"Man can hardly even recognize the devils of his own creation."
                                                                                                -ALBERT SCHWEITZER

Why Do Poisons Matter?

(If distributed, quoted, or republished, please cite UrbanCarnivores.com)

Long after the 1962 publication of Rachel Carson's book, Silent Spring, and the subsequent birth of the environmental movement, the days of concern over the effects of at-home and commercial pesticide use are long from over.  Carson's book described numerous environmental impacts of indiscriminate spraying of DDT in the United States and questioned the logic of releasing large amounts of chemicals into the environment without understanding their effects on the environment or human health. Her book facilitated the ban of the pesticide DDT in 1972 in the United States and the creation of the Environmental Protection Agency.  Through her masterpiece Silent Spring, she accused the chemical industry of spreading disinformation regarding the safety of their products, and public officials of accepting industry claims uncritically.  Forty years later, we can still find certain parallels between DDT and the use and consequences of other commonly used pesticides today.

One of the classes of pesticides of great concern to our wildlife populations, as well as predatory Image created by Jason Clay Lewis. d-CON is one of the brands of anticoagulant rat poisons that are of particular concern for our local wildlife as well as wildlife globally.species worldwide, are anticoagulant rodenticides.  We are particularly interested in this poison because of our research focused on wild carnivore populations, and although we have detected other toxicants such as heavy metals in some animals, the poisons of greatest prevalence, with potential detrimental, population-level effects, seem to be anticoagulant rodenticides.  

Below are facts about anticoagulant rat poisons, some of which are in shocking parallel with the consequences that were found to be associated with the DDT, banned in 1972.  Both classes definitively share that they are indiscriminate killers and they can move through multiple levels of a food chain.  Anticoagulants are also suspected to, like DDT was shown to do, impact animal reproduction and potentially have immunological consequences for those animals chronically exposed.  Finally, as with DDT prior to its banning, the scale of its environmental impacts were unexamined.  Overall, anticoagulant rat poisons may not have the same fear-inducing carcinogenic toxicity as DDT, but there are several shocking parallels between their use and their effects on wildlife populations today.  As a biologist studying this issue,  Laurel Serieys believes that if we would not settle for the consequences associated with poisons like DDT, why should we be content to use poisons like anticoagulants with such brazen abandon?  She advocates that tighter restrictions must be made to regulate the use and availability of these poisons, and has already shared data available from the Santa Monica Mountains with agencies such as Department of Fish and Game and California Department of Pesticide Regulation.  In our at-home pest-control efforts, poisons should- and must- be last resort tools for the control of pest species.  However, they are frequently the first step we seem to take when a pesky rodent issue arises.  Read below to learn why poisons should not be the first step.  If you use poisons at home- do you know the consequences for local wildlife?

First- What Are Anticoagulant Rodenticides?
Rodenticides are a category of pest control chemicals designed to kill rodents, but are used commonly to control many small mammal species including gophers, ground squirrels, rabbits, woodrats, etc.  Anticoagulants are compounds that act by blocking the Vitamin K cycle, which is essential for the production of Vitamin K-dependent blood-clotting factors.  Anticoagulant rodenticides are the most common method used for rodent control worldwide1 and they are frequently used commercially in parks, golf courses, and around office parks.  They are widely available for purchase by any private citizen wishing to apply them within their homes themselves, and pest control companies use, and heavily promote their use, as well.  People use anticoagulant rodenticides both within and around their homes to target the small mammals listed above.
 
Anticoagulant Rat Poisons: The Facts
Here are a few facts that you should know about anticoagulant rat poisons.  Most of the items listed below are in striking parallel with the effects DDT and other poisons presented in Carson's Silent Spring before they were banned.  If you are a user of anticoagulant rat poisons, you should be a well-informed consumer.  The following have been shown by scientific studies in either laboratory and natural settings. We cite each fact so you can read the information for yourself.

1.  An Indiscriminate, Prevalent Killer
These poisons are marketed to control rats and mice.  However, they are used by pest control companies and residents to control anything from gophers, rabbits, grounds squirrels, woodrats, norwegian brown rats, and any other small mammal those living in commercial or residential areas considered a pest mammal. The poisons target the vitamin K cycle, making them toxic to ALL vertebrates2!  Vertebrates include organisms ranging from snakes, birds, lizards, fish, and mammals.  Vitamin K is produced by bacterial flora in the intestinal system of vertebrates- humans included- and is critical to the production of several clotting factors acting throughout our bodies.  Some anticoagulants will include antibiotics as effective ingredients to speed the process of death.  Overall, the effect is that anticoagulant rat poisons are indescriminate killers affecting many nontarget species.

