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PubMed2003

Rat poison and food security in the People's Republic of China: focus on tetramethylene disulfotetramine (tetramine).

The last several years have seen a large number of mass poisonings in mainland China, particularly those caused by illicit rodenticides. One rat poison, tetramine (tetramethylene disulfotetramine) is responsible for a great percentage of death and injury in the People's Republic of China (PRC). Tetramine is an acutely toxic substance with human oral toxicity estimated as low as 0.1 mg/kg, and is widely available in open markets in mainland China--this despite being prohibited for manufacture or sale in the PRC. Being a GABA antagonist, and having an extremely potent effect on the brain stem, many victims can quickly fall into convulsions and die within hours following ingestion. With no known effective antidote at this time, clinical data from the PRC show that acute cases of tetramine poisoning are extremely difficult to treat. The widespread use of tetramine--including its reported sale at a Malaysian outdoor market in September 2002--could exacerbate its hazard to public health, particularly in those areas having large overseas Chinese populations.

Bridged-Ring Compounds↗
PubMed1981

Ocular ergotamine tartrate toxicity during treatment of Vacor-induced orthostatic hypotension.

A 20-year-old woman developed severe orthostatic hypotension after attempting suicide by ingesting the rodenticide, Vacor. Oral ergotamine tartrate, 6 mg a day, was useful in treating the orthostatic hypotension. However, a bilateral toxic retinal vasculopathy, consisting of a severe generalized vasoconstriction and mild macular edema, occurred within three weeks. Additional findings were an extinguished electroretinogram and a reduced dark-adaptation retinal sensitivity; because we performed these two tests after instituting ergotamine therapy we do not know whether to attribute their abnormal results to Vacor toxicity, ergotamine toxicity, or a combination of the two.

Adult↗
PubMed1995

Biochemical biomarkers in ecotoxicology--some recent developments.

Biochemical biomarkers measure the exposure of organisms to environmental chemicals. They can also provide measures of toxic effect, e.g. where they are based on molecular mechanisms which underly toxicity. Ideally, biomarkers should be sensitive, specific, simple to use and suitable for the assay of material obtained by non-destructive sampling procedures (e.g. of blood). Recently, there has been encouraging progress in the development of several different types of biomarker assays: (1) The measurement of inhibition of serum 'B' esterases to monitor exposure of birds to organophosphorus insecticides. (2) The measurement of DNA damage caused by aromatic hydrocarbons. DNA adduct formation has been studied using the 32P-postlabelling technique. Several other techniques are currently under investigation. (3) The measurement of disturbances to the transthyretin-retinol binding protein complex caused by a metabolite of 3,4,3',4',tetrachlorobiphenyl. (4) The measurement of precursors of clotting proteins in blood following the inhibition of the Vitamin K cycle by anticoagulant rodenticides. Of these examples, the first is only a biomarker of exposure but the remaining three examples are, in principle, biomarkers of toxic effect since they all represent measures of molecular mechanisms which underly toxicity. Biochemical biomarkers have considerable potential for measuring effects of chemicals under field conditions--especially where carefully selected combinations of them are used.

Animals↗
PubMed1990

"Superwarfarin" ingestion. A new problem in covert anticoagulant overdose.

For the attention of psychiatric consultants, brodifacoum, a new longer-acting, warfarin-like oral anticoagulant rodenticide, has been used for suicide attempts. The overdose potential with brodifacoum is serious since it is readily available without prescription, and bleeding complications last for weeks to months after a single ingestion. This article reports a case of ingestion and reviews four similar cases from medical literature. Also reviewed are details about mechanism of action, procedures for diagnosis, and treatment requirements. Also, characteristics of persons who ingest long-acting anticoagulants appear to differ from those who ingest short-acting anticoagulants reported from earlier literature.

4-Hydroxycoumarins↗
PubMed1993

Simple and rapid method for the determination of the diastereomers of difenacoum in blood and liver using high-performance liquid chromatography with fluorescence detection.

