1 Aluminium phosphide - draft revised Poisons Information 2 Monograph for peer review 3 4 5 CHEMICAL SUBSTANCES 6 7 1. NAME 8 9 1.1 Substance 10 11 Aluminium Phosphide 12 13 1.2 Group 14 15 1.3 Synonyms 16 17 Celphos, Quickphos, Alphos, Synfume, Chemfume, Phostoxin, Phostek, 18 Delicia 19 20 1.4 Identification numbers 21 22 1.4.1 CAS number 23 20859-73-8 24 25 1.4.2 Other numbers 26 27 vi 867(I)ALP(F)11 28 29 2. SUMMARY 30 31 2.1 Main risks and target organs 32 33 Cardiovascular system is the major system affected and severe hypotension is 34 a major risk. 35 36 2.2 Summary of clinical effects 37 38 Vomiting, abdominal pain, loose motions, restlessness are seen. Cardiovascular 39 complications include thready pulse, tachycardia, tachypnoea, acidosis, marked 40 hypotension. 41 42 Other common complications of aluminium phosphide poisoning include 43 haemorrhage, acute renal failure, disseminated intravascular coagulation and 44 arrhythmias 45 46 Patients remain mentally clear till cerebral anoxia due to shock supervenes 47 resulting in drowsiness, delirium and coma. 48 49 Several ECG changes ranging from ST segment elevation/depression, PR and 50 QRS interval prolongation, complete heart block to ectopics and fibrillation have 51 been observed. Reversible myocardial injury has also been reported. 52 1 1 2.3 Diagnosis 2 3 The following factors alone or in combination would help in the diagnosis. 4 1. Positive history of ingestion 5 2. Symptoms compatible with aluminium phosphide ingestion 6 3. Chemical test for phosphine positive in gastric aspirate and breath 7 The breath of patients who have ingested aluminium phosphide has a 8 characteristic garlic-like odour. Conformation of diagnosis is based on the 9 patient’s history and a positive result (blackening) on tests of the patient's breath 10 with paper moistened with fresh silver nitrate solution or by chemical analysis of 11 blood or gastric acid for phosphine. 12 13 2.4 First-aid measures and management principles 14 15 Gastric lavage is important in the initial stage. 16 The management principles aim to sustain life with appropriate resuscitation 17 measures until phosphine is excreted from the body. 18 The main principles are – 19 1. Carry out methods to absorb phosphine through GI tract. 20 2. Steps to reduce organ toxicity 21 3. Steps to enhance phosphine excretion 22 4. Supportive measures 23 24 3. PHYSICO-CHEMICAL PROPERTIES 25 26 3.1 Origin of the substance 27 This is a synthetic substance. 28 29 3.2 Chemical structure 30 31 AIP (aluminium phosphide) 32 33 3.3 Physical properties 34 35 3.3.1 Colour 36 Dark grey or dark yellow crystals. 37 38 3.3.2 State/Form 39 Solid - crystalline 40 41 3.3.3 Description 42 43 Formulated as a greenish grey tablet of 3 gm which in presence of 44 moisture or HC1 releases phosphine: 45 46 AlP+3H20 = Al(OH)3+PH3 47 AlP+3HC1 = AlC13+PH3 48 49 The residue, Al (OH)3 is non-toxic 50 51 3.4 Hazardous characteristics 52 53 The tablet has typical odour of garlic. 2 1 2 3 4. USES/CIRCUMSTANCES OF POISONING 4 5 4.1 Uses 6 7 4.1.1 Uses 8 9 4.1.2 Description 10 11 Grain fumigant 12 13 4.2 High risk circumstance of poisoning 14 15 Self poisoning is common. Rarely accidental poisoning is seen in grain freight 16 trades. 17 18 4.3 Occupationally exposed populations 19 20 Farmers while using the fumigant, but poisoning is rare. 21 22 23 5. ROUTES OF ENTRY 24 25 5.1 Oral 26 27 Common route 28 29 5.2 Inhalation 30 31 Rare route 32 33 5.3 Dermal 34 Not relevant 35 36 5.4 Eye 37 Not relevant 38 39 5.5 Parenteral 40 Not relevant 41 42 5.6 Others 43 Not relevant 44 45 6. KINETICS 46 47 6.1 Absorption by route of exposure 48 49 In the stomach phosphine is released which is responsible for toxicity. 