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At least 19 recordsLinked to original sources

PubMed1979

Excretion of chlordecone by the gastrointestinal tract: evidence for a nonbiliary mechanism.

Workers exposed to chlordecone (Kepone), a toxic organochlorine pesticide, excreted larger amounts of chlordecone in bile than in stool, suggesting that it may undergo enterohepatic recirculation. We found in a single subject that equal amounts of chlordecone and of its reduced metabolite, chlordecone alcohol, were excreted in bile at a rate four times as great as in stool. When biliary contents were diverted from the intestine through a T tube, fecal excretion of chlordecone alcohol was abolished, presumably due to interruption of its passage via bile to intestine. This change was not accompanied by disappearance of chlordecone from the stool. The amount of chlordecone in stool when bile was diverted was increased six- to tenfold over that when diverted bile was continuously infused into the duodenum. Analogous experiments with [14C]-chlordecone-treated rats in which bile flow was exteriorized through a plastic cannula showed that the excretion of radioactivity in feces was in the same range when bile was reinfused in the duodenum or was totally diverted. Moreover, in rats with bile diverted, cholestyramine, an anion-exchange resin which binds chlordecone in vitro, doubled the excretion of radioactivity in stool. A similar effect was observed in intact animals. We conclude that chlordecone enters the intestinal lumen from a nonbiliary source, probably the gut, and that net excretion of chlordecone from this source can be augmented by cholestyramine.

Bile↗

PubMed1978

Treatment of chlordecone (Kepone) toxicity with cholestyramine. Results of a controlled clinical trial.

Industrial workers exposed to the organochlorine pesticide, chlordecone (Kepone), had signs of toxicity in several organs. The extent of toxicity was proportional to the levels of this chemical in the tissues. In 22 patients, chlordecone was eliminated slowly from blood (half time of 165 +/- 27 days--mean +/- S.E.M.) and fat (half time of 125 days, with a range of 97 to 177), chiefly in the stool. Output of chlordecone in bile was 10 to 20 times greater than in stool, suggesting that chlordecone is reabsorbed in the "ntestine. Cholestyramine, an anion-exchange resin that binds chlordecone, increased its fecal excretion by seven times. In a five-month trial, cholestyramine significantly accelerated elimination of chlordecone from blood, with a half life of 80 +/- 4 days (S.E.M.) (P less than 0.005) and fat (half life of 64 days, with a range of 52 to 85) (P less than 0.05). Cholestyramine offers a practical means for detoxification of persons exposed to chlordecone and possibly to other lipophilic toxins.

Adolescent↗

PubMed1978

Chlordecone intoxication in man. I. Clinical observations.

Industrial overexposure to chlordecone, an organochlorine insecticide, caused tremor in 76 of 148 exposed workers. Chlordecone was absorbed through oral, respiratory, and dermal routes, the last possibly the most significant. Epidemiology of this incident disclosed low-level, widespread environmental exposure of man to chlordecone. In 23 workers with chronic chlordecone intoxication, tremor was associated with opsoclonus, pleuritic pain and arthralgia. No seizures were reported. The site of action of chlordecone on the central nervous system is unknown. It concentrates in human adipose and hepatic tissue but is not biodegradable, either in humans or elsewhere in nature.

Chemical Phenomena↗

PubMed1979

Estrogenic activity of the insecticide chlordecone (Kepone) and interaction with uterine estrogen receptors.

The chlorinated insecticide chlordecone (Kepone) interacts with the estrogen receptor system in the rat uterus in vitro and in vivo. It competes with estradiol for binding to the cytoplasmic receptor in vitro and also induces nuclear accumulation of estrogen receptor sites in uteri in vitro. When injected into immature rats, chlordecone translocates estrogen receptor sites to the uterine nucleus, increases uterine weight, and stimulates the synthesis of the progesterone receptor, an estrogen receptor-mediated process. Its slow onset of action but prolonged duration of interaction with estrogen receptor and stimulation of uterine weight gain and progesterone receptor synthesis indicates that, although it has an affinity for receptor only 0.01-0.04% that of estradiol, its considerable estrogenic activity may likely be derived from its long half-life and bioaccumulative character.

Animals↗

PubMed1978

Cholestyramine: use as a new therapeutic approach for chlordecone (kepone) poisoning.

In rats, as reported in humans, chlordecone (Kepone) is excreted predominantly in the feces. Cholestyramine, an anion exchange resin, binds chlordecone in rat intestine, increases its excretion into the feces, and decreases its content in the tissues. The resin appears to offer a practical method for treating chronic poisoning with this and possibly with other lipophilic toxins.

Animals↗

PubMed1978

Chlordecone intoxication in man. II. Ultrastructure of peripheral nerves and skeletal muscle.

Tremors, mental changes, opsoclonus, muscle weakness, gait ataxia, incoordination, and slurred speech developed in several employees in a Virginia chemical plant during the summer of 1974. Epidemiologic and clinical studies suggested that the chlorinated insecticide chlordecone (Kepone) was responsible. Severity of symptoms seemed directly related to dose and duration of exposure. Five sural nerve and six muscle biopsy specimens were examined by light microscopy and electronmicroscopy. The sural nerves were also evaluated by computerized morphometry, which showed considerable decrease in the number of unmyelinated fibers and lesser abnormalities of myelinated fibers. Compared with the nerves of the control subjects, those of patients may have had an increase in Reich and Elzholz bodies, and a modest increase in endoneurial collagen. There were occasional "collagen pockets," stacks of Schwann cell cytoplasmic membranes, redundant Schwann cell cytoplasmic folds, and fewer unmyelinated axons. The skeletal muscles contained increased amounts of lipofuscin and lipidlike droplets in subsarcolemmal areas and within intermyofibrillary spaces; the significance of this is unknown. Fiber size variability, type I predominance, and type grouping were present in three cases. All results strongly suggest that chlordecone is a neurotoxic agent predominantly affecting Schwann cells and unmyelinated fibers of peripheral nerves.

Adult↗

PubMedDate not supplied

Distribution and excretion of chlordecone (Kepone) in the rat.

Rats received a single, oral, 40-mg/kg dose of 14C-labeled chlordecone in a corn-oil solution. Initially the highest levels of radioactivity were found in the adrenal gland, liver, lung, and fat. While levels declined steadily in all tissues during the course of the study (182 days), the ratio of liver content to that of other tissues increased considerably. The blood half-life was 8.5 days for the first 4 weeks, 24 days for the next 8 weeks, and 45 days for the final 14 weeks, The amount excreted in the feces was 12.7% for the first 24 hr, 2.9% for the second, and 3.3% during the third 24-hr period. By 84 days 65.5% of the dose had been excreted by this route. Total urinary excretion of radioactivity for 84 days was 1.6%. These results indicate that chlordecone is well absorbed and distributed throughout the body, has a long half-life, and disappears more slowly from the liver than from other tissues. The majority of a dose is eliminated slowly in the feces with very little appearing in the urine. The findings are consistent with the expected pharmacokinetics of a chlorinated hydrocarbon, although there was less of a tendency to localize in fat than anticipated.

Animals↗

PubMed1978