Use of Rodenticides Around Aquatic Systems
IAAAM Archive
Lisa A. Murphy
ASPCA Animal Poison Control Center, Urbana, IL


Rodent control is important for prevention of many potential problems; contamination and consumption of foodstuffs, predation on collection animals, transmission of infectious and sometimes zoonotic diseases, and detraction from visitor experience due to plant and building damage.8 Rodent damage to electrical wiring has been cited as the probable cause for certain fires and explosions, as well as an instance of shutting down the Internet.3 Methods of rodent control may include exclusion, habitat management, sanitation, repellents, and removal by trapping, baiting, relocation, and/or euthanasia. Baiting carries the risk of secondary and non-target species toxicity, but trapping is labor intensive and unlikely to be successful in cases of severe rodent overpopulation.8

The objective of this article is to provide an evaluation of commonly used rodenticides, so animal caretakers can make educated decisions about using these agents around aquatic systems. Considerations when choosing a rodenticide around aquatic systems should include: toxicity to exhibit animals, secondary toxicity, environmental and ecological risks, and potential human health hazards.3 This discussion will focus on anticoagulants, bromethalin, cholecalciferol, and zinc phosphide.1-7,9

General Considerations

Rodenticide products can be found as place packs of pellets, wax blocks or tracking powders. The bittering agents and dyes added to many rodenticides to deter children cannot be equally relied upon to deter non-target animals. If the bait can be shaken from stations when they are lifted, stations should be secured with wire or otherwise immobilized. Many bait stations are actually designed with internal bait compartments to minimize spillage. Where bait stations are not feasible, products in place packs or formulated in paraffinized blocks will help reduce primary exposures of birds. Product use should be limited to indoors and against the outside walls of buildings to further limit exposures in non-target wildlife species.3


The first-generation agents' chlorophacinone and diphacinone and the second-generation agents' brodifacoum and bromadiolone are examples of commonly used anticoagulant rodenticides. These are the rodenticides primarily used by pest control operators (PCO's)3 and are available in stores as well. Second-generation agents have greater efficacy in warfarin-resistant rodents because of increased potency and prolonged duration of action,5 and are generally expected to be lethal to rodents following a single ingestion.3

All anticoagulant rodenticides interfere with the vitamin K-epoxide reductase enzyme. Depletion of vitamin K-dependent clotting factors (II, VII, IX, and X) slows the extrinsic, intrinsic, and common coagulation pathways.4 Even though lethal doses of anticoagulant rodenticides can be absorbed dermally,3,7 most cases of anticoagulant poisonings result from oral exposures.

Primary toxicity to mammals is high for all anticoagulant rodenticides, and moderate to high for birds, freshwater fish, and freshwater invertebrates. Rodents poisoned with anticoagulant rodenticides can kill avian and mammalian secondary consumers.3 Although signs have been observed within 1 day of ingestion, there is usually a lag period of 3-5 days between exposure and appearance of clinical signs. Onset of death may be acute, without the presence of other clinical signs. This is most common when hemorrhage occurs in the cerebral vasculature, abdominal cavity, pericardial sac, mediastinum, or thorax. Outward signs of hemorrhage may not exist in these instances. More often, the animal may be initially only depressed, anorexic, and anemic. Animals experiencing prolonged toxicosis may be icteric from breakdown of impoundedblood.1

An elevated prothrombin time (PT) shows up first (24-48 hours post-ingestion) due to the involvement of factor VII. This is followed soon thereafter by an elevated activated partial thromboplastin time (APTT). Platelet count will generally be in the normal to low-normal range. Antemortem sample of choice for confirming anticoagulant poisoning is whole blood (refrigerate) to be sent out for an anticoagulant screen or analysis for a specific anticoagulant. The postmortem sample of choice is liver. Specimens should be wrapped in foil, well identified, sealed in plastic, and frozen (liver) or chilled (blood) during storage and shipment. Continued administration of vitamin K1 for several weeks and monitoring of coagulation parameters is necessary. In the early phase of a poisoning, fresh-frozen plasma may be required as well.7

Anticoagulant rodenticides are generally poorly soluble in water and immobile in soil, so potential contamination of surface and ground water from brodifacoum is low. However, diphacinone's sodium salt is highly water-soluble and actually used to prepare water baits for indoor control of rats and mice. Even though these agents are unlikely to pose a nontarget species risk in a water source, they could still be expected to kill some aquatic animals. Chlorophacinone degrades rapidly in water and soil, and does not accumulate in fish at a significant level3 diphacinone is rapidly decomposed in water by sunlight.7

Even though anticoagulant rodenticides are highly toxic to most animals, one advantage of their use is that a specific antidote does exist. The disadvantage is that early clinical signs are often vague and may lead to an incorrect or delayed diagnosis of intoxication.


