Rodenticides are a heterogeneous group of compounds that exhibit markedly different toxicities to humans and rodents. They are among the most toxic substances regularly found in homes. The varieties of rodenticides used over the years are legion. Before the mid-20th century, heavy metals (arsenic, thallium) were the often-used agents. (See Etiology, Presentation, and Workup.)
Since the mid-20th century, anticoagulant substances have been the mainstays of rodenticide products. In 2014, anticoagulant rodenticides constituted 8833 of the 11,309 case mentions of exposure to rodenticides recorded in the National Poison Data System (NPDS), administered by the American Association of Poison Control Centers (AAPCC). (See Epidemiology.) 
The botanical preparation of red squill, containing a cardiac glycoside as an active ingredient, was used as a rodenticide for many years. In theory, rodents ingest the product and, because they are incapable of vomiting, develop glycoside intoxication and pulmonary edema. Because humans are capable of vomiting, red squill was considered harmless, even to children. This product is not used much today because of its limited effectiveness as a rodenticide.
Alpha naphthyl thiourea
Alpha naphthyl thiourea (ANTU, Dirax) is a rodenticide that can cause pulmonary edema.
Strychnine is a plant alkaloid that, in the past, was used widely as a rodenticide. This agent is not used much today. Consider strychnine toxicity if an individual presents with a generalized seizure-like appearance but without loss of consciousness or extensor posturing with risus sardonicus. Strychnine has been discovered as an adulterant in some street drugs (cocaine, heroin, amphetamines). [2, 3] Strychnine is usually brought into the United States from other countries where its use as a rodenticide is still legal.
Although thallium is not licensed for use in the United States, many case reports document thallium intoxications in developing countries where this product is still used as a rodenticide. Consider thallium toxicity when treating a patient with painful neuropathy and hair loss. Cases of thallium poisoning associated with malicious criminal activity have been reported in the United States.
Arsenic was widely used as a rodenticide until the late 20th century. It may still be found in liquid form in old barns and storage sites.
Worldwide, barium toxicity continues to be occasionally reported. Profound hypokalemia is the most characteristic effect, in addition to abdominal pain, nausea and vomiting, and altered mental status. No commercially available barium-containing rodenticides are currently available in the United States, so exposures are sporadic. The most recent published case of barium toxicity encountered in the United States was due to ingestion of fireworks. 
Cholecalciferol-containing rodenticides produce hypercalcemia. However, overdoses are not likely to occur with this type of rodenticide because these products are not commonly available, and they require extremely large doses to cause toxicity in humans.
Yellow phosphorous was once used as a rat or roach poison. Exposure to this highly combustible toxin can cause signs and symptoms including a garlic odor, oral burns, vomiting, and phosphorescent, smoking feces.
Most rodenticides encountered today are the warfarin-type anticoagulants and the long-acting brodifacoum anticoagulant products. In the United States and various other parts of the world, the long-acting products known as superwarfarins have become the most common rodenticide encountered. [1, 5]
The prolonged anticoagulant effect of superwarfarins presents a challenging and deadly poisoning to manage. In fact, deaths from rodenticide appear to be rare but are almost always associated with exposure to long-acting anticoagulants. In 2011, NPDS reported 2 such deaths and 39 patients experiencing moderate and 15 major clinical effects. 
Rodenticides that are toxic to virtually every organ system in the body have been available. Cyanide, once prevalent but no longer used for rodenticide application, poisons the cytochrome system. Effects of other rodenticides are as follows:
Poison the Krebs cycle (eg, sodium monofluoroacetate)
Destroy the pancreatic beta cell (eg, N -3-pyridylmethyl- Np -nitrophenyl urea [PNU], Vacor)
Serve as antagonists of the neurotransmitter glycine at the postsynaptic spinal cord motor neuron (eg, strychnine)
Drive potassium intracellularly, may lead to hypotonia (eg, barium)
Cause chemical burns (eg, yellow phosphorous)
Combine with sulfhydryl groups, thus blocking numerous enzymatic reactions and cell signaling pathways (eg, arsenic)
Destroy red blood cells (RBCs) by hemolysis (eg, zinc phosphide)
Uncouple oxidative phosphorylation (eg, bromethalin)
Lead to vasoconstriction with ischemia (eg, norbormide)
Block the production of vitamin K–dependent coagulation factors (eg, warfarin, superwarfarins)
The predominant rodenticide exposure is anticoagulant rodenticides, generally the superwarfarin type. In 2014, the AAPCC reported a total of 10,823 single exposures to rodenticides to US poison control centers. Of these, 8372 were to long-acting anticoagulant rodenticides, and 181 were to warfarin type anticoagulant rodenticides. The outcome of rodenticide exposures was generally benign; overall, 12 exposures resulted in major outcomes, and six deaths occurred. Of all the exposures reported, 8809 involved children younger than 6 years. 
Aggregate tabulations for worldwide experience are not available; however, limited data are available from individual countries or regions. The report of the Brazilian National Poisoning Information System, SINITOX, from 1999-2003 revealed that rodenticides were involved in 2.5% of all human exposures, or 3.4% of exposures when pharmaceuticals were removed from the sample. Children younger than age 5 years incurred 31% of rodenticide exposures in SINITOX. Twenty-three exposures resulted in death; 20 of these were intentional suicides. 
As long as the proper duration of therapy is used, acute anticoagulant rodenticide overdoses generally resolve uneventfully.  Deaths usually occur when patients present well after exposure when severe sequelae of anticoagulation have already manifested. Exposures to herbal-based rodenticides, such as red squill, usually present with only gastrointestinal (GI) symptoms, which are also easy to treat, and full recovery is expected.
Metal rodenticides produce serious toxicity and many produce long-term sequelae. Thallium and arsenic are responsible for severe peripheral neuropathies, and fatalities have occurred; thus, the prognosis is guarded and depends on the speed of response.
PNU produces a permanent insulin-dependency syndrome. An autonomic neuropathy is not unusual, further complicating the therapy of diabetes.
Fluoroacetate and zinc phosphide intoxications are potentially fatal. With no true antidote therapy, the mortality rate is considerable. Phosphorus intoxication produces serious corrosive injuries and may require extensive reconstructive surgery.
With anticoagulant rodenticides, the following complications have been reported:
Spontaneous intra-abdominal hemorrhage
Morbidity and mortality
The vast majority of rodenticide exposures are to anticoagulants. According to the 2014 NPDS data, among all rodenticide exposures, 76% of persons treated in a health care facility were exposed to the long-acting superwarfarins. The superwarfarin-exposed individuals experienced 37 moderate and 11 major effects and three deaths. The warfarin-exposed group (181 patients) had one individual experiencing moderate effects, and no major effects or deaths. 
The vast majority of exposed individuals were children younger than age 6 years, in which case, the exposure was most often unconfirmed. Eighty-six percent of the long-acting anticoagulant exposures were in children younger than 6 years.