Three Fatal Sodium Azide Poisonings*

Toxicology Experience Report

Wendy Klein-Schwartz,l Richard L. Gorman, 1 Gary M. Oderda,l Brian P. Massaro, 2 Thomas L. Kurt 3 and James C. Garriott 4 I Maryland Poison Center, University of Maryland School of Pharmacy and School of Medicine, Baltimore, Maryland, USA 2 Frederick Memorial Hospital, Frederick, Maryland, USA 3 North Central Texas Poison Center, Parkland Memorial Hospital, Dallas, Texas, USA 4 Office of the Medical Examiner, San Antonio, Texas, USA

Summary 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 bicarb onate 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 methaemo globin which complexes with azide is discussed.

Sodium azide is a highly toxic chemical which ported previously. In 2 of the fatal cases the amount is lethal in small amounts. It is used both in the ingested was estimated to be 10 to 20g (Abrams et explosive industry to prepare heavy metal azides al. 1987; Albertson et al. 1986). Clinical manifes for shell detonators and as a common preservative tations include neurological, cardiovascular and in laboratory reagents. Sodium azide is a direct va pulmonary toxicity. We report 3 additional fatal sodilator and was used to treat hypertension in the intentional ingestions of sodium azide. 1950s. Sodium azide interferes with mitochondrial phosphorylation and inhibits cytochrome oxidase Case Reports and other oxidative enzymes. 13 cases of sodium azide ingestion, including 4 deaths, have been re- Case I A 38-year-old man intentionally ingested 2 tablespoonsful of sodium azide diluted in water * Presented in part at the annual meeting of the American Association of Poison Control Centers, Santa Fe, New Mexico, (55g, estimated based on density). In the ambul September 28, 1986. ance 30 minutes after ingestion he had a heart rate Fatal Azide Poisonings 220

of 80 beats per minute, blood pressure of 110/ ation revealed a pIa_sma bicarbonate concentration 80mm Hg, respiratory rate of 30 per minute. The of 8 mmol/L as the only abnormality with normal patient had a generalised tonic clonic seizure and complete blood count, prothrombin time, partial his level of consciousness progressively deterio thromboplastin time and other electrolytes. Sali rated. On arrival in the emergency department I cylate level was 4.1 mg/dl (0.30 mmol/L), but blood hour after ingestion, he was comatose and unres and urine were negative for common toxins. The ponsive with heart rate of 160 beats per minute, methaemoglobin level approximately I hour after blood pressure of 130/80mm Hg, respiratory rate administration of sodium nitrite was below 0.5 g/ of 20 per minute. Naloxone was administered dl (within normal physiological range). without response. He was immediately intubated, On admission to the intensive care unit, the placed on 100% oxygen and gastric lavage per patient was comatose with corneal reflexes present. formed. 20 minutes after arrival in the emergency The pupils remained fixed and dilated. Lungs were department he developed ventricular fibrillation clear and he was breathing spontaneously on 100% and hypotension (blood pressure of 84/50mm Hg). oxygen by nasal cannula. Arterial blood gases re He was unresponsive to resuscitative efforts in vealed pH = 7.34, pC02 = 11.4mm Hg, p02 = cluding intravenous dopamine and was pro I 52mm Hg, base excess = -18. His neurological nounced dead 1.5 hours after ingestion. and cardiovascular condition deteriorated rapidly and he became unresponsive to pain with loss of Case 2 corneal and deep tendon reflexes. At 3 hours after A 33-year-old male coworker of case I inten admission, his blood pressure dropped to 80/ tionally ingested an unknown quantity of sodium 40mm Hg and dopamine was started. He remained azide approximately 2 months later. He told his profoundly hypotensive (60/30mm Hg) and oli wife of the ingestion and then collapsed. En route guric despite increasing doses of dopamine. Pre to the emergency department he became uncon mature ventricular contractions developed which scious with muscle rigidity, a heart rate of 120 beats responded to lignocaine (lidocaine). Acidosis (pH per minute, blood pressure of 90/60mm Hg and = 7.2) persisted despite continued administration respiratory rate of 20 per minute. On arrival, he of sodium bicarbonate. At 5 hours after admission was unconscious and diaphoretic. His pupils were he developed respiratory depression and was placed fixed and dilated. Lungs were clear. Cardiac exam on a ventilator; lungs remained clear. Eight hours ination was remarkable only for tachycardia. after admission he became bradycardic (30 beats/ Muscles were flaccid with fasciculations. Electro min) which briefly responded to atropine and sod cardiogram showed sinus tachycardia with non ium bicarbonate. He became profoundly brady specific T -wave changes, and a chest x-ray was un cardic I minute later and did not respond to ad remarkable. The patient was immediately intubated ditional atropine or adrenaline (epinephrine), and and started on 100% oxygen. Orogastric lavage was he was pronounced dead shortly thereafter. performed which recovered a large amount of flaky white material. Later, nasogastric tube drainage was Case 3 grossly bloody. Intravenous therapy was initiated A 52-year-old white man ingested between 1.2 with Ringers lactate and the patient received 300 and 2g of sodium azide in a suicide attempt. The mmol of sodium bicarbonate. Nitrite therapy to in man held a doctorate in pharmacology and was un duce methaemoglobinaemia was initiated with the der severe psychological stress at the time of the cyanide antidote kit: amyl nitrite (0.3ml) by in ingestion. He had access to sodium azide at his halation for 15 seconds, followed by 300mg of sod place of employment in the hospital. On arrival in ium nitrite intravenously. The patient also re the emergency department about 3 hours post ceived 12.5g of sodium thiosulphate. No ingestion he was alert and oriented, moving all ex improvement was noted. Initial laboratory evalu- tremities and ambulating well. 10 minutes after ar- Fatal Azide Poisonings 221

