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PubMed1979

A carcinogenicity study of pesticide dieldrin in hamsters.

Syrian golden hamsters were fed for their lifespan a diet containing 0, 20, 60 and 180 parts per million (ppm) Dieldrin. Tumour-bearing animals totaled 13% among control females and ranged between 3-15% in treated females. Eight per cent of male controls had tumours and between 16-23% of treated males. Incidences of endocrine organ tumours were comparable in all groups. A hepatoma was found in 1 female and 1 male led 180 ppm Dieldrin. The present results show that hamsters tolerate higher doses of Dieldrin than do mice and rats. No significant tumour incidence was observed in treated versus control Syrian golden hamsters.

Animals↗
PubMed1999

Cancer dose-response modeling of epidemiological data on worker exposures to aldrin and dieldrin.

The paper applies classical statistical principles to yield new tools for risk assessment and makes new use of epidemiological data for human risk assessment. An extensive clinical and epidemiological study of workers engaged in the manufacturing and formulation of aldrin and dieldrin provides occupational hygiene and biological monitoring data on individual exposures over the years of employment and provides unusually accurate measures of individual lifetime average daily doses. In the cancer dose-response modeling, each worker is treated as a separate experimental unit with his own unique dose. Maximum likelihood estimates of added cancer risk are calculated for multistage, multistage-Weibull, and proportional hazards models. Distributional characterizations of added cancer risk are based on bootstrap and relative likelihood techniques. The cancer mortality data on these male workers suggest that low-dose exposures to aldrin and dieldrin do not significantly increase human cancer risk and may even decrease the human hazard rate for all types of cancer combined at low doses (e.g., 1 microgram/kg/day). The apparent hormetic effect in the best fitting dose-response models for this data set is statistically significant. The decrease in cancer risk at low doses of aldrin and dieldrin is in sharp contrast to the U.S. Environmental Protection Agency's upper bound on cancer potency based on mouse liver tumors. The EPA's upper bound implies that lifetime average daily doses of 0.0000625 and 0.00625 microgram/kg body weight/day would correspond to increased cancer risks of 0.000001 and 0.0001, respectively. However, the best estimate from the Pernis epidemiological data is that there is no increase in cancer risk in these workers at these doses or even at doses as large as 2 micrograms/kg/day.

Aldrin↗
PubMed1995

Genotype, environment and the asymmetry phenotype. Dieldrin-resistance in Lucilia cuprina (the Australian sheep blowfly).

Dieldrin-resistant (Rdl/Rdl and Rdl/+) and susceptible (+/+) phenotypes of Lucilia cuprina were scored for departures from bilateral symmetry for bristle characters after development at different temperatures, larval densities or concentrations of dieldrin. The asymmetry phenotype of resistant flies was dominant and independent of developmental temperature and larval density. The asymmetry of susceptibles increased for temperatures and larval densities above and below standard rearing conditions. A positive correlation was observed between asymmetry score and dieldrin concentration for all genotypes. The susceptible phenotype did not attain the asymmetry score of resistant in any environment. Resistant phenotypes showed an antisymmetric pattern in each environment; fluctuating asymmetry was observed for susceptibles. The relevance of the results of genetic and general or specific environmental stresses to estimates of developmental perturbation is discussed.

Animals↗
PubMed1977

Mode of inheritance of dieldrin resistance in Anopheles farauti No. 1 and A. farauti No. 2.

The mode of inheritance of dieldrin resistance was studied in Anopheles farauti No. 1 and A. farauti No. 2. In both these species a susceptible strain was crossed with a resistant strain and F1 individuals backcrossed to the susceptible parental strain. After exposure to 0-4% dieldrin for one hour the survivors were again backcrossed to the susceptible. After successive backcrosses it was found that in both species dieldrin resistance was determinded by a single, semi-dominant gene which was not sex-linked.

Animals↗
PubMedDate not supplied

Reduced recovery of dieldrin residues-a shortcoming of sulfuric cleanup of biological samples.