A rapid and sensitive high-performance liquid chromatographic method for the analysis of cis and trans diastereomers of the anticoagulant rodenticide difenacoum has been described. The methodology demonstrates potential for the analysis of diastereomers of related 4-hydroxycoumarin anticoagulants. Separations were achieved by reversed-phase chromatography on a Zorbax ODS column with gradient elution using acetonitrile-water, modified with 0.1% acetic acid, as the mobile phase. Detection of the analytes was effected by fluorescence at excitation and emission wavelengths of 310 and 390 nm, respectively. Sample preparation from both plasma and liver has been simplified to reduce preparation time and manipulation. The minimum detectable concentration of each diastereomer was 5 ng/ml. Recoveries of 100% were obtained from plasma and 93% from liver tissue. This method has been used for the investigation of the pharmacokinetics of difenacoum diastereomers in rats, and for investigation of unexplained hypoprothrombinaemic events encountered clinically.

4-Hydroxycoumarins↗
PubMed1993

The development of a blood clotting response test for discriminating between difenacoum-resistant and susceptible Norway rats (Rattus norvegicus, Berk.).

1. A new test for identifying levels of difenacoum resistance in the Norway rat is described, based upon the differential physiological response to difenacoum administration. 2. This test is based on changes in blood clotting activity over 4 days, following administration of the rodenticide difenacoum in conjunction with menadione (vitamin K3). 3. The anticoagulant effect is reduced only in rats that are resistant or tolerant to difenacoum. 4. This test procedure is quicker than traditional feeding tests, and identifies the degree of resistance in both laboratory and wild rats that have difenacoum resistance genes.

4-Hydroxycoumarins↗
PubMed2005

Planned complex suicide: report of three cases.

This article presents three planned complex suicide cases. The first case was a 46-year-old man, who had taken some antidepressant and antipsychotic drugs before cutting his right wrist and ingesting a large amount of concentrated hydrochloric acid. In the second case, a 34-year-old man was found dead in his home, hanging by his neck, with a suicidal stab wound on the left side of the chest. In the third case, a 22-year-old woman was found dead, hanging by her neck from a ceiling beam of her grandmother's a storage room, after taking of a solid rodenticide. The histories revealed psychiatric problems in all cases. The investigation of scene, the method employed, the autopsy findings and the interview with their relatives altogether pointed toward a suicidal etiology.

Administration, Oral↗
PubMed2006

Alpha-chloralose poisoning in dogs and cats: a retrospective study of 33 canine and 13 feline confirmed cases.

Alpha-chloralose (AC) is an anaesthetic compound also used as a rodenticide, and has dose-dependent central nervous system mixed effects of excitation and depression. The objectives of this study were to detail the clinical and clinicopathological characteristics, as well as the treatment and prognosis, of AC toxicosis in dogs and cats. Medical records were retrospectively reviewed for AC poisoning between the years 1989 and 2004, and 33 dogs and 13 cats were included in the study. The most common clinical signs were seizures, muscle tremor, hyperaesthesia, hypothermia, salivation, myosis, stupor, coma and ataxia. Coma was more common, while salivation and ataxia were less common in cats compared to dogs. Although hypothermia was very common, especially in cats (90.9%), hyperthermia was frequently observed in dogs (21%). Treatment in all patients was supportive and symptomatic, and the most commonly used anticonvulsants were diazepam and barbiturates; however, severe unresponsive seizures in three dogs had to be controlled with inhalant gas anaesthesia. The hospitalisation period was 1-3 days, and the overall mortality rate was 6.5%. Alpha-chloralose poisoning seems to have a favourable prognosis in dogs and cats.

Age Factors↗
PubMed1993

Spontaneous hemorrhage associated with accidental brodifacoum poisoning in a child.

A 36-month-old child had spontaneous hemorrhage from her nose, mouth, and urinary tract, and a fall in hemoglobin of 20 gm/L (2 gm/dl). The prothrombin time and partial thromboplastin time were markedly prolonged with a decrease in the vitamin K-dependent factors. The child had ingested brodifacoum, a long-acting rodenticide. Prolonged follow-up and treatment with vitamin K were necessary.

4-Hydroxycoumarins↗
PubMed1997

Field evidence of secondary poisoning of foxes (Vulpes vulpes) and buzzards (Buteo buteo) by bromadiolone, a 4-year survey.

