in a suicide attempt and developed tachycardia, hypotension, and a severe metabolic acidosis; he quickly deteriorated, and died approximately 8 h later. A 29-year-old woman accidentally drank a solution containing SA while at a college course; she was observed overnight, and released the next day (3). Three days later, she developed dyspnea and chest pain. An electrocardiogram demonstrated STsegment elevation, and a ventriculogram showed diffuse hypokinesia with an ejection fraction of 28%. Despite vasopressor support and a balloon pump, she developed cardiac arrest and could not be further resuscitated. Domestic and international concerns exist regarding future terrorist events (17,18). SA, along with other chemical agents, could be used in a mass poisoning. Because the circumstances regarding how and why SA
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was placed in the iced tea remain unknown, it is possible that the iced tea was deliberately poisoned. Even if the tea was deliberately adulterated, it is unlikely that this was an example of chemical terrorism. However, this does serve as an example of how SA or another chemical agent could be used as a chemical weapon. This further emphasizes the importance of our cases, as our report demonstrates how a joint investigation among multiple agencies was necessary to properly evaluate these patients. The recurrence, and seriousness, of these events suggests a need for continued education of emergency providers. Emergency physicians need to be aware of the possibility of chemical poisonings, as victims will present to the ED (19,20). As such, recognition of these patients as victims of poisonings is important to make the proper diagnosis, deliver an antidote if one is available, and alert the authorities and public health officials. Multiple agencies, including the American College of Medical Toxicology (http://www.acmt.net/cgi/page.cgi/calendar. html?evt=16), the Agency for Toxic Substances and Disease Registry, the Centers for Disease Control and Prevention, and the Radiation Emergency Assistance Center/Training Site, developed courses to educate physicians about toxic industrial chemicals and toxic industrial materials. SA is included as a potential terroristic agent in these courses. Consultation with the health department, poison centers, and forensic and medical toxicologists can assist with outbreak investigation, performing diagnostic studies, assisting with treatment, and arranging patient follow-up. Limitations Biologic samples were not sent for analysis, so we were not able to confirm SA or hydrazoic acid in any of the patients; it is possible that their symptoms were due to something else. However, we did find SA and hydrazoic acid in the iced tea that all the victims drank, and their symptoms were consistent with low-dose poisonings. The police were unable to confirm that the poisonings were intentional, so we cannot be sure that the adulteration was intentional. However, we were not able to find any evidence that would suggest this was an accidental poisoning, either. CONCLUSION We report a cluster of poisonings that occurred at a public restaurant from iced tea that was contaminated with SA and hydrazoic acid. If exposed to a high enough dose, SA can cause life-threatening symptoms and death. A joint investigation by multiple agencies was required to properly investigate the poisonings. 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. Acknowledgments—Joshua G. Schier, MD, Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Centers for Disease Control; David Klein PhD, Linda Gaul PhD, Texas Department of State Health Services; Larry Enmon, Food and Drug Administration; Marc A. LeBeau, PhD, Eileen M. Waninger, Federal Bureau of Investigations laboratory in Quantico, VA; John T. Carlo, MD, Joey Stringer, Tony Jenkins, Dallas County Department of Health and Human Services.
