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Bromethalin
Bromethalin
Bromethalin
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Bromethalin
Names
Preferred IUPAC name
N-Methyl-2,4-dinitro-N-(2,4,6-tribromophenyl)-6-(trifluoromethyl)aniline
Other names
2,4,6-Tribromo-N-[2,4-dinitro-6-(trifluoromethyl)phenyl]-N-methylaniline
Identifiers
3D model (JSmol)
ChemSpider
ECHA InfoCard 100.109.042 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C14H7Br3F3N3O4/c1-21(13-9(16)2-6(15)3-10(13)17)12-8(14(18,19)20)4-7(22(24)25)5-11(12)23(26)27/h2-5H,1H3 checkY
    Key: USMZPYXTVKAYST-UHFFFAOYSA-N checkY
  • InChI=1/C14H7Br3F3N3O4/c1-21(13-9(16)2-6(15)3-10(13)17)12-8(14(18,19)20)4-7(22(24)25)5-11(12)23(26)27/h2-5H,1H3
    Key: USMZPYXTVKAYST-UHFFFAOYAX
  • Brc2cc(Br)cc(Br)c2N(c1c([N+]([O-])=O)cc([N+]([O-])=O)cc1C(F)(F)F)C
Properties
C14H7Br3F3N3O4
Molar mass 577.93 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Bromethalin is a neurotoxic rodenticide that damages the central nervous system.[1]

History

[edit]

Bromethalin was discovered in the early 1980s through an approach to find replacement rodenticides for first-generation anticoagulants, especially to be useful against rodents that had become resistant to Warfarin-type anticoagulant poisons. A structured study was undertaken to develop a substance that would be both poisonous to rodents, but also would be readily eaten by rodents. Bromethalin—N-methyl-2,4-dinitro-N (2,4,6-tribromophenyl)-6-(trifluoromethyl) benzeneamine— was the outcome of that study, as the specific formulation had both desired rodenticidal properties.[1]

Mechanism of action

[edit]

Bromethalin works by being metabolised to n-desmethyl-bromethalin and uncoupling mitochondrial oxidative phosphorylation, which causes a decrease in adenosine triphosphate (ATP) synthesis. The decreased ATP inhibits the activity of the Na/K ATPase enzyme, thereby leading to a subsequent buildup of cerebral spinal fluid (CSF) and vacuolization of myelin. The excess CSF results in increased intracranial pressure, which in turn permanently damages neuronal axons. This damage to the central nervous system can cause paralysis, convulsions, and death.[1][2]

Risk of poisoning to humans and pets

[edit]

Despite risk of severe symptoms and death, most unintentional pediatric exploratory exposures (licking or tasting a pellet) have not shown serious effects, and no deaths have been reported at this time in children, though toxicity is possible if significant amounts are ingested.[3] Due to need for active metabolite generation to produce toxicity, fatal toxicity may be delayed by hours to days.[4] All cases should be managed in consultation with a local poison control center. All intentional ingestions for self harm carry significant risk of death or severe neurologic effects and require monitoring in a hospital setting.[3]

In humans the most common initial effects of unintentional exposure are nausea, vomiting, abdominal pain, and diarrhea, though delayed seizures have been reported.[3] No antidote for bromethalin is known; care is symptomatic and supportive.

In pets, signs to watch for include severe muscle tremors, hyperexcitability, fits, extreme sensitivity to being touched (hyperesthesia) and seizures that appear to be caused by light or noise.[5] Owners of animals that have eaten bromethalin accidentally should seek immediate veterinary attention and be decontaminated. Contacting an animal poison control center can help ensure that timely and appropriate therapy is started. The best treatment is decontamination, but this is only effective if started before symptoms appear.[6]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Bromethalin