Reduced quantitative recovery of dieldrin (1, 2, 3, 4, 10, -10-hexachloro-6, 7-epoxy-1, 4, 4a, 5, 6, 7, 8, 8a-octahydro-1, 4-endo, exo-5, 8-dimethanoaphthalene) while using concentrated sulfuric acid for the cleanup of the extracted samples, has been investigated by gas-liquid chromatography and infrared (IR) spectroscopy. In vitro studies have shown that the servere breakdown in the recovery of dieldrin can be checked if 65% (v/v) H2SO4 is used as opposed to the concentrations greater than 70% sulfuric acid, the epoxide ring attached to the norbornene nucleus of dieldrin undergoes rearrangement to form keto-dihydroaldrin.

Dieldrin↗
PubMed1979

Hazards to wintering geese and other wildlife from the use of dieldrin, chlorfenvinphos and carbophenothion as wheat seed treatments.

Chemical treatments of cereal seeds are used in the United Kingdom to prevent damage by a number of pests including the wheat bulb fly, which is a serious pest of winter wheat. The persistent organochlorine dieldrin was introduced in the 1950s as a seed treatment but caused the death of large numbers of grain eating birds and gave rise to unacceptable environmental contamination. The withdrawal of dieldrin as a seed treatment was made possible by the introduction of two less persistent organophosphate insecticides, chlorfenvinphos and carbophenothion. Although the introduction of these chemicals has been beneficial in reducing environmental contamination, some side-effects on wildlife have still been discernible and carbophenothion has now been withdrawn from use in Scotland owing to the deaths of wintering geese from carbophenothion poisoning. Subsequent laboratory studies have demonstrated that Anser geese are particularly susceptible to carbophenothion poisoning, and the underlying biochemical mechanism has been investigated. The fundamental problem of species variation in toxicity among the organophosphorus and carbamate pesticides which this investigation illustrates presents difficulties for registration authorities when they are considered for clearance for agricultural use. The implications of the environmental problems encountered with dieldrin, chlorfenvinphos and carbophenothion for the pre-clearance testing of new chemicals are discussed and the critical surveillance of the early years of commercial use of a chemical is recommended to support pre-clearance studies aimed at assessing the potential hazard to the environment.

Animals↗
PubMed1990

Flight activity of insecticide resistant and susceptible Anopheles stephensi mosquitoes in actograph chambers lined with malathion, gamma HCH or dieldrin.

The activity and resting behaviour of resistant and susceptible Anopheles stephensi Liston were recorded in acoustic actograph chambers lined with residual deposits of malathion, dieldrin or gamma HCH. In gamma HCH-treated flight chambers, SS and RS mosquitoes became active only after picking up lethal doses of insecticide, which explains why few SS and RS mosquitoes survive release into gamma HCH-treated experimental huts. Similar results were obtained in flight chambers treated with dieldrin; however, more mosquitoes would be expected to survive dieldrin under field conditions because resistance to this insecticide is greater than to gamma HCH. Mosquitoes in contact with malathion showed a three-phase activity pattern: an initial active phase, an inactive phase, and hyper-activity/convulsions. Initial activity or irritability was especially pronounced in SS and RS but absent in RR mosquitoes. Whether or not irritability would protect RS mosquitoes from malathion would probably depend on the ratio of sprayed to unsprayed surfaces in treated huts.

Animals↗
PubMed1982

Dieldrin poisoning and botulism in Australian pelicans (Pelecanus conspicillatus).

Autopsies and laboratory examinations of material from 24 Australian pelicans found sick or dead in southern coastal Queensland in 1977 to 1979 revealed dieldrin poisoning in 8 from the Brisbane region and botulism in 8 from Brisbane, Bundaberg and Gladstone. In those diagnosed as dieldrin poisoning, brain and liver samples contained 12.1 to 27.4 and 34.0 to 48.1 mg/kg dieldrin respectively. All of these birds were emaciated, 2 had convulsed and 1 had muscle tremors. Low and probably insignificant residues of DDE were detected in many birds. Type C botulism was confirmed in 4 of the 6 birds tested with specific antiserums. A large number of parasites including mites, lice, nematodes, cestodes, trematodes, coccidia and Sarcocystis sp were found but were thought to have had only a limited effect on the health of these birds.

Animal Population Groups↗
PubMed1987

Dieldrin toxicity in housed merino sheep.