50 51 6.2 Distribution by route of exposure 52 53 6.3 Biological half-life by route of exposure 3 1 2 6.4 Metabolism 3 4 6.5 Elimination by route of exposure 5 6 7. TOXICOLOGY 7 8 7.1 Mode of Action 9 10 The exact mechanism is not known. It is suggested to produce non-competitive 11 inhibition of the cytochrome oxidase of mitochondria, blocking the electron 12 transfer chain and oxidative phosphorylation producing an energy crisis in the 13 cells. (Cherfuka W et al.1976) 14 15 Recently Chugh et al. found inhibiton of catalase and induction of SOD in 16 humans leading to free radicals stress brought out lipid peroxidation and 17 protein denaturation of cell membrane leading to hypoxic cell damage 18 19 7.2 Toxicity 20 21 7.2.1 Human data 22 23 7.2.1.1 Adults 24 25 1/4th tablet is lethal. 26 Cardiotoxicity (Toxic chemical myocarditis is manifested as depressed 27 left ventricular ejection fraction, ECG changes varying from ST segment 28 elevation/depression, PR prolongation, broad QRS complexes, and right 29 or left bundle branch block, supraventricular ectopics or fibrillation. 30 (Mathur A, et al. 1999) 31 32 Biochemical changes include rise in AST, CPK-MB and LDH. 33 Histopathology shows myocytolysis, multiple areas of necrosis, 34 congestion. 35 (Karanth S & Nayyar V. 2005) 36 37 7.2.1.2 Children 38 Toxicity, biochemical changes and histopathological changes are similar 39 to adults. 40 41 7.2.2 Relevant animal data 42 43 LD50 mice (Inhalation of fumes) 44 Rat: 0.68gm/m3 - 65-75 min. exposure. 45 1.47gm/m3 - 35-50 min. exposure 46 Cat: 25ppm (2-4hrs daily during 3 days) 47 48 7.2.3 Relevant in vitro data 49 Data not available 50 51 7.2.4 Workplace standards 52 Data not available for aluminium phosphide. 53 4 1 For phosphine: TLV: 0.3 ppm as TWA; 1 ppm as STEL. EU OEL: 0.1 ppm 2 and 0.14 mg/m³ as TWA; 0.2 ppm and 0.28 mg/m³ as STEL (WHO/ICSC 3 2006) 4 5 7.2.5 Acceptable daily intake (ADI) and other guideline levels 6 Data not available 7 8 7.3 Carcinogenicity 9 10 Not known 11 12 7.4 Teratogenicity 13 14 Not known 15 16 7.5 Mutagenicity 17 18 Not known 19 20 7.6 Interactions 21 Not known 22 23 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS 24 8.1 Material sampling plan 25 8.1.1 Sampling and specimen collection 26 8.1.1.1 Toxicological analyses 27 Gastric lavage - test for phosphine. 28 8.1.1.2 Biomedical analyses 29 8.1.1.3 Arterial blood gas analysis 30 8.1.1.4 Haematological analyses 31 8.1.1.5 Other (unspecified) analyses 32 8.1.2 Storage of laboratory samples and specimens 33 8.1.2.1 Toxicological analyses 34 Send immediately to laboratory after properly covering the sample. 35 8.1.2.2 Biomedical analyses 36 8.1.2.3 Arterial blood gas analysis 37 8.1.2.4 Haematological analyses 38 8.1.2.5 Other (unspecified) analyses 39 8.1.3 Transport of laboratory samples and specimens 40 8.1.3.1 Toxicological analyses 41 8.1.3.2 Biomedical analyses 42 8.1.3.3 Arterial blood gas analysis 43 8.1.3.4 Haematological analyses 44 8.1.3.5 Other (unspecified) analyses 45 8.2 Toxicological analyses and Their Interpretation 46 8.2.1 Tests on toxic ingredient(s) of material 47 8.2.1.1 Simple Qualitative Test(s) 48 Determine the phosphine liberated by acid treatment, measure by GLC. 49 8.2.1.2 Advanced Qualitative Confirmation Test(s) 50 Determine the phosphine liberated by acid treatment, measure by GLC. 51 8.2.1.3 Simple Quantitative method(s) 52 8.2.1.4 Advanced Quantitative method(s) 53 8.2.2 Tests for biological specimens 5 1 8.2.2.1 Simple Qualitative test(s) 2 Heat the lavage at 50 degree C for 15-20 minutes and place a silver nitrate 3 impregnated filter paper (0.1M) on the mouth of flask. On drying the paper 4 turns black indicating the presence of phosphine. 