Rodenticides are designed to kill nuisance rodents such as rats, mice, moles, voles, ground squirrels, gophers, and prairie dogs. These animals may damage crops in the field or in storage and can transmit disease to humans and other animals through their droppings or bites. A wide variety of organic and inorganic chemicals have been used to control rodents. Plant-derived materials such as strychnine and red squill or inorganic compounds such as thallium or arsenic trioxide were among chemicals used early for rodent control. Newer agents tend to be synthetic organic compounds. All pose particular risks for accidental poisonings. Since these agents are designed to kill mammals, their toxicity is often similar for the target rodents and for humans. Also, since rodents often share environments with humans and other mammals, the risk of accidental exposure to the rodenticide is high because of their placement in those environments. As rodents have become resistant to some chemicals, more toxic chemicals have been developed, exposing those applying them and those living in areas where they are used to increased risk of toxicity. There are over 150 trade name rodenticides in the United States alone, many with very similar names. While important for all poisonings, in rodenticide poisoning, having the label to guide therapy is critical.

Long-acting anticoagulants are responsible for nearly 80% of human rodenticide exposures reported in the United States. Introduced in the 1970s, they have essentially replaced warfarin-based products. They have the same mechanism of action as warfarin but are more potent and have longer half-lives. They are effective in a single feeding (or a limited number of feedings) and in animals that have developed resistance to the older anticoagulants.

Treatment of superwarfarin ingestion depends on the dose. A child who ingests a few pellets or grains of the material can be observed at home for the development of bleeding. A person with a bleeding disorder or who takes an anticoagulant is at much greater risk of excess bleeding, even with a small exposure. Patients with large ingestions (>0.1 mg/kg) should have gastric decontamination if they are seen within an hour or two of the ingestion. If there has been a longer delay, activated charcoal is indicated. Prothrombin time (PT) and partial thromboplastin time (PTT) should be measured at 24 and 48 hours after a significant ingestion. If any value is elevated, phytona-dione (vitamin K1) should be started (1 to 5 mg for children and 15 to 20 mg for adults) by subcutaneous injection and repeated as necessary. Critically ill adults can be given 50 to 200 mg via slow intravenous infusion (0.5 mg/min). The PT and PTT should be checked every 4 hours until stable and then every 24 hours. Once the PT and PTT are stable, the phytonadione may be switched to the oral form (15 to 25 mg daily for adults, 5 to 10 mg for children), tapering the dose as the PT levels decline to normal (over a period sometimes as long as 6 months).

Warfarin-based products are still available, but single exposures, unless large amounts (>0.5 mg/kg) are ingested, can be observed without therapy. Recent large exposures should be treated with activated charcoal. The PT and PTT should be measured at 12 and 24 hours. If the PT is two times normal or more, phytonadione should be given (1 to 5 mg for children, 10 mg for adults orally or intramuscularly and repeated as necessary. The PT should be measured every 4 hours until stable, then every 24 hours until normalized (13).

Bromethalin, a relatively new rodenticide introduced in 1985, is a neuro-toxin that produces its effect by uncoupling mitochondrial oxidative phos-phorylation. This results in increased intracranial pressure, decreased nerve impulse conduction, paralysis, and eventual death. No human exposures have been reported. Its effectiveness as a rodenticide is based on the rodent's consuming a relatively larger dose per kilogram than other larger animals. There is no antidote, so treatment of poisoning would be symptomatic and supportive.

Cholecalciferol (vitamin D3) takes advantage of the fact that rodents are sensitive to small percentage changes in calcium levels in their blood. Chole-calciferol increases serum calcium by mobilizing calcium from bone, resulting in calcium deposition in tissues and nerve and muscle dysfunction and cardiac dysrhythmias. Ingestion of several bait pellets or treated seeds should not be toxic, and no treatment is necessary. Larger ingestions should be treated with gastric lavage if recognized early and activated charcoal in several doses if after 1 to 2 hours of ingestion. Serum calcium should be checked at 24 and 48 hours and treatment initiated if hypercalcemia develops. Forced diuresis with furosemide and a low-calcium diet should be initiated along with prednisone (5 to 15 mg every 6 hours). Calcitonin and/or mithramycin may be necessary for patients unresponsive to above measures.

Red squill is a botanic rodenticide derived from the red sea onion (Urginea maritima). It contains two cardiac glycosides that produce effects similar to digitalis. Treatment of ingestion is the same as for digitalis toxicity, including the use of Digibind.

Strychnine is another botanical, found in seeds of Strychnos nux-vomica, a tree native to India. Used in Germany in the 16th century as a poison for rats and other animals, it is still available in many rodenticides. It is a neurotoxin, producing twitching of facial (risus sardonicus) and neck muscles, reflex excitability and generalized seizures. Treatment should include activated charcoal and anticonvulsants (diazepam, phenobarbital, or phenytoin if unresponsive to diazepam). Stimulation of the patient should be minimized; respiratory support including intubation and mechanical ventilation may be required.

Thallium rodenticides are not used in the United States, but are available around the world. Treatment of poisoning is difficult. Gastric decontamination should be attempted with lavage and activated charcoal. Fluid support with potassium chloride theoretically displaces thallium and increases its excretion.

Zinc and aluminum phosphides are used to protect stored grains from rodents and other pests. On contact with moisture, phosphides release phos-phine gas, which is the primary cause of toxicity. Oral exposures to phosphides occur as a result of intentional ingestion for suicidal purposes. Phosphine inhibits oxidative phosphorylation, leading to cell death, manifested by severe GI irritation, hypotension, and cardiac and respiratory dysfunction. Management is by activated charcoal and gastric lavage. Intragastric sodium bicarbonate and/or potassium permanganate have been suggested to decrease phosphine gas release. Oxygen should be supplemented (100% via rebreather). Treatment is otherwise symptomatic and supportive (14).

The fifth edition of Recognition and Management of Pesticide Poisoning, edited by Drs. Routt Reigart and James Roberts of the Medical University of South Carolina, contains a table that lists manifestations caused by specific pesticides, which may be useful in evaluating possible pesticide exposures and toxicities. The entire textbook is available on the Environmental Protection Agency Web site at handbook.htm (see "Index of Signs and Symptoms" or pages 213 to 224) by request from the Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances at 703-305-7666.

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