View on Grokipedia
from Grokipedia
Bromethalin is a synthetic neurotoxic designed to kill rats and mice through disruption of their , providing lethality from a single feeding dose in targeted species. It is formulated as a pale, odorless crystalline powder with the chemical name N-methyl-2,4-dinitro-N-(2,4,6-tribromophenyl)-6-(trifluoromethyl)benzenamine and the molecular formula C14H7Br3F3N3O4, typically incorporated into at concentrations of 0.01% to 0.025% (0.1–0.25 mg/g). As a non-anticoagulant alternative, it targets warfarin-resistant populations and is applied in residential, agricultural, and structural settings, including stations and loose pellets. Developed in the mid-1970s by Company, bromethalin emerged as a response to growing resistance against first-generation anticoagulants like , achieving approximately 90% efficacy against resistant strains. It gained widespread use in the United States starting in the mid-1980s and became the most common following the U.S. Environmental Protection Agency's (EPA) 2008 risk mitigation measures that restricted second-generation anticoagulants for consumer use. These regulations classified bromethalin as a restricted-use in many formulations, limiting its availability to certified applicators while allowing certain consumer products with tamper-resistant stations; however, it has been banned in the since 2008. The compound's mechanism involves bioactivation in the liver to desmethylbromethalin, which uncouples mitochondrial , thereby depleting cellular (ATP) and impairing the sodium-potassium pump function. This leads to osmotic dysregulation, , increased , and demyelination of nerves, resulting in and typically within 24–36 hours in , though effects can be delayed up to several days. Bromethalin exhibits high to non-target mammals, with median lethal doses (LD50) of 0.4–0.71 mg/kg in cats (highly sensitive) and 2.38–5.6 mg/kg in dogs (moderately sensitive), causing dose-dependent syndromes such as acute convulsions (tremors, seizures) or delayed (lethargy, ). exposures are rare but can result in severe neurological effects including and , with no specific available; treatment relies on , osmotic diuretics like , and supportive care. Environmental concerns include secondary poisoning in wildlife, such as , prompting ongoing EPA evaluations of its ecological impacts.

Chemical properties

Structure and formula

Bromethalin is a synthetic organohalogen compound classified as a substituted diphenylamine, featuring a central N-methyl nitrogen atom linking two aromatic rings with multiple halogen and nitro substituents. Its molecular formula is C14H7Br3F3N3O4C_{14}H_7Br_3F_3N_3O_4, and the molar mass is 577.93 g/mol. The preferred IUPAC name for bromethalin is N-methyl-2,4-dinitro-N-(2,4,6-tribromophenyl)-6-(trifluoromethyl)aniline. Structurally, it consists of a 2,4,6-tribromophenyl group connected via the N-methyl bridge to a ring bearing nitro groups at the 2- and 4-positions and a trifluoromethyl group at the 6-position. Bromethalin is identified by 63333-35-7 and CID 44465.

Physical and chemical characteristics

Bromethalin appears as a pale white to off-white, odorless crystalline solid or powder at . It has a melting point of 150–151°C, indicating thermal stability up to moderately elevated temperatures under standard conditions. Bromethalin exhibits very low solubility in water, with a value of less than 0.01 mg/L at 20°C, which limits its mobility in aqueous environments. In contrast, it is highly soluble in various organic solvents, such as (300–400 g/L), (200–300 g/L), and acetone, facilitating its formulation in non-aqueous systems. The compound is generally stable under normal storage conditions and resistant to across 5-9. However, it degrades under exposure to light. Bromethalin has a pKa of 9.0, suggesting it exists predominantly in its neutral form under physiological conditions. Its (logP) is approximately 7.68, reflecting high that contributes to its ability to cross the blood-brain barrier.

History

Development

Bromethalin was developed in the mid-1970s by researchers at Lilly Research Laboratories, a division of , as a response to the growing problem of resistance in populations. The motivation stemmed from reports of anticoagulant resistance first identified in rats in the and , which reduced the efficacy of multi-feed rodenticides and necessitated a single-feed alternative with a novel non- mechanism. This effort aimed to provide effective control against resistant strains while minimizing bait shyness in target s such as rats and mice. The compound emerged from a systematic screening program focused on N-alkyldiphenylamine derivatives for their potential neurotoxic effects on . Key researcher Barry A. Dreikorn led the synthesis and structure-activity relationship studies, identifying bromethalin (N-methyl-2,4,6-tribromo-N-(2,4-dinitro-6-trifluoromethylphenyl)) as a highly potent candidate after evaluating various substitutions for and . The development process involved multi-step , including coupling of substituted with benzotrifluorides, followed by bromination, , and N-methylation to optimize rodent-specific lethality. Initial laboratory testing confirmed bromethalin's efficacy, with acute oral LD50 values around 2.0 mg/kg in rats, demonstrating rapid onset of neurotoxic symptoms and death within days after a single feeding at concentrations of 50-100 ppm in bait. Animal studies, including non-choice and choice feeding trials on warfarin-resistant Norway rats and house mice, achieved over 90% mortality, validating its performance against resistant strains without inducing bait avoidance. These results supported patent filings, with US Patent 4,084,004 granted in 1978 and US Patent 4,187,318 issued in 1980 to Eli Lilly and Company for the rodenticidal N-alkyldiphenylamines.

