QUESTION:
Could you tell me a little about rodenticides? A history of the transition from multiple dose to single dose, acute vs. anticoagulants, their toxicity to humans and the different classes of them?
ANSWER:
This is a pretty wide topic, so this will be a very abbreviated history as I can remember it. Certainly the first toxicants used to kill pest rodents were natural substances that were available in plants or minerals, such as arsenic (a mineral), cyanide (from a family of salts but also present in many plants), and strychnine (from the seeds of a tree). These are all extremely acute poisons that killed any animal that ate the bait laced with them, and bait avoidance due to eating sub-lethal doses was a possible concern along with the deaths of too many unintended animals. Other early active ingredients included Red Squill, Thallium sulfate, ANTU, and 1080, and each had its benefits and its problems. Another early product was zinc phosphide, and of course this and strychnine are still used in a limited number of rodent baits today.
In the 1940’s anticoagulants were more or less discovered by accident, when “dicoumarin” was isolated as a chemical responsible for internal bleeding in livestock that ate spoiled clover hay. The potential for using this “anti-coagulant” as an animal toxin was then investigated by the Wisconsin Alumni Research Foundation, and eventually WARFarin (named after that group) was created as our first rodenticide anticoagulant. The benefits of anticoagulants include the fact that the active ingredient has essentially no foul taste that would cause bait avoidance, has a delayed reaction so that the rodent will eat more bait before effects begin to take place, thus avoiding bait shyness, and there is an “antidote” that can overcome the effect of the toxin. This is Vitamin K, and I prefer the word “treatment” to “antidote” since an animal may need to continue to receive Vitamin K treatments until the toxin is finally flushed from its system, which can take awhile for some of the anticoagulants.
The anticoagulants actually are still highly toxic substances, but they are so diluted with food ingredients, taking the actual bait formulations down to an a.i. of less than 1% toxin, that it reduces the risk to non-targeted animals. As animals will eventually do, resistance began to develop to these early “multiple feeding” anticoagulants, which also include diphacinone, chlorophacinone, indandione, and others, and efforts began to find new anticoagulants that offered the same benefits on no bait shyness or avoidance, but which could get a lethal dose into the rodent with a single feeding, and difenacoum and brodifacoum, still in a number of our current rodent baits, were the first two Single Feeding anticoagulants to be developed. From these bromadiolone and difethialone were developed, also current actives in our rodent baits. These are often referred to as the “Second Generation” active ingredients and their oral toxicity generally is much higher than the First Generation actives, so they may be present in the finished baits at even lower concentrations.
An effort continues to develop rodent baits that are fairly specific to rodents, or which offer some other safety features that reduce the chances for non-targeted animal poisoning or secondary poisoning, and one of these features is found in the “stop feed” actives such as bromethalin. According to manufacturers of the products with this a.i. a rodent loses its appetite shortly after consuming enough bait to kill it, and thus it does not fatten up on more bait and toxicant than is needed, hopefully reducing the chance for secondary poisoning when another animal eats that rodent. Bromethalin also is not an anticoagulant, and thus bypasses any resistance that may be developing in rodents to the anticoagulants. Instead, it acts to stop the production of energy packets (ATP) at the cellular level, essentially causing the rodent to die as its organs fail due to lack of nerve activity.
Another active that followed the anticoagulants and which is still in our arsenal today is cholecalciferol. This a.i. causes the release of stores of calcium into the blood and results in heart failure. This a.i. and bromethalin are also considered to be “chronic” toxins, as are all of the anticoagulants, in that the effect in the rodent takes time to progress. The safety feature here is that medical treatment can be given when a child or a pet eats one of the baits, whereas the “acute” toxins like strychnine and zinc phosphide may not offer that time delay.
I’ve probably forgotten something of value here, but hopefully this is a decent synopsis of where we were and where we are with rodent baits.
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