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


Why Do Poisons Matter?

Written by Dr. Laurel Serieys (caracal [at] capeleopard.org.za)

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 far 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.

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.

One of the classes of pesticides of great concern to our wildlife populations, as well as predatory 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 chemical classes (anticoagulants and DDT) share that they are indiscriminate killers and they can move through multiple levels of a food chain.  Anticoagulants may also impact animal reproduction and have immunological consequences for those animals chronically exposed.  Finally, as with DDT prior to its banning, the scale of its environmental impacts is unexamined. 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?  Tighter restrictions must be made to regulate the use and availability of these poisons. 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.  If you use poisons at home- do you know the consequences for local wildlife?

Anticoagulant Rat Poisons: The Facts

Rodenticides, or rat poisons, are used to control many small mammal species including gophers, ground squirrels, rabbits, and woodrats, etc. in the southern California area.  Anticoagulant rat poisons in particular act by blocking the Vitamin K cycle, which is essential for the production of certain critical blood-clotting proteins. Anticoagulant rodenticides are the most common method used for rodent control worldwide and they are frequently used in both residential and commercial areas, as well as in parks, cemeteries, and golf courses. 

Here are a few facts that you should know about anticoagulant rat poisons.

1.  An Indiscriminate, Prevalent Killer

These poisons are used by pest control companies and residents to control a number of small mammals that may include gophers, rabbits, ground squirrels and woodrats that are considered a pest mammal. However, the poisons may be toxic to any veterbrate species (mammals, snakes, birds, fish, etc.) that consume them, either directly or indirectly. 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.

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 is well documented in a wide range of animals including owls, buzzards, coyotes, feral cats, mountain lions, otters, endangered European mink, bobcats, bald eagles, and polecats....just to name a few. However, the vast majority of nontarget anticoagulant rodenticide 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 opportunistic samples from an animal that recently died (ie., not too decomposed) is rarely possible for field studies unless that animal has first been radiocollared and is being tracked through radio-telemetry. A second problem is that many animals do not exhibit any obvious signs of poisoning, so poisons may go undetected without specific testing. 

However, when testing is done, anticoagulant exposure in nontarget wildlife often high. In Britain,  31% of polecats livers tested were positive for anticoagulants.  In California, 70% of mammals from across the State in a 2002 study were found exposed to anticoagulants. In southern California, our recent work has found that a shocking 92% of bobcats tested are exposed to anticoagulants for samples collected between 1996-2012.  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 exposure. Although some predatory animals may die directly from the effects of anticoagulant poisoning, many others do not. Among the 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."

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!  During the delay between poison ingestion and death, a couple things may occur:  

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). 

  •  The poisoned animal may continue to feed on the poison baits and accumulate the poisonous compounds over a period of days, thus becoming super toxic!  
  •  Although you may have applied the poison only in your home, animals that have consumed those poisons may run outside your home where it can become an easy snack for a predatory animal. Some studies have found small mammals exposed to the poisons more than 100 meters (300 feet) from the nearest human structure. 
  •  The rats, or other species targeted by the poisons remain attractive to predators, and in becoming weakened by the poisons, may actually become easier to capture. 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 result.

3.  Anticoagulants: The Potential To Inhibit Reproduction in Our Wildlife   

Contaminant exposure that interferes with the reproductive success of wildlife populations may be a critical conservation issue since this exposure can lead directly to population declines. Reproductive consequences associated with anticoagulant exposure in some species have included increased probability of miscarriage, fetal poisoning, and decreased sperm counts in humans, dogs (Canis familiaris), and sheep (Oves aries). Fetuses are considered more susceptible to the toxic effects of anticoagulants.  In humans, prenatal exposure to coumarin (an anticoagulant sometimes used for medical treatment) at therapeutic doses has been associated with abortions, stillbirths, neonatal deaths, and increased risk of central nervous system abnormalities. Similarly, pregnant sheep dosed with anticoagulants had increases in stillborn, nonviable lambs.

In wildlife, it is difficult to assess the reproductive effects of poisons in natural populations without taking them into a controlled, laboratory setting. So, it is unknown the impacts of these rat poisons on the reproductive success of wildlife. However, In southern California, we have documented two fetal bobcats (found in a female bobcat hit by a car) to be exposed to multiple anticoagulant rat poison compounds. These findings show that rat poison exposure, for wildlife, may even begin before they are born, raising the question– how does this impact their health and probability of survival once they are born?  