Commercial introduction

Bromethalin received approval from the U.S. Environmental Protection Agency (EPA) in 1984 as a restricted-use under the Federal , , and Act (FIFRA), marking its entry into the market as a non-anticoagulant alternative for rodent control. Initially developed by Research Laboratories, it was commercialized by , which launched the first product under the brand name in 1985. This pelleted formulation, containing 0.01% bromethalin, targeted warfarin-resistant rodents and quickly gained traction due to its single-feed efficacy. By the late 1980s, bromethalin had achieved widespread use in the United States for both urban and agricultural rodent management, particularly against Norway rats and house mice in diverse field conditions. Its adoption was driven by field trials demonstrating high efficacy, with baits placed in bait stations or broadcast applications proving effective in controlling commensal rodent populations. Over time, the product line expanded through various manufacturers, leading to continued availability under the Assault brand and similar formulations. Global expansion began in the late 1980s with introductions in by Ciba-Geigy under the trade name DORATID, featuring 0.005% to 0.01% grain-based baits and weather-resistant blocks registered in countries including , , , and . By the , bromethalin reached and other regions, with adapted formulations to meet local regulatory and environmental needs, such as varying concentrations for field . This international rollout supported its role in programs beyond the U.S. The compound's popularity surged in the post-1990s era, fueled by increasing resistance to rodenticides like and second-generation variants, positioning bromethalin as a key option for effective, resistance-independent control.

Uses

Rodent control

Bromethalin serves as a primary for controlling commensal populations, particularly targeting rats of the genus Rattus (such as Norway rats, Rattus norvegicus, and roof rats, Rattus rattus) and house mice (Mus musculus). It is especially effective against strains resistant to and other first-generation anticoagulants, addressing a key challenge in urban and agricultural pest management. The compound is formulated for single-feed application, with a typical lethal dose achieved at concentrations of 50-250 ppm in bait, often standardized at 0.01% (100 ppm) bromethalin in palatable matrices. In rats, the oral LD50 is approximately 2 mg/kg, while for mice it is approximately 5.3 mg/kg; these values underscore its high potency against target species. Key advantages of bromethalin include its rapid onset, with mortality occurring in 2-7 days post-ingestion due to its neurotoxic action disrupting cerebral edema. Unlike anticoagulants, it induces no bait shyness, as rodents do not associate the bait with illness before death, and resistance development remains low, even in populations previously exposed to other rodenticides. For effective deployment, bromethalin baits are placed in tamper-resistant stations to minimize access by non-target and domestic animals, suitable for both indoor and outdoor urban environments such as buildings, sewers, and perimeters. Stations should be positioned along runways, renewed every few days to ensure consumption, and spaced according to species—typically 8-12 feet for mice and 15-50 feet for rats—to cover active areas comprehensively. Field trials demonstrate high efficacy, with bromethalin reducing rodent populations by over 90% in controlled evaluations against Norway rats and house mice under diverse conditions, including anticoagulant-resistant infestations.