An outbreak of nervous disease with deaths and reproductive failure was investigated in a fully housed flock of 640 super fine wool (Sharlea) Merino sheep. During the 4 months after the flock was dipped in dieldrin, 70 adult sheep died and no live lambs were produced by the ewes. The diagnosis of poisoning with dieldrin was based upon the presence of characteristic clinical signs, pathological findings and the detection of residues of dieldrin in tissues. Deficiency of vitamin A was confirmed in 2 sheep and may have contributed to the reproductive failure.

Animals↗
PubMed1966

Dieldrin: interaction with nerve components of cockroaches.

We have evidence that the nerve components of the dieldrin-resistant German cockroach have less binding capacity for dieldrin than those of the susceptible cockroach; the highest interstrain difference was in the crudenucleus fraction. The dieldrin-nerve complexes are not extracted by many organic solvents.

Animals↗
PubMed1968

Aldrin and dieldrin: loss under sterile conditions.

After their application to sterile nutrient agar, both aldrin and dieldrin disappeared rather rapidly from the agar in glass-covered petri dishes. In most instances this disappearance was considerably retarded from agar inoculated with either fungi or bacteria. In the presence of microorganisms, aldrin was also epoxidized into dieldrin. Half of the applied aldrin volatilized from the agar during the first day of incubation; dieldrin volatilized more slowly and at a constant rate.

Agar↗
PubMed2002

The toxicity of exposure to the organochlorine, dieldrin, at a sympathetic junction and on the skin of the frog, Caudiverbera caudiverbera.

The effects of the organochlorine, dieldrin, were tested on a noradrenergic synapse of the frog, Caudiverbera caudiverbera. Nerve stimulation induced a transient increase in short circuit current (SCC) and in the potential difference (PD), which consisted of a rapid and then a slow component. Dieldrin in the concentration range 0.01-1.0 mM caused a concentration-dependent block of both components to 32% of their control values, which was partially reversed by washout. In some experiments, this blocking effect was preceded by an initial increase in the magnitude of the electrical parameters of the nonstimulated skin and also in the synaptic response to stimulation when the lowest dieldrin concentration (0.01 mM) was applied; higher concentrations (0.1-1.0 mM) led to progressive reduction of the responses. Results are interpreted as a perturbation of the lipid bilayer structure, which affects the functionality of lipid-protein complexes, leading, on one hand, to glandular Cl- channel inactivation and epithelial Na+ channel blockade and, on the other hand, to transient glandular Cl- activation, opening of a putative Na+ channel, and subsequent blockade.

Administration, Topical↗
PubMed1999

Conversion of dieldrin to aldrin by intestinal bacteria in rats.

The present study provides the evidence that dieldrin is reductively metabolized to aldrin by intestinal bacteria in rats. When dieldrin was incubated with the cecal contents of rats, aldrin, a reduced metabolite of the epoxide, was isolated from the incubation mixture. The metabolite was identified unequivocally by UV and mass spectral comparison with an authentic sample, and on the basis of its TLC and HPLC behavior. The cecal contents of rats exhibited epoxide reductase activity toward dieldrin under anaerobic conditions. However, only marginal activity was observed under aerobic conditions. Four pure strains of intestinal bacteria exhibited epoxide reductase activities to varying degrees under anaerobic conditions. The highest activity was observed in Clostridium sporogenes. Cell-free extracts of the intestinal bacteria in rat cecal contents showed reductase activity when supplemented with both NAD(P)H and FMN under anaerobic conditions.

Aldrin↗
PubMedDate not supplied

Interaction of the organochlorine pesticide dieldrin with phospholipid bilayers.

Dieldrin is an organochlorine insecticide highly toxic for human beings. Although its exact mechanism of action is not well known, there is evidence that it acts at the cell membrane level. In fact, the lipophilicity of the pesticide as well as that of the phospholipid bilayer present in biological membranes makes the latter a most likely target for the interaction of dieldrin with living organisms. In order to evaluate its perturbing effect upon cell membranes the pesticide was made to interact with human erythrocytes and molecular models. These studies were performed by scanning electron microscopy on erythrocytes, fluorescence spectroscopy on dimyristoylphosphatidylcholine (DMPC) large unilamellar vesicles and X-ray diffraction on multilayers of dimyristoylphosphatidylcholine (DMPC) and dimyristoylphosphatidylethanolamine (DMPE). It was observed that dieldrin particularly interacted with DMPC liposomes and multilayers perturbing its molecular arrangements. However, no effect was noticed on erythrocytes, which might be due to its high cholesterol content.