rival he experienced a generalised tonic clonic treatments with the cyanide antidote kit with 5- seizure which was controlled with intravenous di minute infusions of 300mg sodium nitrite followed azepam. by 3-minute infusions of 12.5g of sodium thiosul He was admitted to a medical intensive care unit phate. An autopsy showed bilateral pulmonary with a diagnosis of acute sodium azide ingestion. oedema and congestion, brain swelling and ery His condition upon admission was described as thema of the gastric lining but no other cause of flaccid with no response to deep pain. Pupils were death. The conclusion of the medical examiner was 3mm and unreactive. He was intubated, a venous that the death was a result of acute intoxication line was placed into a central vein and an indwell with sodium azide. ing urethral catheter was placed. Initial laboratory The maximum methaemoglobin level was 16.1 % evaluation revealed a plasma bicarbonate concen which was obtained 1 hour after the second treat tration of 8 mmol/L with normal prothrombin ment. The methaemoglobin level ranged from 9 to time, partial thromboplastin time and other elec 14% for the other courses of therapy. trolytes. After consultation with the Poison Center, treatment with the cyanide antidote kit (sodium Discussion nitrite and sodium thiosulphate) was initiated. Plasma cyanide ion concentration obtained at this Sodium azide is a neutral, stable, white crystal time was 1.6 mg/L; the minimum toxic concentra line solid which is hydrolysed in aqueous solutions tion is 0.5 mgfL and the lethal concentration is 2.0 to release hydrazoic acid (Reinhardt & Brittelli mg/L. The blood and urine were negative for com 1981). It is rapidly absorbed from the gastrointes mon toxic substances. The contents of the vial from tinal tract, skin and respiratory tract. Sodium azide which he ingested the powder were analysed and is highly toxic, with an LDso of 27 mg/kg in mice were negative for cyanide. The vial was not ana (Christensen & Luginbyhl 1974). Toxicity results lysed for sodium azide. During the first 12 hours, from inhalation of the gas (hydrazoic acid) or sodium nitrite 300mg and sodium thiosulphate ingestion of the sodium salt. Ingestion produces 12.5g were administered intravenously 3 times. neurological, cardiovascular and pulmonary tox Seven hours after admission, the patient was de icity. Neurological symptoms include headache, scribed as responsive to pain, making purposeful restlessness, faintness, muscle weakness, hypo- or movements and responding to commands. Plasma areflexia, convulsions, coma and respiratory fail cyanide ion concentration 12 and 18 hours after ure. The cardiovascular effects include profound admission were 1.7 mg/L and 0.6 mg/L, respec hypotension and tachycardia. tively. 24 hours after admission the patient was re The severity of the poisoning is dose dependent. sponsive and 'mouthed' around his endotracheal Table I summarises 13 previously reported cases tube that he had taken sodium azide and was aware and the 3 cases reported herein. Ingestions of 40mg that he was in an intensive care unit. At this time or less result in headache which resolves within 1 his plasma cyanide ion concentration was 0.1 mg/ to 2 hours of the ingestion (Edmonds & Bourne L and he again received sodium nitrite 300mg and 1982; Richardson et al. 1975; Roberts et al. 1974). sodium thiosulphate 12.5g intravenously. Ingestion of 50 to 60mg in a 39-year-old male re 30 hours after admission, he became tachy sulted in a brief loss of consciousness, nausea, cardic and unresponsive. Arterial blood gases on sweating, pallor, severe headache and hypotension 60% oxygen showed a pH of 7.28 with a pC02 of (Richardson et al. 1975). The patient was asymp 32mm Hg and p02 of 74mm Hg. He again re tomatic the next day. Following the ingestion of ceived sodium nitrite 300mg and sodium thiosul 80mg of sodium azide a 24-year-old man devel phate 12.5g intravenously. Shortly thereafter he be oped chest pain and tightness (Edmonds & Bourne came hypotensive and bradycardic, and could not 1982). A woman ingested 150mg which resulted in be resuscitated. The patient received a total of 5 breathlessness, increased pulse, nausea, vomiting, Table I. Summary of sodium azide ingestions ~ [ Age (years) Sex Circumstance/amount ingested Clinicel manifestations/treatment Outcome Reference ~ is.: 18 F Accidental ingestion of one mouthful of 5 minutes: headache, faintness, sweating Survived Richardson et at (1975) n 'Isoton' (0.1% sodium azide); approx. symptoms passed rapidly without treatment "1:1 5- 0 10mg of sodium azide Uj' 0 ::I Adult ? Accidental ingestion of a small amount of Tachycardia, hyperventilation, hypotension; Survived Roberts et al. (1974) S· GO TRIS buffering agent (4% sodium azide) complete recovery within 24 hours without '" specifiC treatment

