Second-generation anticoagulant rodenticides were developed in the 1970s after rodents began evolving resistance to first-generation compounds such as warfarin. These newer compounds, including bromadiolone and difethialone, work by interfering with the vitamin K cycle, specifically the VKORC1 enzyme complex, which is essential for recycling vitamin K1 and producing functional clotting factors. A poisoned animal ultimately dies from internal hemorrhaging, but the process is slow, often taking several days. During that time, the animal can accumulate a lethal body burden of the compound and continue moving through the environment. Because SGARs are extremely persistent in liver tissue, with half-lives that can stretch from weeks to months, they do not simply vanish when the target rodent dies. Instead, they linger in the carcass and in the tissues of any animal that consumed the poisoned prey, creating a pathway for secondary poisoning up the food chain.

The research team, led by Luigi F. Richardson and Albrecht I. Schulte-Hostedde of Laurentian University, set out to answer a deceptively simple question: are the bait stations that pest management professionals deploy around buildings in urban and suburban settings leaking poison into the surrounding wild rodent community? To find out, they used snap traps to capture white-footed mice in urban wildland areas of Toronto and Vaughan, deliberately choosing trapping locations near ongoing professional baiting programs that used products containing bromadiolone and difethialone. White-footed mice are an ideal sentinel species for this kind of work. They are abundant, territorial, and have relatively small home ranges, which means that any residue found in their tissues likely reflects local exposure rather than long-distance movement from a contaminated area far away.

The results were unambiguous, if modest in absolute numbers. Out of 111 mice tested, nine carried detectable residues of bromadiolone and two carried difethialone. That is roughly one in ten animals carrying a potent anticoagulant poison in a population that was never the intended target. Concentrations in liver tissue ranged from 0.008 to 0.03 micrograms per gram for bromadiolone and from 0.008 to 0.023 micrograms per gram for difethialone. While these figures may sound vanishingly small, the authors note that concentrations in this range may be sublethal for raptors, meaning that a bird of prey feeding regularly on contaminated mice could accumulate a toxic burden over time even if no single mouse delivers a lethal dose.

Perhaps the most striking spatial finding is how far from the bait stations the contaminated mice were caught. SGAR residues were detected in individuals trapped at distances of 0 meters, 5 meters, 20 meters, 40 meters, 70 meters, and 100 meters from active rodenticide stations. This pattern suggests that the compounds are not simply leaking a few centimeters into the surrounding soil or being picked up only by animals that wander directly into a bait box. Instead, the exposure appears to be distributed across the landscape, likely through a combination of mechanisms. Poisoned commensal rodents may disperse into wildland areas before dying, contaminated carcasses may be scavenged or partially consumed by mice, and bait itself may be carried out of stations by target rodents or other animals. Invertebrates that feed on bait have also been proposed in the broader literature as a potential vector, though the present study did not directly test that pathway.

When the researchers compared the SGAR-positive mice with the SGAR-negative ones, they found no significant differences in sex, age, body condition, distance to the rodenticide source, capture date, or capture site. In other words, there was no obvious profile of the contaminated mouse. Exposure did not concentrate in juveniles, in animals in poor condition, or in individuals trapped closest to bait stations. This lack of pattern is itself informative. It suggests that exposure risk is broadly distributed across the local mouse population rather than confined to a particular demographic subset or a narrow zone around bait deployment. It also complicates any attempt to predict which individuals or areas are most at risk based on simple proximity measures.

That said, the study did note that four of the exposed individuals were classified as being in poor body condition. While the sample size is too small to draw firm conclusions about a causal relationship between rodenticide burden and physical condition, the observation is consistent with the possibility that sublethal exposure imposes physiological costs. Anticoagulant poisoning, even at doses that do not kill outright, can cause chronic internal bleeding, anemia, and reduced fitness. For a wild mouse, those costs could translate into reduced survival or reproductive output, and for the predators that depend on mice as prey, a population of weakened or poisoned rodents represents a hidden hazard embedded in a normal food source.

The broader context of this work is a growing body of evidence that anticoagulant rodenticides have become pervasive contaminants in urban and suburban food webs. Studies in Chicago have documented widespread exposure among common urban mesopredators, while research in British Columbia has found these compounds in endangered American badgers and fishers. Raptors in Ontario have already been shown to carry SGAR residues, and the compounds have been detected in unexpected places, from urban reptiles in Australia to frogs and freshwater fish in Germany. What has been missing, particularly in Ontario, is a clear understanding of the exposure pathways, the specific mechanisms by which the poison moves from a locked bait station to a hawk’s bloodstream. By demonstrating that nontarget wild rodents near professional baiting programs carry SGAR residues, this study helps fill that gap and points to a plausible link between routine pest control and the contamination of predators.

