<?xml version="1.0" encoding="UTF-8"?><rss version="2.0"
	xmlns:content="http://purl.org/rss/1.0/modules/content/"
	xmlns:wfw="http://wellformedweb.org/CommentAPI/"
	xmlns:dc="http://purl.org/dc/elements/1.1/"
	xmlns:atom="http://www.w3.org/2005/Atom"
	xmlns:sy="http://purl.org/rss/1.0/modules/syndication/"
	xmlns:slash="http://purl.org/rss/1.0/modules/slash/"
	>

<channel>
	<title>wildlife toxicology &#8211; Science</title>
	<atom:link href="https://scienmag.com/tag/wildlife-toxicology/feed/" rel="self" type="application/rss+xml" />
	<link>https://scienmag.com</link>
	<description></description>
	<lastBuildDate>Mon, 12 Oct 2026 09:26:55 +0000</lastBuildDate>
	<language>en-US</language>
	<sy:updatePeriod>
	hourly	</sy:updatePeriod>
	<sy:updateFrequency>
	1	</sy:updateFrequency>
	<generator>https://wordpress.org/?v=7.1.3</generator>

<image>
	<url>https://scienmag.com/wp-content/uploads/2024/07/cropped-scienmag_ico-32x32.jpg</url>
	<title>wildlife toxicology &#8211; Science</title>
	<link>https://scienmag.com</link>
	<width>32</width>
	<height>32</height>
</image> 
<site xmlns="com-wordpress:feed-additions:1">73899611</site>	<item>
		<title>Bobcats Are Loading Up on Rat Poison Across the Northeast, Study Finds</title>
		<link>https://scienmag.com/bobcats-are-loading-up-on-rat-poison-across-the-northeast-study-finds/</link>
		
		<dc:creator><![CDATA[Gavin Prescott]]></dc:creator>
		<pubDate>Mon, 12 Oct 2026 09:26:55 +0000</pubDate>
				<category><![CDATA[Science News]]></category>
		<category><![CDATA[anticoagulant rodenticides]]></category>
		<category><![CDATA[bioaccumulation]]></category>
		<category><![CDATA[bioaccumulation of poisons in food webs]]></category>
		<category><![CDATA[bobcat exposure to anticoagulant rodenticides]]></category>
		<category><![CDATA[bobcats]]></category>
		<category><![CDATA[contamination hot spots]]></category>
		<category><![CDATA[effects of rodenticide on predator species]]></category>
		<category><![CDATA[environmental health hazards of anticoagulant poisons]]></category>
		<category><![CDATA[environmental impact of rat poison]]></category>
		<category><![CDATA[food web contamination]]></category>
		<category><![CDATA[illegal or unintended rodenticide exposure in wild animals]]></category>
		<category><![CDATA[long-term wildlife contamination study]]></category>
		<category><![CDATA[Lynx rufus]]></category>
		<category><![CDATA[mesocarnivores]]></category>
		<category><![CDATA[Northeastern United States]]></category>
		<category><![CDATA[PLOS One]]></category>
		<category><![CDATA[regulatory effectiveness of rodenticide restrictions]]></category>
		<category><![CDATA[rodenticide contamination in wildlife]]></category>
		<category><![CDATA[role of bob]]></category>
		<category><![CDATA[second-generation rodenticides]]></category>
		<category><![CDATA[spread of chemical toxins in northeastern US ecosystems]]></category>
		<category><![CDATA[wildlife health]]></category>
		<category><![CDATA[wildlife poisoning from second-generation anticoagulants]]></category>
		<category><![CDATA[wildlife toxicology]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=264214</guid>

					<description><![CDATA[A decade-long analysis of 352 bobcats across four northeastern states found that 59 percent carried anticoagulant rodenticide residues, with exposure rates climbing about 25 percent per year despite federal restrictions on the most toxic compounds.]]></description>
										<content:encoded><![CDATA[<p>A quiet chemical crisis is unfolding in the forests, suburbs, and farmlands of the northeastern United States, and the bobcat is its most telling sentinel. A new study published in PLOS One has documented widespread contamination of bobcats (Lynx rufus) with anticoagulant rodenticides, the compounds designed to kill rats and mice by disrupting blood clotting. Drawing on more than a decade of samples collected between 2013 and 2024, researchers detected seven different rodenticide compounds in 352 bobcats across four states, with 59 percent of the animals showing evidence of exposure. The findings reveal not only how deeply these poisons have penetrated wild food webs, but also a troubling trajectory: despite federal restrictions on the most toxic second-generation compounds taking effect during the study period, detection rates climbed steadily, rising by roughly 25 percent per year.</p>
<p>Anticoagulant rodenticides work by interfering with the vitamin K cycle, effectively preventing blood from clotting and causing fatal internal hemorrhage in the target rodents. The problem for wildlife is that these compounds do not stay where they are deployed. Rodents that consume poisoned bait often die slowly, sometimes days later, wandering into the open where predators and scavengers encounter them. In the process, the poison moves up the food chain. Second-generation anticoagulants, developed after rodents evolved resistance to earlier formulas, are particularly insidious because they are far more potent and persist in liver tissue for months. A single poisoned rodent can deliver a lethal or sublethal dose to a fox, an owl, a fisher, or a bobcat, and repeated exposure compounds the risk through bioaccumulation.</p>
<p>The research team, led by Jennifer A. Grauer and colleagues from institutions across the Northeast, took advantage of an unusual but powerful resource: opportunistic samples from bobcats harvested by hunters and trappers, along with animals recovered as roadkill, collected across New Hampshire, Vermont, New York, and New Jersey. Liver tissue, where anticoagulant residues concentrate, was analyzed for the presence of seven rodenticide compounds. Because the samples came from animals already dead, the study avoided the ethical and logistical challenges of trapping and sampling live carnivores, while still providing a statistically rich picture of exposure across a large region and a long time span. The approach also allowed the researchers to compare exposure between animals taken by hunters and those killed on roads, a distinction that turned out to matter.</p>