Adult ? Drank a half cup of tea made with water 'Vaguely unwell'; recovered after 2 hours in Survived Edmonds & Bourne (1982) treated with sodium azide; approx. 20mg of casualty department sodium azide

Adult F Drank one cup of tea made with water 3 minutes: headache; ~ecoveredafter 2 Survived Edmonds & Bourne (1982) treated with sodium azide; approx. 40mg hours in casualty department

Adult F Drank one cup of tea made with water Approx. 5 minutes: headache; recovered Survived Edmonds & Bourne (1982) treated with sodium azide; approx. 40mg after 2 hours in casualty department

39 M Accidential ingestion of 'Isoton' (0.1% 5 minutes: collapsed, briefly lost Survived Richardson et at (1975) sodium azide); approx. 50-60mg of sodium consciousness; incontinent of urine azide 10 minutes: pale, sweating, felt hot, nauseated, severe headache. HR = 120; BP = 100/60 1 hour: persistent headache; HR = 90; BP = 120/85 Lavaged within 1 hour; asymptomatic by next morning

24 M Drank 2 cups of tea made with water Violent cramp-like pains in chest radiating Survived Edmonds & Bourne (1982) treated with sodium azide; approx. 80mg of down arms; tingling in legs; recurrence of sodium azide chest pain 3 days, 2 months and 6 months later (possible psychogenic component)

Adult F Pipetted and swallowed 1.5ml of a 10% 5 minutes: breathless, increased pulse Survived Burger & Bauer (1985) sodium azide solution; 150mg of sodium 20 minutes: nausea, vomiting, headache, azide restlessness, diarrhoea; polydipsia, T-wave changes, leucocytosis 10 days: increased perspiration; slight numbness N N N 20 M Put unknown amount of sodium azide in Breathed loudly and was very pale Died Kozlicka-Gajdzinski & ~ §. water and drank it (inebriated at time of Died within 40 minutes at home without Brzyski (1966) ingestion; probably accidental) medical attention. Autopsy - brain and lung ~ swelling s.: '" 19 F Put an unknown amount of sodium azide in 1.5 hours: fainted; loss of vision, nausea, Died Emmitt & Ricking (1975) 'J ~. water and drank it; intentional ingestion hyperventilating ::s 4.5 hours: restless, hyporeflexic, :j" hypothermic, responding only to pain; ~ diffuse rhonchi; chest x-ray showed pulmonary oedema; aCidotic 7.5 hours: hypotension Approx. 11 hours: bradycardia, asystole, death Treatment included ipecac and lavage, amyl nitrite and sodium nitrite in the emergency department. Sodium nitrite was repeated at approx. 5 hours postingestion. Received oxygen, sodium bicarbonate, noradrenaline (norepinephrine). Autopsy - pulmonary oedema and gastrointestinal oedema