The authors also raise the possibility that some of the exposure they detected may have come from residential SGAR use rather than from the professional baiting programs they focused on. In Ontario, as in many jurisdictions, consumers can purchase rodenticide products for home use, and these products are often deployed with less oversight than professional applications. Distinguishing between professional and residential sources of exposure is methodologically difficult, but the finding underscores that the problem is not confined to any single sector of the pest control industry. It is a landscape-scale contamination issue driven by the sheer volume of persistent anticoagulants being deployed across urban environments, whether by licensed technicians or by homeowners dealing with a mouse in the garage.

The implications for policy and practice are significant. Several jurisdictions, including parts of the United States and the European Union, have already moved to restrict public access to SGARs or to limit their use in certain settings, and Health Canada has imposed restrictions on commercial-class rodenticides in agricultural contexts. This study adds weight to the argument that urban and suburban baiting practices deserve similar scrutiny, particularly near wildland fragments that support native rodent populations and the predators that feed on them. The authors suggest that the pest management industry’s use of rodenticides in these settings is likely causing some degree of nontarget spillover in Toronto and the Greater Toronto Area. As cities continue to densify and the boundary between built and natural habitat grows ever more porous, the question is no longer whether rodenticides reach nontarget wildlife, but how much exposure ecosystems can absorb before the cumulative toll on predators and other wildlife becomes unsustainable. For now, the white-footed mice of Toronto’s ravines are carrying the answer in their livers, one contaminated individual at a time.

Subject of Research: Nontarget exposure of white-footed mice to second-generation anticoagulant rodenticides in urban Ontario

Article Title: Exposure of nontarget white-footed mice (Peromyscus leucopus) to second-generation anticoagulant rodenticides in an urban context

Article References: Exposure of nontarget white-footed mice (Peromyscus leucopus) to second-generation anticoagulant rodenticides in an urban context. (n.d.). https://doi.org/10.1007/s10661-026-16038-x

Image Credits: AI Generated

DOI: 10.1007/s10661-026-16038-x

Keywords: anticoagulant rodenticides, SGARs, white-footed mouse, Peromyscus leucopus, bromadiolone, difethialone, urban wildlife, ecotoxicology, secondary poisoning, Toronto, pest control, nontarget exposure

The birds in the study were not killed for research. All 24 cadavers arrived opportunistically between June 2022 and November 2023, a window that coincided with regional mouse infestations. Some were donated by the university’s Veterinary Teaching Hospital after being euthanised for medical reasons, while others were roadkill collected during unrelated fieldwork. Ten raptor species and one nightjar were represented, with Eastern Barn Owls dominating the sample at ten individuals, followed by three Australian Boobook Owls. Two Wedge-tailed Eagles, two Black-shouldered Kites, a Peregrine Falcon, a Powerful Owl, a Grey Goshawk, a Brown Goshawk, a Nankeen Kestrel, a Black Kite and a Tawny Frogmouth rounded out the list. Thirteen birds were male, ten female and one of undetermined sex; fourteen were adults and ten immature.

The analytical centrepiece of the study was liquid chromatography mass spectrometry, or LC-MS, performed at the CSIRO Ecosciences Precinct in Brisbane. Because decay alters the water content of tissue, the researchers homogenised and freeze-dried liver samples before extraction, then used a multi-step process involving formic acid, cold acetonitrile and lipid-removal cartridges to isolate the rodenticide residues. The instrument, an Agilent 6546 liquid chromatography quadrupole time-of-flight mass spectrometer, ran in a data-independent mode called quadrupole-resolved all-ions analysis, screening for eight rodenticides including warfarin, brodifacoum, difethialone, flocoumafen, bromadiolone, difenacoum, coumatetralyl and pindone. Calibration curves spanning 0.01 to 1,000 parts per billion achieved correlation coefficients between 0.9683 and 0.9971, and quality-control samples spiked with known concentrations of the compounds verified the method’s accuracy across low, mid and high ranges.

The results were striking. Thirteen of the 24 birds, just over half, tested positive for rodenticides registered for use in Australia. The most frequently detected compound was warfarin, a first-generation anticoagulant, found in eleven birds. Second-generation anticoagulants, which are far more toxic and persistent, also appeared: brodifacoum in three samples, difethialone in one and flocoumafen in one. Three birds carried warfarin alongside a second-generation compound, meaning they had been exposed to multiple poisons. Perhaps most telling, only six of the thirteen rodenticide-positive birds had rodent remains in their digestive tracts at the time of death. The researchers interpret this as evidence that the poisons can bioaccumulate in liver tissue over time, lingering from past meals of poisoned prey rather than reflecting a single recent exposure.

None of the detected concentrations reached the lethal dose thresholds established for other bird species. Brodifacoum levels in the Barn Owls and a Wedge-tailed Eagle fell below the reported oral LD50 range for owls of 0.15 to 9.68 milligrams per kilogram, and the difethialone concentration in the Tawny Frogmouth, 0.1 milligrams per kilogram, sat below the LD50 values of 0.26 to 23.4 milligrams per kilogram documented for Bobwhite, Japanese Quail and Mallard. Warfarin concentrations were similarly far below the 525 to 2,150 milligrams per kilogram lethal range reported for those same test species. But sublethal does not mean harmless. Second-generation anticoagulants are highly lipid-soluble and resist metabolic breakdown, and brodifacoum has been shown to cause persistent coagulopathy in birds for up to eleven days even at doses below the lethal threshold.

