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At least 397 records · Page 22Linked to original sources
PubMed1988

N-3-pyridylmethyl-N'-p-nitrophenylurea ocular toxicity in man and rabbits.

Ingestion of the rat poison N-3-pyridylmethyl-N'-p-nitrophenylurea (PNU) produced ocular toxicity in three humans and in an animal model, the Dutch Belted rabbit. The electroretinogram b wave was especially susceptible to the effects of the rodenticide, and the target tissue appeared to be the retinal pigment epithelium. Injection of PNU itself did not produce ocular toxicity. The poison had to be administered orally. Gentamicin administered orally with PNU prevented the ocular toxicity. Presumably this antibiotic killed those gastrointestinal bacteria responsible for PNU's metabolism into an ocular toxin. L-tryptophan, a known antidote for the lethal effects of PNU, was an antidote for the ocular toxicity when administered orally but not when administered parenterally.

Adolescent↗
PubMed1982

Pesticide poisoning of livestock: a review of cases investigated.

The cases of suspected poisoning of livestock by a range of organic chemicals, mainly pesticides, investigated at the Central Veterinary Laboratory during the period 1977 to 1980 are reviewed. The incidences of poisoning by various types of compound and the species most at risk are discussed. Organophosphorus pesticides and rodenticides were the commonest causes of poisoning. Pesticides accounted for one in 25 of all fatal poisonings listed by the veterinary investigation diagnosis analysis (VIDA) of the Ministry of Agriculture, Fisheries and Food.

Acetaldehyde↗
PubMed1982

Effects of packaging and appearance on childhood poisoning. Vacor rat poison.

Over a 13-month period, 14 patients were hospitalized at Milwaukee Children's Hospital for rodenticide ingestions. Ten of the 14 patients ingested Vacor Rat Poison (N-3-pyridylmethyl N'-p-nitrophenyl urea). Small children could easily mistake Vacor, which resembles corn meal, for breakfast cereal. To intervene for safer packaging of toxic substances, pediatricians need to be aware of the health hazard posed to children by attractive packaging.

Child↗
PubMed1992

Difenacoum poisoning as a cause of haematuria.

A man presented with frank haematuria and a grossly prolonged prothrombin time. He was later found to have taken an overdose of difenacoum--a 'superwarfarin' rodenticide. The diagnosis was confirmed by a serum concentration of difenacoum of 0.6 micrograms ml-1. Overdosage with superwarfarins is discussed and the need for prolonged treatment with vitamin K1 highlighted.

4-Hydroxycoumarins↗
PubMed2003

Superwarfarin and glass ingestion with prolonged coagulopathy requiring high-dose vitamin K1 therapy.

A 23-year-old man was brought to the emergency department after eating four boxes of brodifacoum-containing rodenticide over a 4-day interval and pieces from approximately two bottles of glass over the previous 2 weeks. He was asymptomatic but his prothrombin time was markedly elevated with an international normalized ratio (INR) of 37.8. A plain abdominal film showed diffuse radiopaque foreign bodies, presumably glass, in the large and distal small intestines. Treatment for ingested glass consisted of stool softeners and bulk-forming laxatives. The patient developed mild gingival bleeding and received fresh frozen plasma (FFP) infusions and vitamin K1 orally. At a vitamin K1 dosage of 300 mg/day, the INR corrected to less than 2.0 and the patient was discharged taking that dosage. He returned 26 days later with hematuria and flank pain, and his INR was 189. He was administered FFP and packed red blood cells, and his vitamin K1 dosage was increased to 800 mg/day; his INR returned to baseline. Compliance with taking the vitamin K1, which required ingestion of 60-160 tablets/day, was a serious problem, requiring numerous follow-up calls and visits to the patient at home and work. At 5-month follow he was doing well. Compliance with large daily doses of vitamin K1 for treatment of "superwarfarin" ingestion may be poor because of the duration of treatment and large number of pills required. A more concentrated formulation may be advantageous for management of patients with brodifacoum poisoning.

4-Hydroxycoumarins↗
PubMed1989

Studies on the fate of flocoumafen in the Japanese quail (Coturnix coturnix japonica).

1. 14C-Flocoumafen, administered to Japanese quail as a single oral or i.p. dose, was rapidly and extensively eliminated in excreta; most was eliminated within 24 h. Extensive metabolism of the rodenticide was seen, with at least 8 metabolites detected; unchanged flocoumafen comprised 9% dose. The elimination kinetics and metabolic profiles were qualitatively similar after oral and i.p. dosing. 2. The major metabolites (60% dose) were labile to beta-glucuronidase, liberating aglycones with identical chromatographic mobilities to those of the unchanged flocoumafen isomers. 3. Radioactivity was retained mostly in the liver; largely as unchanged flocoumafen associated with the mitochondrial and microsomal fractions. Elimination of radioactivity from most tissues was biphasic with an initially rapid depletion (5 days) followed by a slow terminal elimination phase. The elimination half life from liver was greater than 100 days. 4. Livers of quail receiving extended dietary exposure to flocoumafen at 5, 15 and 50 ppm had concentrations of flocoumafen (1.0 nmol/g) that were independent of dose, indicating a capacity-limited binding site. These hepatic concentrations were similar to those after a single oral dose and were also similar to those in rats. The data indicate the presence in quail liver of a saturable high affinity flocoumafin binding site with similar characteristics and capacity to that in the rat. 5. The selective toxicity of flocoumafen to rats (highly toxic) and quail (moderately toxic) appears to arise from differences in metabolism rather than from anticoagulant binding in the liver. When hepatic binding sites of rats are saturated anticoagulant action becomes lethal, whereas quail are able to survive and extensively metabolize the compound.