5 6 8.2.2.2 Advanced Qualitative confirmation Test(s) 7 8.2.2.3 Simple Quantitative Method(s) 8 8.2.2.4 Advanced Quantitative Method(s) 9 8.2.2.5 Other Dedicated Method(s) 10 8.2.3 Interpretation of toxicological analyses 11 8.3 Biomedical investigations and their interpretation 12 8.3.1 Biochemical analysis 13 8.3.1.1 Blood, plasma or serum 14 8.3.1.2 Urine 15 8.3.1.3 Other fluids 16 8.3.2 Arterial blood gas analyses 17 8.3.3 Haematological analyses 18 8.3.4 Interpretation of biomedical investigations 19 8.4 Other biomedical (diagnostic) investigations and their interpretation 20 8.5 Overall Interpretation of all toxicological analyses and toxicological 21 investigations 22 8.6 References 23 24 9. CLINICAL EFFECTS 25 26 9.1 Acute poisoning 27 28 9.1.1 Ingestion 29 30 This is the most common mode of poisoning. 31 32 Vomiting, abdominal pain, loose motions, restlessness are seen. 33 Cardiovascular complications include thready pulse, tachycardia, 34 tachypnoea, acidosis, marked hypotension. ECG changes can be seen. 35 Other common complications of aluminium phosphide poisoning 36 include haemorrhage, acute renal failure, disseminated intravascular 37 coagulation and arrhythmias. 38 39 Patients remain mentally clear till cerebral anoxia due to shock 40 supervenes resulting in drowsiness, delirium and coma. 41 42 9.1.2 Inhalation 43 44 Rarely inhalation of phosphine (PH3) can occur. 45 46 9.1.3 Skin exposure 47 Not relevant 48 49 9.1.4 Eye contact 50 Not relevant 51 52 9.1.5 Parenteral exposure 53 Not relevant 6 1 2 9.1.6 Other 3 4 9.2 Chronic poisoning 5 6 9.2.1 Ingestion 7 Not relevant 8 9 9.2.2 Inhalation 10 Not relevant 11 12 9.2.3 Skin exposure 13 Not relevant 14 15 9.2.4 Eye contact 16 Not relevant 17 18 9.2.5 Parenteral exposure 19 Not relevant 20 21 9.2.6 Other 22 23 Chronic poisoning not seen. 24 25 9.3 Course, prognosis, cause of death 26 Features of hepatotoxicity usually develop 72 hours after poisoning. Death due to 27 acute hepatocellular toxicity and fulminant hepatic failure has also been reported 28 in acute poisoning. Cardiovascular changes and respiratory system changes 29 (ARDS) can also lead to death. 30 31 9.4 Systematic description of clinical effects 32 33 9.4.1 Cardiovascular 34 35 Various changes in ECG ST segment elevation/depression, PR and QRS interval 36 prolongation, complete heart block to ectopics and fibrillation have been observed. 37 Reversible myocardial injury has also been reported, biochemical, 38 histopathological changes in heart, hypotension and shock. 39 40 9.4.2 Respiratory 41 42 Acute respiratory distress syndrome (ARDS) and exudative plural effusions can 43 develop. A possible explanation for the exudative pleural effusion might be that 44 when aluminium phosphide comes in contact with moisture, it releases 45 phosphine (PH3) gas which is absorbed by simple diffusion. This phosphine gas 46 due to non competitive inhibition of cytochrome oxidase system of mitochondria 47 or damage by free radicals causes global hypoxia. This global hypoxia leads to 48 an increase in capillary permeability that could lead to pleural effusion.