Formulation and application

Bromethalin is commonly formulated as rodenticidal baits containing 0.01% active ingredient by weight, including blocks, pellets, granules, place packs, tablets, and impregnated materials designed for palatability to target rodents. As of 2025, EPA restrictions prohibit pelleted baits in consumer markets, emphasizing enclosed or block formulations in tamper-resistant stations. These baits are often mixed with attractive substances such as grains, fats, peanut butter, or molasses to encourage consumption by rats, mice, and moles. Examples include Fastrac All-Weather Blox and Bromethalin-100 Conservation Blocks, which are solid forms optimized for weather resistance and ease of deployment. Application methods emphasize secure placement to target while minimizing non-target exposure, typically using tamper-resistant bait stations positioned in and around structures, burrows, or sewers. For rats, 2–12 blocks or place packs (ranging from 0.53 oz to 3 oz each) are placed at intervals of 16–328 feet; for mice, 1–5 units are used at 8–12 foot intervals, with direct insertion into active burrows for place packs. In sewer systems or hard-to-reach areas, may be deployed using poles, slingshots, or unmanned aerial vehicles by trained personnel, adhering to label-specified minimum amounts of 1–2 ounces per station. Safety protocols require certified applicators for professional products, while consumer products are available for general use with tamper-resistant bait stations, personal protective equipment such as gloves, long pants, and shoes, especially for loose formulations like pellets or granules that may produce dust. Product labels mandate tamper-resistant stations for most applications, warning signs at treated sites, and regular monitoring to replace consumed bait and remove remnants, with all uses limited to within 50–100 feet of buildings depending on consumer or professional status. Storage guidelines recommend keeping bromethalin products in their original containers in cool, dry areas away from , feed, and domestic supplies to prevent and maintain stability. While specific varies by product, formulations remain effective under proper conditions, with no liquid concentrates identified for sewer applications in standard registrations.

Mechanism of action

Biochemical pathway

Bromethalin, a neurotoxic , undergoes rapid absorption from the following ingestion and is primarily metabolized in the liver via P450-mediated N-demethylation to its , desmethylbromethalin (DMB). This hepatic bioactivation process converts the parent compound into DMB, which is equipotent or more toxic than bromethalin itself and serves as the primary agent responsible for cellular toxicity. The metabolism occurs efficiently, with peak plasma concentrations of bromethalin achieved within 4 hours in , facilitating quick distribution to target tissues. The core biochemical mechanism of bromethalin's toxicity involves DMB uncoupling in neuronal mitochondria, disrupting the electron transport chain's ability to drive ATP production. Normally, this process couples proton gradient dissipation to the of ADP to ATP; however, uncoupling dissipates the gradient as without ATP synthesis, leading to severe depletion in high-demand cells like neurons. ADP+Pi+nH+→ATP+H2O\text{ADP} + \text{P}_\text{i} + \text{nH}^+ \rightarrow \text{ATP} + \text{H}_2\text{O} This reaction is inhibited, resulting in ATP shortages that impair pumps and cellular . Bromethalin's high (log P ≈ 6.7) and that of DMB (log P ≈ 4.3) enable both compounds to readily cross the blood-brain barrier, leading to selective accumulation in the where mitochondrial disruption is most pronounced. Biochemical effects begin within hours of ingestion due to rapid absorption and bioactivation, with energy depletion and related cellular stress peaking at 24-48 hours as the concentrates in neural tissues.

Effects on the nervous system

Bromethalin's interference with neuronal energy metabolism leads to rapid depletion of (ATP) in the (CNS), primarily through the action of its metabolite desmethylbromethalin (DMB). This uncoupling of in neuronal mitochondria reduces ATP availability, impairing the function of sodium-potassium pumps essential for maintaining cellular ionic gradients. As a result, neurons experience cytotoxic due to sodium influx and osmotic imbalance, causing cellular swelling and disrupted neural signaling. The accumulation of fluid within myelin sheaths exacerbates these effects, resulting in intramyelinic edema and increased from swelling. This compresses neural tissues, further inhibiting axonal transmission and contributing to widespread CNS dysfunction. Pathological examinations reveal characteristic spongiform degeneration and vacuolation in the of the and , with fluid-filled spaces forming without significant or neuronal . These disruptions manifest as a progressive of neurological impairment, beginning with hindlimb weakness and , advancing to tremors and muscle rigidity, and culminating in convulsions, , and as intensifies. The onset and severity vary by species, with smaller mammals like rats and cats exhibiting faster progression due to their higher metabolic rates and greater sensitivity to ATP depletion compared to larger species such as dogs.