4-Hydroxycoumarins↗
PubMed1988

Evaluation of coagulation factor abnormalities in long-acting anticoagulant overdose.

Newer Rodenticides of the long-acting anticoagulant or "superwarfarin" class are gaining popularity. Since few cases of severe, prolonged anticoagulation after ingestion have been reported, the course of toxicity is not precisely understood. In this case of an intentional ingestion of brodifacoum, a longitudinal analysis of specific coagulation factor derangements was carried out in an attempt to guide a future treatment strategy for this type of toxicity. Results of this analysis demonstrated a profound decrease in levels of factors II, VII, IX, and X, lasting at least 43 days post ingestion. Treatment with subcutaneous vitamin K1 in doses up to 100 milligrams per day was without complication and was effective in reversing the coagulopathy produced by brodifacoum.

4-Hydroxycoumarins↗
PubMed1998

Ultrastructure of neuromuscular junction in vacor-induced diabetic rats.

OBJECTIVES: Rodenticide Vacor causes a severe peripheral neuropathy in humans. Electrophysiologic studies on a peripheral motor nerve-skeletal system of Vacor-treated rat showed decreased amplitude of muscle action potential without conduction velocity abnormalities. The ultrastructural studies of the neuromuscular junction were performed to clarify the anatomic site of the Vacor-induced peripheral neuropathy in male Wistar rats. METHODS: After oral administration of a single dose of Vacor, 80 mg/kg of body weight, to the experimental animals, neuromuscular junctions within the interosseous muscles of the hind foot were observed in time. RESULTS: No axon terminal change was noted until 24 hours after the administration of Vacor. Remarkable loss of presynaptic vesicles and swollen endoplasmic reticulum in the axon terminal were developed at 3 days after Vacor treatment. Progressive degenerative changes consisting of marked loss of presynaptic vesicles, focal disruption of membrane in the axon terminal with disappearance of the number of the damaged axon terminal appeared, and flattening of postsynaptic folds was also seen. CONCLUSIONS: These results suggest that degenerative changes in axon terminal at neuromuscular junction may contribute to the peripheral neuropathy developed in the early phase of Vacor poisoning.

Animals↗
PubMed1975

Fluoroacetamide (1081) oisoning in wild birds.

An outbreak of poisoning in four greylag geese (Anser anser) and 35-45 teal (Anas crecca) is described. Laboratory findings led to the conclusion that a wheat bait containing the rodenticide fluoracetamide (1081) caused the poisoning. Circumstantial evidence incriminated fluoracetamide as the cause of death in white-fronted geese (Anser albifrons), mallards (Anas platyrhynchos), and chukars (Alectoris chukar).

Acetamides↗
PubMed2005

Zinc phosphide intoxication of wild turkeys (Meleagris gallopavo).

Zinc phosphide (Zn3P2) is a rodenticide used to control a variety of small mammal species. It is available over-the-counter or as a restricted-use pesticide depending on how it is to be applied. The toxicity of Zn3P2 is dependent on the species exposed, whether the animal is able to vomit or not, and whether it is ingested on a full or empty stomach. Nontarget species can be exposed through inadvertent or intentional product misapplication. In this article we describe four mortality events in which wild turkeys (Meleagris gallopavo) were believed to have been intoxicated following the ingestion of baits containing Zn3P2.

Animals↗
PubMed2000

Surreptitious superwarfarin ingestion with brodifacoum.

Physicians must have a high index of suspicion when patients have unexplained prolongation of the prothrombin time and bleeding in the absence of detectable warfarin. Several common rodenticides contain modified versions of warfarin that are not detectable in standard warfarin assays. We present a case of surreptitious brodifacoum ingestion in a patient who had years of unexplained bleeding and negative warfarin levels.

4-Hydroxycoumarins↗
PubMed2000

[Pesticide poisoning].

Pesticide intoxications are mainly accidental with a benign course, such as ingestions of diluted fertilizers or low concentration antivitamin K rodenticides, ant-killing products or granules of molluscicides containing 5% metaldehyde. Voluntary intoxications by chloralose, strychnine, organophosphorus or organochlorine insecticides, concentrated anti-vitamin K products, herbicides such as paraquat, chlorophenoxy compounds, glyphosate or chlorates may be severe. Toxicity is due to active substances but also to solvents or surfactants included in the composition. Analysis done in a toxicology laboratory help in establishing diagnosis, prognosis and treatment. Poison centres may be called constantly to help for the evaluation of these intoxications.