Bromethalin was introduced in 1985 as an acute, single-feeding, non-anticoagulant rodenticide. The suspected biochemical mechanism of action of bromethalin is an uncoupling of oxidative phosphorylation. The subsequent loss of Na+-K + ion channel pump function results in the development of cerebral edema. Lethal bromethalin toxicosis in the dog and rat also produces increased cerebrospinal fluid pressure.4 Sublethal doses of bromethalin given to dogs and cats results in delayed CNS depression, hind limb ataxia, paresis, and paralysis. Higher doses given to dogs resulted in rapid severe muscle tremors and generalized seizures.3

Primary toxicity to mammals, birds, freshwater fish, and freshwater invertebrates is very high for bromethalin. Luckily, bromethalin has an extremely low solubility in water, particularly when formulated into "weather-resistant" paraffinized blocks.3 Lesions observed in dogs and target rodents include vacuolation and edema of the cerebellum. Swelling of the brain and spinal cord occurs. Frozen liver, kidney, and brain may be analyzed using gas chromatography with an electron capture detector to confirm exposure.

In animals significantly exposed (e.g., 10% of an LD50 or more), an emetic should be given early on. Repeated oral administration of a super activated charcoal/sorbitol mixture was the only effective therapy for bromethalin toxicosis in the dog. The uses of corticosteroids, mannitol, and furosemide have been ineffective at reversing the toxic syndrome (paralysis, depression) once clinical signs develop. Therapy to abolish seizures is indicated, though may not be clinically rewarding for severely affected animals.1

Bromethalin is an effective single feeding rodenticide, and is readily available in forms that will not readily dissolve in water and discourage feeding by non-target species. The major disadvantage of this agent is that the signs it can cause are difficult to treat once they become severe.


The introduction of cholecalciferol-containing rodenticides has led to many cases of acute vitamin D toxicosis. Fat-soluble cholecalciferol is metabolized by the liver to 25- hydroxycholecalciferol (25-OH-D3). Further metabolism of 25-OH-D3 occurs in the kidney Where calcitriol [1,25-(OH)2-D3] is produced. Calcitriol is the most potent cholecalciferol metabolite in terms of enhancing bone resorption and intestinal calcium transport. The resultant hypercalcemia leads to dystrophic calcification.4

Clinical signs most commonly associated with cholecalciferol-induced hypercalcemia include neurologic, cardiovascular, gastrointestinal, and especially renal effects. Clinical signs generally develop within 18-36 hours post-exposure and include: anorexia, lethargy, nausea, weakness, vomiting (+ blood), diarrhea (+ blood), polyuria, polydipsia, and rarely neurological disturbances (e.g., seizures). Clinical signs become more severe as serum calcium levels increase. Hypercalcemia can result in EKG changes and vasoconstriction and hypertension may occur. Hypercalcemia and hypercalciuria cause decreased renal sodium-chloride reabsorption leading to a degree of medullary washout. Clinically, polyuria and hyposthenuria are observed. In dogs with induced hypercalcemia, vasoconstriction of glomerular afferent arterioles occurs with a resultant decrease in GFR. Death is thought to result from hypercalcemia, calcification of tissues, and renal and heart failure.1

The most profound alteration in serum chemistry is elevated serum calcium. Elevations in serum phosphorous occur at 12 hours post-ingestion and often precede serum calcium rise. Increased BUN and creatinine are also seen. Urine specific gravity may be in the hyposthenuric range. Proteinuria and glycosuria may be seen. Adjusted calcium values (adjusted for protein binding by albumin) may need to be considered: corrected calcium = Ca (mg/dl) - albumin (gm/dl) + 3.5.1

Objectives of treatment are to control hypercalcemia. Several treatment agents have been recommended, including intravenous normal saline, corticosteroids, and furosemide. Thiazide diuretics should not be used because they may contribute to or cause hypercalcemia. In severe cases, salmon calcitonin or pamidronate may be necessary to normalize serum calcium levels.1 Cholecalciferol is practically insoluble in water, but oxidized and inactivated by moist air within a few days. The formulated product is stable for over 1 year at ambient temperatures in sealed packages.7

The advantages to cholecalciferol are that relay toxicosis is not a large concern, and that the product is easily inactivated in the environment. The disadvantage is that intoxication rapidly results in severe signs that can be very labor-intensive and expensive to treat.

Zinc Phoshide

Zinc phosphide is available as grain-based baits, pastes, and tracking powders. Zinc phosphide toxicosis is due primarily to the liberation of phospine gas in the gastrointestinal tract when the compound hydrolyzes. Zinc phosphide is a direct irritant of the gastrointestinal tract, with a 2 peculiar odor that resembles acetylene, garlic, or rotten fish or eggs.