<p>The spatial results were striking. Exposure was not uniform across the landscape. New Hampshire and Vermont recorded the highest levels of contamination, and a spatial clustering algorithm identified localized hot spots of rodenticide detection in those two states as well as in New Jersey. New York, by contrast, emerged as comparatively cold in the analysis, with fewer clusters of positive detections. This patchiness matters because it suggests that rodenticide exposure is driven by local conditions, likely the density of human development, pest-control practices, and the structure of the food web connecting poisoned rodents to wild predators, rather than by broad regional factors alone. The hot spots provide concrete targets for mitigation efforts, from restrictions on consumer-grade poisons to public education campaigns in the affected areas.</p>
<p>Within individual animals, the picture was one of multiple, accumulating exposures. Bobcats that tested positive carried between one and four different rodenticide compounds in their systems, with a mean of 1.07 compounds among exposed individuals and a standard deviation of 1.17. Co-exposure to several compounds is particularly concerning from a toxicological standpoint, because different anticoagulants act through the same physiological pathway and their effects can be additive. An animal carrying multiple compounds may face a substantially higher risk of hemorrhage than one carrying a single residue, especially under stressors such as injury, disease, or starvation. The presence of several compounds in a single bobcat also indicates repeated encounters with poisoned prey over time, painting a picture of chronic, ongoing contamination rather than a one-off accident.</p>
<p>Age emerged as one of the clearest predictors of exposure. The researchers&#8217; statistical models showed that the predicted odds of anticoagulant rodenticide exposure increased by approximately 35 percent, and the predicted number of compounds in an animal&#8217;s system rose by roughly 17 percent, for each additional year of bobcat age. This pattern is consistent with bioaccumulation: older animals have had more years to accumulate persistent residues from contaminated prey, and they may also occupy higher positions in the food web, taking larger prey that themselves carry accumulated burdens. Exposure rates varied by state, by age, and by sampling source, with harvested animals differing from roadkill in their likelihood of testing positive, but the models found no difference between male and female bobcats. That absence of a sex effect suggests that both sexes face similar dietary exposure risks across their ranges.</p>
<p>Perhaps the most sobering finding is the temporal trend. Second-generation anticoagulant rodenticides, the most potent and persistent class, have faced federal restrictions in the United States that went into effect during the course of the study, limiting their availability to professional applicators and removing them from many consumer products. Yet detection rates in bobcats did not decline. Instead, they increased steadily at a rate of approximately 25 percent per year across the 2013 to 2024 sampling window. The researchers are careful not to over-interpret the mechanism behind this rise, but the pattern suggests that current regulations have not yet translated into reduced contamination of wild predators. Possible explanations include lag effects from the persistence of residues in the environment, continued legal use by licensed professionals, illegal or off-label use, and the movement of regulated compounds across jurisdictions where rules differ.</p>
<p>The study gains additional weight from a comparison with another northeastern carnivore. The spatial patterns of exposure observed in bobcats closely mirrored those previously documented in fisher (Pekania pennanti), a mustelid predator with very different habitat preferences and hunting behavior. Fishers tend to occupy deep forest interiors, while bobcats range across a broader mosaic of forest edge, farmland, and suburban development. If two predators with such divergent ecologies show similar geographic fingerprints of contamination, the implication is that rodenticides have become ubiquitous in the northeastern food web, reaching animals regardless of how or where they hunt. The poisoned rodent, in effect, has become a common item on the menu of the region&#8217;s mesocarnivores.</p>
<p>For wildlife managers and conservationists, the study provides something that has been lacking: a long-term, region-wide baseline for a species of growing public interest. Bobcats have been recovering across the Northeast in recent decades, expanding back into areas where they were once eliminated, and their return has been celebrated as a conservation success. That recovery now carries a hidden cost, as expanding populations intersect with landscapes saturated with rodenticides. Sublethal exposure can impair health, reduce survival, and potentially affect reproduction, even when it does not kill outright, and the cumulative burden across a population remains difficult to quantify. The baseline established by this research will allow future monitoring to track whether regulatory changes eventually bend the exposure curve downward.</p>
<p>The broader lesson is one about the reach of human chemicals into ecosystems that seem, on the surface, far removed from suburban garages and city basements. Rodenticides are deployed to solve a narrowly human problem, yet their residues now appear in more than half of the bobcats tested across a four-state region, in hot spots that map onto the interface of development and wild land, and in concentrations that grow with every passing year of an animal&#8217;s life. As evidence accumulates across species, from fishers to bobcats to birds of prey, the case for rethinking how these compounds are used, regulated, and replaced grows stronger. The bobcats of the Northeast, silently carrying seven different poisons in their livers, are delivering a message that regulators and consumers alike cannot afford to ignore.</p>
<p><strong>Subject of Research:</strong> Anticoagulant rodenticide exposure in bobcats across the northeastern United States</p>
<p><strong>Article Title:</strong> Spatiotemporal patterns of anticoagulant rodenticide exposure in bobcats across the northeastern United States</p>