REFERENCES 1. Graham JD. Actions of sodium azide. Br J Pharmacol Chemother 1949;4:1–6. 2. Edmonds O, Bourne M. Sodium azide poisoning in five laboratory technicians. Br J Ind Med 1982;39:308–9. 3. Judge KW, Ward NE. Fatal azide-induced cardiomyopathy presenting as acute myocardial infarction. Am J Cardiol 1989;64:830–1. 4. Klein-Schwartz W, Gorman RL, Oderda GM, Massaro BP, Kurt TL, Garriott JC. Three fatal sodium azide poisonings. Med Toxicol Adverse Drug Exp 1989;4:219–27. 5. Gussow L. Toxicology rounds: the case of the contaminated coffee pot. Emerg Med News 2010;32:8. 6. Gordon SM, Drachman J, Bland LA, Reid MH, Favero M, Jarvis WR. Epidemic hypotension in a dialysis center caused by sodium azide. Kidney Int 1990;37:110–5. 7. Bogucka K, Wojtezak L. Effect of sodium azide on oxidation and phosphorylation processes in rat liver mitochondria. Biochim Biophys Acta 1966;122:381–92. 8. Smith RP, Louis CA, Kruszyna R, Kruszyna H. Acute neurotoxicity of sodium azide and nitric oxide. Fundam Appl Toxicol 1991;17: 120–7. 9. Smith RP, Wilcox DE. Toxicology of selected nitric oxide-donating xenobiotics, with particular reference to azide. Crit Rev Toxicol 1994;24:355–77. 10. Emmett EA, Ricking JA. Fatal self-administration of sodium azide. Ann Intern Med 1975;83:224–6. 11. Centers for Disease Control and Prevention (CDC). Sodium azide poisoning at a restaurant – Dallas County, Texas, 2010. MMWR Morb Mortal Wkly Rep 2012;61:457–60. 12. Okumura T, Ninomiya N, Ohta M. The chemical disaster response system in Japan. Prehosp Disaster Med 2003;18:189–92. 13. Chang S, Lamm SH. Human health effects of sodium azide exposure: a literature review and analysis. Int J Toxicol 2003;22:175–86. 14. Lawson K. Sodium azide. Clin Toxicol Rev 1993;15:1–2. 15. Watanabe K, Hirasawa H, Oda S, et al. A case of survival following high-dose sodium azide poisoning. Clin Toxicol (Phila) 2007;45: 810–1. 16. Richardson SG, Giles C, Swan CH. Two cases of sodium azide poisoning by accidental ingestion of Isoton. J Clin Pathol 1975; 28:350–1. 17. Stoddard FJ Jr, Gold J, Henderson SW, et al. Psychiatry and terrorism. J Nerv Ment Dis 2011;199:537–43. 18. Malakoff D. Scientific paper pulled over terrorism concerns. NPR, Weekend Edition Saturday; May 28, 2005. Available at: http:// www.npr.org/templates/story/story.php?storyId=4670948. Accessed November 1, 2013. 19. Gensheimer KF, Rea V, Mills DA, Montagna CP, Simone K. Arsenic poisoning caused by intentional contamination of coffee at a church gathering—an epidemiological approach to a forensic investigation. J Forensic Sci 2010;55:1116–9. 20. Meggs WJ, Hoffman RS, Shih RD, Weisman RS, Goldfrank LR. Thallium poisoning from maliciously contaminated food. J Toxicol Clin Toxicol 1994;32:723–30.
http://dx.doi.org/10.1016/j.jemermed.2013.08.082
Selected Topics: Toxicology
MULTIPLE POISONINGS WITH SODIUM AZIDE AT A LOCAL RESTAURANT Evan S. Schwarz, MD,* Paul M. Wax, MD,† Kurt C. Kleinschmidt, MD,† Kapil Sharma, MD,† Wendy M. Chung, MD,‡§ Gabriela Cantu, MPH,§ Erin Spargo, PHD,k and Elizabeth Todd, PHDk *Division of Emergency Medicine, Washington University School of Medicine, St. Louis, Missouri, †Division of Emergency Medicine, University of Texas Southwestern School of Medicine, Dallas, Texas, ‡Department of Pediatrics, University of Texas Southwestern School of Medicine, Dallas, Texas, §Dallas County Department of Health and Human Services, Dallas, Texas, and kDallas County Southwestern Institute of Forensic Sciences, Dallas, Texas Reprint Address: Evan S. Schwarz, MD, Division of Emergency Medicine, Washington University School of Medicine, 660 South Euclid, Campus Box 8072, St. Louis, MO 63110
, Abstract—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. Ó 2014 Elsevier Inc.