34 M 10-20g; intentional ingestion Time since ingestion unknown. Found Died Alberton et al. (1986) unresponsive to painful stimulus. Intubated. Gastrointestinal decontamination. Profound metabolic acidosis. Was exchange transfused, charcoal haemoperfused to remove toxin. Increasing infusion of noradrenaline (norepinephrine) necessary to maintain blood pressure. Haemodialysis instituted to control intractable acidosis. Lactic aCidosis persisted and arterial blood pressure continued to fall. Approximately 30 hours after admission, profound hypotension and asystole unresponsive to resuscitation. Autopsy - cerebral and pulmonary oedema

N Continued overleaf N W Table I. contd

Age (years) Sex Circumstance/amount ingested Clinical manifestations/treatment Outcome Reference ~ 30 M 10-20g with large amount of alcohol; 2 hours: coma, flaccid, pupils fixed and Died Abrams et al. (1987) ~ intentional ingestion dilated; rapidly worsening acidosis despite N is.: bicarbonate and intubation. Treatment ~ '"Cl included sodium nitrite. Developed sinus 0 C;;. bradycardia to ventricular fibrillation and 0 ::I death less than 5 hours after ingestion. No :r QQ autopsy '" 38 M Put 2 tablespoonsful (estimated dose = 30 minutes: seizure, CNS depression Died Case 1 55g) in water and drank it; intentional 1 to 1.5 hours: comatose, unresponsive; ingestion ventricular fibrillation, hypotension, death

33 M Put unknown amount of sodium azide in Within 1 hour: unconscious, hypotensive, Died Case 2 water and drank it; intentional ingestion tachycardic, aCidotic Approx. 4 hours: unresponsive with loss of reflexes; hypotension, oliguria, premature ventricular contractions, acidosis Approx. 6 hours: respiratory depression Approx. 9 hours: bradycardia, death Treatment included lavage, amyl nitrite, sodium nitrite and sodium thiosulphate and sodium bicarbonate in the ED; received additional sodium bicarbonate, dopamine, lignocaine (lidocaine), atropine, adrenaline (epinephrine)

52 M Took 1-2g of a powder; intentional Seized approximately 4 hours after Died Case 3 ingestion ingestion. Intubated. Flaccid Approx. 11 hours: improved. Responsive to pain Approx. 28 hours: responsive to commands and mouthing words around endotracheal tube despite increased metabolic acidosis Approx. 30 hours: increasingly tachycardic, tachypnoeic, followed by bradycardic and ventricular standstill despite full resuscitative efforts Treatment included sodium bicarbonate and 5 courses of sodium nitrite and sodium thiosulphate Autopsy - minimal brain swelling, marked IV pulmonary oedema IV .j:> Fatal Azide Poisonings 225

