Rodenticide Toxicity 

  • Author: Derrick Lung, MD, MPH; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Nov 16, 2011
 

Background

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 midcentury, anticoagulant substances have been the mainstays of rodenticide products. In 2009, 14,025 case mentions of exposure to rodenticides were recorded in the National Poison Data System (NPDS), administered by the American Association of Poison Control Centers (AAPCC). (See Epidemiology.)[1]

Red squill

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 another rodenticide that is said to produce pulmonary edema in rodents but not in higher mammals.

Strychnine

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 seizurelike appearance but without loss of consciousness or extensor posturing with risus sardonicus. Strychnine can be found as an adulterant in some street drugs (cocaine, heroin, amphetamines).[2, 3] It is speculated that strychnine is a common contaminant in lysergic acid diethylamide (LSD). Strychnine is usually brought into the United States from other countries where its use as a rodenticide is still legal.

Thallium

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

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.

Barium-containing rodenticides

Interest in these rodenticides is purely academic. No commercially available barium-containing rodenticides are currently available in the United States.

Cholecalciferol-containing rodenticides

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 phosphorus

Yellow phosphorous was once used as a rat or roach poison. Symptoms include a garlic odor, oral burns, vomiting, and phosphorescent, smoking feces.

Warfarin-type anticoagulants

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 superwarfarin shave become the most common rodenticide encountered.[1]

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 2009, NPDS reported 1 such death and 36 moderate and 12 major clinical effects.[1]

Reports have been documented of rodenticide lacing of marijuana in an effort to enhance the effects. Individuals using this combination have been reported to have coagulopathies as a result.[4, 5]

Patient education

For patient education information, see the First Aid and Injuries Center, as well as Activated Charcoal, and Poison Proofing Your Home.

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Etiology

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)
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Epidemiology

The predominant rodenticide exposure is anticoagulant rodenticides, generally the superwarfarin type. In 2009, the AAPCC reported a total of 13,922 reports of rodenticide exposure to US poison control centers. Of these, 80% were anticoagulants and 97% of these were of the superwarfarin type. The outcome of these exposures was generally benign; however, 11 of the superwarfarin exposures resulted in a major effect, and 1 death from such an exposure occurred. About 85% of the rodenticide exposures occurred in children younger than 6 years.[1]

International occurrence

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, 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.

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Prognosis

As long as the proper duration of therapy is used, acute anticoagulant rodenticide overdoses generally resolve uneventfully. 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.

Complications

With anticoagulant rodenticides, the following complications have been reported:

  • Spontaneous intra-abdominal hemorrhage
  • Hematuria
  • Hematemesis
  • Spontaneous hemoperitoneum
  • Intracerebral hemorrhage
  • Death

Morbidity and mortality

The vast majority of rodenticide exposures are to anticoagulants. According to the 2009 NPDS data, among all rodenticide exposures, 75% of persons treated in a health care facility were exposed to the long-acting superwarfarins. The superwarfarin-exposed individuals experienced 42 moderate or major effects and 1 death, while the warfarin-exposed group had no individuals with any more than minor effects.[1]

The vast majority of exposed individuals were children younger than age 6 years, in which case, the exposure was most often unconfirmed. Eighty-eight percent of the long-acting anticoagulant exposures were in children younger than 6 years.[1]

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Contributor Information and Disclosures
Author

Derrick Lung, MD, MPH  Fellow, Medical Toxicology, University of California, San Francisco, School of Medicine; Clinical Instructor, Division of Emergency Medicine, Stanford University Medical Center

Derrick Lung, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Steven Marcus, MD  Professor, Department of Preventive Medicine and Community Health, Associate Professor, Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey; Executive and Medical Director, New Jersey Poison Information and Education System; Consulting Staff, Departments of Pediatrics and Internal Medicine, University Hospital, University of Medicine and Dentistry of New Jersey; Consulting Staff, Department of Pediatrics, Newark Beth Israel Medical Center

Steven Marcus, MD is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Clinical Toxicology, American Academy of Pediatrics, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, and Medical Society of New Jersey

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Fred Harchelroad, MD, FACMT, FAAEM, FACEP Director of Medical Toxicology, Allegheny General Hospital

Disclosure: Nothing to disclose.

Assaad J Sayah, MD Chief, Department of Emergency Medicine, Cambridge Health Alliance

Assaad J Sayah, MD is a member of the following medical societies: National Association of EMS Physicians

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

References
  1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol (Phila). Dec 2010;48(10):979-1178. [Medline]. [Full Text].

  2. Decker WJ, Baker HE, Tamulinas SH, Korndorffer WE. Two deaths resulting from apparent parenteral injection of strychnine. Vet Hum Toxicol. Jun 1982;24(3):161-2. [Medline].

  3. O'Callaghan WG, Joyce N, Counihan HE, Ward M, Lavelle P, O'Brien E. Unusual strychnine poisoning and its treatment: report of eight cases. Br Med J (Clin Res Ed). Aug 14 1982;285(6340):478. [Medline].

  4. Spahr JE, Maul JS, Rodgers GM. Superwarfarin poisoning: a report of two cases and review of the literature. Am J Hematol. Jul 2007;82(7):656-60. [Medline].

  5. La Rosa FG, Clarke SH, Lefkowitz JB. Brodifacoum intoxication with marijuana smoking. Arch Pathol Lab Med. Jan 1997;121(1):67-9. [Medline].

  6. Nelson LS, Perrone J, DeRoos F, Stork C, Hoffman RS. Aldicarb poisoning by an illicit rodenticide imported into the United States: Tres Pasitos. J Toxicol Clin Toxicol. 2001;39(5):447-52. [Medline].

  7. Bruno GR, Howland MA, McMeeking A, Hoffman RS. Long-acting anticoagulant overdose: brodifacoum kinetics and optimal vitamin K dosing. Ann Emerg Med. Sep 2000;36(3):262-7. [Medline].

  8. [Guideline] Caravati EM, Erdman AR, Scharman EJ, Woolf AD, Chyka PA, Cobaugh DJ, et al. Long-acting anticoagulant rodenticide poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2007;45(1):1-22. [Medline]. [Full Text].

  9. Papin F, Clarot F, Vicomte C, Gaulier JM, Daubin C, Chapon F. Lethal paradoxical cerebral vein thrombosis due to suspicious anticoagulant rodenticide intoxication with chlorophacinone. Forensic Sci Int. Mar 2 2007;166(2-3):85-90. [Medline].

  10. Laposata M, Van Cott EM, Lev MH. Case records of the Massachusetts General Hospital. Case 1-2007. A 40-year-old woman with epistaxis, hematemesis, and altered mental status. N Engl J Med. Jan 11 2007;356(2):174-82. [Medline].

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