<p><strong>Article References:</strong> Grauer, J. A., Needle, D. B., Schuler, K. L., Connelly, P. J., Fowles, G., Miller, E. A., Furfey, B., Royar, K., Watson, M. B., DeBow, J., &amp; Frair, J. L. (2026). Spatiotemporal patterns of anticoagulant rodenticide exposure in bobcats across the northeastern United States. <em>PLOS One, 21</em>(10), e0360055. <a href="https://doi.org/10.1371/journal.pone.0360055" rel="noopener noreferrer">https://doi.org/10.1371/journal.pone.0360055</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1371/journal.pone.0360055" rel="noopener noreferrer">10.1371/journal.pone.0360055</a></p>
<p><strong>Keywords:</strong> bobcats, anticoagulant rodenticides, wildlife toxicology, Lynx rufus, northeastern United States, second-generation rodenticides, bioaccumulation, mesocarnivores, PLOS One, contamination hot spots, food web contamination, wildlife health</p>
]]></content:encoded>
					
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">264214</post-id>	</item>
		<item>
		<title>Evolution of Estrogen Receptors Explains Why Species Respond Differently to Chemicals</title>
		<link>https://scienmag.com/evolution-of-estrogen-receptors-explains-why-species-respond-differently-to-chemicals/</link>
		
		<dc:creator><![CDATA[Gavin Prescott]]></dc:creator>
		<pubDate>Mon, 12 Oct 2026 07:13:54 +0000</pubDate>
				<category><![CDATA[Biology]]></category>
		<category><![CDATA[binding pocket]]></category>
		<category><![CDATA[bioinformatics]]></category>
		<category><![CDATA[cetaceans]]></category>
		<category><![CDATA[chemical effects on wildlife]]></category>
		<category><![CDATA[ecological lifestyle and hormone receptor variation]]></category>
		<category><![CDATA[endocrine disruption]]></category>
		<category><![CDATA[endocrine disruption in mammals]]></category>
		<category><![CDATA[environmental toxicology and risk assessment]]></category>
		<category><![CDATA[ER alpha receptor diversification]]></category>
		<category><![CDATA[estrogen receptor alpha]]></category>
		<category><![CDATA[estrogen receptor evolution]]></category>
		<category><![CDATA[hormone receptor ligand binding]]></category>
		<category><![CDATA[in silico modeling]]></category>
		<category><![CDATA[in vitro assays]]></category>
		<category><![CDATA[Machine learning]]></category>
		<category><![CDATA[mammalian evolution]]></category>
		<category><![CDATA[mammalian lineage hormone receptor differences]]></category>
		<category><![CDATA[molecular basis of chemical sensitivity]]></category>
		<category><![CDATA[molecular mechanisms of hormone receptor sensitivity]]></category>
		<category><![CDATA[new approach methodologies]]></category>
		<category><![CDATA[predicting species response to endocrine disruptors]]></category>
		<category><![CDATA[species-specific hormone disruption]]></category>
		<category><![CDATA[species-specific sensitivity]]></category>
		<category><![CDATA[wildlife toxicology]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=263994</guid>

					<description><![CDATA[An integrated study of estrogen receptor alpha evolution across 169 mammalian species reveals how ecological traits and structural mutations drive species-specific sensitivity to estrogenic chemicals.]]></description>
										<content:encoded><![CDATA[<p>One of the most persistent puzzles in environmental toxicology is why a chemical that disrupts the hormones of one mammal may leave a closely related species largely unaffected. Regulatory risk assessment has long struggled with this problem, because safety thresholds established in laboratory rodents cannot simply be extrapolated to whales, bats, elephants, or the thousands of other mammals that share the planet. A new peer-reviewed study published in Environmental Science &amp; Technology by researchers at Ehime University, led by Hisato Iwata, now offers a molecular explanation rooted in evolution itself. By tracing how the estrogen receptor alpha protein has diversified across mammalian lineages, and by linking that diversification to the ecological lifestyles of different species, the team has taken a substantial step toward predicting, rather than merely observing, species-specific chemical sensitivity.</p>
<p>The centerpiece of the research is the estrogen receptor alpha, or ERα, a ligand-activated transcription factor that binds estrogenic molecules and switches on suites of genes governing reproduction, development, and metabolism. Because many environmental contaminants, from natural phytoestrogens to synthetic industrial compounds, can interact with this receptor, ERα sits at the heart of endocrine disruption biology. The ligand-binding domain of the receptor contains a pocket whose shape and chemical properties determine which molecules fit and how strongly they bind. Even a single amino acid substitution in this region can alter the geometry of the pocket, changing the receptor&#8217;s affinity for particular chemicals. The Ehime University team reasoned that if evolutionary pressures have reshaped ERα differently in different mammalian lineages, those structural changes should translate into measurable differences in chemical responsiveness, and that these differences could be mapped and predicted systematically.</p>
<p>To test this idea, the researchers assembled an unusually broad comparative dataset. They collected ERα protein sequences from 169 mammalian species and paired this genetic information with 107 ecological traits for each species, encompassing diet, habitat, reproductive strategy, and other life-history characteristics. The scale of this comparison matters. Most earlier studies of receptor evolution focused on a handful of model organisms, which limited their ability to detect patterns tied to ecology. By casting the net across nearly the entire mammalian class, the team could ask whether species that share similar lifestyles also share similar receptor architectures, a pattern that would suggest common evolutionary pressures acting on hormone signaling.</p>
<p>The bioinformatic analysis revealed exactly such a pattern. When ERα sequences were clustered according to their amino acid composition, the resulting groupings aligned with the ecological profiles of the animals rather than simply with their phylogenetic relatedness alone. Species occupying comparable ecological niches, facing comparable diets and environments, tended to carry receptors with comparable sequence features. This finding implies that ecological factors have exerted selective pressure on the structure of the estrogen receptor, fine-tuning its sensitivity to the endogenous and exogenous molecules each species encounters in its environment. In other words, the receptor is not a static, universal sensor of estrogen; it is an evolving interface between an animal&#8217;s biology and its world.</p>
