Pival, an anti-coagulant rodenticide.
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The effectiveness of the single-dose poison treatments of farm rat infestations, analysed by comparing the weights of the post-treatment census bait takes in covariance with the weights of the prebait takes, showed that treatments with 2-5% zinc phosphide, 0-3% thallium sulphate or 0-3% gophacide were equally effective and significantly better than were treatments with 1% zinc phosphide or 0-1% thallium sulphate. The methodology and sensitivity of different analyses are also considered.
Short laboratory feeding tests were carried out with the anticoagulants warfarin, difenacoum, and brodifacoum on a number of European rodent species: Clethrionomys glareolus, Microtus agrestis, M. arvalis, Apodemus flavicollis, A. sylvaticus, Mus musculus, Rattus rattus and R. norvegicus. It was found that the toxicity to all species was highest with brodifacoum and lowest with warfarin, and that only 0.005% brodifacoum would give a complete mortality in most species after one day's feeding. The potential of this compound for the control of microtine field rodents is suggested.
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Three probabilistic models were developed for characterizing the risk of mortality and subacute coagulopathy to Poouli, an endangered nontarget avian species, in broadcast diphacinone-baited areas on Hawaii, USA. For single-day exposure, the risk of Poouli mortality approaches 0. For 5-d exposure, the mean probability of mortality increased to 3% for adult and 8% for juvenile Poouli populations. For Poouli that consume snails containing diphacinone residues for 14 d, the model predicted increased levels of coagulopathy for 0.42 and 11% of adult and juvenile Poouli populations, respectively. Worst-case deterministic risk characterizations predicted acceptable levels of risk for nonthreatened or endangered species such as northern bobwhite quail and mallards. Also, no acute toxicity was noted for snails and slugs that feed on diphacinone baits.
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1. Appreciable penetration of radioacticity occurred through rat skin following percutaneous administration of 14C-flocoumafen. At 7 days after dosing 12% of the administered radioactivity remained at the site of application, while 25% was located in the liver as unchanged flocoumafen. 2. Excretion of flocoumafen metabolites via the urine accounted for 10% dose over the 7 day experiment, this is some 30-fold greater than that seen after a single oral dose. 3. Unchanged flocoumafen comprised the major product detected in faeces. Biliary elimination was a very minor route of excretion and did not account for all of the unmodified flocoumafen present in faeces. 4. Considerable amounts of unchanged flocoumafen found associated with the contents of the large intestine after intraperitoneal administration to rats fitted with biliary fistulae indicates that, in the intact rat, flocoumafen enters the intestine by a non-biliary intestinal excretion mechanism.
The oral LD50 of indomethacin for a seven-day observation was found to be 12.58 +/- 1.15 mg/kg. At LD10 of 6.61 mg/kg, a dose to weight ratio of 28 was obtained for a 240 g rat, while at a maximum single dose of 3 mg/kg in man it is only 0.04. Neither diazepam nor phenobarbital influenced death at the doses of both drugs used. However, cholestyramine 2 g/kg/day was found to protect by 50% from the LD100 of indomethacin. Gross pathological studies showed dose-dependent ulceration and perforation (P < 0.001, 12 vs 24 mg/kg) and such lesions occurred in starved rats, were low in bile duct-ligated compared to sham-operated rats (P < 0.001) and were also low in cholestyramine-treated rats. Indomethacin-induced lethality in rats was found to be dose-dependent.