49 Furthermore, this phosphine gas is eliminated through the lungs, hence due to 50 high concentration in the respiratory alveoli, it is responsible for direct alveolar 51 damage. This alveolar damage (acute lung injury) causes ARDS. Studies in the

7 1 past have shown increased levels of inflammatory markers (cytokines and 2 interleukins) in ARDS which increase the capillary permeability. This combined 3 effect of increase in capillary permeability due to global hypoxia and ARDS 4 could be responsible for the exudative effusion seen predominantly in the 5 pleural cavity and not in other serous cavities. 6 (Suman RL & Savani M 1999) 7 8 9 10 9.4.3 Neurological 11 12 9.4.3.1 CNS 13 Restlessness, drowsiness and delirium, all due to shock and acidosis 14 9.4.3.2 Peripheral nervous system 15 16 No data available 17 18 9.4.3.3 Autonomic nervous system 19 No data available 20 21 9.4.3.4 Skeletal and smooth muscle 22 No data available 23 24 9.4.4 Gastrointestinal 25 26 Vomiting, abdominal pain can occur initially. 27 28 9.4.5 Hepatic 29 Death due to acute hepatocellular toxicity and fulminant hepatic failure 30 has also been reported in acute poisoning. 31 32 Features of hepatotoxicity usually develop 72 hours after poisoning. 33 During this time the patient may not have any gastrointestinal system 34 problem at all. 35 36 Initially the patient would have icterus and soft, non-tender hepatomegaly. 37 Investigations would reveal alteration of liver enzymes. Abdominal 38 ultrasonography may reveal hepatomegaly with increased echotexture 39 with areas of sparing and ascites (Karanth S & Nayyar V. 2005). 40 41 42 43 9.4.6 Urinary 44 45 9.4.6.1 Renal 46 47 Acute renal failure due to shock could occur (Chugh SN 1998). 48 49 9.4.6.2 Others 50 51 9.4.7 Endocrine and reproductive systems 52 No data available 8 1 2 9.4.8 Dermatological 3 Nil 4 5 9.4.9 Eye, ears, nose, throat: local effects 6 7 Nil 8 9 9.4.10 Haematological 10 11 Haemoconcentration 12 13 9.4.11 Immunological 14 15 Nil 16 17 9.4.12 Metabolic 18 19 9.4.12.1 Acid-base disturbances 20 21 Metabolic acidosis occurs. 22 23 9.4.12.2 Fluid and electrolyte disturbances 24 25 9.4.12.3 Others 26 27 9.4.13 Allergic reactions 28 29 Nil 30 31 9.4.14 Other clinical effects 32 33 Oedema 34 35 9.4.15 Special risks 36 37 Cardiotoxicity 38 Hypotension 39 ARDS 40 41 9.5 Others 42 43 10. MANAGEMENT - 44 45 10.1 General principles 46 47 Supportive treatment mainly gastric lavage, vasoactive substances. 48 49 10.2 Life supportive procedures and symptomatic treatment 50 51 The following conditions should be anticipated and supportive measures should 52 be tailor made according to the individual’s condition. 53 9 1 1. Hypoxia- blood gas monitoring should be done. 2 3 2. Shock - blood pressure should be maintained above 70 mmHg using IV fluids. 4 low dose dopamine (4-6ug/kg/min) and intravenous hydrocortisone 5 (200-400mg after 4-6 hours) have been found to be effective. (Chugh SN 1998) 6 7 3. Arrythmias- conventional drugs such as digoxin, xylocaine are ineffective. 8 atropine is not useful in bradyarryhtmias. Magnesium sulphate has been 9 effective in both tachy and bradyarrythmias due to its membrane stabilizing 10 effect (Chugh SN 1998). 11 12 13 4. Metabolic acidosis- moderate to severe metabolic acidosis can be seen 14 15 5.ARDS- 100% O2 can be delivered via a face mask. Mechanical respiratory 16 support and positive end-expiratory pressure therapy is given for 17 haemodynamically unstable patients. 18 19 Magnesium sulphate has been shown to reduce organ toxicity produced by PH3 20 mediated oxidative injury. The antioxidative, antihypoxic and antiarrhythmic 21 properties all come into play in the management of aluminium phosphide toxicity 22 (Chugh SN 1998). 