<p>Sequence comparisons alone cannot show how amino acid differences translate into three-dimensional structure, so the researchers turned to in silico modeling. Using computer-based structural analysis of the ERα ligand-binding domain, they examined how the binding pocket, the cavity where estrogenic chemicals dock, varies across species with different diets. The results were striking: omnivorous mammals tended to possess larger binding pockets than either carnivores or herbivores. A broader pocket plausibly accommodates a wider chemical repertoire, which fits the ecological reality that omnivores ingest a more chemically diverse diet than specialists. This structural observation provides a mechanistic bridge between what an animal eats and how its hormone receptor responds to chemicals, connecting ecology to molecular pharmacology in a single framework.</p>
<p>Structural modeling, however, remains a prediction until it is tested in living systems, and this is where the study&#8217;s experimental component becomes decisive. The team conducted cell-based in vitro assays using ERα from six mammalian species, exposing the receptors to both natural and synthetic estrogenic chemicals and measuring the resulting activation responses. The experiments demonstrated marked interspecies differences in sensitivity. Receptors that appeared structurally similar in some regions behaved distinctly when challenged with the same compounds, confirming that the amino acid variations documented in the sequence analysis have functional consequences. These assays transform the study from a purely comparative exercise into an empirical demonstration that evolution has produced receptors with genuinely different chemical sensitivities across mammals.</p>
<p>Among the most notable discoveries was a unique mutation found in cetaceans, the group that includes whales and dolphins. In human ERα, the 349th amino acid position is occupied by asparagine; in cetaceans, the team found that this position carries serine instead. This substitution alters the structure of the receptor and is linked to aquatic adaptation as well as changes in chemical responsiveness. The finding is particularly significant for wildlife risk assessment, because cetaceans are apex predators in marine ecosystems and are known to accumulate persistent organic pollutants at high concentrations. If their estrogen receptors have evolved structural properties that change how they respond to estrogenic chemicals, then risk models built on terrestrial mammal data may systematically misjudge the vulnerability of these ocean giants.</p>
<p>The final analytical layer brought artificial intelligence into the framework. Using machine learning, the researchers built models designed to identify which factors best predict variation in ERα structure and, by extension, differences in chemical sensitivity among species. Among the variables examined, one emerged as especially promising: the brain-to-body mass ratio, the proportion of an animal&#8217;s total body weight accounted for by brain tissue. That a neurological and life-history trait should correlate with receptor structure and chemical responsiveness is an intriguing result, suggesting that the evolution of endocrine signaling is entangled with broader physiological and ecological adaptations. Machine learning proved capable of integrating these multidimensional data, sequence features, structural parameters, and ecological variables, into predictive models, which is precisely the kind of capability needed for forward-looking risk assessment.</p>
<p>The methodological architecture of the study is as important as its individual findings. The work exemplifies New Approach Methodologies, or NAMs, an advanced framework that combines bioinformatic sequence analysis, in silico structural modeling, artificial intelligence and machine learning, and in vitro cell-based assays into a single integrated pipeline. NAMs are gaining momentum in toxicology because they promise to reduce reliance on animal testing while increasing the breadth and speed of chemical safety evaluation. This study demonstrates the power of that promise: no single method could have connected 169 species&#8217; genomes, 107 ecological traits, protein structures, and functional receptor responses, but the integrated approach made those connections visible. Each layer of analysis constrained and validated the others, producing conclusions more robust than any component could deliver alone.</p>
<p>The implications reach well beyond academic evolutionary biology. Environmental regulators currently depend heavily on data from a small set of laboratory species, and the study shows why that dependence is hazardous: receptor evolution has embedded species-specific sensitivities that no single-model extrapolation can capture. With the predictive factors identified here, including binding pocket architecture, key amino acid positions, and traits such as brain-to-body mass ratio, it becomes conceivable to estimate the chemical vulnerability of poorly studied wildlife before contamination occurs, rather than after populations show harm. For conservation biologists, the cetacean mutation offers a concrete example of how adaptation to one environment, in this case aquatic life, can reshape sensitivity to human-made chemicals in another. For the broader field of endocrine disruption research, the message is that the molecular targets of chemical action are themselves products of evolution, and understanding that evolutionary history is not optional but essential. By revealing the ecological and structural determinants of species-specific chemical sensitivity, the Ehime University team has outlined the molecular mechanisms required to predict chemical risks to wildlife with high precision, marking a meaningful advance toward a new generation of ecologically informed toxicology.</p>