Image provided by Jason Clay Lewis. d-CON is one brand of poisons of particular concern for our local wildlife.The unintentional poisoning of nontarget species has been documented globally, and includes both primary, secondary, and even tertiary poisoning of nontarget animals.  Primary poisoning occurs when an animal directly consumes the poisons themselves.  Secondary poisoning occurs when a predatory animal consumes a poisoned animal, and thus ingests the poisons secondarily.  For example, if a bobcat consumes a gopher that has been poisoned, the bobcat is thus secondarily exposed to the poison.  Tertiary poisoning would occur when a predatory animal consumes another predatory animal that is secondarily poisoned.  This could occur, for example, if a mountain lion eats a coyote that has eaten poisoned rats.

A Ventura County Star article highlighted the effects of anticoagulants on two local mountain lions. The lions died directly of anticoagulant rat poison toxicity and were thought exposed to the poisons from consuming coyotes that were exposed to the poisons. This suggests tertiary exposure rather through the secondarily exposed coyotes.Secondary anticoagulant poisoning of nontarget animals has already been well documented in a wide range of animals including both birds and mammals1-14.  This long list of unintended poisoning includes owls
15, buzzards12, coyotes3,13, feral cats16, mountain lions4,14,17, otters, endangered European mink, and polecats18. However, the vast majority of this poisoning undoubtedly remains undetected for several reasons. We must remember what is required to get the data, including the fact that to test animals for the presence of anticoagulants (or any other poison), we must first have the tissue from animals to first test for poisons.  In the case of anticoagulant rat poisons, we most frequently use liver tissue collected from an animal that has already died.  Obtaining samples from an animal that is in a state (ie., not too decomposed) is rarely possible for field studies unless that animal has first been radio-collared and is being tracked through radio-telemetry19. A second problem is that many animals do not exhibit any obvious signs of poisoning, so poisons may go undetected without specific testing (e.g., 20). Finally, these tests are often expensive, and in the case of anticoagulant rodenticide exposure testing, each test costs $100.  The funds required to perform a study examining exposure rates can quickly grow beyond budget feasibility.  

However, when testing is done, in the case of anticoagulant rat poisons, anticoagulant occurrence is often high. In Britain,  31% of polecats livers tested were positive for anticoagulants.  In California, Hosea
8 found that 70% of the mammals (including coyotes and bobcats) tested in California, USA, were exposed to anticoagulants, and locally around Los Angeles, our work shows a shocking 95% of bobcats tested are exposed to anticoagulants for samples collected between 1996-2010.  In New York, 49% of predatory birds tested from 1998 to 2001 were positive for anticoagulants.  Further, 81% of the great horned owls tested for the study in New York were positive for exposure7. Although some predatory animals may die directly from the effects of anticoagulant poisoning, many others do not. Among the Anticoagulant exposure rates are high for bobcats in the Santa Monica Mountains, and even those sampled from protected state park areas were found exposed. Figure created by Laurel Serieys using data generated by Riley et al., 2007 and Serieys et al., unpublished data..examples include that 86% of the predatory birds (e.g., hawks and owls) exposed to anticoagulants in New York did not show evidence of death directly from exposure. However, according to Stone et al. (2003:37), "the impact of anticoagulant exposure must extend well beyond those cases in which acute lethal hemorrhage is the proximal cause of death."

Given the challenges mentioned above for studying this issue, little is known about what constitutes a lethal dose for wildlife species, what the sub-lethal, chronic effects may be of anticoagulant exposure.  Typically, wildlife studies only report incidence of poisoning while laboratory studies must generally be performed to understand the sublethal consequences of exposure to poisons
22.  We should consider that poisons are not the only stressors for wildlife.  Habitat fragmentation, combinations of other pesticides wildlife are exposed to, disease carried by domestic animals that may spillover into wildlife populations, in addition to the inherent challenges wildlife face in living in a wild environment where they may have to fend for territory, must hunt their own food, and face the elements including potential droughts, competition with other individuals or species, predation, etc. are all potential daily stressors that could interact with poison exposure to increase the consequences of sublethal, chronic exposure.

