A few updates on my anticoagulant rodenticide research

Recently, a lot of interest has been swirling around the topic of anticoagulant rat poison use on public and private lands. This interest revolves around some recent legislative changes in the regulations regarding the availability and use of second-generation anticoagulants in California. Additionally, P22, the Griffith Park mountain lion, was recently captured and tested for anticoagulant exposure. Much to the surprise of many, two types of first generation anticoagulants (which are less toxic than the second-generation compounds, and to which the new California regulations do not apply) were detected in P22's blood.  So, this has raised a lot of questions for people, concerned about the potential impacts of the first-generation compounds on wildlife, and the meaning of detecting those compounds in P22's blood.  A few people recently emailed me to ask specific questions about what I thought about the P22 findings, and how much risk the first-generation compounds pose. Additionally, folks have been curious about whether the detection of the first-generation anticoagulants is common.  I figured I'd put my email response here, and also add some updates about the anticoagulant research I've been doing on bobcats over the past 8-years.

For this research, I tested 195 bobcat blood samples for exposure to anticoagulants. 39% of animals were exposed, and diphacinone (a first-generation anticoagulant) was the most frequently detected compound. In 77% of blood samples of the 39% in which we detected exposure, diphacinone was detected.  In terms of other first-generation compounds, we also detected chlorophacinone and coumachlor in the blood samples. Diphacinone was detected 3 times as frequently as as second-generation compounds. Given our findings, we concluded that diphacinone, a first-generation compound, is probably the most frequent compound that bobcats are exposed to across our study areas, which included a significant number of samples from Ventura, Los Angeles, and Orange Counties, but also some samples from Santa Barbara and San Diego Counties.

During this study, I also tested 172 bobcat liver samples, and in those samples, I most frequently detected second-generation compounds brodifacoum and bromadiolone. We probably do not detect diphacinone in the liver as frequently because it has a significantly shorter half-life than either second-generation compound (up to several months for diphacinone vs.  6+ months for second-generation compounds).    

During previous research by the National Park Service, and more recently, by myself, we have found a strong association between notoedric mange, an ectoparasitic disease, and anticoagulant exposure in bobcats.  Although we have not found a specific association between mange and first-generation anticoagulants, we have tested for an association only using results from anticoagulant testing using liver samples (we don't have enough blood samples from mangy animals to do the same testing using blood). And as mentioned above, we do not detect first-generation compounds as frequently in liver samples because they have much shorter half-lives than the second-generation compounds. One of our significant findings using this method is that we learned we have been underestimating wildlife (or at least bobcat) exposure to first-generation anticoagulants by relying solely on liver samples to do the testing.  In summary, we use liver samples to test for an association between mange and anticoagulants, and because we underestimate first-generation anticoagulant exposure when we test liver samples, a lack of association between mange and first-generation anticoagulants could potentially be driven by a bias in the shorter tissue half-life of first-generation compounds compared to second-generation compounds. 

Overall, in terms of relationships between mange and anticoagulants, we did find evidence that multiple exposure events to anticoagulant may be the critical component in the development of severe mange. In bobcats with mange, we typically find higher residue concentrations and exposure to more different compounds compared with bobcats without mange, suggesting that multiple exposure events could be a critical factor. In fact, we find a strong association between bobcat exposure to 2 or more compounds, and mange- where bobcats that are exposure to 2 or more compounds are more than 7 times more likely to die of mange than other sources of mortality.

Another interesting note- we more frequently detected anticoagulant exposure in blood samples (and those detections were most frequently first-generation compounds) during the dry season (May- October). Bobcats are 2.6 times more likely to be exposed during the dry season, and we detect 55% more anticoagulant exposure during the dry season. Interestingly, we also 67% more mange cases during the dry season (which I speculate could be related to increased exposure to anticoagulants).

Finally, during some more recent literature research I've done, I discovered that diphacinone itself could potentially pose dangers aside from its effect as an anticoagulant. Similar to warfarin (or coumadin), it has been used therapeutically to prevent thrombosis in humans.  But because a small, but significant, percentage of the human population who have used the drug develop a hypersensitive, immune-stimulated reaction, the drug is banned in the US.  It is still used in Europe, however, but some papers have been published showing that human use of the drug can also result in suppression of certain types of immune-related cells and kidney failure.  Whether these effects occur for animals that are exposed to diphacinone is unknown, but of potential concern. Overall, diphacinone, or other first-generation anticoagulants, should not be viewed as a safe alternative to second-generation anticoagulants.