23 24 25 10.3 Decontamination 26 27 Gastric lavage with saline or sodium bicarbonate or potassium permanganate 28 (1:1000) (Chugh SN 1998). 29 30 31 10.4 Enhanced Elimination 32 Phosphine is excreted through the breath and urine, therefore, adequate 33 hydration and renal perfusion by low dose dopamine 4-6 microg/kg/min must be 34 maintained. Diuretics are not useful in the presence of profound shock. However, 35 if blood pressure is stable around 80 mmHg, the frusemide (20 mg IV) may be 36 tried. 37 38 10.5 Antidote treatment 39 40 10.5.1 Adults 41 42 Nil 43 44 10.5.2 Children 45 46 Nil 47 10.6 Management discussion 48 49 No specific antidote available. The treatment with Magnesium sulphate is not 50 correlated with serum magnesium levels. Early treatment of shock and 51 magnesium therapy results in better prognosis. 52 53 10 1 2 3 4 11. ILLUSTRATIVE CASES 5 6 11.1 Case reports from literature 7 8 CASE REPORTS: 9

10 1. A 25 years old male was admitted to the medical intensive care unit 4 hours after ingestion 11 of a tablet of Celphos (aluminium phosphide). He had a fight with his relatives prior to that. 12 He was restless irritable, drowsy, and poorly responding to simple verbal commands. He had 13 cold clammy skin, non-palpable pulses, respiratory rate 14/min, BP 60 mmHg systolic, and 14 peripheral cyanosis. Cardiac examination revealed tachycardia, normal first and second heart 15 sounds and left ventricular third heart sound. Chest examination showed bilateral normal 16 vesicular breathing with no added sound. Investigations revealed: haemoglobin 8.5 g%, TLC 17 7,900/ mm3, blood urea 96 mg%, and normal chest x-ray. Arterial blood gas analysis revealed 18 severe metabolic acidosis with blood pH 6.91, PaO2 98. In view of hypotension, an urgent 19 ECG was done which revealed incomplete RBBB and generalized ST-T changes. 20 Subsequent ECG showed idioventricular rhythm and complete RBBB. Serum Mg++ could not 21 be done. Thus a diagnosis of toxic myocarditis was made. He was managed with intravenous 22 fluids, MgSo4, sodium bicarbonate, and inotropic support. Dialysis could not be done due to 23 haemodynamic instability. Patient developed cardiac arrest on the same day and could not be 24 revived. The ALP on contact with water liberates phosphine gas ALP + 3H2 . Al (HO)3 + PH3 25 Phosphine inhibits cytochrome oxidase and thereby hampers cellular oxygen utilization. The 26 average time interval between poisoning and death is 3 hours with a range of 1-48 hours. As 27 many as 95% of fatalities occur within first 24 hours. Common causes of death are ventricular 28 fibrillation, ARDS, hepatic failure, acidosis, and dyselectrolytaemia. Our patient presented with 29 anteroinferior wall ischaemia with incomplete RBBB which progressed to idioventricular 30 rhythm, complete RBBB, and T-wave flattening simulating myocardial ischaemia. These 31 changes were due to toxic injury to myocardium. Various ECG changes such as atrial 32 arrhythmias, ventricular arrhythmia, ST-T changes, AV dissociation, bundle blocks, etc., have 33 been described in ALP poisoning1.No specific antidote is available as yet. MgSO4 and 34 corticosteroids have been used. However, there is no hard data to support their use2. 35 Recently animal studies have shown xanthinol nicotinate to reduce mortality secondary to ALP 36 poisoning3.Thus, our case amply illustrates the importance of immediate ECG recording in 37 every case of ALP poisoning to diagnose myocardial involvement in order to formulate early 38 treatment strategies.( Ranga GS et al.2004) 39 40 41 42 2. A 21 years housewife consumed a phosphorus-based rodenticide six days prior to 43 admission into our ICU. Following the ingestion no immediate first-aid was administered. 