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Aluminum Phosphide
Poisoning
By
Yasmin Aziz Badi
Supervised by
Dr. Ammar Ali hussien
Introduction
Aluminum phosphide (AlP) is a solid fumigant pesticide sold as tablets in use since the
1940s. It is considered to be an ideal pesticide because of its cheapness, efficiency and
easy availability in the market and is widely used as a grain preservative worldwide
Although the chemical does not accumulate in the food chain, aluminum phosphide
poisoning is one of the most common forms of poisoning in India. The incidence of
the poisoning has been increasing steadily, and most of the poisoning is from suicide
in the agricultural community. Occupational exposure or accidental exposure of
individuals in railroad boxcars, cargo ships or close proximity to grain storage facilities
has been reported. The mortality in cases of aluminum phosphide poisoning varies
between 60% and 90%, even in experienced and well-equipped hospitals.
None of the patients who had ingested more than three tablets survived. The average
time interval between ingestion of AlP and death is 3 h (1–48 h), 95% of the patients
die within 24 h and the most common cause of death in this group is cardiac
dysrhythmia. Death is reported to result from profound shock, myocarditis and
multiorgan failure. In some countries, the use of AlP is strictly controlled, and it
cannot be freely supplied. Aluminum phosphide is capable of releasing phosphine gas
if it comes in contact with moisture in the air. Phosphine gas is colorless, extremely
flammable and explosive; very toxic to insects; and useful as a fumigant for stored
products for controlling pests; it has a unique smell of garlic or decaying fish, with an
odor threshold of 0.14 ppm and a vapor density of 1.17. Phosphine poisoning
following inhalation has also been reported. The fatal dose of aluminum phosphide
was stated to be in the range of 150–500 mg/ 70 kg
Toxicokinetic:
Phosphine can easily be distributed into all tissues and excreted in the urine and
expelled through the lungs .The most important urine metabolites of phosphine are
phosphite and hypophosphite. Phosphine toxicity to humans occurs with a common
mechanism of respiratory inhibition .Phosphine is a noncompetitive inhibitor of
cytochrome oxidase in mitochondria, with electron transfer blockage, which inhibits
oxidative phosphorylation and, in turn, cellular respiration and production of peroxide
radicals. This inhibits oxidative respiration by 70% and ultimately results in a marked
decrease in the mitochondrial membrane potential .Phosphine can inhibit catalase and
deplete glutathione, which may result in cellular wall and canal dysfunction as well .It is
likely that interference with cellular respiration may lead to multisystem toxicity.
Clinical Finding :
Human phosphine poisoning occurs after inhalation of phosphine generated from
metal phosphides pellets used as fumigants, leading to systematic clinical symptoms
including the damage of the nervous system and respiratory system. Acute phosphine
poisoning has a quick onset; severe poisoning symptoms occur in a few minutes,
although some patients have a long latency to response of 48 h. It mainly causes
dizziness, headache, fatigue, nausea, vomiting, loss of appetite, cough, chest tightness,
dry throat, abdominal pain and diarrhea, and patients often recover in one week with
appropriate treatment. Severe poisoning can cause coma, convulsions, pulmonary
edema, shock, significant myocardial damage, and significant liver and kidney damage .
The symptoms of respiratory and nervous system damage occur quickly after
inhalation of phosphine, while the gastrointestinal symptoms occur early, in
particular in acute poisoning caused by ingestion of zinc phosphide or
aluminum phosphide. Acute phosphine poisoning can be diagnosed according
to the history of exposure, clinical examination, on-site investigation, with
other diseases excluded, and it is rather difficult for diagnosis of phosphine
poisoning in children .
Clinical Finding :
Management:
Management should be started as soon as history and clinical examination
support AlP poisoning, and should not be delayed for the confirmatory
diagnosis . Unfortunately, due to no known specific antidote, management
remains primarily supportive care. As each poison has a definite elimination
time, so also is the case with AlP. Early arrival, resuscitation, diagnosis, intensive
monitoring and supportive therapy may result in good outcome. Care of
patients with severe poisoning can be enhanced by consultation with a medical
toxicologist or a regional poison center.
Case Study :
Case 5 A 7-year-old girl presented with clinical symptoms of vomiting and
abdominal pain in the morning; her grandmother presented with mild vomiting
symptom. She was sent to the hospital and back home after treatment. She was
dead at midnight that night, and phosphine poisoning was suspected because
she lived near a granary. Furthermore, it had been rainy for a week. Forensic
autopsy indicated no trauma or fatal disease. The metabolites of phosphine
were found in the liver and bladder flush fluid by GC–MS.
References :
1- Journal of Analytical Toxicology, 2018;42:330–336 doi: 10.1093/jat/bky005
Advance Access Publication Date: 25 January 2018 Article.
