Malathion is a chemical belonging to the organophosphate class of insecticides. This compound is employed across various sectors, including large-scale agriculture for crop protection and public health programs for mosquito control. It is also found in specific residential products, such as treatments for head lice. Understanding its toxicity is important due to its common application.
Sources of Exposure and Mechanism of Action
Poisoning occurs through several routes, including skin absorption, inhalation of sprays or dusts, and accidental or intentional ingestion. Dermal absorption is significant, particularly in occupational settings where workers handle the chemical without adequate protection. While malathion itself has low toxicity, the body metabolizes it into a much more potent compound called malaoxon.
Malaoxon is responsible for the poisoning by inhibiting the acetylcholinesterase enzyme in the nervous system. This enzyme normally breaks down the neurotransmitter acetylcholine to terminate nerve signals. When inhibited, acetylcholine accumulates at the nerve endings, leading to continuous and excessive stimulation of the nervous system and causing the symptoms of poisoning.
Recognizing the Signs of Acute Poisoning
The signs of acute malathion poisoning result from nervous system overstimulation and are categorized by the type of nerve receptor affected. Muscarinic effects involve excessive secretions and involuntary muscle function. These manifest as pinpoint pupils, increased salivation and tearing, excessive sweating, nausea, vomiting, abdominal cramps, and diarrhea.
Nicotinic effects involve the skeletal muscles and autonomic ganglia. Initial symptoms include muscle fasciculations (fine muscle twitching) followed by generalized weakness and cramps. In severe cases, this progresses to profound muscle paralysis, including the diaphragm, which leads to respiratory failure.
Central Nervous System (CNS) effects are common and indicate serious poisoning. Symptoms include anxiety, confusion, headache, and tremors. As toxicity progresses, the person may develop seizures, slurred speech, loss of consciousness, and coma. The severity of these symptoms depends on the dose and the route of exposure.
Emergency Response and Clinical Treatment
Immediate action is required in suspected malathion exposure to minimize absorption. First, call emergency services, such as a poison control center or 911, and move the victim away from the contamination source into fresh air. Rescuers must prioritize their own safety by wearing protective gear, as malathion can be absorbed through the skin.
Decontamination must be performed rapidly. All contaminated clothing, shoes, and accessories should be removed and double-bagged to prevent secondary exposure. The skin must be washed with soap and water for at least 15 minutes, paying special attention to hair and fingernails. Exposed eyes must be flushed immediately with clean water.
In a clinical setting, professionals focus on supportive care, establishing a clear airway, and providing ventilatory support if breathing is compromised. Primary treatment involves specific antidotes. Atropine is given to block excessive acetylcholine effects at the muscarinic receptors. It controls life-threatening symptoms like excessive bronchial secretions, which can cause death.
The second antidote, pralidoxime (2-PAM), attempts to reactivate the inhibited acetylcholinesterase enzyme. It is most effective when given early, ideally within 24 to 48 hours of exposure, before the enzyme complex becomes permanently bound. Pralidoxime helps reverse both muscarinic and nicotinic effects, including muscle weakness. Large doses of atropine are often required and titrated until secretions are controlled.
Recovery and Long-Term Prognosis
A full recovery is expected when malathion poisoning is treated quickly. The speed with which decontamination and antidotal therapy are initiated is the most important factor determining a positive outcome. Patients who show continuous improvement within the first few hours of treatment usually have a good prognosis.
Even with successful initial treatment, some patients may require prolonged supportive care, including an extended stay in an intensive care unit. A potential complication is Intermediate Syndrome, a delayed muscle weakness that develops one to three days after acute symptoms resolve. Severe or chronic exposure may also lead to residual effects, such as long-term cognitive issues, memory impairment, or depression. These long-term effects underscore the importance of minimizing exposure and ensuring prompt medical intervention.