Onset of clinical signs is variable, though toxicosis is usually evident 15 minutes to 4 hours following ingestion of a toxic dose of zinc phosphide. Occasionally, onset of clinical signs may be delayed for up to 18 hours after ingestion. Death usually occurs in 3-48 hours. No definitive clinical signs characterize zinc phosphide toxicosis. Anorexia, lethargy and vomiting are early clinical signs. Ataxia, weakness, prostration, gasping, struggling, convulsions and hyperesthesia also are seen in some cases. An acetylene or faint garlic odor to the breath also may be noted.2 Acute death is probably due to hypoxia from pulmonary irritation following absorption of phosphine gas.1 In animals surviving for more than a few hours, intact zinc phosphide may also be absorbed, directly effecting the liver and kidneys.2

Zinc phosphide has a high nonspecific toxicity for all forms of animal life9 and has caused deaths in many nontarget animal species and man. Animals have been poisoned by feeding directly on treated bait or on the carcasses of zinc phosphide poisoned rodents.2 Zinc phosphide is slightly corrosive to metals and stable for long periods of time when kept dry, potentially remaining toxic for several months.9 Deterioration is rapid under acid or damp conditions.2

Whenever possible in suspected cases of zinc phosphide poisoning, carcasses should be sent unopened to a diagnostic laboratory as quickly as possible for toxicological examination.2 Source material should be packed and frozen in airtight containers to prevent loss of phosphine gas.1 Elevated zinc levels may be detected in the blood, liver and kidney. Intact zinc phosphide may also be detected in the kidney and liver.2

There is no specific antidote for zinc phosphide poisoning. Gastric lavage with 5% sodium bicarbonate solution2 or administration of aluminum plus magnesium hydroxide gel (Maalox®) can help limit acid hydrolysis of zinc phosphide. Metabolic acidosis may be treated with sodium bicarbonate. Anticonvulsants may be needed to control seizure activity.1 Oxygen administration may assist with respiratory difficulties. Corticosteroids may help with shock and possibly restore micro vascular integrity.2

Even though zinc phosphide quickly degrades in a moist environment, the severe acute health risks it poses to humans and nontarget animal species probably outweighs any benefits it may provide as part of a rodent control program.

Even though zinc phosphide quickly degrades in a moist environment, the severe acute health risks it poses to humans and nontarget animal species probably outweighs any benefits it may provide as part of a rodent control program.

Human Handling Risks

In their re-registration eligibility decision covering chlorophacinone, diphacinone, brodifacoum, and bromadiolone,3 the EPA is concerned about potential dermal and inhalation exposures to fine particles and dusts for handlers loading and applying these chemicals. People should probably wear gloves while handling all rodenticide chemicals not already contained in place packs to reduce dermal exposures. Protective eyewear and dust mask/mist respirators may also be advisable when handling non-paraffinized meal or grain-based baits not contained in place packs.


Rodenticides are potentially toxic to all animal species. Although rodenticide poisoning is rare in freshwater fish or invertebrates, it can occur due to accidental mixing of the bait into the water system. A diagnosis of rodenticide poisoning can be made based upon clinical signs and analysis for detection of the bait in foods, water, body fluids and tissues.


1.  Beasley, V.R., et al. 1999. A Systems Affected Approach to Veterinary Toxicology. University of Illinois, Champaign, IL.

2.  Casteel, S.W. and Bailey, E.M., Jr. 1986. A Review of Zinc Phosphide Poisoning. Veterinary and Human Toxicology 28(2): 151-154.

3.  EPA. 1998. Reregistration eligibility decision (RED). Rodenticide Cluster. U.S. Environmental Protection Agency, Washington DC.

4.  Dorman DC. 1990. Anticoagulant, cholecalciferol, and bromethalin-based rodenticides. Veterinary Clinics of North America: Small Animal Practice 20(2): 339-52.

5.  Duvall, M.D., Murphy, M.J., Ray, A.C., Reagor, J.C. 1989. Case studies on second-generation anticoagulant rodenticide toxicities in nontarget species. Journal of Veterinary Diagnostic Investigation 1:66-68.

6.  James, S.B., Raphael, B.L., Cook, R.A. 1998. Brodifacoum toxicity and treatment in a White-winged Wood Duck (Cairina scutulata). Journal of Zoo and Wildlife Medicine 29(3): 324-327.

7.  Pelfrene, A.F. 1991. Synthetic Organic Rodenticides. In: Hayes, W.J., Jr., Laws, E.R., Jr. Handbook of Pesticide Toxicology Volume 3 Classes of Pesticides. Academic Press, Inc., San Diego, pp. 1271-1316.

8.  Spelman, L.H. 1999. Vermin Control. In: Fowler, M.E. and Miller R.E. Zoo & Wild Animal Medicine: Current Therapy 4. W.B. Saunders Company, Philadelphia, pp.114-120.

9.  Thomson, W.T. 1995. Agricultural Chemicals Book III - Miscellaneous Agricultural Chemicals. Thomson Publications, Fresno, CA.

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Lisa A. Murphy