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PubMed1970

Aldrin: removal from lake water by flocculent bacteria.

Floc-forming bacteria isolated from Lake Erie adsorb and concentrate aldrin from colloidal dispersion so that the settling of the bacterial flocs removes aldrin from the water phase. Contemporary sediments forming in Lake Erie contain aldrin and could adsorb more. The sediments consist of a conglomerate floc of bacteria, diatoms, and inorganic and detrital particles. Flocculent bacteria also adsorb microparticulates, and this adsorption capacity represents a mechanism for sediment formation and for the removal of suspended particles including aldrin from the water column.

Adsorption↗

PubMed1991

Percutaneous absorption and metabolism of aldrin by rat skin in diffusion cells.

Using a static diffusion cell with varying receptor fluids the viability of isolated rat skin mounted as whole skin or as split thickness skin has been studied. Skin viability decreased with time with phosphate buffer or Eagles MEM and was not supported with ethanol/water as the receptor fluid. The pesticide aldrin was absorbed through the skin into ethanol/water but not the aqueous receptor fluids. With viable skin preparations aldrin was metabolised to dieldrin and absorbed aldrin and the metabolite remained in the skin. Viable skin preparations must be used to assess in vitro, the degree of metabolism of xenobiotics which occurs during percutaneous absorption.

Aldrin↗

PubMed1991

Levels of aldrin and dieldrin in environmental samples from Delhi, India.

Aldrin and dieldrin residues in soil, earthworms, water, fish and clams from different sites in Delhi were monitored. Concentrations of aldrin and dieldrin were found to be higher in earthworms than in soil. Concentrations of dieldrin were higher in fish than the ambient water, but the concentration of aldrin in the ambient water was the same as that in fish and clams.

Aldrin↗

PubMed1975

The comparative cytogenetic effects of aldrin and phosphamidon.

An organochlorinated pesticide (aldrin) and an organophosphorus one (phosphamidon) were administered in human lymphocyte cultures, and the cytogenetic effects were related to the compound concentration. The comparative estimation of the number and type of chromosome aberrations observed in the treatments with various doses of drugs permits the following statements. (a) The aldrin showed a narrow range of clastogenic doses, between 19.125 and 38.25 mug/ml. Since these doses are near the limit for cell survival, the observed chromosome lesions are probably not perpetuated in other abnormal cells. (b) Comparatively, the range of phosphamidon clastogenic doses is very large, scattered between 1.9 and 122 mug/ml. Since, in the phosphamidon treatments, the cellular death begins at a concentration above 244 mug/ml, the chromosome aberrations, induced especially by the low doses, could be maintained in other abnormal cells. In a smaller number of experiments, chromosome examinations were performed after intraperitoneal injections of the drugs into rats and mice, 24 h before harvesting of the bone marrow. The administered doses were low, as compared with those of the experiments in vitro: the minimal doses inducing chromosome aberrations in vivo were, in the aldrin treatments 9.56, and in the phosphamidon treatments, 0.07 mug/g body weight. In the experiments both in vitro and in vivo, the analysis of the frequencies of the abnormal cells and of the chromosome lesion types support the existence of a dose-response correlation. The genetic peril due to low doses of pesticides with a general weak toxic effect is discussed.

Aldrin↗

PubMed1976

Enhancement of microsomal monooxygenase, epoxide hydrase and UDPglucuronyltransferase by aldrin, dieldrin and isosafrole administrations in rat liver.