4.  A Disease Epizootic (ie., epidemic) in Bobcats is Statistically Associated with Anticoagulant Rat Poison Exposure

A photo of a bobcat with severe mange in San Diego County.  This bobcat died of mange, likely 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 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 across the state of California.  Bobcats exposed to anticoagulant rat poisons are more than 5 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 with 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, 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 move through the food web  

Locally, both National Park Service and University of California, Los Angeles biologists studying carnivores have found numerous carnivore species exposed to these poisons. Because some of these carnivores such as mountain lions and bobcats are obligate carnivores that generally eat live, or recently dead, prey and are not omnivores, that eat fruits and nuts, it is very unlikely that they are consuming rodent baits directly. We thus expect bobcat exposure to ARs to be predominantly, if not all, secondary for bobcats and mountain lions. Although more omnivorous carnivores like coyotes, gray foxes, and raccoons may opportunistically consume bait that are flavored to be tasteful to wild animals, they likely too are secondarily exposed to the poisons when they consume poisoned prey species. Numerous other studies that have documented anticoagulant rodenticide exposure in predatory species have suspected the exposure to be primarily secondary. Birds of prey such as owls and hawks, and other obligate carnivores such as polecats, are also unlikely to eat the baits directly. These data strongly suggest that these poisons move through food webs, and not just in southern California. 

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.  This extends to anticoagulant rat poisons.  The bottom line is that without rigorous studies done both in the field (documenting exposure in wild animal populations) and the lab (where researchers may test what would happen to animals when they are dosed with the poisons), it is impossible to know the full extent of the ecological impact these poisons have when we use them in and around our homes and in open spaces that are utilized by wild animals. 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. 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 frostbite.

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.

What has research in southern California taught us about anticoagulant exposure risk for wildlife?

In southern California, more than a decade of research in and around Santa Monica Mountains National Recreation Area (SMMNRA), a national park near Los Angeles, has documented widespread AR exposure in multiple carnivore species. AR exposure was the second leading cause of mortality during a 9-year coyote study and 83% of individuals tested were exposed. Ninety percent of mountain lions during recent research were also found exposed. Most recently, 92% of bobcats were found exposed during a large-scale anticoagulant study by National Park Service and University of California biologists. Anticoagulant toxicant load, or the amount of anticoagulant residues detected in liver tissue, was positively associated with the use of developed areas for radio-collared bobcats and mountain lions suggesting that urban areas are a major source of anticoagulant contamination.

Although high rates of exposure were documented for bobcats in southern California, death by anticoagulant toxicity occurred has been documented in the study area only in one case. However, secondary anticoagulant exposure at ≥ 0.05 ppm was significantly associated with death due to severe notoedric mange, an ectoparasitic disease, and a precipitous population decline and genetic bottleneck occurred as a result of the mange outbreak from 2002-2006 (Riley et al. 2007; Serieys et al. in revision). Notoedric mange was previously only reported in isolated cases in free-ranging felids (Pence et al. 1982; Maehr et al. 1995; Pence et al. 1995), although the disease may now be an increasing issue for bobcats across California (Stephenson et al. 2013; Serieys et al. 2013). One hundred percent of bobcats with severe mange that have been tested for anticoagulants were exposed  (N = 19, Riley et al. 2007; N = 11, Serieys et al. 2013). These findings have led researchers to hypothesize that chronic, sublethal exposure to ARs may predispose bobcats to other medical conditions such as decreased immune competence, thus increasing their susceptibility to severe mange infestation (Riley et al. 2007).

Most recently, biologists have been examining risk factors for anticoagulant exposure in urban bobcat populations. These risk factors examined include animal sex, age, the location that they were sampled, the year the animal was sampled, and the types of urban development in close proximity to where the animal was sampled. These results are being prepared for publication, but thus far, biologists have found that diphacinone appears to be the most commonly used anticoagulant poison in southern California.  Although this compound is less toxic than second-generation anticoagulant rat poisons, death due to exposure to diphacinone and other similar compounds has been reported for some wildlife species, including in the Santa Monica Mountains.  Additionally, animal proximity to residential areas appears to be one of the primary risk factors to anticoagulant exposure in multiple southern California Counties, suggesting that residential areas are among the most important contributors to chemical contamination of the environment (anticaogulant use is greatest in these areas).  More details of this research will be reported when the results are published.  



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. 

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 and brand names to keep an eye out for include:

1. Bromadiolone

  • Bromone
  • Maki
  • Supercaid
  • Boothill
  • Contrac

2. Brodifacoum

  • Biosnap 
  • d-Con
  • Finale 
  • Fologorat 
  • Havoc
  • Jaguar 
  • Klerat 
  • Matikus 
  • Mouser
  • Pestanal (Sigma-Aldrich BT)
  • Pestoff
  • Ratak+ 
  • Rodend 
  • Ratsak 
  • Talon
  • Volak 
  • Vertox 
  • Volid

3. Difethialone

  • Hombre
  • Generation
  • FastDraw
  • FirstStrike

4. Diphacinone

  • Diphacin
  • Ditrac 
  • Promar
  • Ramik
  • TomCat

5. Chlorophacinone

  • Rozol
  • Wilson Riddex
  • Ground Force
  • Ratol
  • RAT-XC



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