Toxicology

Acute toxicity in target species

Bromethalin demonstrates high acute toxicity in target rodent species, primarily rats and mice, with oral LD50 values reported as 2.11 mg/kg for male rats, 3.17 mg/kg for female rats, and 5.3 mg/kg for house mice. These values indicate that a single ingestion of a formulated bait containing approximately 0.01% bromethalin can deliver a lethal dose to most individuals, reflecting its design as a single-feed rodenticide. At doses equivalent to the LD50, death occurs within 1-3 days in , primarily due to neurotoxic effects leading to , though higher doses exceeding the LD50 can accelerate onset to 8-12 hours with preceding clonic convulsions. Sublethal exposures result in hind-limb weakness, , and loss of tactile sensation, potentially impairing mobility and survival without causing immediate fatality. Clinical signs in affected progress from initial and to more severe manifestations such as tremors and convulsions, culminating in and death from . These symptoms arise from the compound's disruption of neuronal function, though detailed biochemical pathways are addressed elsewhere. Bromethalin's resistance profile remains robust, with low documented incidence in target populations owing to its acute, single-feeding that limits survival and reproduction of exposed individuals; no cross-resistance with rodenticides has been observed, as its mechanism differs fundamentally. Post-mortem findings in poisoned rodents consistently include cerebral edema and spongy degeneration of the white matter in the brain and spinal cord, with intramyelinic edema visible on ultramicroscopic examination but without associated inflammation or neuronal destruction.

Toxicity to non-target organisms

Bromethalin presents significant risks to non-target organisms through secondary poisoning, as predators and scavengers ingest rodents containing residues of the compound and its toxic metabolite, desmethylbromethalin. This metabolite accumulates in the fatty tissues of poisoned prey, facilitating transfer up the food chain to species such as owls, hawks, foxes, and bobcats. Due to bromethalin's lipophilic properties, residues can persist and concentrate in predators, increasing the potential for biomagnification, though exact factors in terrestrial ecosystems remain understudied. Avian species are highly susceptible to bromethalin toxicity, with acute oral LD50 values indicating variable sensitivity across taxa; for example, bobwhite exhibit an LD50 of 4.56 mg/kg, while mallard ducks have a dietary LC50 of 620 mg/kg. Raptors appear particularly vulnerable, with tolerances similar to small mammals, and exposure often manifests as neurological impairment including , tremors, and hindlimb , progressing to death from within hours to days. A 2023 study detected bromethalin exposure in approximately 30% of sampled , underscoring the compound's role in wildlife morbidity. Non-target mammals, including domestic and wild species, face comparable risks to target , given similar profiles; dogs, for instance, have an oral LD50 of approximately 4 mg/kg (range 2.4–5.6 mg/kg), similar to the 2.11–3.17 mg/kg reported for rats. A 2025 retrospective study confirmed the oral LD50 in dogs as 2.4–5.6 mg/kg. Chronic sublethal exposures at levels exceeding the (NOAEL) of 0.025 mg/kg/day, such as the LOAEL of 0.125 mg/kg/day, may cause neurological effects like tremors and , potentially impairing behavior in affected populations. Ecological assessments reveal broader impacts on predator communities, with 52 documented wildlife poisoning incidents involving bromethalin between 2010 and 2018, including raptors such as great horned owls and red-tailed hawks. These exposures contribute to elevated mortality in localized populations, exacerbating declines from cumulative effects. The persistence of desmethylbromethalin in tissues, with a of approximately 5.6 days in mammalian models but detectable for weeks in adipose, prolongs secondary exposure risks and amplifies ecological disruptions.