INTRODUCTION Sodium azide (NaN3) is a colorless, odorless, and tasteless, highly water-soluble crystal or powder that forms hydrazoic acid (HN3) when combined with water (1). It is used as a laboratory preservative and in air bags (2,3). Historically, it was used as an antihypertensive due to its vasodilatory effects (4). Most poisonings from sodium azide (SA) occur during suicide attempts, or are accidental and occur in the laboratory or health care setting, when a vessel containing SA in a clear solution is confused with water and consumed by a victim (4–6). Similar to cyanide, SA inhibits oxidative phosphorylation (3,4,7). However, it is postulated that the formation of nitric oxide from SA may also be responsible for the vasodilatation and central nervous system toxicity (8,9). Standard treatments for cyanide toxicity, such as sodium thiosulfate and sodium nitrite, do not improve outcomes of patients poisoned by SA (4,10). We report a cluster of poisonings that occurred at a public restaurant, and the subsequent investigation that identified iced tea and SA as the foodborne vehicle and agent, respectively (11).
, Keywords—poisoning; sodium azide; hydrazoic acid; terrorism; metabolic inhibitors
RECEIVED: 26 April 2013; FINAL SUBMISSION RECEIVED: 23 July 2013; ACCEPTED: 16 August 2013 491
492
E. S. Schwarz et al.
CASE REPORT In April 2010, a city health department was notified of four people who were transferred to the same Emergency Department (ED) over a period of 4 h after developing similar symptoms while drinking iced tea at a local restaurant. The city health department was notified by the hospital and by the city fire and police departments that originally responded to the scene. Symptoms included lightheadedness, nausea, diaphoresis, headache, syncope, a sense of impending doom, and hypotension (Table 1). All of their symptoms developed within minutes of drinking iced tea at the restaurant. All of the patients arrived at the restaurant separately and did not know one another. They arrived at different times over the 4-h period. The times when they arrived at the restaurant and became symptomatic did not overlap with one another. That evening, city officials conducted a site visit at the restaurant, temporarily suspended further sales of the iced tea, and collected samples of iced tea from restaurant tea urns and from 2 of the patients that brought cups of iced tea with them to the ED. The patients brought iced tea with them due to their suspicion that the tea was responsible for their symptoms. They did not bring samples of any other food items with them. Three of the four patients were examined by the same emergency physician. Due to 2 of the 3 being hypotensive (92/64 and 89/54 mm Hg), he thought that the patients had been poisoned with an antihypertensive agent (Table 1). Laboratory and radiologic diagnostics performed in the ED did not reveal an etiology for their illness; chemistry analysis was normal. ED toxicologic
evaluation consisted of urine drug of abuse screens for all patients and a serum ethanol concentration in one patient. The urine drug screens were negative for all patients, and the one serum ethanol concentration ordered was < 1 mg/dL. All received intravenous fluids and hemodynamic monitoring, and were discharged home either that night, or after an overnight admission (Table 1). Upon learning of the cases, the Dallas County Health and Human Services epidemiology and environmental health staff members (DCHHS) obtained and reviewed medical records, interviewed patients and restaurant staff members, and conducted a site visit. Due to a high suspicion for a chemical etiology, DCHHS consulted multiple agencies, including the county crime laboratory (Dallas County Southwestern Institute of Forensic Sciences [SWIFS]), the Food and Drug Administration, the Texas state health department, and local medical toxicologists at the University of Texas Southwestern School of Medicine (UTSW), regarding testing for possible etiologic agents. A comprehensive list of potential agents was developed. Toxicologists at SWIFS assisted in identification of a laboratory capable of conducting the appropriate testing. A fifth case (Table 1; patient #3) was identified 4 days after the initial health department notification by the Electronic Surveillance System for the Early Notification of Community-based Epidemics (ESSENCE). To assess the extent to which others were affected, ESSENCE was searched for patients presenting to any of 18 area EDs with similar symptoms during that time frame. Of 1827 ED visits recorded in ESSENCE during that time, 81 patients presented with chief complaints of altered mental status, dizziness, syncope, tingling, or hypotension. One
Table 1. Case Patients’ Demographic, Exposure, and Clinical Outcome Data