The effects of intraperitoneal administration of aldrin (10 mg/kg), dieldrin (10 mg/kg) and isosafrole (50 mg/kg) were investigated on the activities of drug biotransformation enzymes in rat liver. All the compounds studied were found to enhance the activities of microsomal monooxygenase (e.g. p-nitroanisole O-demethylase, aryl hydrocarbon hydroxylase), epoxide hydrase (styrene oxide as substrate) and UDPglucuronyltransferase (p-nitrophenol as aglycone). Dieldrin, the epoxidized derivative aldrin, the eposidized derivative of aldrin, was a more potent inducer than the parent compound itself. NADPH CYTOCHROME C REDUCTASE ACTIVITY WAS EHANCED 2.5-FOLD, P-NITROANISOLE O-demethylase 7-fold, benzpyrene hydroxylase 2-fold, and epoxide hydrase 5-fold after treating rats with dieldrin for 6 days. The increase in activity of the microsomal UDPglucuronyltransferase could be only detected after an in vitro digitonin treatment of microsomal membranes, the enhancement being about 1.5-fold after administering dieldrin for 6 days. The administration of isosafrole to rats increased especially p-nitroanisole O-demethylase activity in liver microsomes (10-fold in 3 days). NADPH cytochrome c reducatase activkty was increased 2-fold, cytochrome P-450 content 1.2-fold, benzpyrene hydrozylase activity 2.5-fold and epoxide hydrase activity 1.2-fold after treatment of rats for 3 days. UDPglucuronyltransferase activity increased 2.2-fold by treating rats for 6 days with isosafrole. This increase was, however, only to be seen in in vitro digitonin-activated microsomes due to the latency of UDPglucuronyltransferase.

Aldrin↗

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↗

PubMed1991

Interactive effects of aldrin, cyclohexylamine, 2,4-diaminotoluene and two phorbol esters on metabolic cooperation between V79 cells.

The in vitro V79/metabolic cooperation assay measures the extent of gap-junctional transfer of metabolites from wild-type to mutant V79 cells. The assay is currently being explored as a short-term test to screen for tumor promoting chemicals, many of which inhibit metabolic cooperation. In this study, the assay was used to determine whether chemical interactions affect detection of tumor promoters in mixtures and to investigate types of interactions that may occur between chemicals. Several two-chemical mixtures were examined. The effects of phorbol-12-myristate-13-acetate (PMA) and phorbol-12,13-dibutyrate, two inhibitors of metabolic cooperation that operate through the same receptor-mediated pathway, were additive at concentrations below the maximally effective concentrations of either. A summation effect was observed in mixtures of two other inhibitors of metabolic cooperation, the pesticide aldrin and the principal metabolite of sodium cyclamate, cyclohexylamine. Synergistic effects were noted when PMA was combined with either aldrin or cyclohexylamine, demonstrating that chemicals in a mixture may yield a much stronger response than expected based on individual chemical exposures. Interactions were also examined between PMA, aldrin, cyclohexylamine and 2,4-diaminotoluene, a chemical that appears to enhance metabolic cooperation. 2,4-Diaminotoluene reversed effects of all inhibiting chemicals to some extent, although the pattern of response was different for each combination. In the most dramatic case, the powerful tumor promoter PMA was completely masked by 2,4-diaminotoluene. These results suggest that the V79/metabolic cooperation assay must be applied with caution in mixture testing because detection of tumor promoting chemicals can depend on other chemicals present.

Aldrin↗

PubMed1997

Mortality of workers exposed to dieldrin and aldrin: a retrospective cohort study.

OBJECTIVE: To investigate the occurrence of long term health effects in humans exposed to aldrin and dieldrin, with an update of an earlier retrospective cohort mortality study. METHODS: A group of 570 workers employed between 1 January 1954 and 1 January 1970 either in a production or formulation plant were followed up for mortality until 1 January 1993. There were extensive industrial hygiene data available and biological monitoring data of aldrin and dieldrin for most of the workers. From these data individual estimates were made of the total intake of dieldrin. A total number of 2539.37 person-years at risk was added to the original study. RESULTS: 118 deaths were observed compared with 156 expected. No increase in mortality from liver cancer was found. However, there was an excess in mortality from rectal cancer. This excess was inversely related to the dose gradient. An analysis by job title did not show any excess cancer in any particular job. CONCLUSION: The study does not support a carcinogenic effect of dieldrin and aldrin in humans.