Poisoning in humans and animals

Symptoms and diagnosis

Bromethalin poisoning in humans typically begins with initial gastrointestinal symptoms such as , , , and , often occurring within 2-24 hours of exposure. These may progress to neurological manifestations including , , agitation, , , tremors, , seizures, , and respiratory depression, particularly in cases of higher doses or intentional ingestion. Accidental exposures in children are usually mild and self-limited, resolving without severe outcomes, but severe cases can lead to and increased . In dogs and cats, symptoms vary by dose and species but generally involve central nervous system effects due to brain edema. High doses in dogs (>3.5 mg/kg) cause an acute convulsant syndrome within 4-36 hours, featuring hyperexcitability, muscle tremors, hyperthermia, grand mal seizures, and hindlimb hyperreflexia, often progressing to death. Lower doses lead to a delayed paralytic syndrome in 1-5 days, with ataxia, hindlimb paresis or paralysis, mild tremors, and possible seizures. Cats exhibit primarily paralytic signs regardless of dose, including depression, anorexia, vomiting, ataxia, decreased intestinal motility, pelvic limb weakness progressing to paralysis, tremors, seizures, and coma, with onset in 1-7 days. Symptoms can be exacerbated by stimuli like light or noise. Diagnosis of bromethalin relies on a history of exposure to the , combined with compatible clinical signs appearing within hours to days. Confirmatory testing involves detection of bromethalin or its , desmethylbromethalin, in serum, fat, liver, kidney, or brain tissue using or , though such assays are available only at specialized labs and often postmortem. Serum chemistry may show nonspecific changes, including elevated from muscle activity during tremors or seizures and from stress response; baseline blood glucose and electrolyte panels are recommended. () can reveal brain edema, such as T2 hyperintensities in , supporting the antemortem. Differential diagnosis includes other neurotoxins and must rule out rodenticides via and tests, and organophosphates or carbamates via serum or activity assays. Additional considerations encompass lead toxicity, , , , , tremorgenic mycotoxins, and other causes of seizures like trauma or infectious diseases. Prognosis is poor once neurological symptoms develop, with high fatality rates in severe cases, often requiring or resulting in death despite intervention. Milder exposures may allow recovery over weeks, though permanent neurological deficits can persist. In humans, unintentional low-dose exposures are rarely fatal, but severe ingestions carry grave risk.

Treatment and management

Treatment of bromethalin poisoning lacks a specific antidote, unlike anticoagulant rodenticides that respond to vitamin K, necessitating aggressive decontamination to prevent absorption and comprehensive supportive care to manage symptoms such as seizures and cerebral edema. Decontamination protocols prioritize early intervention; in asymptomatic animals, emesis is induced within 2-4 hours post-ingestion using agents like apomorphine (dogs) or hydrogen peroxide (dogs), followed by multiple doses of activated charcoal (1-3 g/kg orally every 6-8 hours for 1-3 days) to adsorb the toxin and counter its enterohepatic recirculation. In humans, activated charcoal is administered promptly to inhibit absorption, with gastric lavage considered under poison control guidance if ingestion is recent and large. For clinically affected patients, IV fluid therapy supports hydration and diuresis, while monitoring for electrolyte imbalances and aspiration risk is essential during charcoal administration. Supportive care focuses on neurological stabilization; anticonvulsants such as or benzodiazepines are used to control seizures in both animals and humans, with (0.25-0.5 g/kg IV over 20-30 minutes, repeatable every 4-8 hours) or hypertonic saline employed to reduce from in hydrated patients. Hospitalization for at least 24-48 hours in animals and 12 hours or more in humans with suspected significant exposure allows for continuous monitoring of neurological status, , and , with prognosis improving markedly if intervention occurs before severe symptoms develop. In veterinary cases, particularly for dogs, intravenous lipid emulsion therapy (e.g., 1.5 mL/kg 20% solution as a bolus followed by infusion) is an experimental adjunct for severe toxicity due to bromethalin's , potentially reducing serum toxin levels by up to 75% in reported cases, though it is reserved for non-responders to standard therapies and requires careful monitoring for complications. Human guidelines emphasize consultation with poison control centers for tailored management, including potential use of lipid emulsion in life-threatening neurological cases, underscoring the need for rapid and symptom control to mitigate irreversible brain damage.