This paper presents the result of a 4 year survey in France (1991-1994) based on the activity of a wildlife disease surveillance network (SAGIR). The purpose of this study was to evaluate the detrimental effects of anticoagulant (Ac) rodenticides in non-target wild animals. Ac poisoning accounted for a very limited number of the identified causes of death (1-3%) in most species. Predators (mainly foxes and buzzards) were potentially exposed to anticoagulant compounds (especially bromadiolone) via contaminated prey in some instances. The liver concentrations of bromadiolone residues were elevated and species-specific diagnostic values were determined. These values were quite similar to those reported in the literature when secondary anticoagulant poisoning was experimentally assessed.

4-Hydroxycoumarins↗
PubMed2000

Stimulated pulmonary cell hyperplasia underlies resistance to alpha-naphthylthiourea.

The rodenticide alpha-naphthylthiourea (ANTU) causes pulmonary edema and pleural effusion that leads to death via pulmonary insufficiency. Rats become resistant to the lethal effect of ANTU if they are first exposed to a small, nonlethal dose of ANTU. Young rats are also resistant to ANTU. The mechanism by which rats develop resistance by a prior, small dose exposure has yet to be determined. Growth factor induced-pulmonary hyperplasia has been demonstrated to attenuate ANTU-induced lung leak. We hypothesized that a small dose of ANTU protects against a large dose through pulmonary cell hyperplasia induced by the protective dose. Furthermore, we hypothesized that this hyperplasia is associated with altered transcription of growth factors. Male Sprague-Dawley rats (175-225 g) were treated with a low dose of ANTU (5 mg ANTU/kg; ANTU(L)) 24 h before challenge with a 100% lethal dose of ANTU (70 mg ANTU/kg; ANTU(H)) resulting in 100% protection against the lethal effect of ANTU(H). ANTU(L) protection against ANTU(H) lasted for 5 days, slowly phased out, all being lost by day 20. Injury was assessed by estimating pulmonary vascular permeability and through histopathological examination. ANTU(H) alone resulted in an increase in pulmonary edema leading to animal death. However, injury was prevented if the rats were first treated with ANTU(L). There was a stimulation of pulmonary cell hyperplasia in the lungs of ANTU(L) treated rats as measured by [3H]-thymidine and bromodeoxyuridine incorporation. Treatment with the antimitotic agent colchicine abolished ANTU(L)-induced resistance to ANTU(H). ANTU resistant rats were also resistant to the lethal effect of paraquat. Paraquat is not taken up by pneumocytes if they are undergoing hyperplasia. ANTU(L) administration resulted in an up regulation of gene transcription for keratinocyte growth factor, transforming growth factor-beta, keratinocyte growth factor receptor and epidermal growth factor receptor as determined through reverse transcription-polymerase chain reaction. A significant increase in transforming growth factor-alpha was not observed. These findings collectively suggest that ANTU(L)-induced pulmonary cell hyperplasia underlies resistance to ANTU(H). Furthermore, the stimulation of hyperplasia may be due to altered growth factor and growth factor receptor expressions.

Animals↗
PubMed1997

Determination of warfarin in the yolk and the white of hens' eggs by reversed-phase high-performance liquid chromatography.

A procedure for the determination of warfarin, an anticoagulant rodenticide, in the white and the yolk of hens' eggs, using reversed-phase high-performance liquid chromatography is described. Liquid chromatography was performed on an octadecylsilane cartridge using methanol and ammonium acetate triethylamine buffer as the mobile phase, with UV detection at 281 nm. Samples (5 g) were analysed after liquid-phase extraction using a mixture of acetone and diethyl ether. Linearity, precision and accuracy of the method were determined in the range of 0.5-8.0 microg. Limits of quantitation for warfarin in the white and the yolk were 0.020 and 0.015 microg/g, respectively. Mean recoveries of warfarin from spiked white and yolk samples were 84.6 and 87.4%, respectively. The analytical method was applied to a fourteen-day experimental study conducted in laying hens that had been orally dosed with warfarin.

Animals↗
PubMed1999

Testing for alpha-chloralose by headspace-GC/MS. A case report.

A case is presented involving an acute fatality resulting from self-administered alpha-chloralose, a rodenticide. A 18-year-old man was found dead at home, with several stains of vomit on the carpet. An empty box of three bags of 5 g 100% alpha-chloralose (Corbeaux nuisibles, Rhône Poulenc) was found near the body. The compound was identified and quantified by headspace gas chromatography coupled to mass spectrometry. Alpha-chloralose was converted by concentrated sulphuric acid into chloral, a volatile compound, that was, after chromatography on a HP5-MS capillary column, identified by the following ions, m/z 82, 111 and 148. Peripheral blood concentration was 175.7 mg/l. Alpha-chloralose was quantified in several tissues, indicating kidney sequestration. No other drugs, including ethanol, were detected.