<p><strong>Subject of Research:</strong> Evolutionary determinants of species-specific chemical sensitivity in mammalian estrogen receptor alpha</p>
<p><strong>Article Title:</strong> Uncovering species-specific chemical sensitivity: Insights from mammalian hormone receptor evolution and new approach methodologies</p>
<p><strong>Article References:</strong> Uncovering species-specific chemical sensitivity: Insights from mammalian hormone receptor evolution and new approach methodologies. (n.d.). <a href="https://www.eurekalert.org/news-releases/1145719" rel="noopener noreferrer">Original publication</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> Not provided</p>
<p><strong>Keywords:</strong> estrogen receptor alpha, species-specific sensitivity, New Approach Methodologies, endocrine disruption, mammalian evolution, bioinformatics, in silico modeling, machine learning, in vitro assays, cetaceans, wildlife toxicology, binding pocket</p>
]]></content:encoded>
					
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">263994</post-id>	</item>
		<item>
		<title>Rat Poison Found in Half of Dead Birds of Prey in Queensland Study</title>
		<link>https://scienmag.com/rat-poison-found-in-half-of-dead-birds-of-prey-in-queensland-study/</link>
		
		<dc:creator><![CDATA[Margaret Porter]]></dc:creator>
		<pubDate>Sun, 04 Oct 2026 19:01:39 +0000</pubDate>
				<category><![CDATA[Climate]]></category>
		<category><![CDATA[anticoagulant rodenticide impact on raptors]]></category>
		<category><![CDATA[anticoagulant rodenticides]]></category>
		<category><![CDATA[Australia]]></category>
		<category><![CDATA[bird mortality due to rodenticide in Australia]]></category>
		<category><![CDATA[brodifacoum]]></category>
		<category><![CDATA[coagulopathy]]></category>
		<category><![CDATA[conservation]]></category>
		<category><![CDATA[conservation concerns for Australian raptors]]></category>
		<category><![CDATA[effects of rodenticide on predatory birds]]></category>
		<category><![CDATA[environmental impact of antico]]></category>
		<category><![CDATA[LC-MS]]></category>
		<category><![CDATA[mouse plague management and ecological implications]]></category>
		<category><![CDATA[owls]]></category>
		<category><![CDATA[predator-prey dynamics and chemical risks]]></category>
		<category><![CDATA[Queensland]]></category>
		<category><![CDATA[raptors]]></category>
		<category><![CDATA[rat poison poisoning in Queensland wildlife]]></category>
		<category><![CDATA[roadkill and wildlife poisoning studies]]></category>
		<category><![CDATA[rodenticide exposure in Australian birds of prey]]></category>
		<category><![CDATA[secondary poisoning]]></category>
		<category><![CDATA[sublethal pesticide exposure in birds of prey]]></category>
		<category><![CDATA[warfarin]]></category>
		<category><![CDATA[wildlife toxicology]]></category>
		<category><![CDATA[wildlife toxicology and rodenticide contamination]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=235418</guid>

					<description><![CDATA[Researchers found anticoagulant rodenticides, most often warfarin, in 13 of 24 deceased predatory birds from south-east Queensland, revealing widespread sublethal exposure that may contribute to road mortality and fitness decline.]]></description>
										<content:encoded><![CDATA[<p>A quiet chemical crisis may be unfolding in the skies over eastern Australia. When researchers at The University of Queensland examined the bodies of 24 predatory birds collected around south-east Queensland and northern New South Wales, more than half of them carried anticoagulant rodenticides in their livers, the potent rat and mouse poisons designed to kill rodents but increasingly implicated in the deaths of the very predators that keep those rodents in check. The study, published in December 2024 in the journal Discover Toxicology, offers one of the most detailed looks yet at sublethal rodenticide exposure in Australian birds of prey, and its findings carry uncomfortable implications for how the nation manages its periodic mouse plagues.</p>
<p>The birds in the study were not killed for research. All 24 cadavers arrived opportunistically between June 2022 and November 2023, a window that coincided with regional mouse infestations. Some were donated by the university&#8217;s Veterinary Teaching Hospital after being euthanised for medical reasons, while others were roadkill collected during unrelated fieldwork. Ten raptor species and one nightjar were represented, with Eastern Barn Owls dominating the sample at ten individuals, followed by three Australian Boobook Owls. Two Wedge-tailed Eagles, two Black-shouldered Kites, a Peregrine Falcon, a Powerful Owl, a Grey Goshawk, a Brown Goshawk, a Nankeen Kestrel, a Black Kite and a Tawny Frogmouth rounded out the list. Thirteen birds were male, ten female and one of undetermined sex; fourteen were adults and ten immature.</p>
<p>The analytical centrepiece of the study was liquid chromatography mass spectrometry, or LC-MS, performed at the CSIRO Ecosciences Precinct in Brisbane. Because decay alters the water content of tissue, the researchers homogenised and freeze-dried liver samples before extraction, then used a multi-step process involving formic acid, cold acetonitrile and lipid-removal cartridges to isolate the rodenticide residues. The instrument, an Agilent 6546 liquid chromatography quadrupole time-of-flight mass spectrometer, ran in a data-independent mode called quadrupole-resolved all-ions analysis, screening for eight rodenticides including warfarin, brodifacoum, difethialone, flocoumafen, bromadiolone, difenacoum, coumatetralyl and pindone. Calibration curves spanning 0.01 to 1,000 parts per billion achieved correlation coefficients between 0.9683 and 0.9971, and quality-control samples spiked with known concentrations of the compounds verified the method&#8217;s accuracy across low, mid and high ranges.</p>
<p>The results were striking. Thirteen of the 24 birds, just over half, tested positive for rodenticides registered for use in Australia. The most frequently detected compound was warfarin, a first-generation anticoagulant, found in eleven birds. Second-generation anticoagulants, which are far more toxic and persistent, also appeared: brodifacoum in three samples, difethialone in one and flocoumafen in one. Three birds carried warfarin alongside a second-generation compound, meaning they had been exposed to multiple poisons. Perhaps most telling, only six of the thirteen rodenticide-positive birds had rodent remains in their digestive tracts at the time of death. The researchers interpret this as evidence that the poisons can bioaccumulate in liver tissue over time, lingering from past meals of poisoned prey rather than reflecting a single recent exposure.</p>