Adult↗

PubMed2002

Cancer mortality in workers exposed to dieldrin and aldrin: an update.

This study was conducted to investigate the possible long-term health effects, in particular carcinogenic effects, of occupational exposure to the organochlorine insecticides dieldrin and aldrin. We updated an earlier cohort mortality study of 570 employees involved in the production of these insecticides. All of the employees had worked in the production plants between 1 January 1954 and 1 January 1970 and were followed for cause-specific mortality until 1 January 2001. Based on dieldrin levels in blood samples taken during the exposure period, available for 343 workers, individual estimates of the total intake of dieldrin were estimated for all individual subjects in the cohort. The estimated total intake ranged from 11 to 7755 mg of dieldrin, with an average of 737 mg. One hundred and seventy-one workers had died before 1 January 2001, compared with an expected number of 226.6, giving a standardized mortality ratio (SMR) of 75.6 [95% confidence interval (CI): 64.6-87.7]. This deficit in total mortality was mainly attributable to a deficit in cardiovascular disease mortality, but cancer mortality was also lower than expected. The observed number of deaths from rectal cancer was significantly higher than expected (SMR = 300.0; 95% CI: 109.5-649.3), but was most pronounced in the low-intake subgroup and appears to be unrelated to exposure to dieldrin and aldrin. This study reinforces the earlier findings that occupational exposure of workers to significant amounts of dieldrin and aldrin has not led to a higher cancer mortality than would be found in an unexposed population.

Aldrin↗

PubMed1975

The effects of 1, 2, 3, 4, 10, 10-hexachloro-1, 4, 4a, 5, 8, 8a-hexahydroxy endo, exo-5, 8-dimethionaphthalene (aldrin) and sodium ethylenebisdithiocarbomate (nabam) on the chick.

Fertile White Leghorn chicken eggs were injected on the tenth day of incubation with either 0, 10, 20, 30, 40 or 50 p.p.m. Aldrin or 0, 5, 10 or 15 p.p.m. Nabam and allowed to hatch. Aldrin neither did induce any deformities nor had any effect on hatchability, thyroid weight and histology. However, within three days after hatching, there was greater mortality in chicks treated with higher concentrations of the pesticide. Aldrin at higher concentrations significantly reduced 125I uptake by the thyroids. This was evident in the iodine fractions after chromatographic separation of the thyroid extracts. Nabam not only reduced hatchability but also induced deformities in the higher concentration groups. The thyroids showed an increase of resorption vacuoles in the colloid. Even though the thyroid weights increased in all experimental groups, a significant increase in 125I uptake was seen only in the 15 p.p.m. injected animals. This group also showed a reduction in radioactivity of thyroxine fraction but an increase of 125I in tyrosines. The significance of these results are discussed.

Abnormalities, Drug-Induced↗

PubMed1991

Human aldrin poisoning.

Sixteen patients acutely poisoned with aldrin were examined to evaluate a possible correlation between serum aldrin and dieldrin levels and clinical complaints. The patients were classified as having mild (N = 8), moderate (N = 5) or severe (N = 3) poisoning according to clinical symptoms. Concentrations of less than 20 micrograms/l were usually associated with mild poisoning, which involved complaints such as nausea, vomiting and epigastric pain, whereas concentrations of 100 to 200 micrograms/l were considered to represent moderate intoxication and were associated with nausea, vomiting, epigastric pain, headache, dizziness, and convulsions. Severe or fatal cases were associated with levels above 700 micrograms/l. Taken together, these results suggest that serum aldrin and dieldrin levels can be used as indicators of clinical prognosis after acute poisoning with these insecticides and that convulsions could suddenly occur even in the absence of prodromal signs or symptoms.

Acute Disease↗

PubMed1989

Effect of a specific stress (aldrin) on rat progeny behavior.

