Toxicology of Glufosinate Ammonium Herbicide

Abstract

Glufosinate ammonium is a non-selective herbicide widely used in Thailand's agricultural sector. An increasing number of poisoning cases, both accidental and from intentional self-poisoning, have been reported. The primary toxic mechanism involves inhibition of the enzyme glutamine synthetase, leading to hyperammonemia, which causes severe central nervous system toxicity. A hallmark clinical feature is a "latent period" during which patients may initially present with mild gastrointestinal symptoms before rapidly developing severe neurological manifestations within 8 to 32 hours. These include seizures, amnesia, coma, and respiratory failure. Laboratory evaluation of electrolytes, renal and hepatic function, and serum ammonia is essential, as ammonia levels correlate with the risk of neurological complications and mortality. As no specific antidote exists, management is primarily supportive and symptomatic. Key interventions include avoiding the induction of emesis, considering activated charcoal in appropriate cases, airway management as needed, fluid resuscitation and vasopressors for hypotension, and benzodiazepines for seizures. The role of hemodialysis is considered on a case-by-case basis. Therefore, hospital admission for at least 24-48 hours for close neurological monitoring is essential to ensure timely intervention and patient safety.