<p>None of the detected concentrations reached the lethal dose thresholds established for other bird species. Brodifacoum levels in the Barn Owls and a Wedge-tailed Eagle fell below the reported oral LD50 range for owls of 0.15 to 9.68 milligrams per kilogram, and the difethialone concentration in the Tawny Frogmouth, 0.1 milligrams per kilogram, sat below the LD50 values of 0.26 to 23.4 milligrams per kilogram documented for Bobwhite, Japanese Quail and Mallard. Warfarin concentrations were similarly far below the 525 to 2,150 milligrams per kilogram lethal range reported for those same test species. But sublethal does not mean harmless. Second-generation anticoagulants are highly lipid-soluble and resist metabolic breakdown, and brodifacoum has been shown to cause persistent coagulopathy in birds for up to eleven days even at doses below the lethal threshold.</p>
<p>The clinical consequences of such exposure can be subtle but deadly. Birds suffering sublethal anticoagulant toxicosis have been documented to show lethargy, reduced agility and wing droop, impairments that degrade hunting performance and spatial navigation. For a fast-flying owl hunting at night, a momentary lapse in coordination can be fatal in a different way: collision with a vehicle. Twelve of the fifteen birds in the study showing traumatic injuries were found on roadsides, and the authors suggest that some of these roadkill birds may have been compromised by sublethal poisoning before they ever met a car. Peak coagulopathy after a single lethal ingestion typically occurs one to four days later, and after sublethal ingestion the effects may take even longer to manifest, widening the window of vulnerability.</p>
<p>Disentangling poisoning from trauma is one of the study&#8217;s central methodological challenges. Internal bleeding looks much the same whether it stems from a blunt impact or a drug-induced failure of the clotting cascade, and decomposition or scavenging can destroy clots that would otherwise distinguish the two. Ten birds showed haemocoelom, a coelomic cavity filled with uncoagulated blood, and in six of those there were no grossly obvious external signs of trauma such as fractures or lacerations. Yet only four of the ten haemocoelom cases were rodenticide-positive, and the statistical association between anticoagulant presence and postmortem evidence of coagulopathy was not significant. Alternative causes of bleeding disorders complicate the picture further: three birds carried low-burden apicomplexan parasites consistent with avian malaria, two had chronic enteritis with coccidian oocysts possibly of the genus Goussia, and heavy metal toxicity and bacterial infections such as salmonellosis can produce similar pathology in wild raptors.</p>
<p>One statistically significant pattern did emerge, and it concerned age. Immature birds were significantly more likely to carry higher brodifacoum concentrations than adults, a correlation with an f-value of 5.15 and a p-value of 0.03. The authors offer several non-exclusive explanations: inexperienced young hunters may target weakened, poisoned prey more readily; older birds may metabolise or eliminate the compound more efficiently or simply have longer intervals between exposures; or heavily affected juveniles may never survive to adulthood at all. The researchers caution, however, that the small sample size and a confidence interval hovering near zero mean the finding should be treated as a hypothesis generator rather than a settled conclusion. Species-level dietary differences add another layer of complexity, since rodent specialists such as Barn Owls and Black-shouldered Kites face theoretically higher exposure risk than bird-eating specialists like goshawks.</p>
<p>The conservation stakes extend beyond the species examined, all of which are currently listed as Least Concern by the International Union for Conservation of Nature. The Powerful Owl, despite its global status, numbers only an estimated 2,200 to 2,800 mature individuals, and the Grey Goshawk is estimated at fewer than 10,000 birds with a declining trend and Endangered classification in several Australian states. Sublethal poisoning that reduces foraging success, body condition and reproductive output, effects documented in vulture studies in the Pacific Northwest, could push such populations toward localised declines long before outright poisoning deaths register. Australian raptor populations remain poorly studied overall, making it difficult to assess how much hidden damage rodenticides are doing.</p>
<p>The study&#8217;s most policy-relevant finding may be its challenge to current Australian guidelines, which favour first-generation rodenticides such as warfarin over second-generation products on the assumption that they break down faster in rodents and pose less secondary risk. Warfarin was, after all, the most common residue in these Queensland birds. The authors point instead to coumatetralyl, another first-generation anticoagulant regarded as safer for predatory birds: mammals are generally more sensitive to it than birds, allowing lower effective doses, and while warfarin resistance has been documented in Australian rodents, no coumatetralyl resistance has yet been recorded there. The team calls for physiological studies of exposed raptors, rodent toxicity testing to track resistance, and surveys of rodenticide users to map what, how much and how often is being deployed. Until then, the poisons meant for mice appear to be quietly accumulating in the livers of the owls, eagles and falcons that share those fields, a debt the ecosystem may only now be beginning to itemise.</p>
<p><strong>Subject of Research:</strong> Sublethal anticoagulant rodenticide exposure in deceased predatory birds in south-east Queensland, Australia</p>
<p><strong>Article Title:</strong> Evaluating sublethal anticoagulant rodenticide exposure in deceased predatory birds of South-East Queensland, Australia</p>