The clinical consequences of such exposure can be subtle but deadly. Birds suffering sublethal anticoagulant toxicosis have been documented to show lethargy, reduced agility and wing droop, impairments that degrade hunting performance and spatial navigation. For a fast-flying owl hunting at night, a momentary lapse in coordination can be fatal in a different way: collision with a vehicle. Twelve of the fifteen birds in the study showing traumatic injuries were found on roadsides, and the authors suggest that some of these roadkill birds may have been compromised by sublethal poisoning before they ever met a car. Peak coagulopathy after a single lethal ingestion typically occurs one to four days later, and after sublethal ingestion the effects may take even longer to manifest, widening the window of vulnerability.

Disentangling poisoning from trauma is one of the study’s central methodological challenges. Internal bleeding looks much the same whether it stems from a blunt impact or a drug-induced failure of the clotting cascade, and decomposition or scavenging can destroy clots that would otherwise distinguish the two. Ten birds showed haemocoelom, a coelomic cavity filled with uncoagulated blood, and in six of those there were no grossly obvious external signs of trauma such as fractures or lacerations. Yet only four of the ten haemocoelom cases were rodenticide-positive, and the statistical association between anticoagulant presence and postmortem evidence of coagulopathy was not significant. Alternative causes of bleeding disorders complicate the picture further: three birds carried low-burden apicomplexan parasites consistent with avian malaria, two had chronic enteritis with coccidian oocysts possibly of the genus Goussia, and heavy metal toxicity and bacterial infections such as salmonellosis can produce similar pathology in wild raptors.

One statistically significant pattern did emerge, and it concerned age. Immature birds were significantly more likely to carry higher brodifacoum concentrations than adults, a correlation with an f-value of 5.15 and a p-value of 0.03. The authors offer several non-exclusive explanations: inexperienced young hunters may target weakened, poisoned prey more readily; older birds may metabolise or eliminate the compound more efficiently or simply have longer intervals between exposures; or heavily affected juveniles may never survive to adulthood at all. The researchers caution, however, that the small sample size and a confidence interval hovering near zero mean the finding should be treated as a hypothesis generator rather than a settled conclusion. Species-level dietary differences add another layer of complexity, since rodent specialists such as Barn Owls and Black-shouldered Kites face theoretically higher exposure risk than bird-eating specialists like goshawks.

The conservation stakes extend beyond the species examined, all of which are currently listed as Least Concern by the International Union for Conservation of Nature. The Powerful Owl, despite its global status, numbers only an estimated 2,200 to 2,800 mature individuals, and the Grey Goshawk is estimated at fewer than 10,000 birds with a declining trend and Endangered classification in several Australian states. Sublethal poisoning that reduces foraging success, body condition and reproductive output, effects documented in vulture studies in the Pacific Northwest, could push such populations toward localised declines long before outright poisoning deaths register. Australian raptor populations remain poorly studied overall, making it difficult to assess how much hidden damage rodenticides are doing.

The study’s most policy-relevant finding may be its challenge to current Australian guidelines, which favour first-generation rodenticides such as warfarin over second-generation products on the assumption that they break down faster in rodents and pose less secondary risk. Warfarin was, after all, the most common residue in these Queensland birds. The authors point instead to coumatetralyl, another first-generation anticoagulant regarded as safer for predatory birds: mammals are generally more sensitive to it than birds, allowing lower effective doses, and while warfarin resistance has been documented in Australian rodents, no coumatetralyl resistance has yet been recorded there. The team calls for physiological studies of exposed raptors, rodent toxicity testing to track resistance, and surveys of rodenticide users to map what, how much and how often is being deployed. Until then, the poisons meant for mice appear to be quietly accumulating in the livers of the owls, eagles and falcons that share those fields, a debt the ecosystem may only now be beginning to itemise.

Subject of Research: Sublethal anticoagulant rodenticide exposure in deceased predatory birds in south-east Queensland, Australia

Article Title: Evaluating sublethal anticoagulant rodenticide exposure in deceased predatory birds of South-East Queensland, Australia

Article References: Low, Z., Murray, P. J., Naseem, N., McGilp, D., Doneley, B., Beale, D. J., Biggs, L., & Gonzalez-Astudillo, V. (2024). Evaluating sublethal anticoagulant rodenticide exposure in deceased predatory birds of South-East Queensland, Australia. Discover Toxicology, 1(1), Article 13. https://doi.org/10.1007/s44339-024-00016-4

Image Credits: AI Generated

DOI: 10.1007/s44339-024-00016-4

Keywords: anticoagulant rodenticides, raptors, owls, warfarin, brodifacoum, secondary poisoning, wildlife toxicology, LC-MS, Australia, Queensland, coagulopathy, conservation