2- Hashemi-Domeneh, B., Zamani, N., Hassanian-Moghaddam, H., Rahimi, M.,
Shadnia, S., Erfantalab, P., et al. (2016) A review of aluminium phosphide poisoning
and a flowchart to treat it. Arhiv za higijenu rada i toksikologiju, 67, 183–193
3- Kalawat, S., Thakur, V., Thakur, A., Punjabi, N.D. (2016) Cardiovascular profile of
aluminium phosphide poisoning and its clinical significance. International Journal of
4- Advances in Medicine, 3, 859–864. 12. Meena, M.C., Mittal, S., Rani, Y. (2015) Fatal
aluminium phosphide poisoning. Interdisciplinary Toxicology, 8, 65–67

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Aluminum phosphide poisoning

  • 1. Aluminum Phosphide Poisoning By Yasmin Aziz Badi Supervised by Dr. Ammar Ali hussien
  • 2. Introduction Aluminum phosphide (AlP) is a solid fumigant pesticide sold as tablets in use since the 1940s. It is considered to be an ideal pesticide because of its cheapness, efficiency and easy availability in the market and is widely used as a grain preservative worldwide Although the chemical does not accumulate in the food chain, aluminum phosphide poisoning is one of the most common forms of poisoning in India. The incidence of the poisoning has been increasing steadily, and most of the poisoning is from suicide in the agricultural community. Occupational exposure or accidental exposure of individuals in railroad boxcars, cargo ships or close proximity to grain storage facilities has been reported. The mortality in cases of aluminum phosphide poisoning varies between 60% and 90%, even in experienced and well-equipped hospitals.
  • 3. None of the patients who had ingested more than three tablets survived. The average time interval between ingestion of AlP and death is 3 h (1–48 h), 95% of the patients die within 24 h and the most common cause of death in this group is cardiac dysrhythmia. Death is reported to result from profound shock, myocarditis and multiorgan failure. In some countries, the use of AlP is strictly controlled, and it cannot be freely supplied. Aluminum phosphide is capable of releasing phosphine gas if it comes in contact with moisture in the air. Phosphine gas is colorless, extremely flammable and explosive; very toxic to insects; and useful as a fumigant for stored products for controlling pests; it has a unique smell of garlic or decaying fish, with an odor threshold of 0.14 ppm and a vapor density of 1.17. Phosphine poisoning following inhalation has also been reported. The fatal dose of aluminum phosphide was stated to be in the range of 150–500 mg/ 70 kg
  • 4. Toxicokinetic: Phosphine can easily be distributed into all tissues and excreted in the urine and expelled through the lungs .The most important urine metabolites of phosphine are phosphite and hypophosphite. Phosphine toxicity to humans occurs with a common mechanism of respiratory inhibition .Phosphine is a noncompetitive inhibitor of cytochrome oxidase in mitochondria, with electron transfer blockage, which inhibits oxidative phosphorylation and, in turn, cellular respiration and production of peroxide radicals. This inhibits oxidative respiration by 70% and ultimately results in a marked decrease in the mitochondrial membrane potential .Phosphine can inhibit catalase and deplete glutathione, which may result in cellular wall and canal dysfunction as well .It is likely that interference with cellular respiration may lead to multisystem toxicity.
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  • 7. Clinical Finding : Human phosphine poisoning occurs after inhalation of phosphine generated from metal phosphides pellets used as fumigants, leading to systematic clinical symptoms including the damage of the nervous system and respiratory system. Acute phosphine poisoning has a quick onset; severe poisoning symptoms occur in a few minutes, although some patients have a long latency to response of 48 h. It mainly causes dizziness, headache, fatigue, nausea, vomiting, loss of appetite, cough, chest tightness, dry throat, abdominal pain and diarrhea, and patients often recover in one week with appropriate treatment. Severe poisoning can cause coma, convulsions, pulmonary edema, shock, significant myocardial damage, and significant liver and kidney damage .
  • 8. The symptoms of respiratory and nervous system damage occur quickly after inhalation of phosphine, while the gastrointestinal symptoms occur early, in particular in acute poisoning caused by ingestion of zinc phosphide or aluminum phosphide. Acute phosphine poisoning can be diagnosed according to the history of exposure, clinical examination, on-site investigation, with other diseases excluded, and it is rather difficult for diagnosis of phosphine poisoning in children . Clinical Finding :
  • 9. Management: Management should be started as soon as history and clinical examination support AlP poisoning, and should not be delayed for the confirmatory diagnosis . Unfortunately, due to no known specific antidote, management remains primarily supportive care. As each poison has a definite elimination time, so also is the case with AlP. Early arrival, resuscitation, diagnosis, intensive monitoring and supportive therapy may result in good outcome. Care of patients with severe poisoning can be enhanced by consultation with a medical toxicologist or a regional poison center.
  • 10. Case Study : Case 5 A 7-year-old girl presented with clinical symptoms of vomiting and abdominal pain in the morning; her grandmother presented with mild vomiting symptom. She was sent to the hospital and back home after treatment. She was dead at midnight that night, and phosphine poisoning was suspected because she lived near a granary. Furthermore, it had been rainy for a week. Forensic autopsy indicated no trauma or fatal disease. The metabolites of phosphine were found in the liver and bladder flush fluid by GC–MS.
  • 11. References : 1- Journal of Analytical Toxicology, 2018;42:330–336 doi: 10.1093/jat/bky005 Advance Access Publication Date: 25 January 2018 Article. 2- Hashemi-Domeneh, B., Zamani, N., Hassanian-Moghaddam, H., Rahimi, M., Shadnia, S., Erfantalab, P., et al. (2016) A review of aluminium phosphide poisoning and a flowchart to treat it. Arhiv za higijenu rada i toksikologiju, 67, 183–193 3- Kalawat, S., Thakur, V., Thakur, A., Punjabi, N.D. (2016) Cardiovascular profile of aluminium phosphide poisoning and its clinical significance. International Journal of 4- Advances in Medicine, 3, 859–864. 12. Meena, M.C., Mittal, S., Rani, Y. (2015) Fatal aluminium phosphide poisoning. Interdisciplinary Toxicology, 8, 65–67