<p><strong>Article References:</strong> Low, Z., Murray, P. J., Naseem, N., McGilp, D., Doneley, B., Beale, D. J., Biggs, L., &amp; Gonzalez-Astudillo, V. (2024). Evaluating sublethal anticoagulant rodenticide exposure in deceased predatory birds of South-East Queensland, Australia. <em>Discover Toxicology, 1</em>(1), Article 13. <a href="https://doi.org/10.1007/s44339-024-00016-4" rel="noopener noreferrer">https://doi.org/10.1007/s44339-024-00016-4</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1007/s44339-024-00016-4" rel="noopener noreferrer">10.1007/s44339-024-00016-4</a></p>
<p><strong>Keywords:</strong> anticoagulant rodenticides, raptors, owls, warfarin, brodifacoum, secondary poisoning, wildlife toxicology, LC-MS, Australia, Queensland, coagulopathy, conservation</p>
]]></content:encoded>
					
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">235418</post-id>	</item>
		<item>
		<title>California&#8217;s Rodenticide Crackdown Is Working, Seven-Year Owl Study Finds, but a New Threat Emerges</title>
		<link>https://scienmag.com/californias-rodenticide-crackdown-is-working-seven-year-owl-study-finds-but-a-new-threat-emerges/</link>
		
		<dc:creator><![CDATA[Gavin Prescott]]></dc:creator>
		<pubDate>Sat, 03 Oct 2026 16:11:16 +0000</pubDate>
				<category><![CDATA[Policy]]></category>
		<category><![CDATA[Barred Owls]]></category>
		<category><![CDATA[biomonitoring]]></category>
		<category><![CDATA[California Ecosystems Protection Act]]></category>
		<category><![CDATA[California rodenticide restrictions]]></category>
		<category><![CDATA[cholecalciferol]]></category>
		<category><![CDATA[conservation science and legislation]]></category>
		<category><![CDATA[decline in rat poison exposure in wild owls]]></category>
		<category><![CDATA[emergence of replacement rodenticide compounds]]></category>
		<category><![CDATA[environmental pollution]]></category>
		<category><![CDATA[environmental pollution and wildlife]]></category>
		<category><![CDATA[forest food web]]></category>
		<category><![CDATA[forest food web contamination]]></category>
		<category><![CDATA[impact of legislation on wildlife health]]></category>
		<category><![CDATA[Integral Ecology Research Center]]></category>
		<category><![CDATA[Integral Ecology Research Center research]]></category>
		<category><![CDATA[Northern Spotted Owl]]></category>
		<category><![CDATA[owl biomonitoring study]]></category>
		<category><![CDATA[pesticide regulation]]></category>
		<category><![CDATA[rodenticides]]></category>
		<category><![CDATA[second-generation anticoagulants]]></category>
		<category><![CDATA[seven-year owl study findings]]></category>
		<category><![CDATA[wildlife toxicology]]></category>
		<category><![CDATA[wildlife toxicology and ecosystem health]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=230758</guid>

					<description><![CDATA[A seven-year study of more than 1,000 Barred Owls shows California's rodenticide restrictions sharply reduced second-generation anticoagulant exposure in wildlife, while the less-regulated poison cholecalciferol rose in its place.]]></description>
										<content:encoded><![CDATA[<p>In one of the most consequential wildlife toxicology studies ever conducted in North America, researchers have documented a striking decline in the exposure of wild owls to the deadliest class of rat poisons following California&#8217;s landmark restrictions, while simultaneously raising the alarm about a less-regulated replacement compound that is quietly spreading through forest food webs. The study, led by the Integral Ecology Research Center (IERC) and published in the journal Environmental Pollution, analyzed liver tissue from 1,003 Barred Owls collected across northwestern California between 2019 and 2025, making it the largest rodenticide biomonitoring dataset ever assembled for a single wildlife species on the continent. The findings offer something exceedingly rare in conservation science: direct, quantifiable evidence that legislation, when grounded in rigorous field data, can measurably reduce contamination in wild animal populations within just a few years.</p>
<p>The scale and design of the study are what set it apart from previous work. Most rodenticide surveys rely on animals that are found sick, dying, or dead, which means the samples skew toward the worst cases and overestimate exposure in the broader population. This new research took a fundamentally different approach. The owls in the dataset were removed as part of an ongoing regional conservation program targeting Barred Owls, an invasive species that competes with the threatened Northern Spotted Owl, rather than recovered as carcasses. As a result, the sample represents apparently healthy birds going about their normal lives, providing a far more accurate cross-section of what is actually circulating through the population. Dr. Vitek Jirinec, lead author of the study and research scientist at IERC, emphasized that this distinction gives researchers much greater confidence that the observed trends are real and population-wide rather than artifacts of sampling bias.</p>
<p>The headline result concerns second-generation anticoagulant rodenticides, or SGARs, an extremely potent class of compounds that prevent blood clotting and can kill predators through a single feeding on a poisoned rodent. Because these chemicals persist in the tissues of poisoned prey, they bioaccumulate up the food chain, devastating owls, fishers, bobcats, mountain lions, and other carnivores that never touched the original bait. Among young owls sampled in the study area, exposure to SGARs fell from roughly 50 percent of birds in 2019 to about 20 percent in 2024. That steep decline aligns closely with California&#8217;s phased statewide restrictions, most notably the California Ecosystems Protection Act, known as AB 1788, which was passed in 2020 and banned most second-generation anticoagulant use, along with a 2024 law, AB 2552, that extended restrictions to older-generation anticoagulant compounds as well.</p>