Cell Membrane↗
PubMed1980

Distribution and biliary excretion of carbaryl, dieldrin and paraquat in rats: effect of diets.

Carbaryl and dieldrin were accumulated mostly in the liver, and paraquat was accumulated in the kidney of normal diet (casein 24.5%) rats at 1 hr after the oral administration. At 5 hr after the administration, the concentration of carbaryl in liver or fat, and that of paraquat in kidney were markedly decreased. However, dieldrin in liver, kidney, lung, fat or others was signficantly increased at the same period. The absorption of paraquat from gastrointestinal tract was the least among the chemicals used. Biliary excretion of carbaryl was the highest and that of paraquat was the least by 5 hr after intravenous administration. The excretion ratio was about 100: 10: 1 for carbaryl, dieldrin and paraquat in normal diet rats. Biliary excretion of these chemicals was higher in high protein diet (casein 45%) rats and retention of the chemicals in tissue was higher in low protein diet (casein 5%) rats.

Animals↗
PubMed1987

Effect of dieldrin on catalytic potential of field mouse Mus booduga brain acetylcholinesterase.

Substrate kinetics of acetylcholinesterase (AChE) were investigated in control and dieldrin-treated Mus booduga brains. Non competitive inhibition with respect to activation by acetylcholine was indicated by decreased maximal velocity (V) without change in Michaelis-Menten constant (Km). Activation energies (delta E) were found to be increased suggesting decreased efficiency of enzyme in dieldrin-treated mouse brains. Fall in the activity potential of AChE may account for the interference of dieldrin or its metabolites with the acetylcholine (ACh)--AChE system and deserve consideration in contributing to the neurotoxicity.

Acetylcholinesterase↗
PubMed1980

Significance of acute and chronic renal disease in Osborne-Mendel rats ingesting dieldrin or aldrin.

Renal lesions developed in Osborne-Mendel male and female rats ingesting dieldrin or aldrin in the diet. Chronic interstitial nephritis was seen in rats surviving for 52 wk or longer. The incidence of nephritis was highest and the lesion was most severe in male rats given the higher dose levels of dieldrin, 50 ppm or higher. Over one-half of the rats fed dieldrin or aldrin at 150 ppm, and many fed 100 ppm, died from renal necrosis and sometimes hepatic necrosis during the first year. More female rats died from renal necrosis than did male rats. Rats dying from renal necrosis did not develop tumors; those from severe chronic nephritis either did not have tumors or had preneoplastic lesions that would have become tumors if the animal had lived longer. Thus acute and chronic effects should both be examined carefully when evaluating the safety of a chemical. In addition to causing the death of the animal, acute and chronic toxic effects can prevent the development of malignant tumors by shortening the animal's life span or by causing illness and inhibiting the development of a tumor that otherwise might occur in a healthy animal.

Aldrin↗
PubMed1978

Dieldrin, Ca and P balance, and characteristics of the egg in the quail (Coturnix coturnix japonica).

A study was made of the Ca and P balance, Ca and P content in the femur, physical characteristics of the egg, mineral structure of the shell, and the number of eggs in quails treated with dieldrin (20 mg/kg of diet) for 48 days. The diet contained 3.24% Ca and 0.72% P. The Ca and P balance, the bone contents of Ca and P and the calcemia in the males were not changed by the pesticide. In the females, the pesticide decreased the amount of excreted Ca and Ca in the egg, for which reason the coefficient of nutritive utilization (CNU), the coefficient of corporal retention (CCR), and the Ca level in the femur were greater in treated laying quails. The calcemia remained stable, and the balance of P was not significantly modified by the dieldrin. The study of weight, size, and strength of the egg did not reveal any influence of the dieldrin, and egg production fluctuated throughout the test period.

Animals↗