2.  A Slow Killer that Creates Easy, Lethal Prey For Predatory Species
Once an animal has ingested a LETHAL dose of anticoagulant rat poisons, death of the animal may not occur for up to 10 days
23!  During the delay between poison ingestion and death, a couple things may occur:  

    a)  The poisoned animal may continue to accumulate the poisonous compounds over a period of days, consuming more than the lethal dose of poison.  The fact of their delayed onset of lethality and thus, accompanying symptoms, is exactly one reason this class of poisons remains effective and the most commonly used method of rodent control worldwide.  Since the rats, or other target species, do not immediately feel ill after eating the poison bait, they do not associate the poison with something to "avoid."  So, they continue to eat the poisons, possibly considering it a nice, easy food source until they die days later, while simultaneously potentially ingesting more than a lethal dose of the poison.

    b)  Although you may have applied the poison ONLY in your home, whatever you have poisoned may run outside your home where it can become an easy snack for a predatory animal.

    c)  The rats or other target species we aim to poison remain attractive to predators, and in becoming weakened by the poisons, become easier to capture
23-24. We must remember- before there were poisons- there were owls, hawks, bobcats, foxes, snakes, coyotes, etc. that were our relied-upon pest control.   Those pests we target with poisons are, if not a primary food source, at least an opportunistic meal for some of these predatory animals.  So- for predatory species that consume prey items targeted by pesticides, chronic secondary exposure to the poisons may occur as a result22.

3.  Anticoagulants: The Potential To Inhibit Reproduction in Our Wildlife        
Anticoagulant poisons have been demonstrated to affect the reproduction of at least one non-target specie.  The effects of anticoagulants have been tested only on sheep (to our knowledge) and found to cause decreased sperm counts in males and increased abortion rates in females
25.  Although studies on the effects of these poisons on reproduction are limited, we should consider that similar effects may occur in any cherished wildlife that consume these poisons.  Given the widespread use of these poisons and how many nontarget animals we are daily learning are exposed to the poisons, we must question how we are affecting the reproduction of the wildlife species that exist near urban and agricultural areas.  

4.  A Disease Epizootic (ie., epidemic) in Bobcats is Statistically Associated with Anticoagulant Rat Poison Exposure
We must consider the possibility of other sublethal affects these poisons may have.  The lethal dose for the small mammal species we target with these poisons, and the bobcat, coyote, owl, or A photo of a bobcat with severe mange in San Diego County. This bobcat died of mange, likley associated with anticoagulant rat poison exposure.mountain lions that may be secondarily exposed to the poisons will differ.  So, larger predatory species that consume a poisoned rat will likely ingest a sublethal dose of the poison.  For instance, DDT was noted to affect the immune system of wildlife exposed to the poisons, and although the chemical compounds that make DDT vs. anticoagulants are quite different, we are exploring the possibility that anticoagulants are linked to a disease epidemic we have noted observed in bobcats accross the state of California.  Bobcats exposed to anticoagulant rat poisons are more than 7 times likely to die of notoedric mange, a typically benign disease for wild cats!  See 'Notoedric mange' page for more information.  The disease itself is not caused by anticoagulants, but instead by a microscopic mite, Notoedres cati, that burrows in the skin of the bobcats.  Severe infections are typically associated wtih immune suppressed states.  What we have observed is mass mortalities of bobcats with severe notoedric mange, a disease that until now, has never been documented to cause populations declines in any wild cat species globally.  Thus, we ask the question
This illustration proposes a simple food web for the Santa Monica Mountains. Even though depicting only a few of the potential relationships that exist between wildlife species in the Santa Monica Mountains, many wildlife species can be affected when a single home uses anticoagulant rat poisons (rodenticides). , what is the significance of the disease, and is it possible that sublethal, chronic exposure to anticoagulant rat poisons are decreasing bobcat immunity, increasing their susceptibility to this disease?  This forms the basis for the UCLA bobcat disease susceptibility study (see 'Projects' for more information).