The effect of dam exposure to aldrin, an organochlorinated compound (1.0 mg/kg, sc, daily), during pregnancy or lactation was studied in young rat pups (11, 15, 18 and 22 days of age) and in adult animals (90 days of age). Locomotor activity was significantly greater in both young and adult animals when compared to controls. Male rats that received aldrin during lactation also showed reduced plasma corticosterone levels. Maternal behavior was not affected by treatment during either period. The results suggest that aldrin may act as a perinatal stress factor.

Aldrin↗

PubMedDate not supplied

Monooxygenase-catalyzed aldrin epoxidation and dihydroisodrin hydroxylation in monkey liver needle-biopsy specimens. Assay and properties.

Aldrin epoxidation and dihydroisodrin (1,8,9,10,11,11-hexachloro-2,3-7,6-endo-2,1-7,8-endo-tetracyclo [6.2.1.1(3), (6).0(2), (7)]dodec-9-ene (DHI) hydroxylation have been studied in 0.2-ml liver monooxygenase preparations. Liver biopsy specimens of rhesus (Macaca mulatta) and bonnet (M. radiata) monkeys obtained with a 1.9-mm Menghini needle were the primary enzyme sources. Dieldrin and monohydroxydihydroisodrin (DHI-OH) were the only metabolites detected by electron-capture GLC analysis of hexane extracts of incubation media. Incubation, extraction, and analysis could be done in the same vessel. Maximum rates were obtained in the presence of NADPH and O2, and both transformations were inhibited by CO. The apparent KM and Vmax (+/-SD) for epoxidation was 1.2 +/- 0.2 X 10(-5) M aldrin and 210 +/- 20 pmol of dieldrin per mg of protein per min, and the corresponding values for hydroxylation were 2.3 +/- 0.4 X 10(-5) M DHI and 150 +/- 20 pmol of DHI-OH per mg of protein per min. Aldrin epoxidation and DHI hydroxylation activities of rhesus monkey liver biopsy and rat liver preparations were evaluated after phenobarbital treatment. The assay procedures can be used in protocols in which animals serve as their own controls.

Aldrin↗

PubMedDate not supplied

Aldrin epoxidation, a highly sensitive indicator specific for cytochrome P-450-dependent mono-oxygenase activities.

Aldrin epoxidation was studied in rat liver microsomes. The assay is very sensitive; amounts of less than 1 microgram of microsomal protein were sufficient for activity determination. The very low background, stability of the metabolite, and the complete separation of substrate and metabolite permit estimation of mono-oxygenase activities of less than 1 pmol per mg of protein per min by a simple procedure. Pretreatment of animals with the mono-oxygenase inducer phenobarbital (PB) increased the epoxidation rate 3-fold, whereas 3-methylcholanthrene (MC) treatment markedly depressed enzyme activity. Induction with MC did not change the apparent Km of the reaction, which was 18 muM. The Km in microsomes from PB-treated animals was 28 muM. These data suggest that the same or (a) similar form(s) of mono-oxygenase catalyze(s) the epoxidation in the three different microsomal preparations. SKF 525-A, metyrapone, and 7,8-benzoflavone were almost similarly active as inhibitors in microsomes from control and inducer-treated rats. Sensitivity to these inhibitors was low; 0.7 mM SKF 525-A and 0.4 mM 7,8-benzoflavone were necessary to reduce enzyme activity by 50%, whereas 0.5 mM metyrapone caused an inhibition of 10-45%. The activity of aldrin epoxidation in untreated rats increased almost parallel to the activity of ethylmorphine demethylation between 3 and 10 weeks of age. The rate of benzo[a]pyrene hydroxylation remained unchanged during this period. The results demonstrate that aldrin epoxidation offers a selective and sensitive assay for the activity of mono-oxygenases dependent on cytochrome P-450 forms.

Aging↗

PubMed1982

Bone growth during chronic aldrin intoxication in goats.