Acetaldehyde↗
PubMed1975

Problems of rodent control in rural tropical areas.

Rodent control strategies, techniques, and research needs in rural tropical environments are reviewed and discussed with special reference to Mastomys natalensis, the possible reservoir of Lassa fever in West Africa.Public health rodent problems are far more serious and widespread in rural tropical areas than in developed countries. In the latter, only the commensal rodents constitute a major problem, whereas in rural tropical areas, native semidomestic species also serve as disease reservoirs and sources of infection to man. The success of rodent control programmes in developed countries depends in large part on the willingness and ability of people and governments to spend relatively large sums on research and control, on an acquired intolerance of people to rats and disease, and on a substantial economic base. These prerequisites are not usually to be found in rural tropical areas. Consequently, the rodent control techniques and programme organizations of developed countries are not directly applicable to such areas, even though the principles are the same. For this reason, it is suggested that a well-funded, integrated research and control programme should be undertaken in a known Lassa fever area, stressing public education, personnel training, and environmental management as well as rodenticidal approaches.

Africa, Western↗
PubMed2000

Acute inhalation toxicity study of 2-fluoroacetamide in rats.

One of the most potent rodenticides is 2-fluoroacetamide (2-FA). Toxicity of this chemical is well documented. However, its inhalation toxicity data is not available in the literature. Hence, acute inhalation toxicity study was carried out by exposing male and female rats to aerosols of 2-FA at different concentrations for 4 h in a dynamically operated whole body inhalation exposure chamber. During and after the inhalation exposure the rats were less active, and showed mild tremors and convulsions. At higher concentrations the rats died after 2-3 days. The estimated 4-h LC50 for male and female rats was 136.6 and 144.5 mg.m-3 respectively. Exposure to 0.7 LC50 for 4 h duration showed an increase in the liver weight of male and female rats 7 days after exposure. Various haematological and biochemical variables determined were within the normal limits. However, histological findings showed injured lung as indicated by desquamation and necrosis of the epithelium of the respiratory tract. Marked hypertrophy of hepatocytes displaying strong acidophilic granulated cytoplasm was observed. Focal dilatation of renal proximal tubules in kidney with cytoplasmic vacuolation, and irregularly placed pyknotic nuclei were seen. The present study shows that 2-FA is a highly toxic chemical through the inhalation route based on the LC50 value. Consequently necessary precautions should be taken during its handling.

Animals↗
PubMed2002

Intoxication with sodium monofluoroacetate (compound 1080).

The highly toxic sodium monofluoroacetate (SMFA) was banned as a rodenticide in the U.S. in 1972. We report the first case of intentional ingestion in this country in over 15y. A 47-y-old male was brought to the emergency room status post tonic clonic seizure. At 34 h post ingestion, he responded ony to noxious stimuli and at 48 h, he was unresponsive to painful stimuli, was intubated and placed on a ventilator. Over the following 3 d, he was became minimally responsive to external stimuli with bouts of agitation and hypertension. Two days later he was discharged with no evidence of neurologic sequelae. We report this patient to increase awareness of SMFA toxicity, and its ability to cause anion gap metabolic acidosis.

Drug Overdose↗
PubMed2002

[Serial determination of crimidine by HPLC/SE/SM in a patient ingesting a "mouse trap"].

Crimidine (2 chloro, 4 methyl, 6 dimethyl amidopyrine) is a synthetic rodenticide which causes acute poisonings after oral ingestion in human. Major toxic effects are consciousness disorders, hypertonic coma and convulsions. Toxic level in human is about 5 mg/Kg. An intoxication case is reported. Five serums collected at different times were analyzed with HPLC/ES/MS. Crimidine was extracted with ethylacetate with recovery over 80%. Linearity was up to 800 micrograms/L. LOQ and LOD were 0.5 and 0.3 microgram/L respectively. The coefficients of variation were less than 10% for repeatability and reproductibility. Serum levels varied from 368 micrograms/L for H0 to 64 micrograms/L for H10 and elimination of crimidine was linear in time.

Chromatography, High Pressure Liquid↗
PubMed1960

Epidemiology of accidental poisoning.

In San Jose, California, studies of cases of accidental poisoning showed that the greatest hazard was to children 1 through 3 years of age. Drugs accounted for half the cases, household products for another third, and insecticides and rodenticides and others for the remainder. Most often poison material was within easy reach of the children. An analysis of families in which an accident occurred indicated that accidental poisoning might happen to any family. Since there was little after-effect of poisoning in cases in which treatment was obtained promptly, education directed toward getting prompt treatment seems most advisable. Community agencies interested in poison control need to focus their attention on parents of pre-school children.

California↗