5.  Anticoagulants bioaccumulate and move through the food web  
Our focal area of research is studying carnivores, and we are finding numerous carnivore species affected to these poisons- in other words, species that don't directly consume the poison bait, but rather, consume animals that consume the poison baits.  As mentioned above, numerous nontarget predatory species are already documented to be exposed to anticoagulant rat poisons and the list includes mountain lions, bobcat, coyotes, weasels, stoats, domestic cats, owls, hawks, eagles, etc.

6. These Poisons HAVE BEEN Studied BUT Much Remains Unknown-And Their Widespread Use Remains Legal
The effects of prolonged exposure to toxicants are generally examined in controlled laboratory settings, whereas field studies typically report only the incidence of poisoning cases
22.  This extends to the class of toxicants that we are concerned about- anticoagulant rat poisons.  The bottom line is that without people out studying the wild animals that are ultimately being affected by these poisons, we don't know what the poisons are doing once we put them in and around our homes and in open spaces that wild animals consider their home.

In the case of anticoagulants, little is known about what constitutes a lethal dose to wildlife or the consequences of chronic exposure to predatory species. Further, the physiological effects of anticoagulant exposure vary greatly between the species exposed, the duration and magnitude of exposure, and interactions with other stressors. For example, brodifacoum, one of the most commonly used anticoagulant poisons, has an elimination half-life of approximately 130 days in rats  and 6 days in dogs
26. Dogs are also 100x more susceptible to some anticoagulants than cats, and coyotes and kit foxes are known to suffer high mortality associated with anticoagulant exposure. Cats, on the other hand, can accumulate sublethal levels of anticoagulants without showing symptoms of toxicosis. However, laboratory experiments have shown that interactive effects between sublethal exposure to anticoagulants and other stressors can induce mortality. For example, for laboratory rat and rabbit populations, sublethal anticoagulant doses produced 40-70% mortality when combined with other stressors, such as frostbite27.

The EPA has been working to impose restrictions on the ability of anticoagulant rodenticide companies to sell the poisons in quantities that are used by private homeowners.  This is an uphill battle however.

Are you using anticoagulants around your home?  The packaging for anticoagulant poisons can vary between brand names, and is not just sold as rat poison, but also sold to target other small mammals such as gophers.  Common ingredients to keep an eye out for include:
 

Bromadiolone
Brand names: Bromone, Maki, Supercaid, Boothill, Contrac
 
Brodifacoum
Brand names: Biosnap, d-Con, Finale, Fologorat, Havoc, Jaguar, Klerat, Matikus, Mouser, Pestanal (Sigma-Aldrich BT), Pestoff, Ratak+, Rodend, Ratsak, Talon, Volak, Vertox, Volid

Difethialone
Brand names: Hombre, Generation, FastDraw, FirstStrike

Diphacinone
Brand Names: Diphacin, Ditrac, Promar, Ramik, TomCat

Chlorophacinone

Brand Names: Rozol, Wilson Riddex, Ground Force, Ratol, RAT-XC

 

Locally Observed Secondary Poisoning By Anticoagulant Rodenticides
Primary poisoning occurs when an animal directly consumes the rodenticide bait. Secondary poisoning occurs when a predator consumes poisoned prey
10. Within Santa Monica Mountains National Recreation Area, bobcats, mountain lions, and coyotes have been secondarily poisoned by anticoagulant rodenticides4,14,15.

We have been asked if there are safe poisons safe levels for these common poisons.  The answer is that there is NO safe level at which you can use anticoagulants to control pests, and there are no other poisons we recommend as a replacement.  One reason that anticoagulants are so dangerous is because they have a very long half-life in the liver of an animal that ingests the poison.  For some species, these poisons can remain in the liver for months or even a year.  Even if you use very low levels of the poison or only use it intermittently, the compounds remain in the livers of the animals that have ingested the poison.  

Although local biologists have not yet documented the secondary poisoning of other wildlife species, it is possible that other predatory animals such as owls, hawks, snakes, raccoons, foxes and weasels could also be affected. Worldwide, other nontarget wildlife are documented to have been poisoned by anticoagulants including hawks and coyotes in New York, endangered kit foxes in Bakersfield, CA, weasels and owls in Europe, and owls and hawks in New Zealand and Australia. The issue is global. 
 

