Poisoning from malathion and parathion exposure is becoming less common. Despite this, it is important to be alert and look out for the following symptoms if you have handled a product containing either pesticide.1,2
*It is important to note that symptoms of poisoning for both compounds are the same:
- diarrhoea
- blurred vision
- nausea/vomiting
- abdominal cramps
- excessive sweating or salivation
- seizures
- muscle weakness, twitching or tremors
- In severe cases, loss of consciousness or respiratory arrest, which can cause death
Next Steps
Please seek medical advice if you have any of the symptoms above. Take packaging from the product with you when seeking help – this will be helpful for the medical professionals treating you. Depending on your symptoms, you may be prescribed atropine, pralidoxime or benzodiazepines.1,2
More About Medication
Fast medical intervention is important to prevent long term complications or death. Nevertheless, we understand taking a new medication can be daunting. Press below to learn more about what you have been prescribed.
Atropine
This drug is important in reducing excessive secretions in the lower airways.3 Excess mucus production is often the leading cause of death after malathion/parathion exposure.1,2
How does it work?
Atropine is a competitive antagonist of muscarinic receptors, this means it blocks certain receptors in the body called muscarinic receptors.3 Muscarinic receptors are sites of binding for chemicals in the body.3 Binding of chemicals is our body’s way of sending messages from one part to another, so when this is blocked, issues can arise.3
How and when is it administered?
Intravenously with a dose dependent on clinical symptoms. This must be done by a medical professional.1
Pralidoxime
Like atropine, this drug controls secretions in the lower airways, but also helps with any muscle weakness that you may experience after poisoning. It is used in patients with severe poisoning, and used more commonly to treat parathion due to its higher toxicity.1,2,4
How does it work?
When you are exposed to malathion/parathion, an organophsophate – AChE complex forms.5,6 This is where the pesticide (the organophosphate), binds to the acetylcholinesterase, an important enzyme which is present in your body. This means the enzyme cannot function normally.5,6
Pralidoxime works by breaking up the pesticide complex, meaning the enzyme can work normally again.6,7
How and when is it administered?
Intravenously (IV) over 30 to 60 minutes. Intramuscularly if IV cannot be established. It is most effective with early administration. This must be done by a medical professional.1
Benzodiazepines
This drug is very fast acting as it’s absorbed in the GI tract and crosses the blood-brain barrier.8 It acts on GABA receptors.8
How does it work?
GABA is the main inhibitory chemical messenger in the central nervous system, and is important for its calming effect on the brain.9 Sometimes the neurons in our brain are over active and this can lead to seizures, but GABA plays a role in reducing this activity.9
Benzodiazepines enhance the effects of GABA.9 They do this because GABA receptors and benzodiazepines form a complex which causes an influx of negative ions into the cells. This is necessary after exposure of either pesticide to reduce activity of neurons and preventing the chance of seizures happening.1,2,9
How and when is it administered?
As soon as possible, to prevent seizures. This must be done by a medical professional.1,2
References
- ATSDR. Medical Management Guidelines for Malathion [Internet]. Available from: https://wwwn.cdc.gov/TSP/MMG/MMGDetails.aspx?mmgid=517&toxid=92 [Cited: 1st November 2024].
- ATSDR. Medical Management Guidelines for Parathion [Internet]. Available from: https://wwwn.cdc.gov/TSP/MMG/MMGDetails.aspx?mmgid=1140&toxid=246 [Cited: 2nd November 2024].
- Ahmed E.A., Alkuwayti M.A., Ibrahim H-I.M.. Atropine is a suppressor of epithelial–mesenchymal transition (EMT) that reduces stemness in drug-resistant breast cancer cells. 2022;23/17 [Cited: 18th November 2024]. Available from: https://pubmed.ncbi.nlm.nih.gov/36077256/
- Koca, Y. O., Üstündağ, A. Ö., Yalcin, M., & Turgut, C. (2024). Assessing malathion residue impact on poultry health, human safety, and production performance. Heliyon, 10(7), e28438. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10979103/
- Araújo M .F., Castanheira E.M.S., Sousa S.F. The Buzz on Insecticides: A Review of Uses, Molecular Structures, Targets, Adverse Effects, and Alternatives. Molecules. 2023; 28/8 [Cited: 18th November 2024] Available from: https://www.mdpi.com/1420-3049/28/8/3641
- Lotti M. Chapter 72 – Clinical Toxicology of Anticholinesterase Agents in Humans. In: Krieger R, editor. Hayes’ Handbook of Pesticide Toxicology (Third Edition). New York: Academic Press; 2010. p. 1543-89.
- Wong L., Radić Z., Brüggemann R.J.M., Hosea N., Berman H.A., Taylor P. Mechanism of oxime reactivation of acetylcholinesterase analyzed by chirality and mutagenesis. Biochemistry. 2000 May 1;39(19):5750-7. [Cited: 15th November 2024]
- Griffin C.E., Kaye A.M., Bueno F.R., Kaye A.D. Benzodiazepine pharmacology and central nervous system–mediated effects. The Ochsner Journal. 2013;13/2:214-23. [Cited: 13th November 2024].
- Zhu S., Noviello C.M., Teng J., Walsh R.M. Jr, Kim J.J., Hibbs R.E. Structure of a human synaptic GABAA receptor. Nature. 2018;559(7712):67-72. [Cited: 12th November 2024].