<p>For Dr. Greta M. Wengert, co-founder and co-director of IERC and principal investigator on the study, the results represent the culmination of more than a decade of work connecting contamination data to policy action. She noted that illegal use and unregulated products had driven rodenticide exposure in these forests for years, and that seeing anticoagulant exposure actually decline within a few years of the regulations taking effect demonstrates that policy grounded in good data from effective biomonitoring efforts can improve outcomes for wildlife. The study embodies what researchers describe as a feedback loop central to IERC&#8217;s mission: supplying the science that informs legislative decisions, and then documenting the real-world benefit that those decisions deliver on the ground.</p>
<p>But the study is not simply a victory lap. For the first time in this species, the researchers screened for cholecalciferol, commonly known as vitamin D3, a rodenticide that works through an entirely different mechanism than anticoagulants. Rather than disrupting blood clotting, cholecalciferol in toxic doses causes life-threatening hypercalcemia, raising calcium levels in the blood until organ failure occurs. The compound turned up in nearly one in five owls, at 18.5 percent of the sample, and detections rose over precisely the same period that anticoagulant exposure was falling. The researchers interpret this inverse pattern as evidence of product substitution: as older, regulated compounds became harder to access, users appear to have shifted toward cholecalciferol-based products, which currently face fewer restrictions in California.</p>
<p>The overall contamination picture remains sobering. When all rodenticide compounds were counted together, as much as 46 percent of the owls sampled carried at least one rodenticide in their system. This means that even as the most lethal anticoagulants recede, nearly half of the owls in the study area are still being exposed to some form of poison through the prey they consume. The data also revealed telling patterns within the population: female Barred Owls and older adults carried the highest exposure levels and the widest mix of compounds, a result consistent with pesticides accumulating in tissues over a lifetime of feeding on contaminated rodents.</p>
<p>That demographic pattern carries particular weight for conservation, because the individuals with the highest burdens, breeding-age females and established territory holders, are exactly the animals a population depends on most to sustain itself. The implications extend beyond Barred Owls to the species they share the forest with. Northern Spotted Owls, a closely related and federally threatened species, have a higher proportion of rodents in their diets, which may place them at even greater risk of accumulating these compounds. The new findings reinforce and extend earlier IERC research: a 2012 study first documented widespread anticoagulant exposure in Pacific fishers linked to trespass cannabis cultivation on public lands, and a 2018 study found rodenticides in 70 percent of sampled Northern Spotted Owls in the same region. Barred Owls, Spotted Owls, fishers, and other sensitive wildlife all feed from the same contaminated food web, and this much larger dataset adds substantial weight to that earlier evidence.</p>
<p>The authors are careful to caution that the exact sources of ongoing exposure are not fully resolved, and this uncertainty points to significant gaps in regulatory oversight. State pesticide-use records capture only licensed commercial applicators, leaving household purchases and illegal use entirely invisible to regulators. Trespass cannabis cultivation, which IERC has long documented as a major source of rodenticide contamination on public and tribal lands, remains untracked by any regulatory database. Legacy contamination from past illicit grow sites may also continue cycling through these forest ecosystems long after active cultivation has stopped, as persistent compounds move from soil and bait stations into rodents and then into the predators that hunt them. Researchers say these hidden and historical sources likely explain at least part of the exposure that persists even as legal, regulated use declines.</p>
<p>Published as Forest food web contamination by rodenticides is pervasive but responsive to regulation: Insights from Barred Owl biomonitoring, the study by Jirinec, Gabriel, Peery, Higley, Hofstadter, Varian, Rex, Franklin, Poppenga, Woods, Volker, and Wengert arrives at a pivotal moment for pesticide policy. It demonstrates that science-based regulation can produce measurable improvements for wildlife within a few years, a finding that should embolden policymakers elsewhere considering similar restrictions. At the same time, the rising tide of cholecalciferol detections serves as a warning that substitution effects can undermine hard-won gains when regulatory frameworks address only one class of compounds at a time. For the old-growth forests of northwestern California and the threatened species that depend on them, the message from more than a decade of IERC research is twofold: the same underlying toxic threat has persisted across multiple species, but for the first time, it is demonstrably responding to policy, and the next chapter of that policy response will determine whether the progress holds.</p>
<p><strong>Subject of Research:</strong> Rodenticide contamination in Barred Owls and the effect of California pesticide regulations on wildlife exposure</p>
<p><strong>Article Title:</strong> Largest-ever study of its kind shows California’s rodenticide restrictions are working, and flags new rodenticides rising in their place</p>
<p><strong>Article References:</strong> Largest-ever study of its kind shows California’s rodenticide restrictions are working, and flags new rodenticides rising in their place. (n.d.). <a href="https://www.eurekalert.org/news-releases/1145785" rel="noopener noreferrer">Original publication</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> Not provided</p>
<p><strong>Keywords:</strong> rodenticides, Barred Owls, California Ecosystems Protection Act, second-generation anticoagulants, cholecalciferol, Northern Spotted Owl, biomonitoring, wildlife toxicology, Integral Ecology Research Center, Environmental Pollution, pesticide regulation, forest food web</p>
]]></content:encoded>
					
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">230758</post-id>	</item>
	</channel>
</rss>
