Wildlife and rodenticides: The new silent spring?


The Griffith Park mountain lion, discovered wandering the urban wilds above Los Angeles in the late winter of 2012, has been celebrated like none other of its kind. While mountain lions menace suburbs in Colorado and distress ranchers in Arizona, in the Santa Monica Mountains of Southern California, the rare cougar is widely viewed as a talisman for ecological renewal, a sign that the natural balance can return to our urban wildlands if we only work to restore it. And among the fantasies the region holds of itself at the moment, is that re-wildling is what we are doing – letting nature come back to the city, with its creeks and birds and native plants; finding a balance between domestic safety and the wildland ecosystem.

It was shocking then, and heartbreaking, to see the most recent remote camera images of the mountain lion, who is no longer the golden, rippling predator stalking the hills below the Hollywood sign shown last November in Steve Winter’s spectacular photographs published in National Geographic. Today, P-22 – the 22nd puma to be collared in a 12-year-old National Park Service study – roams the hills looking sickly and haunted, his coat faded to a flat, sparse gray. When a team led by NPS biologist Jeff Sikich recaptured and sedated the animal, they found him crusted with notoedric mange, an opportunistic parasite that preys on immune-deficient felines. Blood samples sent to the California Animal Health and Food Safety Lab at the University of California-Davis found rat poison coursing through the depleted cougar’s veins.

P-22 was recaptured in late March by National Park Service biologists and treated for mange, a parasitic disease of the hair and skin. Blood tests later showed exposure to anti-coagulant rodenticides, commonly known as rat poison.

P-22 has all along served as a living public-service announcement for the wildland-urban interface in Southern California; through him, NPS biologists have had a chance to school residents in the naturally reclusive habits of pumas and the challenges wild animals face in their hemmed-in habitats. That the animal braved two freeways only to be threatened by urban poisons seems a depressing irony, and the news gave a public-relations boost to the California Department of Pesticide Regulation’s decision to ban the retail sale of some types of rodenticides beginning July 1, 2014 (as did rodenticide manufacturer Reckitt Benckiser’s decision to sue to stop the ruling).

And yet the exact causes of P-22’s condition remain a mystery. Common rat poisons, which interfere with the blood’s clotting mechanism, have been found in wild cats afflicted with mange: An NPS study published in 2007 tested 39 mange-ridden bobcats and found that 35 had been exposed to anti-coagulant rat poison. It's important to emphasize that no one claims a causal link, and that many cougars exposed to rodenticide don't contract mange but die from other, perhaps unrelated, causes. For instance, half the cougars that have died in the Santa Ana Mountains, another isolated ecosystem to the south of the Santa Monicas, have been hit by cars. "And all them had been exposed to rodenticides," says Winston Vickers, a veterinarian at the University of California-Davis Wildlife Health Center, and field lead on the Southern California Cougar Project. "Can you make that link, between rodenticides and vehicle strikes?"

Maybe not – or just maybe not yet. Laurel Klein Serieys, a doctoral candidate at the University of California-Los Angeles, collected blood from five bobcats hit by cars and found that all of them had ingested rat poison, too. Yet only a little more than a third of bobcats caught in live traps had rodenticide in their blood. “It suggests that recent (rodenticide) exposure predisposes bobcats to other sources of mortality,” she says. Biologists have long observed that poisoned rats grow lethargic and have slower reaction times before they die; could the same be true in larger animals? Does the ingestion of rat poison leave small animals more vulnerable to predators and large and small more susceptible to disease?

These are hard questions to answer, and no one can yet say for sure. What researchers do know, however, is that anti-coagulant poisons are building up in the environment at an alarming rate, in part due to the formulation of so-called “second-generation” anti-coagulants such as brodifacoum, the main ingredient in the popular household rat poison d-Con. Second-generation rodenticides work the same as their earlier counterparts — they inhibit the enzyme that triggers the production of vitamin K, which in the bodies of birds and mammals allows blood to clot. But brodifacoum and its analogs have been formulated to persist in their victims much longer. “In some species they have a half life that can extend beyond 160 days,” says Serieys, “which means the compounds themselves can persist for over a year.”

That’s a whole year for cumulative doses of poison to build up in the liver of a coyote every time it kills a rat, and again in every cougar with each coyote kill. Large predators get a concentrated dose. “Mountain lions typically go right for the liver on lots of prey items,” NPS wildlife ecologist Seth Riley writes in an email, “which is also where these chemicals get sequestered.” Riley, one of the leaders of the NPS puma study and Serieys' co-advisor, says that two mountain lions in the Santa Monicas have bled to death from ingesting rodenticides. Both had mange.

The anti-coagulant substances found in P-22’s blood, diphacinone and chlorophacinone, are shorter-lived first-generation rodenticides, but there might have been second-generation exposure, too. “We do know for sure that (the presence of rodenticide in the blood) is reflection of recent exposure events,” Serieys says. “But without getting liver tissue it’s hard to determine whether he’s been exposed to second generation.” (Mange, however non-causally, is usually associated with exposure to second-generation compounds.)

Contrary to claims made in the 1988 patent for brodifacoum – that the chemical only lingers in “target species” tissue and so “non-target” species should be safe – brodifacoum and other second-generation anti-coagulants are decimating wildlife in California, and elsewhere in the American West where urban development presses up against wildlife habitat. The chemical regularly turns up in necropsies of golden eagles, red-tailed hawks, owls, vultures, geese, black bears, foxes, geese and fishers. The California Department of Fish and Wildlife recommended restricting their use as early as 1997, and the U.S. Environmental Protection Agency in 2008 banned their retail sale, a prohibition that has been delayed by lawsuits. California's ban on the retail sale of the chemicals will take second-generation rodenticides off the shelves of Home Depot after July 1, but it won’t eliminate the poison completely: Professional exterminators, who presumably have some higher knowledge that will prevent brodifacoum from entering the food chain, can still get their hands on it.

That will do little to help P-22, who lives in a park bounded on one side by high-density single-family homes and on another by a golf course — “the number one and number two risk factors,” says Serieys, “for anti-coagulant rodenticide exposure.” Jeff Sikich and his crew treated the puma with subcutaneous injections of Vitamin K and six tubes of selamectin — a topical parasite killer often used to control fleas and heartworm in domestic pets – but the puma's future looks impossibly grim. “He’s definitely headed downhill,” Serieys says, and it's hard to imagine him finding any route up.

Judith Lewis Mernit is a contributing editor to High Country News. She tweets @judlew.

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