Microscopic examination of the costochondral junction of goats after chronic aldrin intoxication revealed a drastic reduction in the width of proliferating, maturing and degenerating cartilage cells. The zone of provisional calcification was almost negligible in aldrin treated animals. In contrast, the control animals showed an orderly sequence of endochondral bone formation. Appositional bone growth studied by the tetracycline labelling technique also showed a marked reduction following chronic aldrin intake. It was concluded that decrease in the rate of appositional bone growth at endosteal periosteal and osteonic surfaces might be due to poor synthesis of bone matrix by the osteoblasts.

Aldrin↗

PubMed1989

Organic solvents as modifiers of aldrin epoxidase in reconstituted monooxygenase systems and in microsomes.

To examine the response of individual cytochrome P-450 species catalysing the epoxidation of aldrin (Wolff T and Guengerich FP, Biochem Pharmacol 36: 2581-2588, 1987), monooxygenase systems reconstituted from these species were assayed in the presence of 5% (v/v) = 0.87 M ethanol. The activity of cytochromes P-450PB-B and P-450PB-D, two enzymes inducible by phenobarbital was increased seven-fold. The activity of two other P-450 enzymes purified from these animals was either inhibited by 50%, as observed for cytochrome P-450PB-C or remained unchanged, as noted with cytochrome P-450PCN-E. Two P-450 enzymes purified from untreated rats, cytochromes P-450UT-F and P-450UT-H, showed an inhibition by 50 and 20%, respectively, while the activity of cytochrome P-450UT-A was slightly increased by 50%. Indirect evidence that solvents enhance aldrin epoxidation by interacting with the hemoprotein was obtained by the finding that ethanol stimulated the activity of cytochrome P-450PB-B already, before addition of the lipid component, L-alpha-1,2-dilauroyl-sn-glycero-3-phosphocholine. The Km of cytochrome P-450PB-B for NADPH cytochrome P-450 reductase was not altered by ethanol indicating that the interaction between the two enzymes was not affected by the solvent. Other results indicate that the stimulatory solvent binds to a site, apart from the type I or type II binding site. The potency of various hydrophylic solvents to modify aldrin epoxidase activity was assayed in microsomes of rats pretreated with phenobarbital and of untreated male rats. Ethanol, n-propranol, n-butanol, acetone and tetrahydrofuran enhanced enzyme activity of phenobarbital pretreated rats to a maximal extent of two-fold and, at similar concentrations, inhibited the enzyme activity of untreated rats by 50%. The potency of these solvents correlated with their lipophilicity. Methanol and dimethylsulfoxide only slightly modified the activity of induced and noninduced animals. In the presence of 0.5 M n-propranol as the modifying agent, microsomal epoxidase activity of rats pretreated with pregnenolone-16 alpha-carbonitrile, dexamethasone, 3-methylcholanthrene and of control rats was inhibited by 60-80%, whereas the activity of animals pretreated with phenobarbital, DDT, or the polychlorinated biphenyl mixture, Clophen A 50, was stimulated between two- and three-fold. The results reveal that organic solvents frequently used to dissolve monooxygenase substrates may considerably modify the activity of cytochrome P-450 dependent reactions, in particular when purified enzymes are assayed.

1-Propanol↗

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↗

PubMed1985

Mortality study of industrial workers exposed to aldrin, dieldrin and endrin.

Vital status and cause of death were assessed for 232 of a group of 233 workers engaged in the manufacturing and formulation of aldrin, dieldrin, endrin and (for a limited period) Telodrin. This group is part of the total exposed population of more than 1000 workers and was selected for follow up on account of the high exposures in the initial years of manufacturing and formulation and of the long exposure (mean 11 years) and observation (mean 24 years) periods. Total observed mortality was 25 versus 38 expected on the basis of the death statistics of the male Dutch population. Of the 9 cancer deaths, 3 were caused by lung cancer, while the remaining 6 were each of a different nature. Although in this group exposures have been high and exposure, as well as observation periods, were long enough for meaningful evaluation, this study revealed no indication of a specific carcinogenic activity of aldrin, dieldrin or endrin in manufacturing plant workers exposed to these products.

Aged↗