No Poison Is A Good Poison
Often people inquire, after learning the harmful impacts of anticoagulant poisons, what poisons may be used in substitution for anticoagulants.  The truth is that no poison is a good poison- in other words, no poison available on the market in the United States poses no risk to wildlife.  Beyond considering the impacts of secondary exposure of wildlife to poisons, don't forget that nontarget wildlife can too directly consume the poisons.  

We know a lot more about some poisons than others.  Because anticoagulant rodenticides are the most commonly used method of rodent control used worldwide, more research concerning the negative impacts of this poison on wildlife have been conducted.  However, even for this poison, there are MANY unknowns!  The reality is that it is exceedingly difficult to know what happens to wildlife once they ingest poisons.  If there is an absence of data regarding how some compounds affect wildlife (ie., vitamin D poison, zinc phosphide, or bromethelin), it does not mean it poses no risk to wildlife.

In 2004, two biologists with the Environmental Protection Agency prepared a report for the EPA highlighting the risks of 9 rodenticide compounds on wildlife populations.  The executive summary is provided below in quotes.  The full report is provided here for more information.  In summary, the authors of the report, Erickson and Urban (2004), report that none of the 9 poisons reviewed pose no risk to wildlife.  

"Executive Summary:
This document presents the {Environmental Protection] Agency’s assessment of potential risks to birds and nontarget mammals from 9 rodenticides, including 3 second-generation anticoagulants (brodifacoum, difethialone, bromadiolone), 3 first-generation anticoagulants (diphacinone, chlorophacinone, warfarin), and 3 non-anticoagulant compounds (zinc phosphide, bromethalin, cholecalciferol). These rodenticides are predominantly used to control commensal rats and mice in and around buildings, transport vehicles, and in sewers. Some, mainly zinc phosphide, chlorophacinone, and diphacinone, also have products registered for other outdoor uses against other rodent and small mammalian pests. A major concern in using rodenticides is that they are not selective to the target species; birds and nontarget mammals that feed on grain-based baits (pellets, meal, treated grains, wax blocks) or meat-based, vegetable, or fruit baits are potentially at risk. The available information from laboratory and pen studies, field studies, control programs, reported incidents, and toxicokinetics also indicates that a variety of avian and mammalian predators and scavengers are potentially at risk from consuming animals poisoned with some of these rodenticides.

The assessment focuses on the potential primary and secondary risks to birds and nontarget mammals posed by applications of these 9 rodenticides (11 baits) to control rats and mice in and around buildings (commensal use) and in field and other outdoor settings to control various rodent and other small mammalian pests. Risk is a function of exposure and hazard (toxicity), and data are available to estimate toxicity based on laboratory acute and secondary-hazard tests. However, typical use information used to estimate nontarget organism exposure, such as amount of active ingredient or formulated product applied per unit area, is not available for commensal uses. Thus, exposure estimates are largely based on the amount of active ingredient available per kilogram of the formulated bait (mg ai/kg bait). An assumption is made in most OPP/EFED risk assessments that birds and nontarget mammals are likely to be exposed to the pesticide via consumption of contaminated foods. This assumption is well established for rodenticides, for which ingestion of the formulated bait is the route of exposure.

Refining the exposure assessment to establish a quantitative measure of likelihood of exposure and effects would require a much more extensive data set than registrants have submitted for their rodenticides and for the nontarget species potentially at risk. The Agency provided the preliminary risk assessment to rodenticide registrants in October, 2001 and posted it in the EDocket on EPA’s website for public comments from January 29 to May 30, 2003. No additional data or relevant information to refine the exposure assessment has been provided by the registrants or other stakeholders. Nevertheless, the existence of substantial incident data along with liver-residue analysis confirms that birds and nontarget mammals are being exposed and adversely affected by applications of rodenticide baits. The fact that numerous species of birds and mammals, including predators and scavengers, have been found exposed to these baits indicates that both primary and secondary exposures are occurring.

The risk conclusions are based both on the lines of evidence of the available data and
comparative analysis modeling. Each rodenticide is ranked or categorized and compared to the other rodenticides according to the following criteria:


(1) overall potential risk;
(2) potential primary risk to birds;
(3) potential primary risk to nontarget mammals;
(4) potential secondary risk to avian predators and scavengers;
(5) potential secondary risk to mammalian predators and scavengers.