44 Twenty-four hours later she developed vomiting and abdominal pain for which she was taken 45 to a peripheral hospital where she received primary care in the form of a stomach wash and 46 some other symptomatic therapy before being discharged. Forty-eight hours after the alleged 47 ingestion she again developed intractable vomiting and thus was shifted back to the same 48 hospital where she was admitted this time. On the sixth day after the incident in view of 49 worsening of her sensorium she was referred to our institution. She reached the ICU in shock 50 (with a blood pressure of 80 systolic, pulse rate of 160/minute and cold peripheries), febrile 51 (temperature 100.6°F.) and O2 on saturation 95% on room air. Systemic examination was 52 normal except for the presence of a decreased Glasgow Coma Scale (GCS) of 7/ 15 (Eye 11 1 opening 1, Verbal response 1, Motor response 5). Investigations on admission revealed an 2 acute hepatitis-like picture with a total bilirubin 6.1mg%, ALT 826U/L, AST 389U/ L and 3 prolonged prothrombin time of greater than two minutes. Serum ammonia was also elevated 4 to 46.2 mcg/dl. Arterial blood gases revealed well compensated metabolic acidosis. 5 Sonographic imaging revealed fatty liver with minimal ascites. Thus a diagnosis of acute 6 fulminant hepatic failure secondary to toxic hepatitis following a rodenticide poisoning was 7 made. Accordingly she was started on antihepatic precoma measures, low-dose dopamine 8 and other symptomatic measures. Infective causes of acute hepatitis including malaria, 9 leptospira and other viral markers were negative. Through the next forty-eight hours the 10 patient showed gradual worsening of her sensorium which dropped to a GCS of 4/15 by day 11 three of admission (ninth day following the alleged ingestion of poison). She continued to be in 12 this state till the fifth day following admission (eleventh day after the alleged ingestion), when 13 further worsening of her sensorium was noted. By now she had also developed 14 haemodynamic instability requiring increasing levels of inotropic support. On the following day 15 she had an episode of bradycardia followed by a ventricular fibrillation. She was resuscitated 16 and placed on mechanical ventilation. However through the course of the day, she worsened 17 and expired at 6 PM that day. A post-mortem liver biopsy was done which showed collapsed 18 reticulin framework with fibrosis between the hepatocytes showing a bubbly and vacuolated 19 cytoplasm suggestive of an acute fulminant hepatitis. (Karanth S & Nayyar V. 2005) 20 21 22 3. A 25 years housewife presented with alleged history of ingestion of an unknown quantity 23 of a rodenticide, Ratol (containing 3% yellow phosphorus) mixed with alcohol about five days 24 prior to admission. There were no symptoms immediately following the ingestion. However 25 she confessed to having taken the poison four days after the incident. Following primary care 26 in a nearby hospital she was referred to our institution. Examination revealed her to be icteric, 27 with normal vitals and presence of a soft, non-tender hepatomegaly. Investigations at the time 28 of admission revealed a picture of acute hepatitis with total bilirubin of 7.8mg%, direct bilirubin 29 of 3 mg%, ALT 1055U/L, AST 824U/L, alkaline phosphatase 13 U/L and a prolonged PT of 30 over two minutes. An abdominal ultrasonography revealed hepatomegaly with diffuse 31 increase in echotexture of liver with areas of sparing associated with ascites. Through her stay 32 in the hospital initially there was increasing icterus that was noticed which was also supported 33 by a biochemical evidence showing increasing total bilirubin till about the seventh day of 34 admission, following which there was a gradual decline in the serum bilirubin