Regulatory status

Approval and restrictions

Bromethalin was first registered by the (EPA) in 1984 as a and is classified as a restricted-use (RUP) for professional and agricultural applications, necessitating use only by certified applicators who have completed mandatory training programs. Consumer products containing bromethalin are limited to smaller packaging sizes, typically one pound or less, and are prohibited from sale in general retail outlets like grocery stores, further emphasizing its controlled status to minimize accidental exposures. Internationally, bromethalin is not approved for use in the under Regulation (EC) No 1107/2009, resulting in its effective ban across EU member states due to concerns over health and environmental risks. In the United States, regional variations exist, such as in , where its application is restricted solely to the control of rats and mice, with state-specific formulations required to comply with enhanced regulatory standards for structural pest management. All bromethalin products must adhere to stringent labeling requirements, including the mandatory use of tamper-resistant bait stations designed to withstand tampering by children under six years of age and domestic animals, as well as for formulations accessible to the public. Labels are required to prominently feature warnings about the dangers to pets and non-target wildlife, along with instructions for secure placement and disposal to prevent secondary poisoning. As of 2025, the EPA has opened the docket for bromethalin's registration review, assessing its ongoing safety profile in light of evolving alternatives to second-generation rodenticides, which face increasing limitations; while no nationwide bans are in place, urban use restrictions have been tightened to reduce risks in populated areas. Bromethalin's is governed by general protocols for hazardous pesticides, though it is not included in Annex III of the and thus exempt from the convention's prior informed consent procedure for exports to participating nations.

Environmental considerations

Bromethalin exhibits low solubility, <0.01 mg/L at 25°C, which restricts its mobility in aqueous environments and limits potential runoff into surface waters during typical use scenarios. In , it demonstrates high persistence with an aerobic ranging from 132 to 235 days, depending on environmental conditions, rendering it hardly mobile due to a strong affinity for (Koc ≈ 55,000 L/kg). The primary degradation product is desnitrobromethalin, which can accumulate to up to 64% of the parent compound over time, though its ecological toxicity remains incompletely characterized. Due to its lipophilic nature (log Kow ≈ 7.6), bromethalin shows significant potential for in fatty tissues of organisms, with a measured (BCF) of 120,000 in whole-body tissues under conditions. This affinity raises concerns for secondary risks within food chains, particularly for predators consuming contaminated prey shortly after bait exposure, although rapid elimination (plasma of about 5.6 days) may mitigate long-term residue buildup in some . Ecological impact studies indicate bromethalin poses moderate to high risks to non-target wildlife, especially , with U.S. Environmental Protection Agency (EPA) risk quotients (RQs) for species like the and barn owl ranging from 2.4 to 20, exceeding the agency's level of concern (LOC) of 0.5. Wildlife incident reports from 1996 to 2018 document 56 cases involving non-target species, with over 90% occurring after 2010 and a notable proportion in urban areas such as and New York, where use is intensive. Recent field studies, including a 2023 analysis of adipose tissues from 44 in , detected bromethalin residues in approximately 30% of samples across species like red-tailed hawks and barred owls, suggesting ongoing exposure that may contribute to population-level stresses in raptors. To mitigate these risks, the use of tamper-resistant bait stations is mandated for above-ground applications, effectively reducing accidental exposure to non-target wildlife by containing baits and limiting access. (IPM) approaches are recommended, emphasizing non-chemical methods such as sanitation, exclusion, and monitoring alongside targeted baiting to minimize overall environmental release and ecological disruption. Post-2020 wildlife studies highlighting bromethalin exposure in avian species have prompted increased monitoring efforts, with calls for enhanced in urban ecosystems through 2025 to better assess and long-term effects, including potential accumulation in sediments where gaps persist.

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  36. https://vcahospitals.com/know-your-pet/bromethalin-rodenticide-poisonings-in-dogs
  37. https://vcahospitals.com/know-your-pet/bromethalin-rodenticide-poisoning-in-cats
  38. https://www.aspca.org/news/poison-alert-beware-bromethalin
  39. https://mdpoison.com/media/SOP/mdpoisoncom/ToxTidbits/2014/August%202014%20ToxTidbits.pdf
  40. https://www.aspcapro.org/resource/treating-bromethalin-toxicosis
  41. https://meridian.allenpress.com/jaaha/article/52/4/265/183358/Intravenous-Lipid-Emulsion-Therapy-for-Bromethalin
  42. https://npic.orst.edu/factsheets/rodenticides.html
  43. https://ucanr.edu/blog/pests-urban-landscape/article/rodenticides-further-restrictions-2025
  44. https://www.epa.gov/pesticide-registration/child-resistant-packaging-pesticides
  45. https://downloads.regulations.gov/EPA-HQ-OPP-2016-0077-0010/content.pdf
  46. https://www.pic.int/theconvention/chemicals/annexiiichemicals
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