Conclusions are presented below:
• Brodifacoum and difethialone stand out as the two rodenticides posing the greatest
potential overall risk to birds and nontarget mammals, followed by bromadiolone and
diphacinone. Zinc phosphide also ranked high for overall risk based on the comparative
analysis modeling, primarily because of high potential primary risks.

• Brodifacoum, difethialone, and zinc phosphide pose the greatest potential primary risks to birds that eat bait. A single zinc phosphide or brodifacoum bait pellet provides more than an LD50 dose for a small bird. In contrast, a small bird would need to eat more than twice its body weight in bait pellets to ingest a comparable dose of a first-generation anticoagulant in a single feeding.

• Rodenticide baits are formulated to be lethal to small mammals, and they are not
selective to the target species. All baits pose a high potential primary risk to nontarget
mammals that eat bait. However, the first-generation anticoagulants likely pose less risk
to mammals that only occasionally feed on 1 or just a few bait pellets, because they are
more rapidly metabolized and generally must be eaten for several days to provide a lethal dose.

• Brodifacoum and difethialone pose the greatest potential risks to avian predators and
scavengers that feed on target or nontarget animals poisoned with bait. The available
data indicate that the first-generation anticoagulants are less hazardous than the more
highly toxic and persistent second-generation anticoagulants.

• Mammalian predators and scavengers are at risk from feeding on animals poisoned with anticoagulant baits. Although the non-anticoagulant rodenticides appear to be much less hazardous to secondary consumers, confirmatory data are still needed to make this assumption for bromethalin and cholecalciferol baits.

• The available toxicokinetic data indicate that the second-generation anticoagulants are considerably more persistent in animal tissues than are the first-generation anticoagulants, and bioaccumulation may increase whole-body residues with repeat feedings.

• More than 300 documented wildlife incidents attest to exposure of birds and nontarget mammals, including endangered species, to some rodenticides, especially brodifacoum (244 incidents). Brodifacoum residue has been detected in liver tissue of 27 of 32 endangered kit foxes screened for rodenticide residues from 1999 to 2003. Birds in which rodenticides are most frequently detected include owls, hawks, eagles, and crows; mammals include wild canids and felids, tree squirrels, raccoons, deer, and others."

We recommend that people avoid using poisons altogether.  If your pest problem feels beyond your control, consider finding a pest-control company that uses sustainable practices to assist you.  Let them decide whether poisons are truly a necessary tool.  Companies that practice Integrated Pest Management should use poisons only as a very last resort.  

Remember also- if you have fruit and nut trees in your garden, a vegetable garden, or have domestic animals such as chickens that you feed- these are unnatural things in the Southern California ecosystem.  So, you will attract rats and other rodents that you consider pests.  Maintain perspective that when we alter the landscape, there are consequences that may tip the balance of the system in favor of pest species that thrive in human disturbed landscapes.  Try to minimize your impact and you may find that your rodent problem isn't so bad afterall.  Our natural predators are here too to feed on rodents, thus helping to control their populations.  When we use poisons, we kill those natural predators.  Killing the natural predators has a bigger impact on the predator populations since they have slower generation times and tend to have lower density populations than the pest rodent populations.  Thus, in using poisons, we are actually tipping the scales even further in the favor of those pests we are trying to control.  So, consider using alternatives to poisons, and if the problem remains, get a professional to help you. 

 

References
1. Stone, W.B., J.C. Okoniewski, J.R. Stedelin. 1999.  Poisoning of wildlife with anticoagulant rodenticides in New York.  Journal of Wildlife Diseases, 35: 187-193.

2. Brakes, C. R., & Smith, R. H. 2005. Exposure of non-target small mammals to rodenticides: short-term effects, recovery and implications for secondary poisoning. Journal of Applied Ecology, 42(1), 118-128.

3. Riley, S.P.D., Sauvajot, R.M., Fuller, T.K., York, E.C., Damradt, D.A., Bromley, C., and Wayne, R.K. 2003. Effects of urbanization and habitat fragmentation on bobcats and coyotes in southern California. Conservation Biology, 17: 566-576.

4. Riley, S.P.D., Bromley, C., Poppenga, R.H., Whited, L., Sauvajot, R.M. 2007. Anticoagulant exposure and notoedric mange in bobcats and mountain lions in urban Southern California. Journal of Wildlife Management, 71(6): 1874-1884.