diarrhoea, headache and restlessness (Burger & azide-methaemoglobin complex. It is unclear why Bauer 1965). Although these symptoms resolved, so little of the complex is formed in vivo but may the patient was still complaining of increased per involve azide penetration of other cellular mem spiration and numbness 10 days later. Ofthe 7 re branes more readily than the red cell membrane. ported fatalities, the amount ingested was known In 2 previous reports doses of sodium nitrite in 4 cases: 1 to 2g (20 to 40 mgfkg) [case 3), 10 to were administered without change in the patient's 20g (200 to 400 mgfkg) [Albertson et al. 1986), 15 condition (Abrams et al. 1987; Emmitt & Ricking to 20g (300 to 400 mgfkg) [Abrams et al. 1987) and 1975). In case 2, inhalation of amyl nitrite and 55g (1000 mgfkg) [case I). The other 3 fatalities intravenous sodium nitrite administered in the ingested unknown amounts (Emmitt & Ricking emergency department had no apparent effect on 1975; Kozlicka-Gajdzinski & Brzyski 1966; case 2). the patient's condition. The methaemoglobin level The terminal cardiovascular events in the 6 approximately 1 hour after nitrite administration patients who died under medical care were pro was below 0.5 gfdl (3%). Although there is limited found hypotension, bradycardia and ventricular fi information on the expected methaemoglobin level brillation. The terminal event in case 1 was hypo following the usual dose of sodium nitrite, a 300mg tension and ventricular fibrillation. Bradycardia dose produced a peak methaemoglobin level of 21 % followed by asystole occurred in case 2 and had in a 60kg adult (Shragg et al. 1982). Normal re been previously reported (Emmitt & Ricking 1975). ducing mechanisms within the erythrocyte will take Profound metabolic acidosis was documented in 5 approximately 15 to 20 hours to convert of the ingestions which resulted in death. These methaemoglobin to haemoglobin (Harris & Kel patients died in less than 5 hours (Abrams et al. lermeyer 1970). The methaemoglobin level in case 1987), approximately 9 hours (case 2), 11 hours 2 is much lower than would be expected; there are (Emmitt & Ricking 1975) and 30 hours (case 3; several possible explanations. One consideration is Albertson et al. 1986) after the ingestions. Acidosis that the methaemoglobin-azide complex was not was not reported in the other 2 fatalities; however, measured by the spectrophotometric assay which one of these patients died at home within 40 min uses the change in absorbance on addition of cy utes of the ingestion (Kozlicka-Gajdzinski & anide to determine the methaemoglobin concen Brzyski 1966). In case 1 in this report, the patient tration. In view of the limited binding of azide by died in an emergency department without an ar methaemoglobin demonstrated in animal studies, terial blood gas being drawn. Pulmonary oedema this does not completely explain such a low met occurred in 3 fatal cases previously reported (Al haemoglobin level. In the previously reported case bertson et al. 1986; Emmitt & Ricking 1975; Ko of azide poisoning in which sodium nitrite was ad zlicka-Gajdzinski & Brzyski 1966) and was noted ministered, a methaemoglobin level of 15% was on autopsy of case 3. measured in the presence of azide (Emmitt & Rick Treatment of sodium azide ingestions involves ing 1975). Laboratory error or in vitro reduction of primarily gastric lavage and respiratory and car methaemoglobin to haemoglobin prior to analysis diovascular support. Since azide complexes with of the blood sample are other possible reasons for methaemoglobin in vitro. administration of sod the low methaemoglobin level. ium nitrite to form methaemoglobin which could In case 3, the cyanide antidote kit was used prevent or delay toxicity has been suggested as a multiple times with levels of methaemoglobin potential antidote. Abbanat and Smith (1964) ranging from 9 to 16%. This case occurred at a dif demonstrated a 20% increase in the LDso of sod ferent hospital, which used a different laboratory ium azide in mice by prior administration of sod to determine methaemoglobin levels than in case ium nitrite. While 34% of the haemoglobin was in 2. In case 3 the patient did not have a dramatic the form of methaemoglobin, only 15% of the response to the sodium nitrite and sodium thio available methaemoglobin was in the form of the sulphate, and had persistent metabolic acidosis Fatal Azide Poisonings 226