levels. However 35 all through this period there was a steady decrease in, serum ALT and AST levels associated 36 with an improvement in the prothrombin time suggesting improving hepatic function. smear for 37 MP was repeatedly negative. Hepatotropic viral markers were also negative. Patient was 38 administered vitamin-K for three days along with other symptomatic measures. She was 39 admitted in the hospital for a period of two weeks and later discharged. At the time of 40 discharge her liver function tests read as follows: Total bilirubin 3.5mg%, ALT 245U/L, AST 41 136U/L and prothrombin time 22.3 seconds. (Karanth S & Nayyar V. 2005) 42 43 44 45 12. ADDITIONAL INFORMATION 46 47 12.1 Specific preventive measures 48 These include- 49 Availability of single tablet pack encased in hard plastic material with spikes. 50 -By restricting the free sale of the chemical 51 -Social awareness regarding handling of the substance and its lethality. 52 -Some emetic substance may be added in it. 53 12 1 12.2 Other 2 3 13. REFERENCES 4 5 Bajaj R, Agarwal R, Wasir HS, Bhatia ML. (1988) Clinical toxicity and intensive haemodynamic 6 monitoring in patients of aluminium phosphide poisoning. J Assoc Phys Ind, 36: 23 7 8 Bajaj R, Wasir HS. (1988) Epidemic aluminium phosphide poisoning in Northern India. Lancet, 9 1:820. 10 11 Chopra JS, Kalra OP, Malik VS, Sharma R, Chandra A. (1986) Aluminium phosphide 12 poisoning: a prospective study of 16 cases in one year. Postgrad Med J 62: 1113-1115 13 14 Cherfuka W,Kashi KP, Bond EP (1976) The effect of phosphene on electron transport in 15 mitochondria. Pest Biochem Physiol,6:65-84 16 17 Chugh SN (1998) Aluminium Phosphide in Lall SB, Essentials of Clinical Toxicology, New Delhi, 18 Narosa Publishing House pp 41-46 19 20 Christophers AJ, Singh S, Goddard DG (2002) Dangerous bodies: a case of fatal aluminium 21 phosphide poisoning. MJA ,176 (8): 403 22 23 Dashora VK, Swaroop D. (1985) The dreadful celphos poisoning. J Assoc Phys Ind, 34:227. 24 25 Karanth S, Nayyar V. (2005) Rodenticide-induced Hepatotoxicity. J Assoc Physicians India, 26 51:316-317 27 28 Lall SB, Peshin SS, Seth SD. (1989) Retrospective five year study of acute poisoning cases at 29 The All India Institute of Medical Sciences. J Foren Med Toxicol, 6:1-8 30 31 Mathur A, Swaroop A, Aggarwal A. (1999) ECG changes in aluminium phosphide and organo 32 phosphorus poisoning. The Indian Practitioner, 52: 249-52 33 34 Ranga GS, Dwivedi S, Manish Agarwal, Dharmender Kumar: (2004) Aluminium Phosphide 35 Poisoning in a Young Adult : A Suicidal Cardiotoxin Simulating Myocardial Ischaemia: Journal, 36 Indian Academy of Clinical Medicine, 5(4): 369 37 38 39 Sepaha GC, Bharani AK, Jain SM, Kamath PG. (1985) Acute aluminium phosphide 40 poisoning. J Ind Med Assoc, 83: 378-379 41 42 Singh S, Dilwari JB, Vashist R, Malhotra HS, Sharma BK. (1985) Aluminium phosphide ingestion. 43 Br. Med J, 290: 1110-1111. 44 45 Singh S, Sharma BK, Wahi PL, Anand BS, Chugh KS. (1984) Spectrum of acute poisoning in 46 adults (10 year experience). J Assoc Phys Ind, 32: 561-563 47 48 Siwach SB, Yadav DR, Arora B. (1988) Acute aluminium phosphide poisoning: An 49 epidemiological, clinical and histopathological study. J Assoc Phys Ind, 36:594 50 51 Suman RL , Savani M (1999) Pleural Effusion- A Rare Complication of Aluminium Phosphide 52 Poisoning: Indian Pediatrics,36: 1161-1163 53 13 1 WHO/ICSC (2006) International Chemical Safety Card No. 694 Phosphine. 2 3 4 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 5 ADDRESSES 6 7 First Draft: 8 Dr S. Lall 9 New Delhi Poisons Centre 10 August 1993 11 12 Revision: 13 Prof. Ravindra Fernando 14 National Poisons Information Centre 15 National Hospital of Sri Lanka 16 Colombo 8 17 Sri Lanka 18 19 November 2007 20

14