Age, years Sex Food Drink (iced tea)* Symptoms Headache Syncope Nausea/vomiting Diaphoresis Chest pain Dyspnea Paresthesias Sense of impending doom Heart rate (beats/min)† Blood pressure (mm Hg)† Treatments ED Disposition
Patient #1
Patient #2
Patient #3
Patient #4
Patient #5
46 Male Bite of a sandwich 2 sips
52 Female Cookie 8 ounces
32 Male 1 bite of a sandwich and cookie 1 /4 cup
50 Female Cookie 4 ounces
48 Female 2 bites of a sandwich 2 sips
Yes Yes Yes Yes – Yes – Yes 72 92/64 NS Discharged
– – Yes Yes – – Yes Yes 110 110/68 NS, L, O, P Admitted
Yes Yes Yes Yes Yes – – – 62 84/42 NS, O Discharged
– Yes Yes Yes – Yes Yes Yes 127 89/54 NS, O, P Admitted
– Yes Yes Yes – Yes Yes – 94 86/54 NS, L, O, P Discharged
NS = normal saline; L = lorazepam; O = ondansetron; P = promethazine; ED = emergency department. * None of the patients admitted to drinking anything other than iced tea. † Initial recorded heart rate or blood pressure.
Sodium Azide Poisonings
additional case belonging to this cluster was identified. The patient was initially taken to the same hospital as the four other cases, but left prior to being evaluated. He was later evaluated at an outpatient clinic, and referred to a different ED with a dysrhythmia. Although patients suspected that the iced tea was responsible, due to the initial absence of laboratory confirmation proving this, DCHHS conducted a casecontrol study to assess the epidemiologic association of the illnesses with specific foods. The case-control study concluded that cases were approximately 65 times more likely to have consumed iced tea compared with controls (odds ratio 65.0; 95% confidence interval 2.4–3292). Testing of tea samples by SWIFS was negative for over 100 different chemicals and drugs (e.g., cyanide, arsenic, metoprolol, verapamil), except for caffeine. SWIFS then referred tea samples to the Federal Bureau of Investigation (FBI) laboratories (Quantico, VA). Almost 5 months after the incident, headspace-gas chromatography/mass spectrometry analysis by the FBI laboratory detected hydrazoic acid. The presence of hydrazoic acid led to the use of infrared spectroscopy to detect SA. Both compounds were found in three samples: two from patients’ cups and one from the tea urn in use at the time of the incident. Neither was found in a control sample from a second tea urn used earlier that day. Neither chemical was used at the FBI laboratory or at the restaurant. Filter lines were not recently changed, and the dried tea used for brewing was distributed in individually sealed packets. The tea and soda were connected to a common water line, but no one drinking soda reported feeling ill. The self-service urns were kept in an open location in the restaurant, accessible by customers, and out of the direct line-of-sight of employees. How the tea became contaminated with SA remains unknown. A police investigation was unrevealing and is now closed. After receiving notification of SA as the etiologic agent, all 5 patients were evaluated in the medical toxicology clinic at UTSW. All had improved and were determined not to have any persistent symptoms due to the effects of SA. DISCUSSION Previous reports of SA poisonings are mainly limited to case reports involving ingestion of SA either accidently or during a suicide attempt, and did not take place at a public venue such as a restaurant. There are two reports of previous SA foodborne poisonings; however, neither included clinical or epidemiological information on the victims or the investigation, making our cases important and unique (5,12). Six workers at Harvard Medical School became ill after drinking from a communal coffee pot that was contaminated with SA (5). They had palpitations and diaphoresis within minutes of the inges-
493
tion. Two fainted, but all their symptoms rapidly resolved, and there were no fatalities. The coffee pot was located in the New Research Building on the campus of a medical school. SA was deliberately added to a teapot in Niigata, Japan in 1998; this prompted five other copycat poisonings (12). Where and why these poisonings took place is not discussed. No further clinical data or any other details concerning the poisonings were mentioned in either report, which makes our cases unique. Toxicity from SA is dose dependent (4). Lower doses cause hypotension, palpitations, tachycardia, dyspnea, headaches, syncope, diaphoresis, and nausea and vomiting, whereas higher doses cause prolonged or recurrent hypotension, seizures, dysrhythmias, acidosis, and death (2–4,10,13–16). Our patients developed symptoms similar to other low-dose exposures. Edmonds and Bourne report five laboratory technicians that drank tea made from water that was accidentally treated with SA (2). Dizziness, headache, and nearsyncope were reported by four people; the fifth patient developed severe