Adolescent↗
PubMed1996

Spontaneous hemoperitoneum from brodifacoum overdose.

Brodifacoum is a 4-hydroxycoumarin derivative that is commonly used as a rodenticide. Human exposures have produced severe coagulopathies resulting in hematuria, gastrointestinal bleeding, intracranial hemorrhage, and death. This is the first report of spontaneous hemoperitoneum secondary to brodifacoum ingestion. The patient was successfully managed with fresh frozen plasma, packed red blood cells, and vitamin K1. No surgical intervention was performed. The patient required ongoing daily vitamin K1 therapy for longer than 6 months.

4-Hydroxycoumarins↗
PubMed2001

Pesticide toxicosis in the horse.

Toxicosis from pesticides rarely occurs in horses and is usually the result of inappropriate pesticide use or handling by humans. Organophosphorus and carbamate insecticides inhibit acetylcholinesterase and are the insecticide class most frequently associated with toxicosis in domestic animals. Metaldehyde is a molluscicide, and zinc phosphide is a rodenticide, both of which have caused toxicosis in horses. All three of these pesticides affect the nervous system of horses and can be fatal if not treated promptly.

Acetaldehyde↗
PubMed1978

Field trials of brodifacoum (WBA 8119) against the house mouse (Mus musculus L.).

The anticoagulant rodenticide brodifacoum was tested against house mice (Mus musculus L.) infesting farm buildings. In six trials, treatment success was assessed from the results of census baitings conducted before and after treatment. With 0.005% brodifacoum in canary seed/corn oil bait, the control achieved ranged between 92.7% and 100%, mean 98.8%. Two mouse populations were eradicated in 3 to 4 weeks but a few individuals survived each of the other four treatments which lasted 6 weeks. The effectiveness of brodifacoum against mice is compared with that of 0.1% calciferol and 0.025% warfarin in combination. It is concluded that brodifacoum and calciferol warfarin are equally effective in controlling M. musculus but that brodifacoum treatments need to be conducted for a relatively longer period.

4-Hydroxycoumarins↗
PubMed1974

Field trials of calciferol against warfarin resistant infestations of the Norway rat (Rattus norvegicus Berk).

The effectiveness of calciferol (vitamin D(2)) against Rattus norvegicus was investigated in field trials on twenty-three farms with rat infestations partly resistant to warfarin. At 0.01% combined with warfarin at 0.025% no rodenticidal effect of the calciferol was discernible. At 0.025% with warfarin at the same concentration, results were better, but not appreciably better than is often obtained with warfarin alone against resistant rat populations. When the concentration of calciferol was stepped up to 0.1%, four out of five treatments in which the poison was applied directly gave complete control. The fifth may have partly failed because of poison shyness caused by under-baiting. Five out of six more treatments done after ;pre-baiting' were also successful. The sixth failed for reasons unconnected with the choice of poison.Six further infestations that were not responding adequately to warfarin treatments were quickly controlled when, in three instances, calciferol at 0.1% was used instead and, in three more, it was used together with warfarin. It is concluded that calciferol at 0.1% is an effective poison against R. norvegicus either combined with warfarin or not, but that because at 0.1% its effect is subacute rather than chronic, there may be a case in some environments for using it only after pre-baiting.

Animals↗
PubMed1986

Field trials of flocoumafen against warfarin-resistant infestations of the Norway rat (Rattus norvegicus Berk.).

The anticoagulant rodenticide flocoumafen was tested against warfarin-resistant Norway rats (Rattus norvegicus Berk.) infesting farm buildings. Complete control was obtained in 10-21 days (mean 14.2 days) in six treatments in which baits poisoned with 0.005% flocoumafen were maintained, in surplus, until rats ceased to feed from them. A further six treatments, in which the application of poisoned bait was restricted to periodic placements of 50 g, were also completely successful in 15-30 days (mean 21.0 days). Less poisoned bait was used in the restricted flocoumafen treatments than in the unrestricted treatments but the time taken to control the rat infestations was significantly longer.

4-Hydroxycoumarins↗