which signified progressive cellular dysfunction and thiosulphate. There is no evidence of a role for led to death. thiosulphate in the treatment of sodium azide In case 3 in this report, cyanide was detected in poisoning, and it is unlikely that the thiosulphate plasma; the cyanide ion concentrations were 1.6, had any effect on these patients' conditions. 1.7,0.6, and 0.1 mgfL at 0, 12, 18 and 24 hours, Sodium azide ingestions are rare. In the major respectively. No source of cyanide was identified ity of reported cases the victim had access to the and the patient was not on nitroprusside as part of compound in a laboratory; all 3 patients reported his life support. The method used for determining herein had access to sodium azide. Of interest, 14 plasma cyanide ion concentrations at this hospital of the 16 cases involved laboratory workers. An has been well described and is specific for cyanide additional case involved a patient who was given with no interference from the azide moiety the sodium azide-containing solution by accident (McAnalley et al. 1979). No evidence that cyano by a laboratory technician. Therefore, prevention genesis is a major factor in the mechanism of azide strategies should be aimed at laboratory personnel. toxicity could be found. The majority of the accidental ingestions involved While the presence of cyanide is unexplained, it relatively low concentration solutions of sodium is virtually certain that azide and not cyanide was azide with the ingestions of small quantities re the agent responsible for the demise of patient 3. sulting in only mild toxicity. However, intentional All plasma levels of cyanide ion reported in this ingestions usually involved the ingestion of large case are sublethal (Rumack 1988). The patient had quantities with the development of serious and a doctorate in pharmacology and claimed he in often lethal toxicity. gested sodium azide. Analysis of the vial contents and from which the powder was ingested was negative Conclusions Therapeutic Implications for cyanide. The patient did not respond to the cy Severe neurological, cardiovascular and pul~ anide antidote kit despite adequate production of monary toxicity are manifestations of azide poi methaemoglobin. Finally, the clinical course is not soning. Antidotal therapy with sodium nitrite to consistent with acute cyanide poisoning and does produce methaemoglobinemia has been previously not parallel the declining plasma cyanide ion con recommended. However, sodium nitrite was inef centrations. fective in 4 fatal sodium azide ingestions (2 of which The nitrites did not appear to alter either are reported herein). In addition, the hypotensive patient's condition clinically. It is possible that effect of sodium nitrite may be detrimental in azide production of higher levels of methaemoglobin with poisoning since azide causes profound hypoten larger doses of sodium nitrite might prove bene sion. In view of the unproven efficacy of sodium ficial. However, the results of the animal studies nitrite and its potential adverse effects, sodium ni suggest that the potential for sodium nitrite as an trite should not be used to treat azide poisoning. antidote for sodium azide poisoning is limited. Case Until other specific therapies are developed, man 3 in the present report is remarkably similar in agement of azide poisoning should consist of gas course and outcome to a case where the cyanide tric lavage and intensive support of respiratory and antidote kit was not used. Another concern in the cardiovascular function. use of sodium nitrite is its potential toxicity; its hypotensive effect can complicate the clinical tox Acknowledgement icity and management of azide poisoning. Sodium We would like to thank Bryan Ballantyne, M.D., Ph.D. nitrite was not efficacious in 4 uncontrolled uses for his assistance in reviewing this manuscript. in humans which is further evidence of the limited References usefulness of this therapeutic modality. Abbanat RA. Smith RP. The influence of methemoglobinemia Cases 2 and 3 received the entire contents of on the lethality of some toxic anions I. Azide. Toxicology and the cyanide antidote kit, including the sodium Applied Pharmacology 6: 516-583. 1964 Fatal Azide Poisonings 227

Abrams J, EI-Mallalh RS, Meyer R. Suicidal sodium azide inges fide and cyanide poisoning. Journal of Analytical Toxicology tion. Annals of Emergency Medicine 16: 1378-1380, 1987 3: 111-114, 1979 Albertson TE, Reed S, Sietkin A. A case of fatal sodium azide Reinhardt CF, Briltelli MR. Heterocyclic and miscellaneous ni ingestion. Clinical Toxicology 24 (4): 339-351, 1986 trogen compounds. 3.1 Azides. In Clayton & Clayton (Eds) Burger E, Bauer HM. A case of acute poisoning by the accidental Patty's industrial hygiene and toxicology, 3rd ed., pp. 2778- ingestion of a sodium azide solution. Archiv fOr Toxikologie 2784, John Wiley and Sons, New York, 1981 20: 279-283, 1965 Richardson SGN, Giles C, Swan CHJ. Two cases of sodium azide Christensen HE, Luginbyhl TT (Eds). The toxic substances list, poisoning by accidental ingestion ofisoton. Journal of Clinical p. 718, HEW Publication No. 74-134, Rockville, 1974 Pathology 28: 350-351, 1975 Edmonds OP, Bourne MS. Sodium azide poisoning in five la Roberts RJ, Simmons A, Barrett II DA. Accidental exposures to boratory technicians. British Journal of Industrial Medicine sodium azide. American Journal of Clinical Pathology 61: 879- 39: 308-309, 1982 880, 1974 Rumack BH (Ed.). Cyanide. Poisindex information system, Mi Emmitt EA, Ricking JA. Fatal self-administration of sodium azide. cromedex, Denver, 1988 Annals of Internal Medicine 83: 224-226, 1975 Shragg TA, Albertson TE, Fisher CJ. Cyanide potsoning after bit Harris JW, Kellermeyer. The red cell, pp. 447-523, Harvard Uni ter almond ingestion. Western Journal of Medicine 136: 65- versity Press, Cambridge, 1970 69, 1982 Kozlicka.(lajdzinski H, Brzyski J. A case offatal intoxication with sodium azide. Archiv fOr Toxikologie 22: 160-163, 1966 McAnalley BH, Lowry WT, Oliver RD, Garriott Jc. Determin ation of inorganic sulfide and cyanide in blood using specific Authors' address: Dr Wendy Klein-Schwartz, 20 N. Pine Street, ion electrodes: application to the investigation of hydrogen sul- Baltimore, MD 21201 (USA).