chest pain. All recovered within a few hours without long-term sequelae. Two patients accidentally drank laboratory diluting fluid that contained 0.1% SA (16). The diluting fluid was for a hematology blood counter in the hematology laboratory. In both cases, instead of dissolving folic acid in water, the folic acid was accidentally dissolved in the diluting fluid. The first patient drank the solution as part of an evaluation for macrocytosis; the second patient was a laboratory technician who drank the solution because she liked the taste of folic acid. They developed a combination of diaphoresis, headache, nausea, and syncope. Both recovered rapidly. Deaths are reported after poisoning with SA (3,4,10). A 38-year-old man developed seizures followed by hypotension and ventricular fibrillation; he died within an hour and a half of the ingestion (4). Two months later, a 33year-old co-worker ingested SA in a suicide attempt and developed tachycardia, hypotension, and a severe metabolic acidosis; he quickly deteriorated, and died approximately 8 h later. A 29-year-old woman accidentally drank a solution containing SA while at a college course; she was observed overnight, and released the next day (3). Three days later, she developed dyspnea and chest pain. An electrocardiogram demonstrated STsegment elevation, and a ventriculogram showed diffuse hypokinesia with an ejection fraction of 28%. Despite vasopressor support and a balloon pump, she developed cardiac arrest and could not be further resuscitated. Domestic and international concerns exist regarding future terrorist events (17,18). SA, along with other chemical agents, could be used in a mass poisoning. Because the circumstances regarding how and why SA
494
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was placed in the iced tea remain unknown, it is possible that the iced tea was deliberately poisoned. Even if the tea was deliberately adulterated, it is unlikely that this was an example of chemical terrorism. However, this does serve as an example of how SA or another chemical agent could be used as a chemical weapon. This further emphasizes the importance of our cases, as our report demonstrates how a joint investigation among multiple agencies was necessary to properly evaluate these patients. The recurrence, and seriousness, of these events suggests a need for continued education of emergency providers. Emergency physicians need to be aware of the possibility of chemical poisonings, as victims will present to the ED (19,20). As such, recognition of these patients as victims of poisonings is important to make the proper diagnosis, deliver an antidote if one is available, and alert the authorities and public health officials. Multiple agencies, including the American College of Medical Toxicology (http://www.acmt.net/cgi/page.cgi/calendar. html?evt=16), the Agency for Toxic Substances and Disease Registry, the Centers for Disease Control and Prevention, and the Radiation Emergency Assistance Center/Training Site, developed courses to educate physicians about toxic industrial chemicals and toxic industrial materials. SA is included as a potential terroristic agent in these courses. Consultation with the health department, poison centers, and forensic and medical toxicologists can assist with outbreak investigation, performing diagnostic studies, assisting with treatment, and arranging patient follow-up. Limitations Biologic samples were not sent for analysis, so we were not able to confirm SA or hydrazoic acid in any of the patients; it is possible that their symptoms were due to something else. However, we did find SA and hydrazoic acid in the iced tea that all the victims drank, and their symptoms were consistent with low-dose poisonings. The police were unable to confirm that the poisonings were intentional, so we cannot be sure that the adulteration was intentional. However, we were not able to find any evidence that would suggest this was an accidental poisoning, either. CONCLUSION We report a cluster of poisonings that occurred at a public restaurant from iced tea that was contaminated with SA and hydrazoic acid. If exposed to a high enough dose, SA can cause life-threatening symptoms and death. A joint investigation by multiple agencies was required to properly investigate the poisonings. 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. Acknowledgments—Joshua G. Schier, MD, Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Centers for Disease Control; David Klein PhD, Linda Gaul PhD, Texas Department of State Health Services; Larry Enmon, Food and Drug Administration; Marc A. LeBeau, PhD, Eileen M. Waninger, Federal Bureau of Investigations laboratory in Quantico, VA; John T. Carlo, MD, Joey Stringer, Tony Jenkins, Dallas County Department of Health and Human Services.