5. Riley, S.P.D., Boydston, E.E., Crooks, K.R., Lyren, L.M. 2010. Bobcats (Lynx rufus). In: Urban Carnivores (Gehrt, S.D., Riley, S.P.D., Cypher, B.L., eds.) pp. 121-138 (John Hopkins University Press)

6.  Eason, C.T. and Spurr, E.E. 1995. Review of the toxicity and impacts of brodifacoum on non-target wildlife in New Zealand. New Zealand Journal of Zoology, 22: 371-379

7.  Stone, W. B., Okoniewski, J. C., & Stedelin, J. R. 2003. Anticoagulant Rodenticides and Raptors: Recent Findings from New York, 1998–2001. Bulletin of Environmental Contamination and Toxicology, 70(1), 34-40.

8.  Hosea, R. C. 2000. Exposure of non-target wildlife to anticoagulant rodenticides in California. Proceedings of the Vertebrate Pest Conference, 19:236-244.

9.  Eason, C. T., E. C. Murphy, G. R. G. Wright, and E. B. Spurr. 2002. Assessment of risks of brodifacoum to non-target birds and mammals in New Zealand. Ecotoxicology, 11:35-48.

10. Elmeros, M., Christensen, T. K. r., & Lassen, P. .2011. Concentrations of anticoagulant rodenticides in stoats Mustela erminea and weasels Mustela nivalis from Denmark. Science of The Total Environment, 409(12), 2373-2378.

11.  Berny, P., & Gaillet, J.-R. 2008. Acute poisoning of red kites (Milvus milvus) in France: Data from the Sagir Network. Journal of Wildlife Diseases, 44(2), 417-426.

12.  Berny, P. J., Buronfosse, T., Buronfosse, F., Lamarque,F. and G. Lorgue. 1997. Field evidence of secondary poisoning of foxes (Vulpes vulpes) and buzzards (Buteo buteo) by Bromadiolone, a 4-year survey. Chemosphere, 35:1817-1829.

13.  Gehrt, S.D. and Riley, S.P.D. 2010. Coyotes (Canis latrans). In: Urban Carnivores (Gehrt, S.D., Riley, S.P.D., Cypher, B.L., eds.) pp. 78-95 (John Hopkins University Press).

14.  Beier, P., Riley, S.P.D., and Sauvajot, R.M. 2010. Mountain Lions (Puma concolor).  In: Urban Carnivores (Gehrt, S.D., Riley, S.P.D., Cypher, B.L., eds.) pp. 141-155 (John Hopkins University Press).

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Mendenhall, V. M., and L. F. Pank. 1980. Secondary poisoning of owls by anticoagulant rodenticides. Wildlife Society Bulletin, 8:311-315.

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Alterio, N. 1996. Secondary poisoning of stoats (Mustela erminea), feral ferrets (Mustela furo), and feral house cats (Felis catus) by the anticoagulant poison, brodifacoum. New Zealand Journal of Zoology, 23:331-338.

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Littrell, E. E. 1988. Wild carnivore deaths due to anticoagulant intoxication. California Fish and Game, 74:183.

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McDonald, R. A., S. Harris, G. Turnbull, P. Brown, and M. Fletcher. 1998. Anticoagulant rodenticides in stoats (Mustela erminea) and weasels (Mustela nivalis) in England. Environmental Pollution, 103:17-23.

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23.  Cox, P. and Smith, R.H. 1992 Rodenticide ecotoxicology: pre-lethal effects of anticoagulants on rat behaviour. In: Borrecco JE, Marsh RE (eds) Proceedings of the 15th vertebrate pest conference. University of California, Davis, California, USA. pp 165–170.

24. 
Parmar, G., H. Bratt, R. Moore, and P.L. Batten. 1987. Evidence for a common binding site in vivo for the retention of anticoagulants in rat liver. Human Toxicology, 6:431-43

25.  Petterino, C. and Paolo, B. 2001. Toxicology of various anticoagulant rodenticides in animals. Veterinary and Human Toxicology, 43:353-36.

26.  Woody, B.J., Murphy, M.J., Ray, A.C., Green, R.A. 1992. Coagulopathic Effects and Therapy of Brodifacoum Toxicosis in Dogs. Journal of Veterinary Internal Medicine, 6(1): 23-28.

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