REFERENCES 1. Graham JD. Actions of sodium azide. Br J Pharmacol Chemother 1949;4:1–6. 2. Edmonds O, Bourne M. Sodium azide poisoning in five laboratory technicians. Br J Ind Med 1982;39:308–9. 3. Judge KW, Ward NE. Fatal azide-induced cardiomyopathy presenting as acute myocardial infarction. Am J Cardiol 1989;64:830–1. 4. Klein-Schwartz W, Gorman RL, Oderda GM, Massaro BP, Kurt TL, Garriott JC. Three fatal sodium azide poisonings. Med Toxicol Adverse Drug Exp 1989;4:219–27. 5. Gussow L. Toxicology rounds: the case of the contaminated coffee pot. Emerg Med News 2010;32:8. 6. Gordon SM, Drachman J, Bland LA, Reid MH, Favero M, Jarvis WR. Epidemic hypotension in a dialysis center caused by sodium azide. Kidney Int 1990;37:110–5. 7. Bogucka K, Wojtezak L. Effect of sodium azide on oxidation and phosphorylation processes in rat liver mitochondria. Biochim Biophys Acta 1966;122:381–92. 8. Smith RP, Louis CA, Kruszyna R, Kruszyna H. Acute neurotoxicity of sodium azide and nitric oxide. Fundam Appl Toxicol 1991;17: 120–7. 9. Smith RP, Wilcox DE. Toxicology of selected nitric oxide-donating xenobiotics, with particular reference to azide. Crit Rev Toxicol 1994;24:355–77. 10. Emmett EA, Ricking JA. Fatal self-administration of sodium azide. Ann Intern Med 1975;83:224–6. 11. Centers for Disease Control and Prevention (CDC). Sodium azide poisoning at a restaurant – Dallas County, Texas, 2010. MMWR Morb Mortal Wkly Rep 2012;61:457–60. 12. Okumura T, Ninomiya N, Ohta M. The chemical disaster response system in Japan. Prehosp Disaster Med 2003;18:189–92. 13. Chang S, Lamm SH. Human health effects of sodium azide exposure: a literature review and analysis. Int J Toxicol 2003;22:175–86. 14. Lawson K. Sodium azide. Clin Toxicol Rev 1993;15:1–2. 15. Watanabe K, Hirasawa H, Oda S, et al. A case of survival following high-dose sodium azide poisoning. Clin Toxicol (Phila) 2007;45: 810–1. 16. Richardson SG, Giles C, Swan CH. Two cases of sodium azide poisoning by accidental ingestion of Isoton. J Clin Pathol 1975; 28:350–1. 17. Stoddard FJ Jr, Gold J, Henderson SW, et al. Psychiatry and terrorism. J Nerv Ment Dis 2011;199:537–43. 18. Malakoff D. Scientific paper pulled over terrorism concerns. NPR, Weekend Edition Saturday; May 28, 2005. Available at: http:// www.npr.org/templates/story/story.php?storyId=4670948. Accessed November 1, 2013. 19. Gensheimer KF, Rea V, Mills DA, Montagna CP, Simone K. Arsenic poisoning caused by intentional contamination of coffee at a church gathering—an epidemiological approach to a forensic investigation. J Forensic Sci 2010;55:1116–9. 20. Meggs WJ, Hoffman RS, Shih RD, Weisman RS, Goldfrank LR. Thallium poisoning from maliciously contaminated food. J Toxicol Clin Toxicol 1994;32:723–30.
